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The effects of resistance exercise on lipid peroxidation, bone metabolism, and physical performance in adults aged 60-85 years.

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The effects of resistance exercise on lipid peroxidation, bone metabolism, and physical performance in adults aged 60-85 years.
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Bone density ( jstor )
Bones ( jstor )
Endurance ( jstor )
Exercise ( jstor )
Free radicals ( jstor )
Legs ( jstor )
Older adults ( jstor )
Strength training ( jstor )
Stress tests ( jstor )
Treadmills ( jstor )
Dissertations, Academic -- Exercise and Sport Sciences -- UF ( lcsh )
Exercise and Sport Sciences thesis, Ph.D ( lcsh )
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Thesis (Ph.D.)--University of Florida, 1999.
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Includes bibliographical references (leaves 180-192).
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Typescript.
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Vita.
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by Kevin Robert Vincent.

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THE EFFECTS OF RESISTANCE EXERCISE ON LIPID PEROXIDATION, BONE
METABOLISM, AND PHYSICAL PERFORMANCE IN ADULTS AGED 60-85
YEARS.











By

KEVIN ROBERT VINCENT


A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE
UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE
REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY

UNIVERSITY OF FLORIDA

1999














Copyright 1999

By

Kevin Robert Vincent














This dissertation to dedicated to:

My wife Heather. Her love and support has guided me through this process. For that, I
can never thank her enough.

Michael L. Pollock, Ph.D. I hope that he is as proud of this work as I am of being his
student.

My parents, James and Mary Ellen Vincent. Their love and support has provided me the
foundation for who I have become. I am very proud to be their son.














ACKNOWLEDGMENTS


An endeavor such as this one cannot be accomplished by one person alone.

Throughout my doctoral career at the University of Florida I have been fortunate to meet

and work with many outstanding people. I hope that I have touched their lives as they

have touched mine.

I would like to acknowledge Dr. Michael L. Pollock, my first advisor at the

University of Florida. He was the reason I chose to attend this university. I will always

cherish the opportunity I had to work with and to get to know him. Thank you for

everything "Big Mike"!

I would also like to express my gratitude to Dr. Randy W. Braith. His support,

guidance, and friendship over the past year have been greatly appreciated. Whenever I

had a question or just needed to talk, he was always available. I could not have

accomplished this project without him.

I would like thank my doctoral committee members: Dr. David Lowenthal, Dr. Jeff

Bauer, and Dr. Charles Wood for all of their assistance throughout my doctoral career.

Their advice and friendship helped to guide my studies as well as my life.

The friends that I have made at Florida have made this entire experience

worthwhile. I would like to express my sincerest thanks and appreciation to Shannon

Lennon, Rachel Cutler, Ross Feldman, Pete Magyari, and Chris Hass. You were all there








for me when I needed a shoulder to lean on or some help with data collection. I will

always cherish our friendship.

I would like to thank Michelle Brown for her seemingly endless patience during

this project. She was always there to listen to my frustrations and she allowed me the

time necessary to work on this study. I can never thank her enough for her support.

Finally, I would like to thank my wife, Heather Vincent. I cannot express how

much I appreciate the help and support that she has given me, not only during graduate

school, but with life. I would not be where I am without her.












TABLE OF CONTENTS


ACKNOWLEDGMENTS. .

ABSTRACT .....

CHAPTERS

1 INTRODUCTION ..


Justification for Research .
Purpose and Specific Aims.
Research Hypotheses ..
Significance of Research .


2 REVIEW OF RELATED LITERATURE .. ....
Age-Related Alterations in Muscle Mass, Structure, and Strength
Decreased Muscle Mass .. .....
Motorneuron Decline with Aging ...
Neuromuscular Performance Changes with Aging
Muscle Mass and Strength Increases with Resistance .
Exercise in Older Adults
Postural Control and Aging .. .....
Resistance Exercise and Balance and Physical Function .
Bone Formation and Resorption .. ....
Resistance Exercise and Bone Mineral Density .. ..
Oxidative Stress and Free Radical Production ..
Free Radicals and Aging .. ........
Exercise and Oxidative Stress ...
Exercise Prescription for Older Adults ...

3 METHODS .. .......


Subjects .
Subject Eligibility .
Inclusion Criteria .
Exclusion Criteria .
Study Design .
Experimental Protocol .. ..


. iv


I









Visit 1: Screening/Orientation .
Visit 2: Treadmill Graded Exercise Test .
and Blood Sample Collection
Visit 3: Muscular Strength Assessment .
Visit 4: Muscular Endurance .
Visit 5: Bone Mineral Density .
Visit 6: Balance, Stair Climbing, and Isometric .
Lumbar Extension Strength
Visit 7: Body Composition and Muscular Strength Assessment .
Training Period: Six Months of Dynamic Resistance Exercise
Biochemical Assays .
Markers of Bone Metabolism .... .
Alkaline Phosphatase-B .
Osteocalcin .
Pyridinoline Crosslinks .
Biochemical Indicators of Oxidative Stress .
Lipid Peroxidation Measurements .
Oxidative Challenges in vitro ... .
Xanthine-Xanthine Oxidase System .
(Superoxide Generator)
Hydrogen Peroxide System .
Ferric Chloride System (Hydroxyl Generator) .
Statistical Analyses .

4 RESULTS ........


Subject Characteristics ..
Aerobic Endurance ..
Oxygen Consumption ..
Treadmill Time to Exhaustion.
Time to Ascend One Flight of Stairs .
Changes in Muscular Strength
Chest Press ..
Leg Press .. ...
Leg Curl .
Biceps Curl ..
Seated Row .. ...
Overhead Press ..
Triceps Dip ..
Leg Extension ..
Total Strength .. ..
Muscular Endurance .. ..
Chest Press ..
Leg Press .. ...
Lumbar Extension Strength .


S36
. 37

S 39
S40
S40
S 41

42
44
S 45
S 45
S45
S46
S46
S47
S47
S47
. 48

S 48
S 48
S 48









0 of Lumbar Flexion 59
12 of Lumbar Flexion 59
24 of Lumbar Flexion .. 59
36 of Lumbar Flexion 60
48 of Lumbar Flexion ..... 60
60 of Lumbar Flexion ... 60
72 of Lumbar Flexion .. 60
Total Lumbar Extension Strength. 62
Bone Mineral Density .. 62
Total Body Bone Mineral Density 62
Femoral Neck Bone Mineral Density. 62
Anterior/Posterior Lumbar Spine Bone Mineral Density 62
Lateral Lumbar Spine Bone Mineral Density 63
Ward's Triangle Bone Mineral Density.. .. .. 63
Correlations Between Physiological Performance Variables 63
and Muscular Strength
vo2 ... .. 64
Treadmill Time to Exhaustion. 64
Stair Climbing Time .68
Correlations Between Physiological Performance Variables and 68
Bone Mineral Density
Total Body 68
Femoral Neck. 69
Ward's Triangle....... .69
Anterior/Posterior Lumbar Spine 69
Lateral Lumbar Spine. 70
Biochemical Analyses. 71
TBARS 71
Lipid Hydroperoxides..... 71
Serum Osteocalcin 72
Serum Bone-Specific Alkaline Phosphatase .72
Serum Pyridinoline Crosslinks. 72

5 DISCUSSION 146

Overview and Principal Findings .146
Muscular Strength, Muscular Endurance, and Stair Climbing 147
Muscular Strength. 147
Muscular Endurance 149
Stair Climbing Ability 150
Physiological Significance of Strength Data .. .. 150
Aerobic Endurance 151
VO1 a .. 151
Treadmill Time to Exhaustion. 154
Bone Mineral Density and Bone Metabolism 155









Bone Mineral Density .
Biochemical Markers of Bone Metabolism .
Physiological Significance .
Lipid Peroxidation and Resistance to Oxidative Stress
Physical Challenge in vivo ....
Oxidative Challenge in Vitro ..
Physiological Consequence and Significance .
Major Conclusions .
Physiological Significance ...
Limitations to the Experiment and Future Directions.


APPENDICES


A A-PRIORI SAMPLE SIZE ESTIMATION AND POWER ANALYSIS
B INFORMED CONSENT TO PARTICIPATE IN RESEARCH .
C INSTITUTIONAL REVIEW BOARD APPROVAL FORM TO.
PERFORM RESEARCH

REFERENCES ........

BIOGRAPHICAL SKETCH .......


155
. 157
158
. 159
160
162
. 163
163
164
. 165













Abstract of Dissertation Presented to the Graduate School of the University of Florida in
Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy

THE EFFECTS OF RESISTANCE EXERCISE ON LIPID PEROXIDATION, BONE
METABOLISM, AND PHYSICAL PERFORMANCE IN ADULTS AGED 60-85
YEARS.



By

Kevin Robert Vincent

August 1999


Chairman: Randy W. Braith
Major Department: Exercise and Sport Sciences

The purpose of this investigation was to examine the effects of circuit resistance

exercise training (CWT) at two different intensity levels on physical function, bone

metabolism, and lipid peroxidation in elderly persons. Sixty-two men and women (age

68.16.3 yr.) completed the study. Participants were randomized into three groups: high-

intensity (HEX, 80% of 1RM for 8 repetitions, n=22), low-intensity (LEX, 50% of IRM

for 13 repetitions, n=24) and control (CON, n=16). HEX and LEX groups trained 3x/wk

for 6 months using 11 machines. All groups were tested pre- and post-training for aerobic

capacity (V024,), treadmill time to exhaustion, IRM on the chest press, leg press, leg

curl, leg extension, seated row, overhead press, biceps curl, and triceps dip, chest press

and leg press endurance, time to walk up one flight of stairs, regional bone mineral density

(BMD), serum markers of bone metabolism, and serum lipid peroxidation (LIPOX). Both








training groups significantly increased IRM strength for all 8 exercises (p<0.05). Total

strength increased 17.2 and 17.8% for the LEX and HEX groups, respectively (p<0.05).

VO2.k increased 23.5 and 20.1% for the LEX and HEX groups, respectively (p<0.05).

Treadmill time increased 26.4 (p<0.05) and 23.3% for the LEX and HEX groups,

respectively. Time to ascend one flight of stairs decreased by 7.3 (p<0.05) and 5.79% for

the LEX and HEX groups, respectively. Chest press endurance increased by 75.5 and

68.0%, and leg press endurance increased by 79.2 and 105% for the LEX and HEX

groups, respectively (p<0.05). Femoral neck (BMD) increased significantly for the HEX

group (p<0.05). Osteocalcin increased significantly for the LEX and HEX groups, and

alkaline phosphatase increased for the HEX group (p<0.05). Both the LEX and HEX

groups demonstrated significantly lower levels ofLIPOX immediately after the graded

exercise test when compared to CON (p<0.05). The results of this study indicate that one

set of either low- (50% 1RM) or high- (80% 1RM) intensity resistance exercise is

sufficient to increase strength VO2peak, regional BMD, bone turnover, and decrease

exercise-induced LIPOX in older adults.














CHAPTER 1
INTRODUCTION


Aging is associated with decreases in strength, muscle cross-sectional area, bone

mineral density, and physical function (Fiatarone et al., 1994, and Tseng et al., 1995).

Aging is also associated with an increase in oxidative stress. It has been proposed that

aging is a consequence of the interactions of oxygen free radicals with cell components

throughout life (Ji, 1994). Free radicals have been implicated as contributors to cell

membrane disruption, atherosclerosis, and sarcopenia (Weindruch, 1995).

During the aging process, indices of free radical formation increase (Ji et al.,

1990). This increase results in an increase in antioxidant enzyme levels to act as defense

against oxidative stress (Ji, 1993). An increased rate of free radical generation is a signal

for an increase in antioxidant enzyme activity (Jenkins, 1988). Numerous investigations

have shown that acute and chronic exercise can result in an increase in antioxidant enzyme

activity (Ji, 1993, Ji et al., 1991, and Tullson et al., 1994). Aerobic endurance exercise,

particularly intense endurance exercise, produces free radicals that upregulate antioxidant

enzyme activities (Tullson et al., 1994). It was recently demonstrated that intermittent

sprint cycling performed three times per week for 6 weeks followed by a seventh week

with five sessions increased antioxidant enzyme activity (Hellsten et al., 1996).

Resistance exercise induces a metabolic stress similar to that seen during sprint

exercise. Therefore, resistance exercise may elicit similar increases in antioxidant enzyme








activity observed during sprint exercise. It has also been shown that transient ischemia

followed by reperfusion can also increase antioxidant enzyme activity (Das et al., 1993).

Muscular contractions greater than 40% of the maximal voluntary contraction (MVC), as

seen during resistance exercise, result in transient blood flow occlusion in the exercising

muscle (Donald et al., 1967). Thus, resistance training may subject skeletal muscle to a

form of ischemia/reperfusion that could possibly result in an increase in antioxidant

enzyme activity leading to improved defense against oxidative stress. Since free radical

formation has been implicated as a possible cause for many debilitating conditions

associated with aging, it is important to ascertain which interventions are effective in

decreasing oxidative stress.

Aging has been associated with a decrease in muscle mass and strength (Larsson et

al., 1979). This decrease in strength is linked to decreased mobility, physical function, and

increased risk of falling in older people (Bendall et al., 1989 and Fiatarone et al., 1990).

Resistance exercise has been shown to be effective for increasing muscle mass, strength

and physical function in elderly adults (Fiatarone et al., 1990, Fiatarone et al., 1994, and

Verfaillie et al., 1997). The Surgeon General's Report on Physical Activity and Health

states that developing muscular strength can improve one's ability to perform tasks and

reduce the risk of injury (Surgeon General, 1996). Furthermore, the report states that

"resistance training may contribute to better balance, coordination, and agility that may

help prevent falls in the elderly (Surgeon General, 1996)."

Resistance exercise also improves physical function by decreasing the relative

intensity of tasks performed in daily life. Resistance exercise can decrease the stress








placed on the heart during lifting tasks such as lifting moderate to heavy boxes which has

been implicated as a cause of heart attacks (McCartney et al., 1993).

Osteoporosis is a degenerative disease that is characterized by a decrease in bone

mineral density (BMD). This loss makes the bones more susceptible to fractures.

Research has indicated that bone formation can be stimulated by placing a strain on the

bone such as during resistive exercise (Rubin and Lanyon, 1984). Braith et al. (1996)

examined the effects of 6 months of resistance exercise on BMD following heart transplant

surgery. Typically, BMD decreases during the post-operative period as a consequence of

glucocorticoid therapy. The group that performed strength training was able to return

their lumbar, total body, and femoral neck BMD to near baseline levels while the control

group's BMD remained depressed. Isolated strength training of the lumbar muscles has

also been shown to increase lumbar BMD. Pollock et al. (1992) showed that 6 months of

isolated lumbar training improved lumbar BMD compared to controls in men and women

60 to 79 years of age. Menkes et al. (1993) reported a significant increase in femoral neck

BMD in middle-aged to older men following 16 weeks of strength training. Resistance

exercise can also have a significant effect on biochemical markers of bone metabolism.

For example, Menkes et al. (1993) reported significant increases in osteocalcin and

skeletal alkaline phosphatase isoenzyme (markers of bone formation) and a significant

decrease in tartrate-resistant acid phosphatase (marker of bone resorption) following 16

weeks of training. However, the results of this study were not replicated in another 16

week study by the same group (Ryan et al., 1994). It is possible that the duration of

training was not adequate to elicit a consistent alteration in the levels of these markers.








A factor that makes comparison of many of the investigations mentioned in this

review difficult is that some used high intensity resistance exercise while others used lower

intensity levels. Therefore, comparisons of their results or the ability to make appropriate

recommendations is difficult or impossible. The current intensity recommendation for

adults over 50 years of age corresponds to 14 to 16 (hard) on the Borg RPE scale

(Pollock et al., 1994). The intensity should be perceived as hard by the participant, but

should not be to voluntary failure as is recommended for younger adults (ACSM, 1990).

This recommendation for people over 50 yr. is not based upon scientific evidence and it is

not known if elderly people need to work at the same intensity as younger adults to derive

similar benefits, or if a lower intensity is sufficient. Therefore, the purpose of the proposed

investigation is determine what level of intensity is necessary for improved physical

function, bone metabolism, and defense against oxidative stress.



Justification for Research

Resistance exercise can have a significant impact on bone mineral density, strength,

physical function, and balance. Also, recent studies have demonstrated that elderly

persons can show similar adaptations to resistance exercise when compared to younger

adults. However, what is not known is if there is an intensity threshold for these

adaptations. It is also unknown if the same intensity is necessary to elicit these changes or

if they each respond to a different intensity. Since a large portion of the American

population is growing older, it is important to know what is the threshold intensity that

should be recommended to these people to improve health.








To date, no published investigations have examined if resistance exercise can

improve antioxidant defense systems. It has been shown that endurance exercise can

increase antioxidant enzyme activities (Powers et al., 1994). If resistance exercise can

increase these enzymes it could be recommended as another means of combating oxidative

stress. What is also necessary to determine is if low or high intensity exercise is necessary

to elicit adaptations in the endogenous antioxidant defense system.

It has been shown that resistance exercise can positively impact bone mineral

density, and improve balance and physical function. Although both low and high intensity

resistance exercise can affect all of the previously mentioned parameters, we sought to

determine if a greater impact will be made by high intensity training.



Purpose and Specific Aims

The purposes of this investigation were twofold: (1) To examine the effects of 6

months of dynamic resistance exercise training at two different intensity levels on physical

function, bone metabolism, aerobic endurance, and alterations in lipid peroxidation in

older adults. (2) To determine if the various physiological adaptations to 6 months of

resistance exercise vary between two intensity levels of resistance training. Specifically,

the aims of this study were to examine the consequences of low and high intensity

resistance exercise on:

1. Muscle strength: Measured by 1-repetition maximum (1-RM) for the chest

press, leg press, leg curl, biceps curl, seated row, overhead press, triceps dip, and

leg extension.








2. Muscle endurance: Measured by maximum number of repetitions performed

using 60% of the pre-training 1-RM for chest press and leg press.

3. Physical function: Measured by time to climb one flight of stairs

4. Bone metabolism: Measured by assaying for serum levels of pyridiniline

crosslinks, osteocalcin, and skeletal alkaline phosphatase enzyme.

5. Bone mineral density: Measured by dual-energy photon absorptiometry (DXA)

6. Serum oxidative stress measured by lipid peroxidation.

7. Aerobic endurance measured by a symptom-limited graded exercise test, and

time to exhaustion measured during the graded exercise test.



Research Hypotheses

The purpose of this investigation was to examine how dynamic resistance exercise

training at two different intensity levels affected strength, aerobic endurance, bone

metabolism, and lipid peroxidation older adults. This experiment was designed to test two

hypotheses. The first was that six months of resistance exercise would improve "health-

related" adaptations including bone metabolism, defense against lipid peroxidation, aerobic

endurance, physical function, and strength. The second hypothesis was that high-intensity

resistance exercise would not cause greater improvements in muscle strength and

endurance, aerobic endurance, serum markers of bone turnover, bone mineral density, and

serum lipid peroxidation when compared to low-intensity resistance exercise.








Significance of Research

Aging is associated with decreases in strength, muscle mass, physical function,

balance, and increased oxidative stress. Muscle weakness has been shown to be an

important contributor to risk of falling in older people (Nevitt et al., 1991). It is estimated

that the acute care costs associated with falls is in excess of $10 billion (Tinetti et al.,

1994). It is further estimated that insufficient strength to perform activities of daily living

incurs an additional $7 billion in health care costs (Rowland and Lyons, 1991). Decreased

muscular strength can lead to loss of physical independence, increased risk of injury, and

long term disability or institutionalization. Since the proportion of the population over 60

years of age is increasing, it is important to identify feasible interventions that can maintain

quality of life as people age. Resistance exercise has been shown to be an effective means

of improving strength and physical function in people of all ages. However, it is necessary

to obtain data which indicates what is the appropriate quantity and quality of resistance

exercise necessary to promote improved health and function. It is currently unknown if

there is an intensity threshold for health-related adaptations to resistance exercise for older

adults. The American College of Sports Medicine has recognized that resistance training

is important for quality of life and physical function for older adults (ACSM, 1990, 1998).

However, the recommendations for the quantity or quality of this exercise is not based on

an abundance of scientific evidence, rather it is based on the opinions of experts in the

field. There are data to support the beneficial effects of resistance exercise for this

population, but not what the appropriate intensity level is to attain these benefits. The

current intensity recommendation for adults over 50 years of age corresponds to 14 to 16

(hard) on the Borg RPE scale (Pollock et al., 1994). The intensity should be perceived as







8

hard by the participant, but should not be to voluntary failure as is recommended for

younger adults (ACSM, 1990). However, as stated, this recommendation for people over

50 yr. is not based upon scientific evidence and it is not known if elderly people need to

work at the same intensity as younger adults to derive similar benefits, or if a lower

intensity is sufficient. If a greater impact were to be made by high intensity training then

more definitive recommendations to the public can be made. However, if there is no

difference between groups, then the low intensity exercise would be the best

recommendation because it may be associated with a greater adherence rate as compared

to high intensity.














CHAPTER 2
REVIEW OF RELATED LITERATURE


Age Related Alterations in Muscle Mass. Structure and Strength

Decreased Muscle Mass

Aging is associated with a progressive loss of muscle mass and consequently

strength. This age related decline in muscle mass is termed sarcopenia (Evans, 1995). As

a result of the decrease in muscle mass and strength, older individuals can experience

decreased balance, physical function, bone mineral density, independence, and lowered

metabolic rate which contributes to alterations in body composition (Evans, 1995,

McComas, 1996, and Porter et al., 1995).

Aging is accompanied by a loss in fiber size and number (McComas, 1996). Lexell

et al., (1983) reported that elderly men (70-73yr) had 25% fewer muscle fibers in the

vastus lateralis compared to younger men (19-37 yr.). Lexell et al. (1988) also showed

that men in their 80s have 50% the number of fibers compared to younger individuals. The

results also showed that only 10% of the muscle area was lost by age 50, and that after

that point the loss in mass accelerated.

Numerous investigations have reported that the type II fibers experience the

greatest degree of atrophy ( Grimby et al., 1982, Klitgaard et al., 1990, Lexell et al., 1988,

1991, and Tomlinson et al., 1969). This selective reduction in type I muscle size may be

the result of decreased activity leading to disuse atrophy of the high force motor units.









Lexell et al. (1988) demonstrated that the age related decline in muscle mass is mainly

accounted for by type II fiber atrophy with very little contribution from type I fibers.

However, it has also been shown that although the type II fibers experience more atrophy

(decreased cross-sectional area), the relative proportion of type I to type II fibers remains

largely unchanged with age (Grimby et al., 1982,1984, and Lexell et al., 1988). Lexell et

al. (1988) reported that the proportion of type I fibers was 51% at 20 yr. and 55% at 80

yr. It has also been shown that the "mosaic" muscle pattern that is evident in the muscles

of younger individuals is lost with age (Klitgaard et al., 1990). There is typically an

intermixing of motor units so that similar fiber types are not grouped together in one area.

Data from Klitgaard et al. (1990) indicate that muscle fibers in older adults may

experience histochemical alterations in myosin heavy chain (MHC) expression. They

reported that fibers may contain more that one MHC isoform such that type IIA and IIB

or type I and HA isoforms may be found together. The authors felt that this could be the

result of a dynamic equilibrium between fiber groups resulting from disuse, denervation,

or both.

Other studies have reported further histological alterations in aging muscle

(Tomlinson et al., 1969, McComas, 1996). These alterations include: macrophage

infiltration, hyaline degeneration, disorganized sarcomeres, lipofucshin pigmentation,

decreased mitochondrial size, and increased connective tissue.



Motomeuron Decline with Aging

Aging is accompanied by a decrease in the number ofmotorneurons, particularly

the larger alpha-motorneurons (Ansved and Larsson, 1990, Kawamura et al., 1977, and







11

Tomlinson and Irving, 1977). Once denervated, the muscle quickly atrophies, losing 50%/

of its weight in one month and the rate of decline is more rapid for old animals when

compared to young (Gutmann, 1962, and White and Vaughan, 1991). Ansved et al.

(1991) and Einsiedel and Luff (1992) have shown that older neurons are not able to

demonstrate the same degree of collateral sprouting as compared to younger neurons.

This may be the result of decreased protein synthesis and a decreased rate of axonal

transport that is observed with old age (Ansved et al., 1991). Ansved et al. (1991) also

reported that preferential loss during aging is observed in large, fast-conducting

motorneurons with low oxidative enzyme activity that innervate fast-twitch muscle fibers.

In an examination of the extensor digitorum brevis, Campbell et al. (1973)

reported that prior to the age of 60, the number of functioning motor units shows little

change, but there is a progressive decline in functional motor units beyond that age.

Similar results have also been reported for the biceps, soleus, and the thenar muscles

(McComas, 1996). Campbell et al. (1973) also reported that the mean amplitudes of

motor unit potentials are significantly larger in the elderly when compared to younger

controls. These results indicate that when certain muscle fibers become denervated, other

motorneurons reinnervate the fiber by sending out new axonal branches (McComas,

1996). Studies using electromyography have shown that the number of motor units

decreases while the size of the motor units increases with age (Campbell et al., 1973,

Doherty et al., 1993a, 1993b). Although it has been established that motorneurons

decrease with age, the mechanism for this decline is currently not known. However, there

are several proposed mechanisms for neuronal death with age. These proposed

mechanisms are: ischaemia, accumulation of neurotoxins, free radical damage, and that








neurons may be genetically programmed to die at a certain age (McComas 1996, and

Weindruch, 1995).



Neuromuscular Performance Changes with Aging

The consequence of a decrease in motor units and more homogenous fiber

grouping is a decline in contractile function within the muscle. In an examination of the

triceps surae muscle in elderly subjects, Davies et al. (1986) reported that both the time to

peak tension and the time to relaxation were both significantly increased for evoked

twitches. A similar finding was reported for both the plantar and dorsiflexors

(Vandervoort ad McComas, 1986). The results from Vandervoort and McComas (1986)

also indicated that twitch time increased linearly with age (from 20-100yr.) but that a

significant decrease in muscle strength did not occur until the subjects were in their 60's.

The increase in contraction time is likely the result of a decrease in type II fibers. It is also

interesting to note that in the Vandervoort and McComas (1986) study the gastrocnemius

which contains more fast twitch motor units than the soleus showed a greater age related

decline in contractile function.

Fatigability has also been examined but the results from these investigations has

been equivocal (Davies et al., 1986, Klein et al., 1988, Larsson and Karlsson, 1978,

Lennmarken et al., 1985, and Narici et al., 1991). Narici et al., 1991 reported a decrease in

fatiguability with age while Lennmarken et al.(1985) observed an increase in fatiguability

in a similar study. Klein et al. (1988) reported no differences in fatiguability using the

triceps surae muscle, while Davies et al. (1986) found a decrease in fatiguability using the

same muscle group. These studies may be limited by the fact that although similar muscle









groups were used, the frequency of stimulation for the evoked contractions varied

between investigations. Larsson and Karlsson (1978) had subjects perform a sustained

voluntary contraction, and reported that fatiguability was similar for older and younger

adults. It is interesting to note that although there is an increase in the proportion of type

I fibers with age, fatigability is not altered. This may be the result of decreased physical

activity that is seen with aging.

As a consequence of increased contraction time, the elderly muscle's ability to

generate power is compromised (Bassey et al., 1992), as well as, the ability to generate

force during protective reflexes (Vandervoort and Hayes, 1989). Research has indicated

that the ability to generate force quickly, not the absolute amount of force produced is an

important variable in the prediction of risk of falling (Whipple et al., 1987, Maki and

Mcllroy, 1996).



Muscle Mass and Strength Increases with Resistance Exercise in Older Adults

Numerous recent investigations have demonstrated that resistance exercise is an

effective means for increasing muscle mass and strength (Fiatarone et al., 1990,1994,

Frontera et al., 1988, Klitgaard et al., 1990, Morganti et al., 1995). The purpose of this

section will be to highlight these five studies which represent the findings reported in other

previous, as well as, subsequent investigations.

In a cross-sectional study, Klitgaard et al. (1990) reported that men 68 yr. who

had a history of strength training had similar knee and elbow isometric strengths and

cross-sectional area as compared to 28 yr. endurance trained men. They also reported that

men 68yr. with a history of aerobic exercise or no physical activity had lower knee and









elbow isometric strengths and cross-sectional area as compared to 28 yr. endurance

trained men.

Morganti et al. (1995) resistance trained 20 women (av. age 61yr.) twice per week

for six months. Subjects performed three sets of eight repetitions at 80% of their 1RM for

the double leg press, knee extension, lateral pull-down, trunk extension, and trunk flexion.

Strength was measured for the lat pull-down, leg press, and knee extensions at 6 and 12

months. The results indicated an increase in strength in the training group after 12 months

of 77%, 35%, and 74% for the lat pull-down, leg press, and knee extensions, respectively.

No significant increases in strength were noted at 12 months in the control group.

Fiatarone et al. (1990) resistance trained 10 elderly men and women (mean age

90yr) for 8 weeks. Subjects performed 3 sets of 8 repetitions of knee extensions 3 days

per week. Strength was measured by 1RM and regional body composition was assessed

by computed tomography (CT). The results showed that 1RM knee extension strength

improved by 174%, and that mid-thigh muscle area increased 9%.

Fiatarone et al. (1994) examined the effect of resistance training alone or in

combination with a nutritional supplement in men and women with an average age of 87yr.

Subjects performed 3 sets of 8 repetitions 3 days per week for 10 weeks for the hip and

knee extensors. CT scans of the mid-thigh were obtained to assess changes in muscle

area. The results showed an increase in strength of 113%, but a non-significant increase

of 2.7% in mid-thigh-muscle area. The increase in strength was not related to protein

supplementation.

Frontera et al. (1988) examined the effect of 12 weeks of resistance exercise for

the knee flexors and extensors. They trained 12 men (age range 60-72yr) using 3 sets of 8







15

repetitions performed 3 days per week. At the conclusion of the 12 weeks, knee extension

strength had improved 107% and knee flexor strength had increased 227%. CT scans

revealed an 11% increase total muscle area of the mid-thigh. The authors also reported a

40% increase in urinary 3-methyl-L-histidine which is a marker of protein turnover.

One recent study examined the effects of either high- (80% of IRM for 7

repetitions) or low-intensity (40%/ of IRM for 14 repetitions) on strength, thigh cross-

sectional area, and bone mineral density (Taafe et al., 1996). The subjects were women

aged 65-79 yr. Subjects trained 3 days per week for 52 weeks at one of the two

intensities performing 3 sets of leg press, knee extension, and knee flexion. The authors

reported a mean increase in strength of 59%/ and 41% for the high and low groups,

respectively. Both groups demonstrated a significant and similar increase in type I fiber

area but not type H. Neither group experienced a significant increase in bone mineral

density.

These studies indicate that resistance training is an effective means for improving

strength and muscle mass in older adults. However, the resistance training regimens in

these,as well as, other studies are very similar. Most studies use 3 sets per exercise and

typically 6-15 repetitions, not based on research, but based on either investigator opinion

or studies performed on younger people. It is not known if high volume is necessary to

elicit increases in strength and mass, or if a lower intensity would produce similar results.



Postural Control and Aging

The previously described alterations in muscle mass, strength and motor units that

accompany aging can have deleterious effects on posture and balance. The human body









has been described as a multilink inverted pendulum (Maki et al., 1996). As such, it is

inherently unstable due to the influence of gravity (Maki et al., 1996). Perturbations in

posture or balance are responded to by either controlling the center of mass (COM)

through generating torque at the joints or by altering the base of support (BOS) by

stepping or grasping movements with the limbs (Maki et al., 1996). Perturbations

affecting balance can either be mechanical (i.e. force acting on the body) or informational

(i.e. visual, vestibular, somatosensory) (Maki et al., 1996).

Sensory systems display decreased function with aging. Visual acuity, contrast

sensitivity, depth perception, and dark adaptation are all decreased with aging. Decreased

visual acuity has been implicated as a risk factor for falling because the older person may

not be able to see an obstacle in front of them or see that a curb is ahead while walking on

the street (Alexander, 1996). Other degenerative adaptations such as reduced

proprioception, touch sensitivity, vestibulo-ocular reflex, and the density and sensitivity of

dermal mechanoreceptors are reported with aging (Maki et al., 1996).

As previously mentioned, aging is associated with a decreased skeletal muscle

contraction rate which may impair the ability to rapidly produce force in response to

postural perturbations (McComas, 1996). Available evidence indicates that there is an

association between leg muscle weakness and risk of falling and postural sway (Lord et

al., 1991a, 1991b). Research also indicates that the torque necessary to prevent a fall is

typically within the elderly person's ability. However, what is not, is the ability to

generate the torque quickly (Maki et al., 1996). A common way to measure postural sway

and balance is through measuring changes in center of pressure (COP) during force plate

analysis (Alexander, 1996). Alexander (1996) reported that the maximum peak-to-peak







17

COP excursion or speed of the COP excursion can be used to distinguish between young

and adult postural sway patterns. Maki et al. (1994) reported that the amplitude of

mediolateral COP displacement was found to be the single best predictor of falling risk

compared to other balance measures. The authors indicated that adductor/abductor

strength as well as proprioceptors were most critical to maintaining lateral stability.

Research also indicates that using force plates, and insole pressure sensors provide

a reliable and valid means of assessing balance and postural sway (Alexander, 1996, and

Maki et al., 1996). Other commonly used methods such as questionnaires, one-legged

stance time, and reaching tasks have been shown to measure fear of falling rather than

probability of falling (Alexander, 1996). The use of insole pressure sensors allows for

balance and postural sway during dynamic activities to be measured as well.



Resistance Exercise and Balance and Physical Function

Aging has been associated with a decrease in muscle mass and strength (Larsson et

al., 1979). This decrease in strength is linked to decreased mobility, physical function, and

increased risk of falling in older people (Bendall et al., 1989). Resistance exercise has been

shown to be effective for increasing muscle mass, strength and physical function in elderly

adults (Fiatarone et al., 1990,1994, and Verfaillie et al., 1997). The Surgeon General's

Report on Physical Activity and Health states that developing muscular strength can

improve one's ability to perform tasks and reduce the risk of injury(Surgeon General,

1996). Furthermore, the report states that "resistance training may contribute to better

balance, coordination, and agility that may help prevent falls in the elderly (Surgeon

General, 1996)". Falls have been identified as the most frequent cause of injury related









mortality in the elderly (Fife et al., 1984). Nevitt et al. (1991) conducted a prospective

study to determine the risk factors that lead to injurious falls in the elderly. They reported

that the fallers' ability to protect him- or her-self during the fall affected the risk of injury.

The authors recommended that interventions intended to reduce the risk of falling and

injury should include strength training. Fiatarone et al. (1994) examined the effect of 10

weeks of resistance exercise for the legs only on muscle strength and function in elderly

adults (mean age, 87+ 0.6 yr.). Resistance exercise increased muscle strength, gait

velocity, and stair climbing power. Fiatarone et al. (1990) reported that 8 weeks of

resistance exercise for the leg improved strength and function in nonagenarians (mean age

90+lyr.). Quadriceps strength improved 174% and tandem gait speed increased 48%

following resistance training.



Bone Formation and Resorption

The process of bone remodeling (deposition/resorption) is a continuous and

interdependent process (Marcus, 1991). The two primary cells that are involved in the

process of bone metabolism are the osteoblasts and the osteoclasts. Osteoblasts are

primarily involved in bone formation and come from the differentiation of osteoprogenitor

cells (Mundy, 1993, and Raisz et al., 1993). Osteoclasts are primarily involved with bone

resorption and are formed from tumor cells or leukocytes under the influence of osteoclast

forming cells (Mundy, 1993).

Osteoblasts contain alkaline phosphatase, the protein osteocalcin, and secrete type

I collagen (Calvo et al., 1996). This forms the osteoid which is the site of bone

deposition. Into this collagen matrix Ca" and P04- will be deposited to form







19

hydroxyapatite. As the bone develops it will eventually surround the osteoblast which will

then be incorporated into the bone as the osteocyte. The osteocytes are connected via a

canal system known as the Haversian canals (or canaliculi). These canals allow rapid

communication between the interior and exterior of the bone. The canals allow Ca"and

PO4- to be transmitted from the areas of newly formed interior bone to the outside. This

process is known as osteocytic osteolysis (Marcus, 1991). Osteoblast activity is

stimulated by several factors. Estrogen and testosterone act on response elements

(Estrogen Response Element) within the osteoblast to produce Insulin like Growth Factor

1 (IGF-I) (Martin, 1993). Osteoblasts have membrane receptors for IGF-I and I, and

these receptors can also bind insulin (Martin, 1993). Insulin and the IGFs bind to a

tyrosine kinase receptor that has two sub-units. These sub-units interact with the Insulin

Response Substrate (IRS) to induce glucose uptake and protein transcription. So it can be

seen that insulin helps to promote bone formation. Growth Hormone (GH) also promotes

bone formation and plasma calcium increase because it stimulates the release of IGF-I

from the liver and increases intestinal absorption of Ca" (Arnaud, 1993, and Martin,

1993). IGF-I is an anabolic hormone which stimulates bone growth and formation. The

osteoblast has receptors for IGF and produces it, so the osteoblast can produce a factor

which stimulates osteoblast activity (Raisz et al., 1993). At low levels, Prostaglandin E

helps to promote the formation of osteoblasts and stimulates the production of IGF-I

(Raisz et al., 1993). Other factors which can promote bone formation are gamma

interferon, leukemia inhibitory factor, and retinoic acid. Retinoic acid helps to induce

transforming growth factor beta, and bone morphogenetic protein. Vitamin D3 although

more involved in bone resorption is necessary for bone formation because it increases







20

intestinal absorption of Ca"and P04 ,and increases the number of IGF-I receptors on the

osteoblast membrane (Raisz et al., 1993).

The osteoclast secretes tartrate resistant acid phosphatase which helps to form a

ruffled invagination in the osteoid and facilitate the release of Ca*and P04- (Calvo et al.,

1996). Interestingly, the osteoblast will use this site to deposit new bone. Osteoclast

activity is promoted by several factors. One of the most important is parathyroid hormone

(PTH) which is secreted by the chief cells of the parathyroid gland (Mundy, 1993). PTH

is secreted primarily in response to low serum Ca" levels. Low serum Ca* causes an

increase in cAMP levels in the chief cells which leads to PTH exocytosis (Mundy, 1993).

The release of PTH in response to low Ca" occurs within minutes. PTH release can also

be stimulated by high serum levels of P04- because the P04- can bind to Ca+ so that the

free Ca" levels in serum decrease. PTH stimulates the kidney to increase the reabsorption

of Ca" and increase the excretion ofPO4-. PTH also acts on the osteoblast to cause it to

secrete a factor that stimulates the activity of the osteoclast to increase osteocytic

osteolysis (Mundy, 1993). This will also serve to increase plasma levels of Ca" and PO4-.

PTH cannot stimulate osteoclasts if osteoblasts are not present. This is an example of the

coupling of resorption and formation. Also, PTH inhibits collagen production by the

osteoblast but does promote osteoblast proliferation. PTH also promotes the conversion

of 25-OH-VitD to the active form of 1,25-OH-VitD (VitD3) (Seino et al., 1993). VitD3

formation can be induced by low serum Ca", PO4-, and Vit D3. VitD3 acts in the brush

border of the intestinal villi to increase the number ofCa" transporters enhancing its

absorption (Seino et al., 1993). It also acts to increase the absorption of PO4-. Both PTH

and VitD3 help to increase serum levels of Ca", Vit Da by increasing its intestinal







21

absorption and both by increasing Ca" resorption from bone (Seino et al., 1993). VitD3

acts on cells of the kidney, intestine, liver, and skeletal muscle to produce Calbindin (Seino

et al., 1993). Calbindin acts as a carrier of Ca" effectively decreasing the levels of free

Ca" within cells. Ca" is a very reactive substance and can promote many intracellular

reactions and therefore it is important to keep its free concentration down. VitD3 also

increases Ca" uptake into the sarcoplasmic reticulum in skeletal muscle (Seino et al.,

1993). VitD3 acts on the osteoblast to increase the production ofosteoclast stimulating

factors(Seino et al., 1993). VitD3 is active in bone resorption (stimulates osteoclast

activity), increases serum Ca" (increased intestinal absorption), and bone formation

(increased IGF-I receptors and Ca*/PO4- availability). Once at the site of bone turnover,

several other mechanisms are involved. PTH causes an increase in cAMP within the

osteoblast. This stimulates the production ofPGE2. PGE2 in high levels serves to

increase bone resorption(Raisz et al., 1993). It promotes osteoclast proliferation and

activity. It also helps to initiate the cycle that causes an increase in IGF-I production.

PGE2 increases cAMP levels, which further increases PGE2 levels (autoamplification).

Bone resorption is also stimulated by Interleukin l(IL-1), interleukin-6 (IL-6) and tumor

necrosis factor. IL-6 works by promoting osteoclast congregation.

The final hormone that impacts bone metabolism is calcitonin (Martin, 1993). The

relative effect or importance of calcitonin has not been proved in humans. It responds to

high levels of serum Ca". Its effect is to oppose the actions of PTH and increase Ca"

excretion and possibly promote bone formation.

Estrogen is essential for promoting bone growth (Orimo et al., 1993). Estrogen

increases the osteoblastic production of IGF-I and decreases the production ofIL-1, IL-6,







22

and reduces the sensitivity of the osteoblast to PTH(Hashimoto et al., 1993 and Orimo et

al., 1993). Estrogen also promotes the formation of VitD3. With aging, the production of

estrogen declines (menopause) and the level of PTH in women steadily increases (Orimo

et al., 1993). The age dependent increase in PTH is not seen in men. Also with aging,

glucocorticoid levels increase or are given exogenously. Cortisol decreases the absorption

of Ca" and inhibits bone formation (Raisz et al., 1993). This could also increase the bone

loss in post-menopausal women or in people given glucocorticoids. Another

pathophysiological condition which can cause a large decrease in bone mass is organ

transplantation (Braith et al., 1996). These patients are supplemented with corticosteroids

and cyclosporin which can cause precipitous decreases in bone formation. These patients

are also usually sedentary and the lack of physical activity can decrease bone mass.

Bone formation can be impacted by environmental or pathophysiological factors.

It has been observed that there are seasonal alterations in bone metabolism. During the

winter the elderly or immobile do not go outside. VitD must either be consumed in the

diet or obtained through exposure to sunlight (Seino et al., 1993). If the person is not

exposed to sunlight and this is combined with inadequate VitD intake, then Ca"

absorption and serum levels will be impaired. Under these circumstances, a more

collagenous, soft bone will be deposited due to the lack ofCa" and P04-(Seino et al.,

1993) Winter conditions can also lead to decreased physical activity. Physical activity has

been shown to be a determinant of bone mineral density (BMD). Physical activity such as

strength training and running which cause skeletal loading can increase BMD. The

osteoclasts and lining cells of the bone contain mechanoreceptors. These receptors

respond to increased mechanical or electrical stimulation (Rubin and Lanyon, 1984).









These physical stimuli are translated into biochemical messages. When this occurs an

increase in 2nd messenger activity is observed in the osteoblasts. Within 10 seconds of

mechanical loading, mRNA levels within the osteoclast increase. In the osteoblast, two

second messenger systems are activated. First, adenylate cyclase is activated and cAMP

levels rise. Second, the inositol triphosphate system is activated causing an increase is

inositol diphosphate, protein kinase C, phospholipase A which increase arachidonic acid

entry and formation which leads to the production ofPGE2. PGE2 also increases cAMP

(Raisz et al., 1993). The increase in cAMP and PGE2 causes an increase in IGF-I

production and therefore increased bone formation.


Resistance Exercise and Bone Mineral Density

Osteoporosis is a degenerative disease that is characterized by a decrease in bone

mineral density (BMD). This loss makes the bones more susceptible to fractures.

Research has indicated that bone formation can be stimulated by placing a strain on the

bone as is found during resistive exercise (Rubin and Lanyon, 1984). Hamdy et al.(1994)

reported higher BMD in the upper arm in people that weight trained when compared to

runners, but that there was no difference for lower body BMD between the two groups.

Karlsson et al.(1993) reported that active and retired weightlifters had higher BMD for

the spine, hip, tibia, and forearm when compared to controls.

Kohrt et al. (1997) examined the effect of either exercise involving ground reaction

forces (GRF) or joint reaction forces (JRF) on bone mineral density in women aged 60-74

years. Both groups trained for 11 months with the GRF group performing walking,

jogging, and stair climbing while the JRF group performed resistance training and rowing.







24

The resistance training regimen consisted of 8 exercises performed for 2-3 sets, for 8-12

repetitions two times per week. The results indicated significant and similar increases in

BMD for the whole body, lumbar spine, and Ward's triangle region of the proximal femur

for both groups. Only the GRF group exhibited a significant increase in femoral neck

BMD.

Braith et al. (1996) examined the effects of 6 months of resistance exercise on

BMD following heart transplant surgery. Typically, BMD decreases during the post-

operative period as a consequence of glucocorticoid therapy. The group that performed

strength training was able to return their lumbar, total body, and femoral neck BMD to

near baseline levels while the control group's BMD remained depressed. Isolated

strength training of the lumbar muscles has also been shown to increase lumbar BMD.

Pollock et al. (1992) showed that 6 months of isolated lumbar training improved lumbar

BMD compared to controls in men and women 60 to 79 years of age.

Menkes et al. (1993) reported a significant increase in femoral neck BMD in

middle-aged to older men following 16 weeks of strength training. The mechanism for

how resistance exercise effects BMD has yet to be determined. It is thought that the strain

placed on bone by loading results in a piezoelectric current which causes an increase in

bone formation. Resistance exercise can also have a significant effect on biochemical

markers of bone metabolism. Menkes et al (1993) reported significant increases in

osteocalcin and skeletal alkaline phosphatase isoenzyme (markers of bone formation) and

a significant decrease in tartrate-resistant acid phosphatase following 16 weeks of training.

However, the results of this study were not replicated in another 16 week study by the








same group (Ryan et al., 1994). It is possible that the duration of training was not

adequate to elicit a consistent alteration in the levels of these markers.



Oxidative Stress and Free Radical Production

Free Radicals and Aging

It has been proposed that aging is a consequence of macromolecular disturbances

mediated by oxidative stress (free radical generation)(Harman, 1956, Ji, 1993,and Nohl,

1993, ). Free radicals can be produced in the mitochondria, or in any system that utilizes

oxygen(Yu, 1994). Sites of radical generation are the electron transport chain

(Ubiquinone, Coenzyme Q) and cytochrome P450 in the nucleus as well as other

locations. It has been shown that the mitochondria are prime sites of free radical

production and that damage to DNA is 16 times higher in the mitochondria than in the

nucleus (Yu, 1994). It has also been shown that the mitochondria of aged animals shows

more superoxide (0-) leakage than that of younger animals(Nohl, 1993). Also, free

radicals are produced by xanthine oxidase (XO). During exercise, ATP is converted to

adenosine. At the same time, Xanthine dehydrogenase is converted to XO by the increase

in intracellular calcium seen during exercise. XO acts on the adenosine byproducts to form

uric acid (a free radical) (Yu, 1994).

Oxidative stress is defined as an imbalance between free radical production and the

forces that oppose their production (Jenkins, 1988). Free radicals are also called reactive

oxygen species (ROS). The various forms of free radicals produced are superoxide (02-),

hydroxide (OH), and hydrogen peroxide (H202). These radicals can then take electrons

from other substances and form other radicals and cause damage to biological systems.








Common sites for damage are molecules containing sulfhydryl groups (proteins, gates,

DNA), double bonds (Polyunsaturated Fatty Acids, PUFA in membranes), and

carbohydrates (Reid, 1996, and Yu, 1994). The primary defense against this type of

damage includes the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX)

and catalase (CAT). SOD is an enzyme located in the mitochondrial membrane, cytosol,

and plasma (Jenkins, 1988). It scavenges superoxide radicals and converts them to H202.

Although this is still a ROS, it is less reactive than superoxide. H202 can be rendered

harmless by two other enzymes. The first is GPX which uses glutathione to accept the

extra electron and converts the H202 to H20. The glutathione is then regenerated by

glutathione reductase with the help ofNADPH from the pentose phosphate pathway.

H202 can also react with CAT. CAT also converts H202 to H20. One postulated reason

for having the two enzymes is that GPX is active at lower levels of H202 and CAT

becomes active with higher levels.

Superoxide can also be scavenged by dietary antioxidants such as vitamin E, beta

carotene, and vitamin C. Typically, vitamin E is used to squelch superoxide or to insert

itself into the membrane to inhibit the propagation of membrane disruption. Free radicals

will use the double bond site of PUFAs in the cell membrane as a place to steal an

electron. This can cause disruption in the membrane because that fatty acid tries to steal

an electron from a neighboring fatty acid. Propagation can result in holes in the cell

membrane. These holes can disrupt the ionic balance of the cell, as well as, allow the

entry of calcium which can activate proteases and cause cellular damage. Vitamin E and

beta carotene are lipid soluble and have long hydrophobic tails. The head of the vitamin E

can accept the free radical and prevent the free radicals from continuing to disrupt the cell







27

membrane. Vitamin E is then recycled through the action of vitamin C and lipoic acid or

through GPX. Although vitamin C is a good antioxidant, it does have a limitation in that

at high levels it can act as a pro-oxidant and promote free radical damage. Lipoic acid

does not scavenge radicals by itself, but rather it serves a supportive function by aiding in

the recycling of vitamin E. Glutathione is the primary thiol scavenger in the antioxidant

defense system. Other minor antioxidants are bilirubin and carbohydrates.

Free radicals and ROS have been implicated as major contributors to the aging

process (Harman, 1956). Aging has been defined as a decreased ability for the cells to

proliferate. This decreased proliferation may be the result of an internal timer within the

cell that when expired, will not allow the cell to survive. It may also be due to impaired

codon transcription (Nohl, 1993, and Yu, 1994), as ROS cross-links proteins. If this

occurred in DNA, then the strand would not be readable. Cross-linking mRNA results in

failure of transcription of the genetic message. Therefore, ROS may be responsible for the

inability to correctly translate the messages found in DNA (Jenkins, 1988, Nohl, 1993, and

Yu, 1994). Ultimately, this could inhibit the cell from proliferating or from correctly

functioning.

Aging is associated with a decrease in muscle mass and strength (sarcopenia). One

cause of a decrease in mass is a loss in muscle fiber number, likely due to a loss of motor

neuron innervation. It has been shown that ROS can negatively impact nerves and either

cause their inactivation or their degeneration (Lou Gehrig's Disease, Parkinson's

disease)(Sohal and Orr, 1992). Therefore, ROS are a potential source ofdenervation and

sarcopenia with aging. ROS can damage the SR and inhibit the release and uptake of

Ca", leading to decreased contractile force. It has been shown in skinned fiber







28
preparations that the integrity of the contractile element in the muscle fiber remains intact

with aging and does not decrease in force capability (Powers et al., 1994). What does

show impairment is the excitation-contraction coupling (Reid, 1996). ROS have also been

implicated in type I and II diabetes (Yu, 1994). It has been shown that ROS can attack

and deactivate the beta cells in the pancreas which stimulate the release of insulin. It has

also been shown that SOD activity is lower in persons with diabetes. Diabetes is a risk

factor for cardiovascular disease (Yu, 1994).

According to Evans (1995), elderly people experience exacerbated muscle damage

compared to young people as a consequence of exercise. This may be due to several

factors. First, when damage occurs (typically from eccentric contractions) in young,

healthy muscle, neutrophils and lysozymes infiltrate the area and release free radicals as a

means of breaking down damaged tissue. Satellite cells which decrease with age are non

differentiated cells that are next to muscle fibers (Carlson, 1995). They help to repair the

fiber, or can even form new ones. In younger mammals, damaged fibers are replaced with

contractile elements, where in older mammals, contractile elements are replaced with non-

contractile elements like collagen. This would decrease the muscles integrity leaving it

more susceptible to damage.

It has also been shown that tissue levels of vitamin E decrease with age (Yu,

1994). This could be from decreased intake or increased utilization. As mentioned

earlier, aging is associated with increased free radical production. It may also be

associated with or the result of an accumulation of damage incurred by ROS over time. Ji

(1993) showed that with aging, skeletal muscle antioxidant enzyme (AOE) activity

increases. Since AOE activities increase as a result of ROS production the increase in








AOE must result from accumulated oxidative stress. This stress may accumulate with

time and cause damage that is outwardly seen as the aging process. Several investigators

have shown that increased metabolic activity has been associated with a shorter life span.

The results have been most clearly demonstrated in fruit flies. When allowed to fly and

mate, their life span decreases compared to those that were kept from flying or

sequestered from the opposite sex.



Exercise and Oxidative Stress

During the aging process, the rate of free radical formation increases (Ji et al.,

1990). This stimulus increases antioxidant enzyme levels that act as defense against this

oxidative stress (Ji, 1993). Increased free radical generation is a signal for an increase in

antioxidant enzyme activity (Jenkins, 1988). Numerous investigations have shown that

acute and chronic exercise can result in an increase in antioxidant enzyme activity

(Hammeren et al., 1992, Ji, 1993, Ji et al., 1991, and Tullson et al., 1994). Aerobic

endurance exercise, particularly intense endurance exercise results in an increase in free

radical generation which also results in increased antioxidant enzyme activities (Tullson et

al., 1994). It has been shown that increasing the metabolic rate or flux of oxygen through

the electron transport system (ETS) promotes ROS generation (Ji, 1993, Powers et al.,

1994, and Reid et al., 1993). As oxygen consumption increases, the possibility of ROS

generation increases. Reid et al. (1993) demonstrated that excessive ROS generation was

related to decreased force production. It has also been shown that ROS can interact with

the sulfhydryl groups on the gates on the sarcoplasmic reticulum and either inhibit the

release or the uptake of Ca" (Reid, 1996). This results in disruption of the force









producing capabilities of the muscle and interferes with excitation-contraction coupling

(Reid, 1996). As mentioned earlier, ROS can also cause membrane disruption in the

cellular membrane which would also cause a breakdown in the ionic gradient necessary for

contractions.

Numerous investigators have shown that SOD and GPX levels increase in

response to exercise training (Ji, 1993, Leeuwenburgh et al., 1994, and Powers et al.,

1994). The effects of exercise on CAT activity is not as clear. Therefore, it seems that

ROS generation causes some adaptation which increases antioxidant enzyme (AOE)

activity. This can occur either through promoting the transcription of more enzymes or

through the allosteric modification of existing enzymes allowing them to be more active.

Free radical production can also result from ischemia followed by reperfusion (Das

et al., 1993). During systole, blood flow to the ventricles is momentarily occluded

(ischemia). During diastole, blood flow is restored (reperfusion). During exercise, the

period of diastole and therefore reperfusion is decreased. This type of cycle has been

shown to increase ROS generation and can cause damage to the myocardium or to the

vasculature (Yu, 1994). A similar ischemia/ reperfusion cycle may be present in skeletal

muscle during resistance exercise. Muscular contractions greater than 40% of the maximal

voluntary contraction (MVC) as performed during resistance exercise result in transient

blood flow occlusion in the exercising muscle (Donald et al., 1967). This form of

ischemia/reperfusion could possibly increase antioxidant enzyme activities that leading to

improved defense against oxidative stress. Recently, McBride et al. (1998) demonstrated

that intense resistance exercise causes an increase in free radical production. Subjects

performed 10 repetitions for 3 sets with 1 minute rest periods between sets for 8 exercises.








The results showed an increase in malondialdehyde (MDA) levels which indicates an

increase in free radical production. A recent investigation has also demonstrated that

intermittent sprint cycling performed three times per week for 6 weeks followed by a

seventh week with five sessions resulted in an increase in antioxidant enzyme activity

(Hellsten et al., 1996). The subjects performed fifteen 10 second maximal sprints with a

50 second rest period between each sprint during each training session(Hellsten et al.,

1996). Resistance exercise induces a metabolic stress similar to that seen during sprint

exercise. Therefore, resistance exercise may elicit similar increases in antioxidant enzyme

activity observed during sprint exercise.

The same exercise-induced increases in free radical production and elevations in

antioxidant enzyme activities have been shown in senescent animals (Ji, 1993,

Leeuwenburgh et al., 1994, and Powers et al., 1994). As a consequence of endurance

exercise, AOE activities were upregulated to the same extent as in younger animals.



Exercise Prescription for Older Adults

The American College of Sports Medicine (ACSM) currently recommends that

resistance exercise be incorporated as a component of a well-rounded exercise program

for all healthy adults (ACSM,1990). The ACSM recommends 1 set of 8-12 repetitions for

younger adults and 10-15 repetitions for adults over 50-60yr., using 8-10 exercises,

performed 2-3days per week (ACSM, 1990, 1998). The greater repetitions for older

adults is used to decrease the risk of orthopedic injuries which may result from lifting

increased loads associated with low volume higher intensity efforts, while the range in age

reflects individual differences towards weakness or frailty. When initiating an exercise






32

regimen for older adults, it is recommended that the initial resistance used should be 30-

40% of their one repetition maximum (1-RM) for that exercise(Pollock et al., 1994). If a

I-RM is not available, start with a low resistance and progress slowly allowing time for

muscle and soft tissue adaptation. The current intensity recommendation for older adults

corresponds to an RPE of 12-13 (somewhat hard) initially (first 4-6 wk) and then progress

to 14 to 16 (hard) on the RPE scale (Pollock et al., 1994). The intensity should be

perceived as hard by the participant, but should not be to voluntary failure as is

recommended for younger adults until approximately 12 weeks (ACSM, 1990). This time

period should be taken as an estimate, the 12 weeks could be lengthened or shortened

depending on the health status or level of fitness of the individual. Once older adults adapt

to their resistance training regimen, most will be capable of progressing to 10-15RM.














CHAPTER 3
METHODS


Subjects

The participants for this study were apparently healthy adults between the ages of

60 and 85 years. Eighty-six participants were entered into the study and sixty-two

completed the protocol. Participants were recruited from the Gainesville, Florida and the

surrounding areas. All participants had not participated in in regular resistance training for

at least one year, but may have been engaged in low-intensity aerobic training equal to or

less than 3 times per week.



Subject Eliaibility

Inclusion Criteria

Subjects were considered eligible for participation if they were:

* aged 60 85 years

* not participating in regular resistance exercise for at least one year

* free from any orthopedic or cardiovascular problems that would limit exercise








Exclusion Criteria

Subjects were excluded from study participation if they:

* Participated in regular resistance exercise during the last year or regular moderate

to high intensity aerobic training.

* had known orthopedic, cardiovascular or non-cardiovascular abnormalities that

would preclude participation in exercise.

* Had any abnormalities identified by the American College of Sports Medicine

(ACSM) as absolute or relative criteria for discontinuing exercise as revealed during a

symptom limited graded exercise test (SL-GXT) (3)



Study Design

This investigation was conducted at the Center for Exercise Science located in the

Florida Gym at the University of Florida. Participants were matched and randomly

assigned to 1 of the following three groups:

low-intensity resistance exercise (LEX)

high-intensity resistance exercise (HEX)

wait list control (CON)

Subjects were matched using a composite strength score calculated by adding the chest

press and leg press one-repetition maximum (1RM) values. Three subjects were matched

using the composite strength score when their pre-testing visits were completed and were

then randomly assigned to one of the three groups. Randomization was performed using a

random numbers table. Muscle strength and endurance, bone metabolism, serum lipid







35

peroxidation, and physical function were measured before and after the 6 month training

period.

Participants were scheduled for seven visits prior to the start of the training period.

Visit 1: Participants read and signed an informed consent, and were given an explanation

of the study. They also received an orientation to the resistance exercise machines and the

treadmill protocol that was used during the graded exercise test. Visit 2: Participants

were given an SL-GXT (Naughton protocol) whereby blood pressure, heart rate, ECG,

and symptoms were monitored by a physician. The GXT was terminated upon volitional

fatigue of the subject and/or according to the guidelines established by the American

College of Sports Medicine (3). A blood sample was also collected before and after the

GXT to measure biochemical markers of bone turnover and antioxidant enzyme capacity.

Visit 3: Participants had their maximum strength measured by determining the maximum

load that they could lift for 1 repetition (1-RM) on the leg press, chest press, leg curl, and

biceps curl. Visit 4: Participants had their muscular endurance measured on the leg press

and chest press. They were asked to perform as many repetitions as possible without

assistance while maintaining proper form using 60% of their previously determined 1-RM.

Visit 5: Each subject had their total body and regional bone mineral density measured

using dual-energy X-ray absorptiometry (DXA). Visit 6: Participants were asked to

ascend one flight of stairs as quickly as possible. Two trials were performed. Maximal

isometric strength for the lumbar extensor muscles was measured using a seven angle

lumbar extension test. Visit 7: Body composition was determined using a seven site

skinfold technique. Participants had their maximum strength measured by determining the








maximum load that they could lift for 1 repetition (1-RM) on the seated row, overhead

press, triceps dip, and knee extension.



Experimental Protocol

Visit 1. Screening / Orientation

All potential participants were recruited from Gainesville and the surrounding area.

Those volunteers who had no contraindications (see exclusion criteria) were asked to

participate in the study. All participants received a comprehensive explanation of the

proposed study, its benefits, inherent risks, and expected commitments with regard to

time. Following the explanation of the proposed study, all participants were allowed a

period of questioning. Those participants who were willing to participate were required to

read and sign an informed consent document, complete a self-reported activity, medical

history, and dietary questionnaires. Participants were then given an orientation to the

resistance exercise machines and equipment used during the GXT by trained personnel.

The resistance exercise equipment for this investigation was MedX resistance machines

(MedX Corp., Ocala, FL). These machines were selected because their design allows for

proper positioning and weight increases for frail or diseased populations. The smallest

increment of load increase is 2 ft-pounds as opposed to 5 or 10 pounds found with other

such exercise equipment. Participants were instructed as to the proper positioning and

exercise form for each machine. Participants performed 10-15 repetitions on each

machine using a light load (20 ft-lb). The machines used for this study were abdominal

crunch, leg press, leg extension, leg curl, calf press, seated row, chest press, overhead

press, biceps curl, seated dip, leg abduction, leg adduction, and lumbar extensions. The







37

participants were then allowed to walk on the treadmill and practice breathing through the

headgear which was used to collect expired air used for the determination of VO2,pi

during the GXT. The subjects walked on the treadmill at 2.0 m.p.h. at a 0% grade for 3

minutes followed by 2 minutes at 2.0 m.p.h. at a 3% grade.



Visit 2. Treadmill Graded Exercise Test and Blood Sample Collection

On visit 2, participants reported to the Center for Exercise after a three hour fast.

Upon arrival participants were seated in a quiet room for 15 minutes where after resting

heart rate (HR), and blood pressure (BP) were obtained using standard auscultation

procedures and a Trimline mercury sphygmomanometer (Pymah Co., Somerville, N.J.). A

medical examination was performed by a physician specializing in geriatric medicine. A 30

ml blood sample was collected via venipuncture of an antecubital vein and used for

measuring bone metabolism and lipid peroxidation. The sample was allowed to clot at

room temperature for 10-20 minutes and then centrifuged for 15 minutes at 0C. The

serum was then pipetted into polystyrene tubes and stored at minus 800C for later analysis.

Samples were analyzed for osteocalcin, skeletal alkaline phosphate isoenzyme, and

pyridinoline crosslinks. Osteocalcin and skeletal alkaline phosphate are markers of bone

formation while pyridiniline crosslinks is a marker of bone resorption. All three

biochemical markers have been shown to be valid indicators of bone turnover and sensitive

to changes with exercise (Menkes et al., 1993, Thorsen et al., 1996). The samples were

collected before the test and repeated within 10 minutes following the conclusion of the

GXT.







38

The subject performed a walking SL-GXT using an incremental treadmill exercise

protocol (Naughton) to determine peak oxygen consumption (VOZp,). The initial

workload was 2.0 m.p.h. at 0% grade and was progressed every two minutes by

increasing the grade 3.5%. Once the test time reached 12 minutes, the treadmill speed

increased to 3.0 m.p.h. and the incline decreased to a 12% grade. From this point, the

grade again increased 3.5% every 2 minutes until the subject reached voluntary maximal

exertion or became symptomatic with positive hemodynamic or medical indices (3). The

following criteria recommended by the ACSM were used for termination of the SL-GXT

(3).

Fatigue

Failure of monitoring equipment

Light-headedness, confusion, ataxia, cyanosis, dyspnea, nausea or any peripheral

circulatory insufficiency

Onset of grade II/III angina pectoris (moderate to severe) with exercise

Mild angina pectoris with 2 mm of ST segment depression

Symptomatic supraventricular tachycardia

ST displacement 4 mm or greater in the absence of angina pectoris

Ventricular tachycardia (3 or more consecutive PVC's)

Exercise induced left bundle branch block

Onset of second and/or third degree A-V block

R on T PVC's (one)

Frequent multifocal PVC's (30% of the complexes)








Excessive hypotension (greater than 20mmhg drop in systolic BP during

exercise)

Excessive BP rise: systolic BP greater or equal to 240 or diastolic BP greater

or equal to 110 mm Hg)

Inappropriate bradycardia (drop in HR greater than 10 beats/min) with an

increase or no change in workload.

During the test, expired gases were collected through a low-resistance one-way

valve (Hans Rudolph). Breath by breath analysis of expired gases was performed

continuously throughout the test using a Medical Graphics Corporation Metabolic Cart

(CPS/Max Medical Graphics TM, St. Paul, MN). The oxygen and carbon dioxide

analyzers were calibrated daily and immediately before and after each test using a known

gas mixture of 12.0% 02 and 5% C02. Ventilatory responses (tidal volume and

frequency of breathing) were measured with a pneumotachograph. Volume calibration was

performed with a 3-liter calibration syringe. Twelve lead electrocardiograms (ECG) were

recorded throughout the test using standard lead placement with a Quinton Q 2000 system

(Quinton Instruments, Seattle, WA). Blood pressure measurements were taken every

other minute using a standard sphygmomanometer and RPE was obtained at the end of

each minute throughout the test using Borg's RPE 6-20 point scale.



Visit 3. Muscular Strength Assessment

During visit 3, dynamic muscular strength was measured using four resistance

exercises which included: chest press, leg press, leg curl, and biceps curl. For each

dynamic exercise, a one repetition maximum (1-RM) was determined. Participants were








properly positioned in the machine and performed a dynamic warm-up using a light

weight. The participant began the test by lifting a light weight and then incremental

increases of 5-10 pounds were made according to the difficulty with which the participant

executed the previous lift. Difficulty was measured by having the participant rate his/her

exertion level using the RPE scale. Two to three minutes rest were given between trials to

prevent premature fatigue. The investigator continued to increase the weight lifted until

reaching the maximum weight that could be lifted in one repetition. This was usually

determined in 5 to 6 trials. Maximal strength was defined as the maximum weight that

could be lifted through a full range of motion with proper form.



Visit 4. Muscular Endurance

During visit 4, assessment of muscular endurance was performed on the chest

press and leg press resistance machines. The participants were properly positioned in the

appropriate machine and allowed a dynamic warm-up with a light weight. The subject

then performed as many repetitions as possible with proper form using 60% of their

previously determined 1-RM. The endurance test for the leg press was always performed

first.



Visit 5: Bone Mineral Density

Bone mineral density (BMD) was assessed using dual energy x-ray absorptiometry

(DXA) (DXA model DPX-L, Lunar Radiation Corp., Madison, WI). DXA is a non-

invasive radiologic projection technique which uses both low and higher energy x-ray

tubes as an energy source. However, radiation exposure is minimal (approximately 1/60







41
of the dose of a chest x-ray). DXA also provides body composition information. During

a DXA scan, the subject was positioned either in a supine or lateral position while the x-

ray scanner performed a series of transverse scans, measured at 1-cm intervals from the

top to the bottom of the region. Four separate skeletal regions were scanned: 1)

anterior/posterior (AP) view of the total body; 2) AP view of the lumbar spine; 3) AP

view of the hips; and 4) lateral view of the lumbar spine.



Visit 6. Balance. Stair Climbing, and Isometric Lumbar Extension Strength

On visit 6, participants were assessed for time to walk up one flight of stairs, and

isolated lumbar extension strength. The participants were asked to walk up a flight of

stairs consisting of 23 steps as quickly as possible. The stairs were 6.5 in. high and 11.5

in. wide. After 14 steps the participants made a left-hand wrap-around turn and then

completed the remaining 9 steps. The participants were not allowed to use the handrails.

The time to complete this task was recorded to the nearest hundredth of a second using a

hand held stopwatch. Participants were required step on all of the steps, taking 2 steps at

a time was not allowed. This test was repeated following a 2-3 minute rest period and the

fastest of the two trials was used for data analysis.

Isometric lumbar extension strength was also tested. Prior to the test, participants

performed a series of stretching exercises and a dynamic variable resistance exercise

session designed to stretch and warm-up the low back, hamstrings, and abdominal areas.

For the dynamic exercise, participants were seated in the MedX isolated lumbar extension

machine (MedX, Ocala, FL) and secured in place by restraints positioned under the feet,

anterior thigh, and posterior pelvis. These restraints restrict movement of the pelvis,








which facilitates isolation of the lumbar extensor muscles. The participants then moved

from flexion to extension through a full range ROM. Men warmed-up with 40 pounds and

women with 20 pounds for 10 repetitions. This series of stretching and dynamic exercises

lasted approximately 10 minutes. Following the dynamic exercise session participants

completed an isometric test of lumbar extensor muscle strength. Seven testing points (0,

12, 24, 36, 48, 60, and 72 degrees of lumbar flexion) were measured for participants who

had a full range of lumbar motion. The specific angles were modified for those

participants with limited ROM. A maximum isometric contraction was generated at each

of these angles beginning with 72 of flexion. Participants were instructed to extend back

slowly building up tension over a 2 to 3 second period. Once maximal tension had been

developed, participants were encouraged to maintain maximal force for an additional 1 to

2 seconds, then slowly relax. Following each isometric contraction was a 10 second rest

period while the next position was set. In this manner a force curve was generated

throughout the ROM for each subject. Participants were given verbal encouragement

during the lifts to ensure a maximal effort.



Visit 7. Body Composition and Muscular Strenath Assessment

On visit 7, the participant had their body composition assessed using skinfolds and

1RM muscular strength was determined for the seated row, overhead press, triceps dip,

and knee extension. The procedure for 1RM determination was the same as for visit 3.

Skinfold measurements were taken to the nearest 0.5 mm on the right side of the body

using a Lange caliper (Cambridge Scientific Industries, Cambridge, MD). Seven sites were

measured: chest, axilla, triceps, subscapular, abdomen, suprailiac, and anterior thigh. The








landmarks and techniques of Pollock and Wilmore (35) were used for the skinfold

measurements:

Chest fold: The skinfold thickness of the chest was measured as an oblique fold one half

the distance between the anterior axillary line and the nipple for men and one third of the

distance from the anterior axillary line and the equivalent position for women.

Axilla fold: The axilla skinfold was measured as a vertical fold on the midaxillary line at

the level of the xiphoid process of the sternum.

Triceps fold: The triceps fold was measured as a vertical fold midway between the

olecranon and acromium process on the posterior of the brachium with the elbow relaxed

and extended.

Subscapular fold: The subscapular fold was taken on a diagonal line coming from the

vertebral border to 1-2 cm from the inferior angle of the scapula.

Abdominal fold: The subject stood erect with body weight evenly distributed on both feet.

The abdominal skinfold was measured as a vertical fold taken 2 cm lateral to and at the

level of the umbilicus.

Suprailiac fold: The suprailiac skinfold was measured from a diagonal fold at the anterior

axillary line immediately above the crest of the ilium.

Anterior thigh fold: A thigh skinfold was be taken with the subject standing with his/her

weight on the left foot, with a relaxed and slightly flexed right leg. The measurement was

made as a vertical fold located on the midline of the anterior aspect of the thigh midway

between the inguinal crease and the proximal border of the patella.








Training Period: Six Months of Dynamic Resistance Exercise

Participants in both the high- and low-intensity training groups were asked to

report to the CES three times per week for 6 months to perform dynamic variable

resistance exercise under the supervision of trained personnel for all machines except the

isolated lumbar extension exercise. Isolated lumbar extensions were performed once per

week under the supervision of personnel certified for the use ofMedX rehabilitation

equipment. Each subject received appropriate instruction concerning warm-up and cool-

down techniques, as well as how to monitor the intensity of the exercise using the RPE

scale. Each subject performed one set on each of the following resistance exercise

machines: abdominal crunch, leg press, leg extension, leg curl, calf press, seated row,

chest press, overhead press, biceps curl, seated dip, and lumbar extensions. There was a 2

minute rest period allowed between each machine. Each set consisted of 8 repetitions for

the HEX group and 13 repetitions for the LEX group at the appropriate resistance load.

To examine the effects of training intensity on the outcome variables and criterion

measures, the LEX group trained at an intensity equivalent to 50% of their IRM, while

the HEX group used loads corresponding 80% of their IRM. For the LEX and HEX

groups, the load was increased by 5% when their RPE rating dropped below 18. The

rationale for training the lumbar extensor muscles only one day per week is derived from

previous research in this lab showing that 1 set of this exercise once per week is adequate

for improvements in lumbar strength and that training more often does not provide

superior results. Prior to the dynamic exercise, participants performed the series of

stretches. Participants were then secured in the lumbar extension machine. Once secure

the subject was instructed to complete a warm-up set of dynamic variable resistance








lumbar extension exercise using 50 percent of their current training weight. Participants

began the dynamic exercise in the fully flexed position (72), extending their trunk back

against the back pad lifting the weightload over a 2-3 second count. After pausing briefly

in the fully extended position (0), the subject was instructed to slowly flex their trunk

forward to the starting position over a 4 second count. The combined movement of

extension, brief pause, and flexion constitutes one repetition. The HEX group performed

10 repetitions, while the LEX group performed 15 repetitions.



Biochemical Assays

Markers of Bone Metabolism

Alkaline Phosphatase-B

The bone-specific alkaline phosphatase isoform (BAP) was measured in serum

using an Alkphase-B(r) enzymatic immunoassay kit (EIA) (Metra Biosystems, Mountain

View, CA, USA). The assay is highly specific for BAP, cross-reacting <=8% with liver

AP and not significantly with other AP isoenzymes. The Alkphase-B kit or EIA used

microtiter stripwell format utilizing a monoclonal anti-BAP antibody and the catalytic

activity of the captured enzyme itself to measure BAP activity in serum. BAP in the

sample binds to antibody coated on the stripwell and the reaction is detected with the

substrate, p-nitrophenyl phosphate (pNPP). Color developed during the incubation of

captured BAP and substrate is measured at 405 nm in a microtiter plate reader. BAP

values of unknown specimens are calculated from a calibration curve fit with a quadratic

equation. Values are expressed in U/L; each unit represents one mole of pNPP








hydrolyzed per minute at 250C in 2-amino-2-methyl-l-propanol buffer. 20 pL of serum

per well (assayed in duplicate) was required for determination of BAP.



Osteocalcin

Osteocalcin (OC) also known as bone gla protein was measured with a

NovoCalcin(r) EIA kit (Metra Biosystems, Mountain View, CA, USA), a microtiter

stripwell format utilizing a murine monoclonal anti-OC antibody.[4] OC in the sample

competes for antibody binding sites with OC coated on the stripwell. A rabbit anti-mouse

IgG antibody conjugated to alkaline phosphatase is added and the reaction is detected with

the substrate, p-nitrophenyl phosphate. Color developed during the incubation of

captured enzyme conjugate and substrate is measured at 405 nm in a microtiter plate

reader. OC values of unknown specimens are calculated from a calibration curve fit with a

4-parameter logistic equation. Values are expressed in ng/mL. 25 pL of serum per well

(assayed in duplicate) is required for determination of OC.



Pyridinoline Crosslinks

Serum pyridinoline crosslinks were measured with Serum Pyd(r) EIA kit

purchased from Metra Biosystems (Mountain View, CA, USA). The EIA kit uses a

microtiter stripwell format utilizing a rabbit monoclonal anti-PYD antibody. PYD in the

sample competes for antibody binding sites with PYD coated on the stripwell. A goat

anti-rabbit IgG antibody conjugated to alkaline phosphatase is added and the reaction is

detected with the substrate, p-nitrophenyl phosphate. Color developed during the

incubation of captured enzyme conjugate and substrate is measured at 405 nm in a









microtiter plate reader. PYD values of unknown specimens are calculated from a

calibration curve fit with a 4-parameter logistic equation. Values are expressed in nmol/L.

25 pL of serum per well (assayed in duplicate) is required for determination of serum

PYD.



Biochemical Indicators of Oxidative Stress

Lipid Peroxidation Measurements

Malondialdehyde levels were determined spectrophotometrically using the

thiobarbituric acid-reactive substances (TBARS) method previously described (Uchiyama

and Mihara, 1978). The agent 1,1,3,3-tetraethoxypropane was used as the standard for

this assay. Samples were performed in duplicate.

Lipid hydroperoxides were quantified using the ferrous oxidation/xylenol orange

technique previously reported (Hermes-Lima et al. 1995). Cumene hydroperoxide was

used as the standard for this assay. All samples were performed in triplicate. In our

laboratory, the coefficients of variation for the TBARS and lipid hydroperoxide assays are

~3 and 4 percent, respectively.



Oxidative Challenges in vitro

To investigate the relationship between obesity and myocardial antioxidant

capacity, the serum was subjected to a series of several different ROS-generating systems.

Serum aliquots were incubated at a concentration of 7 mg protein/ml in the presence of an

ROS generating system. Following each challenge, the aliquots were analyzed for lipid

peroxidation using the technique of Uchiyama and Mihara (1978).










Xanthine-Xanthine Oxidase System (Superoxide Generator).

Superoxide radicals were generated by the reactions involved in a xanthine-

xanthine oxidase system similar to the technique described by Reid et al. (1992). One ml

of 1 mM xanthine and 0.1 IU xanthine oxidase were added to a 1 ml aliquot of serum and

incubated at 37C for 15 min.



Hydrogen Peroxide System

One ml of hydrogen peroxide (100 mM) was added directly to a one ml aliquot of

serum and incubated at 37C for 15 min according to the method of Scott et al. (1987).



Ferric Chloride System (Hydroxyl Generator)

Hydroxyl radicals were produced in the serum by adding 0.1 mM ferric chloride

(FeCI3). The choice of these particular concentrations is based on the work ofBernier et

al. (1986).



Statistical Analyses

Statistical analyses were performed using the Statistical Package for the Social

Sciences (SPSS) software (version 9.0). Experimental analysis was performed with a3 x 2

repeated-measures analysis of variance (ANOVA) model to determine differences within

and between groups over time. If a significant (group x time) interaction was found, the

appropriate post-hoc procedures were applied. The post-hoc procedure used for this

investigation was a one-way ANOVA with a Scheff6 post-hoc test to determine if and







49

where there was a difference between the group means. Although no statistical differences

were observed between groups at study entry, an analysis of covariance (ANCOVA) was

performed on outcome variables at conclusion of the study. When the ANCOVA revealed

that the covariate significantly contributed to the outcome, then the predicted means

generated by the ANCOVA were analyzed with a one-way ANOVA and a Scheff6 post-

hoc test. Pearson bivariate correlations were performed to examine the degree of

association between variables. A-priori alpha levels were set at 0.05.














CHAPTER 4
RESULTS


Throughout the results section PRE will refer to testing completed prior to the six

month training or control period, and POST will refer to testing completed after the six

month training or control period. In all tables and figures, the values presented are means

plus and minus standard deviation. At study entry, there were no significant differences

between any of the experimental groups. As a further precaution against the influence of

any pre-training differences, ANCOVAs were performed on all outcome variables.



Subject Characteristics


The characteristics for the participants in this study are presented in Table 4.1.

The groups did not significantly differ with respect to any of the variables listed (p>0.05).

Correlation between pre-training percent body fat measured by skinfold and DXA was

0.86 (p<0.01) with no significant difference between methods. Correlation between post-

training percent body fat measured by skinfold and DXA was 0.91 (p<0.01) with no

significant difference between methods.









Table 4.1. Subject Characteristics


VARIABLES CON (n=16) LEX (n=24) HEX (n=22)


PRE POST PRE POST PRE POST

AGE
AGE 71.04.7 67.66.3 66.66.7
(yrs.)

HEIGHT
169.910 167.211.5 167.19.7
(cm)

WEIGHT
WEHT 73.113.8 71.014.3 77.419.3 74.416.5 74.114.8 74.815
(kg)

SKINFOLD
SKFATLD 30.37.5 28.97.4 30.96.0 29.05.1 32.07.8 29.97.8
O/oFAT

DXA %FAT
33.57.4 34.47.2 34.18.9 34.18.4 35.98.6 36.29.0


FAT FREE
FAT FREE 46.510.5 46.010.6 50.514.6 48.713.3 47.712 47.912
MASS (kg)
Values are mean SD. CON = control group, LEX = low-intensity group, HEX = high-
intensity group. DXA = dual energy x-ray absorptiometry









Aerobic Endurance

Oxygen Consumption

Values for peak oxygen consumption (VOg) are presented in Table 4.2. The

absolute and percent changes for V04. are shown in Figures 1 and 2, respectively. As

shown in Figure 1, both the LEX and HEX groups significantly increased VOpc during

the six months of resistance exercise (p<0.05). However, the CON group did not change

during the control period. Peak oxygen consumption increased 23.5% and 20.1% for the

LEX and HEX groups, respectively (Figure2.), which was significantly greater than the

percent change for the CON group (p<0.05).



Treadmill Time to Exhaustion

Treadmill time to exhaustion during the graded exercise test is presented in Table

4.2 and figures 3 and 4. The CON, LEX, and HEX groups increased treadmill time by

6.2%, 26.4% and 23.3%, respectively. However, only the LEX and HEX groups

significantly increased their treadmill time from PRE to POST (p<0.05).



Time to Ascend One Flight of Stairs

The stairs used for this test consisted of 22 steps which had to be completed by

touching every step and not holding the railing. Climb data can be found in Table 4.4, and

Figures 4 and 5. Both the LEX and HEX groups significantly decreased the time

necessary to ascend one flight of stairs following training (p<0.05). The LEX and HEX

groups decreased stair time by 7.3 and 5.8 percent, respectively. However, only the







53

Table 4.2. Comparison of Peak Oxygen Consumption and Treadmill Time to Exhaustion
br the CONIEXand HEX groups Daring a Graded Exercise Test


Values are mean & SD. *p<0.05 vs PR
'
E, *p<0.05 vs CON. +p<0.05 vs. CON (ANCOVA)
CON= control group, LEX = low-intensity group, HEX = high-intensity group. TREADMILL =
treadmill time to exhaustion during GXT.


VARIABLES CON LEX HEX


PRE POST PRE POST PRE POST


(m.kg".lmin) 22.63.4 22.43.4 20.243 24.74.8* 20.96.1 24.45.8*

V02.k
(O ) -0.412.0 23.514.1** 20.123.7"*

T L 11.52.5 12.112.5 11.212.3 14.03.1 12.23.4 15.04.9*+
(n)114 26.43.7 23.33.1
S 1U ~ 6.211.4 26.423.7-* 23.323.1









percent change from pre- to post-training in the LEX group was significantly different

than the CON group (p<0.05).



Changes in Muscular Strength

Chest Press

Muscular strength were determined by determining the maximum amount of

weight that could be lifted for one repetition with good form (lRM). Chest press strength

adaptations to the six months of training are displayed in Table 4.3. The absolute IRM

values, 1RM normalized for fat free mass (relative), and percent changes in IRM strength

from pre- to post-training are shown in Figures 7, 8, and 9, respectively. Both the LEX

and HEX groups, but not CON, increased absolute and relative IRM strength significantly

from pre- to post-training (p<0.05).



Leg Press

Leg press strength adaptations to the six months of training are displayed in Table

4.3 and Figures 10, 11, and 12. Both the LEX and HEX groups, but not CON, increased

absolute and relative IRM strength significantly from PRE to POST-training (p<0.05).



Leg Curl

Leg curl strength adaptations to the six months of training are displayed in Table

4.3 and Figures 13, 14 and 15. Both the LEX and HEX groups, but not CON, increased

absolute and relative IRM strength significantly from pre- to post-training (p<0.05).









Biceps Curl

Biceps curl strength adaptations to the six months of training are displayed in

Table 4.3 and Figures 16, 17, and 18. Both the LEX and HEX groups, but not CON,

increased absolute and relative 1RM strength significantly from pre- to post-training

(p<0.05).



Seated Row

Seated row strength adaptations to the six months of training are displayed in

Table 4.3 and Figures 19, 20, and 21. Both the LEX and HEX groups, but not CON,

increased absolute and relative IRM strength significantly from pre- to post-training

(p<0.05).



Overhead Press

Overhead press strength adaptations to the six months of training are displayed in

Table 4.3 and Figures 22, 23, and 24. Both the LEX and HEX groups increased absolute

and relative IRM strength significantly from pre- to post-training (p<0.05).



Triceps Dip

Triceps dip strength adaptations to the six months of training are displayed in

Table 4.3 and Figures 25, 26, and 27. Both the LEX and HEX groups, but not CON,

increased absolute and relative 1RM strength significantly from pre- to post-training

(p<0.05).










Table 4.3. Comparison of Changes in Muscular Strength for the CON, LEX, and HEX
Groups Following Six Months of Resistance Training.
CON LEX HEX
PRE POST PRE POST PRE POST
CP IRM 191.792.3 184.990.0 223.7116.2 258.8129.8*+ 254.3141 287.7157.3*+
CPREL 4.11.1 3.91.2 4.11.4 4.91.3* 5.01.6 5.61.7* **+
CP%A -1.219.9 17.513.5"* 16.016.6**
LP IRM 329.178.4 329.282.3 401.0120.1 469.1158.6* **+ 375.4171 469.1196.6"
LPREL 7.01.1 7.22.2 7.92.2 9.32.0*" + 7.71.7 9.72.3 **+
LP %A 1.522.3 15.715.9 27.618.3"*
LC IRM 180.355.2 179.259.2 174.559.4 217.173.8* 209.583.4 246.8108.7*
LC REL 3.810.6 3.80.7 3.50.7 4.4.4+ 4.31 5.01l.1 +
LC %A -0.710 25.313.4** 17.39.5"*
BC IRM 113.848.3 107.1144.6 118.449.8 138.858.2* 114.444.9 143.965.8*
BC REL 2.30.7 2.30.6 2.20.6 2.70.5* 2.40.5 3.00.7* **+
BC %A -3.816.2 17.89.8** 24.614.3"*
SR IRM 252.692.9 268.0101.4 318.9125.5 276.2136.9*+ 228.8109 376.5140*+
SRREL 5.4l1.0 5.81.1 591.3 7.21.10 **+ 6.31.0 7.61.2" **+
SR%A 6.516.4 19.211.4"* 22.115.9**
OP IRM 176.173.9 169.578.5 215.398.4 251.6110.6* 220.5113 257.1135.4*
OPREL 3.71.0 3.61.1 3.91.1 4.81.0*+ 4.51.3 5.21.5* "+
OP %A -3.618.0 18.811.7** 16.610.0"
TD IRM 219.869.4 217.767.7 263.295.7 310.5111" + 265.299.9 307.9123 **
TDREL 4.70.6 4.80.6 4.80.9 5.90.8* **+ 5.41.0 6.21.2* **+
TD%A -0.75.8 18.59** 16.110.0"*
LE IRM 234.0175.4 222.974.7 276.2102 305.6114* 298.1123 347.1167"
LE REL 5.01.0 4.90.9 5.31.0 5.81.0* 5.91.3 6.8.91 **+
LE4%A -4.68 10.87.3** 14.611.8"*
TS IRM 1697537 1678535 1719696 2029818* 1909850 22631078*
TS REL 36.04.4 36.06.6 32.29.2 38.58.8* 38.58.9 45.312.0"+
TS %A -1.16.3 17.29.7"* 17.87.8"*
Values are mean SD. *p<0.05 vs PRE, **p<0.05 vs CON. +p<0.05 vs CON (ANCOVA)CON
= control group, LEX = low-intensity group, HEX = high-intensity group. CP = chest press, LP =
leg press, LC = leg curl, BC = biceps curl, SR= seated row, OP = overhead press, TD = triceps
dip, LE = leg extension. TS = total strength. IRM= one repetition maximum. REL = relative
change (Nm/kg FFM), %A = percent change from PRE to POST.









Leg Extension

Leg extension strength adaptations to the six months of training are displayed in

Table 4.3 and Figures 28, 29, and 30. Both the LEX and HEX groups, but not CON,

increased absolute 1RM strength significantly from pre- to post-training (p<0.05).



Total Strength

The result for total strength was computed by summing the 1RM values for the

chest press, leg press, leg curl, biceps curl, seated row, overhead press, triceps dip, and leg

extension. The means and standard deviations for total strength for each of the three

experimental groups can be found in Table 4.3. The results for total strength expressed in

absolute numbers (Nm), relative to fat free mass (Nm/kg FFM), and as percent change

from pre- to post-training are shown in Figures 31, 32, and 33, respectively. Both the

LEX and HEX groups, but not CON, significantly increased absolute and relative force

output from pre to post-training (p<0.05).



Muscular Endurance

Chest Press

Chest press endurance data can be found in Table 4.4. The results for number of

repetitions and percent change from pre- to post-training for chest press endurance are

shown in Figures 34 and 35, respectively. Both the LEX and HEX groups, but not CON,

significantly increased the number of repetitions performed from pre- to post-training

(p<0.05).










Leg Press

Leg press endurance data can be found in Table 4.4. The results for number of

repetitions and percent change from pre- to post-training for chest press endurance are

shown in Figures 36 and 37, respectively. Both the LEX and HEX groups, but not CON,

significantly increased the number of repetitions performed from pre- to post-training

(p<0.05).


Table 4.4. Comparison of Stair Climbing Time, Chest Press and Leg Press Endurance for
the CON LEX, and HEX Groups Following Six Months of Resistance Training

CON LEX HEX


PRE POST PRE POST PRE POST


STAIRS (s) 9.11.2 9.01.0 9.41.7 8.691.4* 8.231.8 7.771.7+


STAIRS
S -0.5816.7 -7.316.4* -5.797.56
OKA


CHET 17.65.8 16.95.3 16.94.5 28.67.6* **+ 17.18.7 27.412 **+
(reps)

CHEST
CHEST -0.0532 75.547.4** 68.035.2**



LEG(reps) 32.216.3 29.418 26.39.4 45.020*+ 25.113.4 48.324.5*+


LEG %A -5.043.7 79.210.6" 10594.3**

Values are mean SD. *p<0.05 vs PRE, **p<0.05 vs CON. +p<0.05 vs CON (ANCOVA)
CON = control group, LEX = low-intensity group, HEX = high-intensity group. STAIRS = time to
ascend one flight of stairs. CHEST = chest press endurance. LEG = leg press endurance.









Lumbar Extension Strength

Lumbar extension strength was measured isometrically at 7 different angles of

lumbar flexion and is expressed in Newton meters (Nm). The seven angles used for this

test were 0, 12, 24, 36, 48, 60, and 72 degrees of lumbar flexion.



0 of Lumbar Flexion

Lumbar extension strength values at 00 of lumbar flexion can be found in Table 4.5

and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly

increased both absolute and relative force output from pre- to post-training (p<0.05).



12 of Lumbar Flexion

Lumbar extension strength values at 12* of lumbar flexion can be found in Table

4.5 and Figures 38, 39, and 40. Both the LEX and HEX groups, but not CON,

significantly increased both absolute and relative force output from pre- to post-training

(p<0.05).



24 of Lumbar Flexion

Lumbar extension strength values at 24' of lumbar flexion can be found in Table

4.5 and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON,

significantly increased both absolute and relative force output from pre- to post-training

(p<0.05).








360 of Lumbar Flexion

Lumbar extension strength data at 360 of lumbar flexion can be found in Table 4.5

and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly

increased both absolute and relative force output from pre- to post-training (p<0.05).



48 of Lumbar Flexion

Lumbar extension strength data at 480 of lumbar flexion can be found in Table 4.5

and Figures 38, 39, and 40. Both the LEX and HEX groups, but not CON, significantly

increased both absolute and relative force output from pre- to post-training (p<0.05).



600 of Lumbar Flexion

Lumbar extension strength data at 60* of lumbar flexion can be found in Table 4.5

and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly

increased both absolute and relative force output from pre- to post-training (p<0.05).



72' of Lumbar Flexion

Lumbar extension strength data at 720 of lumbar flexion can be found in Table 4.5

and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly

increased both absolute and relative force output from pre to post-training (p<0.05).








61

Table 4.5. Comparison of Changes in Lumbar Extension Strength for the CON, LEX, and
HEX Groups Following Six Month of Resistance Training.
ANGLES CON LEX HEX

PRE POST PRE POST PRE POST
O0ABS 137t76 104191 10369 16575* 9374 172107'

0OREL 2.61.11 1.841.3 2.21.6 3.61.2'**+ 1.81.1 3.41.31-*+

0'%A -33.339 141.4A184" 130.3114"*

12ABS 185183 1601102 13571 20779* 138106 229118*

12"REL 3.71 3.11.3 2.71.4 4.41.2*+ 2.71.5 4.61.4* *+

12'%A -13.940 8787"* 1121110"*

24'ABS 217104 19188 14685 23884* 187115 254125*

240 REL 4.31.1 3.81 2.91.6 5.01.0" *+ 3.81.6 521.3 **+

24% A -10124 136213" 5766

36'ABS 235108 2181104 175102 25994* 207114 270125*

36 REL 4.61.1 4.31.1 3.41.6 5.31.0*+ 4.21.5 5.51.3 **+

36% A -5.8120 76.564*" 40.432**

48'ABS 237100 226107 201103 27492* 233134 273134*

48 REL 4.71 4.51.1 3.71.5 5.510.8*+ 4.71.7 5.51.4"+

48'%A -5.716 5341** 2734

60'ABS 240184 259113 20199 26787* 249t138 278134*

60* REL 4.810.9 5.21.2 3.911.5 5.60.8* 5.11.6 5.71.3*

60 % A 7.019 4837"* 18122

72'ABS 24175 249196 19789 26283* 254125 289138*

72'REL 4.911.9 5.12.4 4.21.7 5.71.0* 5.31.3 6.01.2'

72% A -7.1140 45.3138"* 1717

TSLB ABS 1342400 1245550 1100494 16131495' 1364796 1772887*

TSLB REL 28.214.7 25.816.3 22.39.2 34.36.3*+ 27.59.7 35.98.8' **+

TSLB% A -8.0123 62.644"* 39.530.3**
Values are mean SD. *p<0.05 vs PRE, **p<0.05 vs CON. tp<0.05 vs HEX. +p<0.05 vs. CON
(ANCOVA). CON = control group, LEX = low-intensity group, HEX = high-intensity group.
TSLB = total lumbar strength. REL = relative change (Nm/kg FFM), %A = percent change from
PRE to POST. ABS= absolute value (Nm)








Total Lumbar Extension Strength

The result for total lumbar extension strength was computed by summing the peak

force generated for each of the seven angles tested. Total lumbar strength data for each of

the three experimental groups can be found in Table 4.5 and Figures 41, 42, and 43. Both

the LEX and HEX groups, but not CON, significantly increased absolute and relative

force output from pre to post-training (p<0.05).



Bone Mineral Density

Total Body Bone Mineral Density

The means and standard deviations for total body bone mineral density (BMD) are

shown in Table 4.6. The results for absolute BMD and percent change from pre to post-

training can be found in Figures 44 and 45, respectively. There were no significant

differences either between groups or from pre to post-training (p>0.05).



Femoral Neck Bone Mineral Density

Femoral neck bone mineral density data are shown in Table 4.6 and Figures 46 and

47. The HEX group significantly increased BMD of the Femur Neck from pre to post-

training (p<0.05).



Anterior/Posterior Lumbar Spine Bone Mineral Density

The means and standard deviations for anterior/posterior (AP) lumbar spine bone

mineral density are shown in Table 4.6 and Figures 48 and 49. There were no significant








differences between groups at study entry and AP BMD did not change (p>0.05) after 6

months of training or control period.



Lateral Lumbar Spine Bone Mineral Density

Lateral lumbar spine bone mineral density data are shown in Table 4.6 and Figures

50 and 51. There were no significant differences between groups at study entry and lateral

lumbar spine BMD did not change (p>0.05) after 6 months of training or control period.



Ward's Triangle Bone Mineral Density

Ward's triangle bone mineral density data are shown in Table 4.6 and Figures 52

and 53. There were no significant differences between groups at study entry and Ward's

triangle BMD did not change (p>0.05) after 6 months of training or control period.



Correlations Between Physiological Performance Variables and Muscular Strength

Correlation coefficients relating VO2p, stair climbing time (STAIRS), and

treadmill time to exhaustion (TREADMILL) to leg press 1RM (LP 1RM), leg press

endurance (LP END), leg curl 1RM (LC IRM), leg extension (LE IRM), total strength

(TOTAL STR.), and training volume (TRAINING VOL) can be found in Tables 4.7 and

4.8. Training volume was calculated by multiplying the training weights for each of the

exercises performed on the last day of training times the number of repetitions performed.










The correlation coefficients for absolute and percent changes in VOP,

to changes in muscular strength and endurance can be found in Tables 4.7 and 4.8,

respectively. As shown in Table 4.7, absolute VO4,pk is significantly correlated (p<0.05)

to all muscular strength variables listed except for LP END (p<0.05). This indicates that

resistance training is related to, and can lead to increases in VOp The results from

Table 4.8 show that percent changes in muscular strength are not related to percent

changes in VO. This indicates that the magnitude of change for the two variables may

not be related. In other words, a 25% increase in leg press 1RM may not correspond to a

25% increase in VO However, it is important to note that increased strength is

associated with increased aerobic capacity.



Treadmill Time to Exhaustion

The correlation coefficients for absolute and percent changes in treadmill time to

exhaustion during the GXT and changes in muscular strength and endurance can be found

in Tables 4.7 and 4.8, respectively. As shown in Table 4.7, absolute TREADMILL is

significantly (p<0.05) correlated to all muscular strength variables except for LP IRM and

TRAINING VOL. (p<0.05). These results indicate that resistance training can increase

TREADMILL during a GXT in the absence of endurance training. It is interesting to

notethat LE was the most highly correlated strength variable to treadmill time, while LP

IRM was not significantly correlated at all, even though both are quadriceps exercises.









Table 4.6. Changes in Bone Mineral Density for the CON, LEX, and HEX Groups
Following Six Months of Resistance Training or Control Period.

SITE CON LEX HEX

PRE POST PRE POST PRE POST

TOTAL BMD
(g/cm2) 1.1960.1 1.1870.1 1.1950.1 1.1890.1 1.1920.1 1.1820.1

TOTAL %A -0.731.9 -0.422.1 -0.211.6

FEMNK
(g/cm2) 0.8630.1 0.8480.1 0.8930.2 0.90.18 0.8520.1 0.8690.1*

FEMNK/%A -1.594.89 0.685.57 1.963.33

APSPINE
(g/cm2) 1.2280.2 1.2220.2 1.1860.2 1.1820.2 1.1970.2 1.1880.2

APSPINE %A -.02514.1 -0.4643 -0.9583.5

LTSPN
(g/cm2) 0.6450.2 0.6510.2 0.7150.3 0.720.2 0.6940.3 0.6740.2
LATSPINE
%A*& 0.64413.1 3.2216.91.11715.6
%Ao 1.11715.6
WARD'S
(g/cm2) 0.690.1 0.6760.2 0.7430.2 0.7330.2 0.6770.1 0.6760.1

WARD'S %A -1.948.3 -0.746.4 -0.176.7


vuaues are mean i a. "p group, HEX = high-intensity group. TOTAL = total body. FEMNK = femoral neck.
APSPINE = anterior/posterior spine. LTSPN = lateral spine. WARD'S = Ward's triangle.
%A = percent change from PRE to POST.









Table 4.7. Correlations Between Absolute VOa.k, Treadmill Time, and Stair Time and
Select Strength Measures. r Values are Shown Followed by Significance Value in
Parentheses


VO .k

STAIRS

TREADMILL

LP IRM

LP END

LC 1RM

LE IRM

TOTAL STR.

TRAINING VOL.


VO2,

1.0 (0.00)**

-0.53(0.00)**

0.72(0.00)*

0.45(0.00)**

0.03(0.85)

0.42(0.01)**

0.54(0.00)**

0.40(0.01)**

0.46(0.01)**


STAIRS

-0.53(0.00)**

1.0 (0.00)**

-0.34(0.02)*

-0.73(0.00)**

-0.09(0.6)

-0.67(0.00)**

-0.78(0.00)**

-0.64(0.00)**

-0.54(0.00)**


TREADMILL

0.72(0.00)*

-0.34(0.02)*

1.0 (0.00)**

0.28(0.07)

0.37(0.014)*

0.29(0.054)

0.43(0.01)**

0.31(0.04)*

0.24(0.19)


* correlation significant at p<0.05, **correlation significant at p<0.01. VO k = maximal
oxygen consumption during graded exercise test (GXT). TREADMILL = time to
exhaustion during GXT. STAIRS = time to ascend one flight of stairs. LP 1RM = leg
press 1RM. LP END = leg press endurance. LC IRM = leg curl IRM. LE 1RM = leg
extension 1RM. TOTAL STR. = total strength. TRAINING VOL. = training volume.


--








Table 4.8. Correlations Between Percent Changes in VO k, Treadmill Time, and Stair
Time and Select Strength Measures. r Values are Shown Followed by Significance Value
in Parentheses
VOp STAIRS TREADMILL

VO., 1.0 (0.00)** -0.19(0.22) 0.26(0.09)

STAIRS -0.19(0.22) 1.0 (0.00)** -0.17(0.24)

TREADMILL 0.26(0.09) -0.17(0.24) 1.0 (0.00)**

LP IRM 0.21(0.20) -0.20(0.18) 0.01(0.93)

LPEND 0.13(0.41) -0.31(0.03)* 0.25(0.11)

LC IRM 0.36(0.02)* -0.21(0.15) 0.21(0.17)

LE IRM 0.06(0.72) -0.54(0.00)** 0.25(0.12)

TOTAL STR. 0.23(0.14) -0.40(0.00)** 0.17(0.25)
* correlation significant at p<0.05, **correlation significant at p<0.01. VOzp* = maximal
oxygen consumption during graded exercise test (GXT). TREADMILL = time to
exhaustion during GXT. STAIRS = time to ascend one flight of stairs. LP 1RM = leg
press 1RM. LP END = leg press endurance. LC IRM = leg curl 1RM. LE 1RM = leg
extension IRM. TOTAL STR. = total strength.








Stair Climbing Time

The correlation coefficients for absolute and percent changes in STAIRS to

changes in muscular strength and endurance can be found in Tables 4.7 and 4.8,

respectively. As shown in Table 4.7, absolute STAIRS is significantly (p<0.05) correlated

to all strength variables except for LP END (p>0.05). The correlations are negative

values indicating an inverse correlation. This indicates that as muscular strength increases,

the time necessary to ascend one flight of stairs decreases. STAIRS was also significantly

correlated to the other physiological performance variables of TREADMILL and VO*.k.

Percent change in STAIRS.is significantly (p<0.05) correlated to all muscular strength

variables except for LC IRM (p>0.05). These correlations are also inverse indicators that

the percent increase in muscular strength and endurance is related to a percent decrease in

stair climbing time.



Correlations Between Physiological Performance Variables and Bone Mineral Density

Correlation coefficients relating total body (TOTAL), femoral neck (FEMNK),

Ward's triangle (WARD'S), anterior/posterior lumbar spine (AP SPINE), and lateral

lumbar spine (LAT SPINE) to leg press IRM (LP IRM), overhead press (OP IRM), total

strength (TOTAL STR.), and total lumbar extension strength (TOTAL LMB) can be

found in Tables 4.9 and 4.10.



Total Body

The correlation coefficients for absolute and percent changes in TOTAL to

changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As shown









in Table 4.9, absolute TOTAL was significantly (p<0.05) correlated to all strength

variables. This indicates that greater muscular strength is associated with greater TOTAL

bone mineral density.



Femoral Neck

The correlation coefficients for absolute and percent changes in FEMNK

to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As

shown in Table 4.9, absolute FEMNK was significantly (p<0.05) correlated to all strength

variables except TOTAL LMB. The lack of a correlation between TOTAL LMB and

FEMNK was not surprising because the MedX lumbar extension machine is designed to

isolate the lumbar spine and not involve any other musculature.



Ward's Triangle

The correlation coefficients for absolute and percent changes in WARD'S

to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As

shown in Table 4.9, absolute WARD'S was not significantly correlated to any of the

strength variables (p>0.05). This indicates that greater muscular strength is not associated

with greater WARD'S bone mineral density.



Anterior/Posterior Lumbar Spine

The correlation coefficients for absolute and percent changes in AP SPINE

to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As

shown in Table 4.9, absolute AP SPINE was significantly (p<0.05) correlated to all







70
strength variables. This indicates that greater muscular strength is associated with greater

AP SPINE bone mineral density,



Lateral Lumbar Spine

The correlation coefficients for absolute and percent changes in LAT SPINE

to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As

shown in Table 4.9, absolute LAT SPINE was significantly (p<0.05) correlated to all

strength variables. This indicates that greater muscular strength is associated with greater

LAT SPINE bone mineral density.





Table 4.9. Correlations Between Absolute Changes in Bone Mineral Density and Select
Strength Measures. r Values are Shown Followed by Significance Value in Parentheses

SITE TOTAL STR TOTAL LMB LP 1RM OP 1RM

TOTAL 0.58(0.00)** 0.48(0.00)** 0.60(0.00)** 0.57(0.00)**

FEMNK 0.29(0.04)* 0.18(0.28) 0.29(0.05)* 0.30(0.03)*

WARD'S .07(0.61) 0.05(0.78) 0.22(0.13) 0.16(0.26)

AP SPINE 0.38(0.01)** 0.33(0.05)* 0.43(0.00)** 0.41(0.00)**

LAT SPINE 0.60(0.00)** 0.44(0.01)** 0.61(0.00)** 0.63(0.00)**
* correlation significant at p<0.05, **correlation significant at p<0.01. LP IRM = leg
press IRM. OP IRM = overhead press IRM. TOTAL LMB = total lumbar strength.
TOTAL STR. = total strength. TOTAL = total body. FEMNK = femoral neck.
WARD'S = Ward's triangle. AP SPINE = anterior/posterior spine. LAT SPINE = lateral
spine.









Biochemical Analyses


TBARS

Thiobarbituric acid-reactive substances (TBARS) data are shown in Table 4.11.

The results for absolute TBARS and percent change from pre to post-training can be

found in Figures 62 and 63, respectively. The level of peak exercise TBARS, and

therefore lipid peroxidation was lower in the LEX group compared to the CON group

following the post-training GXT (p<0.05). Also, the percent change from pre- to post-

GXT for the LEX group following the training period was significantly lower than those

of the HEX and CON groups (p<0.05). These results suggest that the exercise training

imparted some measure of protection from oxidative stress on the people in the LEX

group. The results for the in vitro oxidative stress challenges are presented in Table 4.11.

The results indicate that the post-training FeCI3 TBARS response of the HEX group was

significantly greater than those of the LEX and CON groups (p<0.05). However, the

TBARS response following the H202 challenge was lower for the LEX group compared

to the CON group (p<0.05).



Lipid Hydroperoxides

Lipid hydroperoxides values can be found in Table 4.11. The results for lipid

hydroperoxides are shown in figure 64. All groups (CON,LEX, HEX) significantly

increased lipid hydroperoxide levels at peak exercise at study entry (p<0.05). Following

the training or control period, only the CON group showed a significant increase in lipid

hydroperoxides and the the levels for the LEX and HEX groups were significantly lower








than that of the CON group (p<0.05). The percent increase in lipid hydroperoxides

immediately following the post-training GXT was significantly lower for the LEX group

compared to the CON and HEX groups (p<0.05).



Serum Osteocalcin

Serum osteocalcin values are shown in Table 4.12 and Figures 65 and 66. Both the

LEX and HEX groups, but not CON, significantly increased osteocalcin levels from pre to

post-training (p<0.05).



Serum Bone-Specific Alkaline Phosphatase

Serum bone-specific alkaline phosphatase (BAP) data are shown in Table 4.12 and

Figures 67 and 68. The HEX group significantly increased BAP levels from pre to post-

training (p<0.05).



Serum Pyridinoline Crosslinks

Serum pyridinoline crosslinks (PYD) values are shown in Table 4.12 and Figures 69

and 70. None of the groups significantly changed PYD from pre- to post-training

(p






73
Table 4.10. Correlations Between Percent Changes in Bone Mineral Density and Select
Strength Measures. r Values are Shown Followed by Significance Value in Parentheses

SITE TOTAL STR TOTAL LMB LP 1RM OP IRM

TOTAL 0.13(0.36) 0.04(0.81) -0.11(0.45) 0.04(0.80)

FEMNK 0.33(0.02)* -0.09(0.61) 0.25(0.09) 0.23(0.11)

WARD'S 0.15(0.28) 0.28(0.09) 0.01(0.94) 0.18(0.22)

AP SPINE 0.01(0.94)** 0.13(0.45) -0.11(0.47) -0.02(0.87)

LAT SPINE 0.10(0.48) 0.31(0.06) 0.18(0.23) 0.15(0.29)

* correlation significant at p<0.05, **correlation significant at p<0.01. LP IRM = leg
press IRM. OP 1RM = overhead press 1RM. TOTAL LMB = total lumbar strength.
TOTAL STR. = total strength. TOTAL = total body. FEMNK = femoral neck.
WARD'S = Ward's triangle. AP SPINE = anterior/posterior spine. LAT SPINE = lateral
spine.










Table 4.11. Comparison of Changes in Markers of Oxidative Stress for the CON, LEX,
and HEX Groups Following Six Months of Resistance Trainin.
MARKER CON LEX HEX

PRE POST PRE POST PRE POST
TBARS
PRE-XT 0.2340.05 0.2220.05 0.2110.04 0.2070.03 0.240.0.07 0.2110.03
(nmol/mln

%A -4.8511.2 -0.1216.1 -7.8121.6

TBARS
POST- 0.2510.06 0.2540.07 0.2220.06 0.2100.04"* 0.2850.12 0.231t06


%A 1.8511.5 -2.5217.1 -11.628.2

%A PRE-/
POST- 7.116.4 15.924.8 5.113.7 2.414.4"* 20.3141.5 9.9121.8
GXT
3 0.2830.04 0.2790.05 0.2910.06 0.2880.05 0.3170.04 0.340.04**

XO
S 0.2250.06 0.2590.11 0.2530.11 0.2660.11 0.2710.12 0.2350.04
(nmo-ml)
H202
o2 0.5540.36 0.7110.37 0.4330.28 0.4690.25** 0.5790.46 0.678i0.37
(nmolml)
LPD-HPX
L 2.330.62 2.520.56 2.770.78 2.550.72 2.260.64 2.32i0.60"*


%A 12.830.3 -1.9138.8 2.8340.4

LPD-HPX
POST- 2.911.16* 3.410.51* 3.300.90* 2.920.76"* 3.020.77 2.870.5**
GXT
%A PRE-/
POST- 22.517.0 39.227.1 20.421.0 16.918.9**l 34.240.4 33.430.1
GXTI III


Values are mean SD. *p<0.05 vs PRE-GXT. **p<0.05 vs. CON (ANCOVA). :p<0.05
HEX vs. LEX (ANCOVA). CON = control group, LEX = low-intensity group, HEX =
high-intensity group.FECL3 = ferric chloride. XO = hypothanine/xanthine oxidase. H202
= hydrogen peroxide. LPD-HPX = lipid hydroperoxides. PRE-GXT = before graded
exercise test.. POST-GXT = post-graded exercise test. %A = percent change from PRE to
POST-training. TBARS = thiobarbituric acid-reactive substances







75



Table 4.12. Comparison of Changes in Markers of Bone Metabolism for the CON, LEX,
and HEX Groups Following Six Months of Resistance Training.
MARKER CON LEX HEX

PRE POST PRE POST PRE POST
OSCAL
(ngO L 12.325.4 13.235.2 10.744.0 13.587.2* 11.945.0 15.577.4-

%A 6.631.7 25.136.8 39.044.6
ALKPHOS
L 21.1410.4 18.884.6 16.625.6 17.545.7 17.866.6 19.157.5*

%A 3.015.9 7.820.7 7.113.3
PYD
(nmol/L) 1.820.8 1.720.6 1.500.7 1.510.6 1.530.7 1.4510.6

%A -1.334.5 11.352.7 -9.966.4

Values are mean SD. *p<0.05 vs PRE. CON = control group, LEX = low-intensity
group, HEX = high-intensity group. OSCAL = serum osteocalcin. ALKPHOS = bone-
specific alkaline phosphatase. PYD = serum pyridinoline crosslinks. %A = percent change
from PRE to POST-training.












35.0


*
30.0 *




25.0




20.0




15.0 -BCON
LEX
EHEX

10.0




5.0




0.0
PRE POST


Figure 1. Absolute peak oxygen consumption (VO2peak) measured
during a graded exercise test before (PRE) and after (POST) six
months of resistance training.
*p<0.05 vs PRE






















35.0 -


25.0 -


HEX


Figure 2. Percent change in peak oxygen consumption (VO2eak) after
six months of resistance training.
+p

15.0


CON


------X













20.0


18.0
*

16.0


14.0


12.0


10.0


8.0


6.0 CON
ELEX
2HEX
4.0


2.0


0.0
PRE POST


Figure 3. Absolute treadmill time during a graded exercise test
measured before (PRE) and after (POST) six months of resistance
training.
*p<0.05 vs PRE











50.0

+
45.0



40.0



35.0



30.0



25.0-



20.0



15.0



10.0



5.0



0.0
CON LEX HEX

Figure 4. Percent change in treadmill time during a graded exercise
test after six months of resistance training.
+p<0.05 vs CON















II


* CON
ELEX
1 HEX


0.0 --


POST


Figure 5. Absolute stair climbing time measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE










CON LEX HEX
0.0



-2.0



-4.0



-6.0



-8.0



-10.0



-12.0



-14.0

+

-16.0





Figure 6. Percent change in stair climbing time after six months of
resistance training.
+p<0.05 vs CON













450.0


400.0

*
350.0


300.0


250.0


200.0

W CON
150.0 LEX
AHEX
12 HEX I

100.0


50.0


0.0
PRE POST


Figure 7. Absolute chest press IRM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs PRE













8 -



7-

*

6-



5*p<0.05 v. PRE






5 v. CON
3 ELEX
SHEX

2-



1-



0
PRE POST

Figure 8. Relative chest press IRM measured before (PRE) and after
(POST) six months of resistance training.
*p<0,05 vs. PRE
+p<0.05 vs. CON























* CON U LEX

BHEX


Figure 9. Percent change in chest press IRM after six months of
resistance training.
+p<0.05 vs CON


0.0


-10.0




-20.0-




-30.0-












700.0


*+
600.0
*+


500.0



400.0



300.0

M CON
ELEX
200.0- [ HEX



100.0



0.0
PRE POST


Figure 10. Absolute leg press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs PRE
+p<0.05 vs. CON














14


*
12




10




8




6 MCON
MLEX
MHEX

4-




2-




0
PRE POST

Figure 11. Relative leg press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE












60.0

+


50.0




40.0




S30.0




20.0




10.0




0.0
CON LEX HEX


Figure 12. Percent change in leg press IRM after six months of
resistance training.
+p<0.05 vs CON











































POST


Figure 13. Absolute leg curl 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs PRE


350.0



300.0



250.0



200.0



150.0



100.0



50.0



0.0 --


T
T


* CON
MLEX
MHEX























*


7-



6




5-




4"



S3-




2 -




1 -




0 -


POST


Figure 14. Relative leg curl IRM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON
**p<0.05 vs. LEX


* CON
*LEX
BHEX


------ I




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FILES


THE EFFECTS OF RESISTANCE EXERCISE ON LIPID PEROXIDATION, BONE
METABOLISM, AND PHYSICAL PERFORMANCE IN ADULTS AGED 60-85
YEARS.
By
KEVIN ROBERT VINCENT
A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE
UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE
REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY
UNIVERSITY OF FLORIDA
1999

Copyright 1999
By
Kevin Robert Vincent

This dissertation to dedicated to:
My wife Heather. Her love and support has guided me through this process. For that, I
can never thank her enough.
Michael L. Pollock, PhD. I hope that he is as proud of this work as I am of being his
student.
My parents, James and Mary Ellen Vincent. Their love and support has provided me the
foundation for who I have become. I am very proud to be their son.

ACKNOWLEDGMENTS
An endeavor such as this one cannot be accomplished by one person alone.
Throughout my doctoral career at the University of Florida I have been fortunate to meet
and work with many outstanding people. I hope that I have touched their lives as they
have touched mine.
I would like to acknowledge Dr. Michael L. Pollock, my first advisor at the
University of Florida. He was the reason I chose to attend this university. I will always
cherish the opportunity I had to work with and to get to know him. Thank you for
everything “Big Mike”!
I would also like to express my gratitude to Dr. Randy W. Braith. His support,
guidance, and friendship over the past year have been greatly appreciated. Whenever I
had a question or just needed to talk, he was always available. I could not have
accomplished this project without him.
I would like thank my doctoral committee members: Dr. David Lowenthal, Dr. Jeff
Bauer, and Dr. Charles Wood for all of their assistance throughout my doctoral career.
Their advice and friendship helped to guide my studies as well as my life.
The friends that I have made at Florida have made this entire experience
worthwhile. I would like to express my sincerest thanks and appreciation to Shannon
Lennon, Rachel Cutler, Ross Feldman, Pete Magyari, and Chris Hass. You were all there
IV

for me when I needed a shoulder to lean on or some help with data collection. I will
always cherish our friendship.
I would like to thank Michelle Brown for her seemingly endless patience during
this project. She was always there to listen to my frustrationss and she allowed me the
time necessary to work on this study. I can never thank her enough for her support.
Finally, I would like to thank my wife, Heather Vincent. I cannot express how
much I appreciate the help and support that she has given me, not only during graduate
school, but with life. I would not be where I am without her.
v

TABLE OF CONTENTS
page
ACKNOWLEDGMENTS iv
ABSTRACT x
CHAPTERS
1 INTRODUCTION 1
Justification for Research 4
Purpose and Specific Aims 5
Research Hypotheses 6
Significance of Research 7
2 REVIEW OF RELATED LITERATURE 9
Age-Related Alterations in Muscle Mass, Structure, and Strength 9
Decreased Muscle Mass 9
Motomeuron Decline with Aging 10
Neuromuscular Performance Changes with Aging 12
Muscle Mass and Strength Increases with Resistance 13
Exercise in Older Adults
Postural Control and Aging 15
Resistance Exercise and Balance and Physical Function 17
Bone Formation and Resorption 18
Resistance Exercise and Bone Mineral Density 23
Oxidative Stress and Free Radical Production 25
Free Radicals and Aging 25
Exercise and Oxidative Stress 29
Exercise Prescription for Older Adults 31
3METHODS 33
Subjects 33
Subject Eligibility 33
Inclusion Criteria 33
Exclusion Criteria 34
Study Design 34
Experimental Protocol 36
vi

Visit 1: Screening/Orientation 36
Visit 2: Treadmill Graded Exercise Test 37
and Blood Sample Collection
Visit 3: Muscular Strength Assessment 39
Visit 4: Muscular Endurance 40
Visit 5: Bone Mineral Density 40
Visit 6: Balance, Stair Climbing, and Isometric 41
Lumbar Extension Strength
Visit 7: Body Composition and Muscular Strength Assessment . 42
Training Period: Six Months of Dynamic Resistance Exercise ... 44
Biochemical Assays 45
Markers of Bone Metabolism 45
Alkaline Phosphatase-B 45
Osteocalcin 46
Pyridinoline Crosslinks 46
Biochemical Indicators of Oxidative Stress 47
Lipid Peroxidation Measurements 47
Oxidative Challenges in vitro 47
Xanthine-Xanthine Oxidase System 48
(Superoxide Generator)
Hydrogen Peroxide System 48
Ferric Chloride System (Hydroxyl Generator) 48
Statistical Analyses 48
4 RESULTS 50
Subject Characteristics 50
Aerobic Endurance 52
Oxygen Consumption 52
Treadmill Time to Exhaustion 52
Time to Ascend One Flight of Stairs 52
Changes in Muscular Strength 54
Chest Press 54
Leg Press 54
Leg Curl 54
Biceps Curl 55
Seated Row 55
Overhead Press 55
Triceps Dip 55
Leg Extension 57
Total Strength 57
Muscular Endurance 57
Chest Press 57
Leg Press 58
Lumbar Extension Strength 59
vii

0° of Lumbar Flexion 59
12° of Lumbar Flexion 59
24° of Lumbar Flexion 59
36° of Lumbar Flexion 60
48° of Lumbar Flexion 60
60° of Lumbar Flexion 60
72° of Lumbar Flexion 60
Total Lumbar Extension Strength 62
Bone Mineral Density 62
Total Body Bone Mineral Density 62
Femoral Neck Bone Mineral Density 62
Anterior/Posterior Lumbar Spine Bone Mineral Density 62
Lateral Lumbar Spine Bone Mineral Density 63
Ward’s Triangle Bone Mineral Density 63
Correlations Between Physiological Performance Variables 63
and Muscular Strength
V02pc.k 64
Treadmill Time to Exhaustion 64
Stair Climbing Time 68
Correlations Between Physiological Performance Variables and . . . . 68
Bone Mineral Density
Total Body 68
Femoral Neck 69
Ward’s Triangle 69
Anterior/Posterior Lumbar Spine 69
Lateral Lumbar Spine 70
Biochemical Analyses 71
TBARS 71
Lipid Hydroperoxides 71
Serum Osteocalcin 72
Serum Bone-Specific Alkaline Phosphatase 72
Serum Pyridinoline Crosslinks 72
5 DISCUSSION 146
Overview and Principal Findings 146
Muscular Strength, Muscular Endurance, and Stair Climbing 147
Muscular Strength 147
Muscular Endurance 149
Stair Climbing Ability 150
Physiological Significance of Strength Data 150
Aerobic Endurance 151
V02pelk 151
Treadmill Time to Exhaustion 154
Bone Mineral Density and Bone Metabolism 155
viii

Bone Mineral Density 155
Biochemical Markers of Bone Metabolism 157
Physiological Significance 158
Lipid Peroxidation and Resistance to Oxidative Stress 159
Physical Challenge in vivo 160
Oxidative Challenge in Vitro 162
Physiological Consequence and Significance 163
Major Conclusions 163
Physiological Significance 164
Limitations to the Experiment and Future Directions 165
APPENDICES
A A-PRIORI SAMPLE SIZE ESTIMATION AND POWER ANALYSIS 168
B INFORMED CONSENT TO PARTICIPATE IN RESEARCH . ... 169
C INSTITUTIONAL REVIEW BOARD APPROVAL FORM TO. . . . 179
PERFORM RESEARCH
REFERENCES 180
BIOGRAPHICAL SKETCH 193
ix

Abstract of Dissertation Presented to the Graduate School of the University of Florida in
Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy
THE EFFECTS OF RESISTANCE EXERCISE ON LIPID PEROXIDATION, BONE
METABOLISM, AND PHYSICAL PERFORMANCE IN ADULTS AGED 60-85
YEARS.
By
Kevin Robert Vincent
August 1999
Chairman: Randy W. Braith
Major Department: Exercise and Sport Sciences
The purpose of this investigation was to examine the effects of circuit resistance
exercise training (CWT) at two different intensity levels on physical function, bone
metabolism, and lipid peroxidation in elderly persons. Sixty-two men and women (age
68.1±6.3 yr.) completed the study. Participants were randomized into three groups: high-
intensity (HEX, 80% of 1RM for 8 repetitions, n=22), low-intensity (LEX, 50% of 1RM
for 13 repetitions, n=24) and control (CON, n=16). HEX and LEX groups trained 3x/wk
for 6 months using 11 machines. All groups were tested pre- and post-training for aerobic
capacity (V02pak), treadmill time to exhaustion, 1RM on the chest press, leg press, leg
curl, leg extension, seated row, overhead press, biceps curl, and triceps dip, chest press
and leg press endurance, time to walk up one flight of stairs, regional bone mineral density
(BMD), serum markers of bone metabolism, and serum lipid peroxidation (LIPOX). Both

training groups significantly increased 1RM strength for all 8 exercises (p<0.05). Total
strength increased 17.2 and 17.8% for the LEX and HEX groups, respectively (p<0.05).
V02pc,k increased 23.5 and 20.1% for the LEX and HEX groups, respectively (p<0.05).
Treadmill time increased 26.4 (p<0.05) and 23.3% for the LEX and HEX groups,
respectively. Time to ascend one flight of stairs decreased by 7.3 (p<0.05) and 5.79% for
the LEX and HEX groups, respectively. Chest press endurance increased by 75.5 and
68.0%, and leg press endurance increased by 79.2 and 105% for the LEX and HEX
groups, respectively (p<0.05). Femoral neck (BMD) increased significantly for the HEX
group (p<0.05). Osteocalcin increased significantly for the LEX and HEX groups, and
alkaline phosphatase increased for the HEX group (p<0.05). Both the LEX and HEX
groups demonstrated significantly lower levels of LIPOX immediately after the graded
exercise test when compared to CON (p<0.05). The results of this study indicate that one
set of either low- (50% 1RM) or high- (80% 1RM) intensity resistance exercise is
sufficient to increase strength V02peak, regional BMD, bone turnover, and decrease
exercise-induced LIPOX in older adults.
xi

CHAPTER 1
INTRODUCTION
Aging is associated with decreases in strength, muscle cross-sectional area, bone
mineral density, and physical function (Fiatarone et al., 1994, and Tseng et al., 1995).
Aging is also associated with an increase in oxidative stress. It has been proposed that
aging is a consequence of the interactions of oxygen free radicals with cell components
throughout life (Ji, 1994). Free radicals have been implicated as contributors to cell
membrane disruption, atherosclerosis, and sarcopenia (Weindruch, 1995).
During the aging process, indices of free radical formation increase (Ji et al.,
1990). This increase results in an increase in antioxidant enzyme levels to act as defense
against oxidative stress (Ji, 1993). An increased rate of free radical generation is a signal
for an increase in antioxidant enzyme activity (Jenkins, 1988). Numerous investigations
have shown that acute and chronic exercise can result in an increase in antioxidant enzyme
activity (Ji, 1993, Ji et al., 1991, and Tullson et al., 1994). Aerobic endurance exercise,
particularly intense endurance exercise, produces free radicals that upregulate antioxidant
enzyme activities (Tullson et al., 1994). It was recently demonstrated that intermittent
sprint cycling performed three times per week for 6 weeks followed by a seventh week
with five sessions increased antioxidant enzyme activity (Hellsten et al., 1996).
Resistance exercise induces a metabolic stress similar to that seen during sprint
exercise. Therefore, resistance exercise may elicit similar increases in antioxidant enzyme
1

2
activity observed during sprint exercise. It has also been shown that transient ischemia
followed by reperfusion can also increase antioxidant enzyme activity (Das et al., 1993).
Muscular contractions greater than 40% of the maximal voluntary contraction (MVC), as
seen during resistance exercise, result in transient blood flow occlusion in the exercising
muscle (Donald et al., 1967). Thus, resistance training may subject skeletal muscle to a
form of ischemia/reperfiision that could possibly result in an increase in antioxidant
enzyme activity leading to improved defense against oxidative stress. Since free radical
formation has been implicated as a possible cause for many debilitating conditions
associated with aging, it is important to ascertain which interventions are effective in
decreasing oxidative stress.
Aging has been associated with a decrease in muscle mass and strength (Larsson et
al., 1979). This decrease in strength is linked to decreased mobility, physical function, and
increased risk of falling in older people (Bendall et al., 1989 and Fiatarone et al., 1990).
Resistance exercise has been shown to be effective for increasing muscle mass, strength
and physical function in elderly adults (Fiatarone et al., 1990, Fiatarone et al., 1994, and
Verfaillie et al., 1997). The Surgeon General’s Report on Physical Activity and Health
states that developing muscular strength can improve one’s ability to perform tasks and
reduce the risk of injury (Surgeon General, 1996). Furthermore, the report states that
“resistance training may contribute to better balance, coordination, and agility that may
help prevent falls in the elderly (Surgeon General, 1996).”
Resistance exercise also improves physical function by decreasing the relative
intensity of tasks performed in daily life. Resistance exercise can decrease the stress

3
placed on the heart during lifting tasks such as lifting moderate to heavy boxes which has
been implicated as a cause of heart attacks (McCartney et al., 1993).
Osteoporosis is a degenerative disease that is characterized by a decrease in bone
mineral density (BMD). This loss makes the bones more susceptible to fractures.
Research has indicated that bone formation can be stimulated by placing a strain on the
bone such as during resistive exercise (Rubin and Lanyon, 1984). Braith et al. (1996)
examined the effects of 6 months of resistance exercise on BMD following heart transplant
surgery. Typically, BMD decreases during the post-operative period as a consequence of
glucocorticoid therapy. The group that performed strength training was able to return
their lumbar, total body, and femoral neck BMD to near baseline levels while the control
group’s BMD remained depressed. Isolated strength training of the lumbar muscles has
also been shown to increase lumbar BMD. Pollock et al. (1992) showed that 6 months of
isolated lumbar training improved lumbar BMD compared to controls in men and women
60 to 79 years of age. Menkes et al. (1993) reported a significant increase in femoral neck
BMD in middle-aged to older men following 16 weeks of strength training. Resistance
exercise can also have a significant effect on biochemical markers of bone metabolism.
For example, Menkes et al. (1993) reported significant increases in osteocalcin and
skeletal alkaline phosphatase isoenzyme (markers of bone formation) and a significant
decrease in tartrate-resistant acid phosphatase (marker of bone resorption) following 16
weeks of training. However, the results of this study were not replicated in another 16
week study by the same group (Ryan et al., 1994). It is possible that the duration of
training was not adequate to elicit a consistent alteration in the levels of these markers.

4
A factor that makes comparison of many of the investigations mentioned in this
review difficult is that some used high intensity resistance exercise while others used lower
intensity levels. Therefore, comparisons of their results or the ability to make appropriate
recommendations is difficult or impossible. The current intensity recommendation for
adults over 50 years of age corresponds to 14 to 16 (hard) on the Borg RPE scale
(Pollock et al., 1994). The intensity should be perceived as hard by the participant, but
should not be to voluntary failure as is recommended for younger adults (ACSM, 1990).
This recommendation for people over 50 yr. is not based upon scientific evidence and it is
not known if elderly people need to work at the same intensity as younger adults to derive
similar benefits, or if a lower intensity is sufficient. Therefore, the purpose of the proposed
investigation is determine what level of intensity is necessary for improved physical
function, bone metabolism, and defense against oxidative stress.
Justification for Research
Resistance exercise can have a significant impact on bone mineral density, strength,
physical function, and balance. Also, recent studies have demonstrated that elderly
persons can show similar adaptations to resistance exercise when compared to younger
adults. However, what is not known is if there is an intensity threshold for these
adaptations. It is also unknown if the same intensity is necessary to elicit these changes or
if they each respond to a different intensity. Since a large portion of the American
population is growing older, it is important to know what is the threshold intensity that
should be recommended to these people to improve health.

5
To date, no published investigations have examined if resistance exercise can
improve antioxidant defense systems. It has been shown that endurance exercise can
increase antioxidant enzyme activities (Powers et al., 1994). If resistance exercise can
increase these enzymes it could be recommended as another means of combating oxidative
stress. What is also necessary to determine is if low or high intensity exercise is necessary
to elicit adaptations in the endogenous antioxidant defense system.
It has been shown that resistance exercise can positively impact bone mineral
density, and improve balance and physical function. Although both low and high intensity
resistance exercise can affect all of the previously mentioned parameters, we sought to
determine if a greater impact will be made by high intensity training.
Purpose and Specific Aims
The purposes of this investigation were twofold: (1) To examine the effects of 6
months of dynamic resistance exercise training at two different intensity levels on physical
function, bone metabolism, aerobic endurance, and alterations in lipid peroxidation in
older adults. (2) To determine if the various physiological adaptations to 6 months of
resistance exercise vary between two intensity levels of resistance training. Specifically,
the aims of this study were to examine the consequences of low and high intensity
resistance exercise on:
1. Muscle strength: Measured by 1-repetition maximum (1-RM) for the chest
press, leg press, leg curl, biceps curl, seated row, overhead press, triceps dip, and
leg extension.

6
2. Muscle endurance: Measured by maximum number of repetitions performed
using 60% of the pre-training 1-RM for chest press and leg press.
3. Physical function: Measured by time to climb one flight of stairs
4. Bone metabolism: Measured by assaying for serum levels of pyridiniline
crosslinks, osteocalcin, and skeletal alkaline phosphatase enzyme.
5. Bone mineral density: Measured by dual-energy photon absorptiometry (DXA)
6. Serum oxidative stress measured by lipid peroxidation.
7. Aerobic endurance measured by a symptom-limited graded exercise test, and
time to exhaustion measured during the graded exercise test.
Research Hypotheses
The purpose of this investigation was to examine how dynamic resistance exercise
training at two different intensity levels affected strength, aerobic endurance, bone
metabolism, and lipid peroxidation older adults. This experiment was designed to test two
hypotheses. The first was that six months of resistance exercise would improve “health-
related” adaptations including bone metabolism, defense against lipid peroxidation, aerobic
endurance, physical function, and strength. The second hypothesis was that high-intensity
resistance exercise would not cause greater improvements in muscle strength and
endurance, aerobic endurance, serum markers of bone turnover, bone mineral density, and
serum lipid peroxidation when compared to low-intensity resistance exercise.

Significance of Research
Aging is associated with decreases in strength, muscle mass, physical function,
7
balance, and increased oxidative stress. Muscle weakness has been shown to be an
important contributor to risk of falling in older people (Nevitt et al., 1991). It is estimated
that the acute care costs associated with falls is in excess of $10 billion (Tinetti et al.,
1994). It is further estimated that insufficient strength to perform activities of daily living
incurs an additional $7 billion in health care costs (Rowland and Lyons, 1991). Decreased
muscular strength can lead to loss of physical independence, increased risk of injury, and
long term disability or institutionalization. Since the proportion of the population over 60
years of age is increasing, it is important to identify feasible interventions that can maintain
quality of life as people age. Resistance exercise has been shown to be an effective means
of improving strength and physical function in people of all ages. However, it is necessary
to obtain data which indicates what is the appropriate quantity and quality of resistance
exercise necessary to promote improved health and function. It is currently unknown if
there is an intensity threshold for health-related adaptations to resistance exercise for older
adults. The American College of Sports Medicine has recognized that resistance training
is important for quality of life and physical function for older adults (ACSM, 1990, 1998).
However, the recommendations for the quantity or quality of this exercise is not based on
an abundance of scientific evidence, rather it is based on the opinions of experts in the
field. There are data to support the beneficial effects of resistance exercise for this
population, but not what the appropriate intensity level is to attain these benefits. The
current intensity recommendation for adults over 50 years of age corresponds to 14 to 16
(hard) on the Borg RPE scale (Pollock et al., 1994). The intensity should be perceived as

8
hard by the participant, but should not be to voluntary failure as is recommended for
younger adults (ACSM, 1990). However, as stated, this recommendation for people over
50 yr. is not based upon scientific evidence and it is not known if elderly people need to
work at the same intensity as younger adults to derive similar benefits, or if a lower
intensity is sufficient. If a greater impact were to be made by high intensity training then
more definitive recommendations to the public can be made. However, if there is no
difference between groups, then the low intensity exercise would be the best
recommendation because it may be associated with a greater adherence rate as compared
to high intensity.

9
CHAPTER 2
REVIEW OF RELATED LITERATURE
Age Related Alterations in Muscle Mass. Structure and Strength
Decreased Muscle Mass
Aging is associated with a progressive loss of muscle mass and consequently
strength. This age related decline in muscle mass is termed sarcopenia (Evans, 1995). As
a result of the decrease in muscle mass and strength, older individuals can experience
decreased balance, physical function, bone mineral density, independence, and lowered
metabolic rate which contributes to alterations in body composition (Evans, 1995,
McComas, 1996, and Porter et al., 1995).
Aging is accompanied by a loss in fiber size and number (McComas, 1996). Lexell
et al., (1983) reported that elderly men (70-73yr) had 25% fewer muscle fibers in the
vastus lateralis compared to younger men (19-37 yr ). Lexell et al. (1988) also showed
that men in their 80s have 50% the number of fibers compared to younger individuals. The
results also showed that only 10% of the muscle area was lost by age 50, and that after
that point the loss in mass accelerated.
Numerous investigations have reported that the type n fibers experience the
greatest degree of atrophy ( Grimby et al., 1982, Klitgaard et al., 1990, Lexell et al., 1988,
1991, and Tomlinson et al., 1969). This selective reduction in type n muscle size may be
the result of decreased activity leading to disuse atrophy of the high force motor units.
9

10
Lexell et al. (1988) demonstrated that the age related decline in muscle mass is mainly
accounted for by type II fiber atrophy with very little contribution from type I fibers.
However, it has also been shown that although the type II fibers experience more atrophy
(decreased cross-sectional area), the relative proportion of type I to type II fibers remains
largely unchanged with age (Grimby et al., 1982,1984, and Lexell et al., 1988). Lexell et
al. (1988) reported that the proportion of type I fibers was 51% at 20 yr. and 55% at 80
yr. It has also been shown that the “mosaic” muscle pattern that is evident in the muscles
of younger individuals is lost with age (Klitgaard et al., 1990). There is typically an
intermixing of motor units so that similar fiber types are not grouped together in one area.
Data from Klitgaard et al. (1990) indicate that muscle fibers in older adults may
experience histochemical alterations in myosin heavy chain (MHC) expression. They
reported that fibers may contain more that one MHC isoform such that type IIA and IIB
or type I and IIA isoforms may be found together. The authors felt that this could be the
result of a dynamic equilibrium between fiber groups resulting from disuse, denervation,
or both.
Other studies have reported further histological alterations in aging muscle
(Tomlinson et al., 1969, McComas, 1996). These alterations include: macrophage
infiltration, hyaline degeneration, disorganized sarcomeres, lipofucshin pigmentation,
decreased mitochondrial size, and increased connective tissue.
Motomeuron Decline with Aging
Aging is accompanied by a decrease in the number of motomeurons, particularly
the larger alpha-motomeurons (Ansved and Larsson, 1990, Kawamura et al., 1977, and

11
Tomlinson and Irving, 1977). Once denervated, the muscle quickly atrophies, losing 50%
of its weight in one month and the rate of decline is more rapid for old animals when
compared to young (Gutmann, 1962, and White and Vaughan, 1991). Ansved et al.
(1991) and Einsiedel and Luff (1992) have shown that older neurons are not able to
demonstrate the same degree of collateral sprouting as compared to younger neurons.
This may be the result of decreased protein synthesis and a decreased rate of axonal
transport that is observed with old age (Ansved et al., 1991). Ansved et al. (1991) also
reported that preferential loss during aging is observed in large, fast-conducting
motomeurons with low oxidative enzyme activity that innervate fast-twitch muscle fibers.
In an examination of the extensor digitorum brevis, Campbell et al (1973)
reported that prior to the age of 60, the number of functioning motor units shows little
change, but there is a progressive decline in functional motor units beyond that age.
Similar results have also been reported for the biceps, soleus, and the thenar muscles
(McComas, 1996). Campbell et al. (1973) also reported that the mean amplitudes of
motor unit potentials are significantly larger in the elderly when compared to younger
controls. These results indicate that when certain muscle fibers become denervated, other
motomeurons reinnervate the fiber by sending out new axonal branches (McComas,
1996). Studies using electromyography have shown that the number of motor units
decreases while the size of the motor units increases with age (Campbell et al., 1973,
Doherty et al., 1993a, 1993b). Although it has been established that motomeurons
decrease with age, the mechanism for this decline is currently not known. However, there
are several proposed mechanisms for neuronal death with age. These proposed
mechanisms are: ischaemia, accumulation of neurotoxins, free radical damage, and that

12
neurons may be genetically programmed to die at a certain age (McComas 1996, and
Weindruch, 1995).
Neuromuscular Performance Changes with Aging
The consequence of a decrease in motor units and more homogenous fiber
grouping is a decline in contractile function within the muscle. In an examination of the
triceps surae muscle in elderly subjects, Davies et al. (1986) reported that both the time to
peak tension and the time to relaxation were both significantly increased for evoked
twitches. A similar finding was reported for both the plantar and dorsiflexors
(Vandervoort ad McComas, 1986). The results from Vandervoort and McComas (1986)
also indicated that twitch time increased linearly with age (from 20-100yr.) but that a
significant decrease in muscle strength did not occur until the subjects were in their 60’s.
The increase in contraction time is likely the result of a decrease in type II fibers. It is also
interesting to note that in the Vandervoort and McComas (1986) study the gastrocnemius
which contains more fast twitch motor units than the soleus showed a greater age related
decline in contractile function.
Fatigability has also been examined but the results from these investigations has
been equivocal (Davies et al., 1986, Klein et al., 1988, Larsson and Karlsson, 1978,
Lennmarken et al., 1985, and Narici et al., 1991). Narici et al., 1991 reported a decrease in
fatiguability with age while Lennmarken et al.(1985) observed an increase in fatiguability
in a similar study. Klein et al. (1988) reported no differences in fatiguability using the
triceps surae muscle, while Davies et al. (1986) found a decrease in fatiguability using the
same muscle group. These studies may be limited by the fact that although similar muscle

13
groups were used, the frequency of stimulation for the evoked contractions varied
between investigations. Larsson and Karlsson (1978) had subjects perform a sustained
voluntary contraction, and reported that fatiguability was similar for older and younger
adults. It is interesting to note that although there is an increase in the proportion of type
I fibers with age, fatigability is not altered. This may be the result of decreased physical
activity that is seen with aging.
As a consequence of increased contraction time, the elderly muscle’s ability to
generate power is compromised (Bassey et al., 1992), as well as, the ability to generate
force during protective reflexes (Vandervoort and Hayes, 1989). Research has indicated
that the ability to generate force quickly, not the absolute amount of force produced is an
important variable in the prediction of risk of falling (Whipple et al., 1987, Maki and
Mcllroy, 1996).
Muscle Mass and Strength Increases with Resistance Exercise in Older Adults
Numerous recent investigations have demonstrated that resistance exercise is an
effective means for increasing muscle mass and strength (Fiatarone et al., 1990,1994,
Frontera et al., 1988, Klitgaard et al., 1990, Morganti et al., 1995). The purpose of this
section will be to highlight these five studies which represent the findings reported in other
previous, as well as, subsequent investigations.
In a cross-sectional study, Klitgaard et al. (1990) reported that men 68 yr. who
had a history of strength training had similar knee and elbow isometric strengths and
cross-sectional area as compared to 28 yr. endurance trained men. They also reported that
men 68yr. with a history of aerobic exercise or no physical activity had lower knee and

14
elbow isometric strengths and cross-sectional area as compared to 28 yr. endurance
trained men.
Morganti et al. (1995) resistance trained 20 women (av. age 61yr.) twice per week
for six months. Subjects performed three sets of eight repetitions at 80% of their 1RM for
the double leg press, knee extension, lateral pull-down, trunk extension, and trunk flexion.
Strength was measured for the lat pull-down, leg press, and knee extensions at 6 and 12
months. The results indicated an increase in strength in the training group after 12 months
of 77%, 35%, and 74% for the lat pull-down, leg press, and knee extensions, respectively.
No significant increases in strength were noted at 12 months in the control group.
Fiatarone et al. (1990) resistance trained 10 elderly men and women (mean age
90yr) for 8 weeks. Subjects performed 3 sets of 8 repetitions of knee extensions 3 days
per week. Strength was measured by 1RM and regional body composition was assessed
by computed tomography (CT). The results showed that 1RM knee extension strength
improved by 174%, and that mid-thigh muscle area increased 9%.
Fiatarone et al. (1994) examined the effect of resistance training alone or in
combination with a nutritional supplement in men and women with an average age of 87yr.
Subjects performed 3 sets of 8 repetitions 3 days per week for 10 weeks for the hip and
knee extensors. CT scans of the mid-thigh were obtained to assess changes in muscle
area. The results showed an increase in strength of 113%, but a non-significant increase
of 2.7% in mid-thigh-muscle area. The increase in strength was not related to protein
supplementation.
Frontera et al. (1988) examined the effect of 12 weeks of resistance exercise for
the knee flexors and extensors. They trained 12 men (age range 60-72yr) using 3 sets of 8

15
repetitions performed 3 days per week. At the conclusion of the 12 weeks, knee extension
strength had improved 107% and knee flexor strength had increased 227%. CT scans
revealed an 11% increase total muscle area of the mid-thigh. The authors also reported a
40% increase in urinary 3-methyl-L-histidine which is a marker of protein turnover.
One recent study examined the effects of either high- (80% of 1RM for 7
repetitions) or low-intensity (40% of 1RM for 14 repetitions) on strength, thigh cross-
sectional area, and bone mineral density (Taafe et al., 1996). The subjects were women
aged 65-79 yr. Subjects trained 3 days per week for 52 weeks at one of the two
intensities performing 3 sets of leg press, knee extension, and knee flexion. The authors
reported a mean increase in strength of 59% and 41% for the high and low groups,
respectively. Both groups demonstrated a significant and similar increase in type I fiber
area but not type II. Neither group experienced a significant increase in bone mineral
density.
These studies indicate that resistance training is an effective means for improving
strength and muscle mass in older adults. However, the resistance training regimens in
these,as well as, other studies are very similar. Most studies use 3 sets per exercise and
typically 6-15 repetitions, not based on research, but based on either investigator opinion
or studies performed on younger people. It is not known if high volume is necessary to
elicit increases in strength and mass, or if a lower intensity would produce similar results.
Postural Control and Aging
The previously described alterations in muscle mass, strength and motor units that
accompany aging can have deleterious effects on posture and balance. The human body

16
has been described as a multilink inverted pendulum (Maki et al., 1996). As such, it is
inherently unstable due to the influence of gravity (Maki et al., 1996). Perturbations in
posture or balance are responded to by either controlling the center of mass (COM)
through generating torque at the joints or by altering the base of support (BOS) by
stepping or grasping movements with the limbs (Maki et al., 1996). Perturbations
affecting balance can either be mechanical (i.e. force acting on the body) or informational
(i.e. visual, vestibular, somatosensory) (Maki et al., 1996).
Sensory systems display decreased function with aging. Visual acuity, contrast
sensitivity, depth perception, and dark adaptation are all decreased with aging Decreased
visual acuity has been implicated as a risk factor for falling because the older person may
not be able to see an obstacle in front of them or see that a curb is ahead while walking on
the street (Alexander, 1996). Other degenerative adaptations such as reduced
proprioception, touch sensitivity, vestibulo-ocular reflex, and the density and sensitivity of
dermal mechanoreceptors are reported with aging (Maki et al., 1996).
As previously mentioned, aging is associated with a decreased skeletal muscle
contraction rate which may impair the ability to rapidly produce force in response to
postural perturbations (McComas, 1996). Available evidence indicates that there is an
association between leg muscle weakness and risk of falling and postural sway (Lord et
al., 1991a, 1991b). Research also indicates that the torque necessary to prevent a fall is
typically within the elderly person’s ability. However, what is not, is the ability to
generate the torque quickly (Maki et al., 1996). A common way to measure postural sway
and balance is through measuring changes in center of pressure (COP) during force plate
analysis (Alexander, 1996). Alexander (1996) reported that the maximum peak-to-peak

17
COP excursion or speed of the COP excursion can be used to distinguish between young
and adult postural sway patterns. Maki et al. (1994) reported that the amplitude of
mediolateral COP displacement was found to be the single best predictor of falling risk
compared to other balance measures. The authors indicated that adductor/abductor
strength as well as proprioceptors were most critical to maintaining lateral stability.
Research also indicates that using force plates, and insole pressure sensors provide
a reliable and valid means of assessing balance and postural sway (Alexander, 1996, and
Maki et al., 1996). Other commonly used methods such as questionnaires, one-legged
stance time, and reaching tasks have been shown to measure fear of falling rather than
probability of falling (Alexander, 1996). The use of insole pressure sensors allows for
balance and postural sway during dynamic activities to be measured as well.
Resistance Exercise and Balance and Physical Function
Aging has been associated with a decrease in muscle mass and strength (Larsson et
al., 1979). This decrease in strength is linked to decreased mobility, physical function, and
increased risk of falling in older people (Bendall et al., 1989). Resistance exercise has been
shown to be effective for increasing muscle mass, strength and physical function in elderly
adults (Fiatarone et al., 1990,1994, and Verfaillie et al., 1997). The Surgeon General’s
Report on Physical Activity and Health states that developing muscular strength can
improve one’s ability to perform tasks and reduce the risk of injury(Surgeon General,
1996). Furthermore, the report states that “resistance training may contribute to better
balance, coordination, and agility that may help prevent falls in the elderly (Surgeon
General, 1996)”. Falls have been identified as the most frequent cause of injury related

18
mortality in the elderly (Fife et al., 1984). Nevitt et al. (1991) conducted a prospective
study to determine the risk factors that lead to injurious falls in the elderly. They reported
that the fallers’ ability to protect him- or her-self during the fall affected the risk of injury.
The authors recommended that interventions intended to reduce the risk of falling and
injury should include strength training. Fiatarone et al. (1994) examined the effect of 10
weeks of resistance exercise for the legs only on muscle strength and function in elderly
adults (mean age, 87+ 0.6 yr ). Resistance exercise increased muscle strength, gait
velocity, and stair climbing power. Fiatarone et al. (1990) reported that 8 weeks of
resistance exercise for the leg improved strength and function in nonagenarians (mean age
90±lyr.). Quadriceps strength improved 174% and tandem gait speed increased 48%
following resistance training.
Bone Formation and Resorption
The process of bone remodeling (deposition/resorption) is a continuous and
interdependent process (Marcus, 1991). The two primary cells that are involved in the
process of bone metabolism are the osteoblasts and the osteoclasts. Osteoblasts are
primarily involved in bone formation and come from the differentiation of osteoprogenitor
cells (Mundy, 1993, and Raisz et al., 1993). Osteoclasts are primarily involved with bone
resorption and are formed from tumor cells or leukocytes under the influence of osteoclast
forming cells (Mundy, 1993).
Osteoblasts contain alkaline phosphatase, the protein osteocalcin, and secrete type
I collagen (Calvo et al., 1996). This forms the osteoid which is the site of bone
deposition. Into this collagen matrix Ca++ and PO4- will be deposited to form

19
hydroxyapatite. As the bone develops it will eventually surround the osteoblast which will
then be incorporated into the bone as the osteocyte. The osteocytes are connected via a
canal system known as the Haversian canals (or canaliculi). These canals allow rapid
communication between the interior and exterior of the bone. The canals allow Ca' and
P04- to be transmitted from the areas of newly formed interior bone to the outside. This
process is known as osteocytic osteolysis (Marcus, 1991). Osteoblast activity is
stimulated by several factors. Estrogen and testosterone act on response elements
(Estrogen Response Element) within the osteoblast to produce Insulin like Growth Factor
1 (IGF-I) (Martin, 1993). Osteoblasts have membrane receptors for IGF-I and II, and
these receptors can also bind insulin (Martin, 1993). Insulin and the IGFs bind to a
tyrosine kinase receptor that has two sub-units. These sub-units interact with the Insulin
Response Substrate (IRS) to induce glucose uptake and protein transcription. So it can be
seen that insulin helps to promote bone formation. Growth Hormone (GH) also promotes
bone formation and plasma calcium increase because it stimulates the release of IGF-I
from the liver and increases intestinal absorption of CaM (Amaud, 1993, and Martin,
1993). IGF-I is an anabolic hormone which stimulates bone growth and formation. The
osteoblast has receptors for IGF and produces it, so the osteoblast can produce a factor
which stimulates osteoblast activity (Raisz et al., 1993). At low levels, Prostaglandin E
helps to promote the formation of osteoblasts and stimulates the production of IGF-I
(Raisz et al., 1993). Other factors which can promote bone formation are gamma
interferon, leukemia inhibitory factor, and retinoic acid. Retinoic acid helps to induce
transforming growth factor beta, and bone morphogenetic protein. Vitamin D3 although
more involved in bone resorption is necessary for bone formation because it increases

20
intestinal absorption of Ca”and PO4 ,and increases the number of IGF-I receptors on the
osteoblast membrane (Raisz et al., 1993).
The osteoclast secretes tartrate resistant acid phosphatase which helps to form a
ruffled invagination in the osteoid and facilitate the release of Ca”and PO4- (Calvo et al.,
1996). Interestingly, the osteoblast will use this site to deposit new bone. Osteoclast
activity is promoted by several factors. One of the most important is parathyroid hormone
(PTH) which is secreted by the chief cells of the parathyroid gland (Mundy, 1993). PTH
is secreted primarily in response to low serum Ca" levels. Low serum Ca* causes an
increase in cAMP levels in the chief cells which leads to PTH exocytosis (Mundy, 1993).
The release of PTH in response to low Ca" occurs within minutes. PTH release can also
be stimulated by high serum levels of P04- because the PO4- can bind to Ca++ so that the
free Ca” levels in serum decrease. PTH stimulates the kidney to increase the reabsorption
of Ca” and increase the excretion of P04-. PTH also acts on the osteoblast to cause it to
secrete a factor that stimulates the activity of the osteoclast to increase osteocytic
osteolysis (Mundy, 1993). This will also serve to increase plasma levels of Ca” and P04-.
PTH cannot stimulate osteoclasts if osteoblasts are not present. This is an example of the
coupling of resorption and formation. Also, PTH inhibits collagen production by the
osteoblast but does promote osteoblast proliferation. PTH also promotes the conversion
of 25-OH-VitD to the active form of 1,25-OH-VitD (VitD3) (Seino et al., 1993). VitD3
formation can be induced by low serum Ca”, PO4-, and Vit D3. VitD3 acts in the brush
border of the intestinal villi to increase the number of Ca” transporters enhancing its
absorption (Seino et al., 1993). It also acts to increase the absorption of P04-. Both PTH
and VitD3 help to increase serum levels of Ca”, Vit D3 by increasing its intestinal

21
absorption and both by increasing Ca” resorption from bone (Seino et al., 1993). VitD3
acts on cells of the kidney, intestine, liver, and skeletal muscle to produce Calbindin (Seino
et al., 1993). Calbindin acts as a carrier of Ca” effectively decreasing the levels of free
Ca++ within cells. Ca” is a very reactive substance and can promote many intracellular
reactions and therefore it is important to keep its free concentration down. VitD3 also
increases Ca” uptake into the sarcoplasmic reticulum in skeletal muscle (Seino et al.,
1993). VitD3 acts on the osteoblast to increase the production of osteoclast stimulating
factors(Seino et al., 1993). VitD3 is active in bone resorption (stimulates osteoclast
activity), increases serum Ca” (increased intestinal absorption), and bone formation
(increased IGF-I receptors and Ca”/PC>4- availability). Once at the site of bone turnover,
several other mechanisms are involved. PTH causes an increase in cAMP within the
osteoblast. This stimulates the production of PGE2. PGE2 in high levels serves to
increase bone resorption(Raisz et al., 1993). It promotes osteoclast proliferation and
activity. It also helps to initiate the cycle that causes an increase in IGF-I production.
PGE2 increases cAMP levels, which further increases PGE2 levels (autoamplification).
Bone resorption is also stimulated by Interleukin l(IL-l), interleukin-6 (IL-6) and tumor
necrosis factor. IL-6 works by promoting osteoclast congregation.
The final hormone that impacts bone metabolism is calcitonin (Martin, 1993). The
relative effect or importance of calcitonin has not been proved in humans. It responds to
high levels of serum Ca”. Its effect is to oppose the actions of PTH and increase Ca”
excretion and possibly promote bone formation.
Estrogen is essential for promoting bone growth (Orirno et al., 1993). Estrogen
increases the osteoblastic production of IGF-I and decreases the production of IL-1, IL-6,

22
and reduces the sensitivity of the osteoblast to PTH(Hashimoto et al., 1993 and Orimo et
al., 1993). Estrogen also promotes the formation of VitD3. With aging, the production of
estrogen declines (menopause) and the level of PTH in women steadily increases (Orimo
et al., 1993). The age dependent increase in PTH is not seen in men. Also with aging,
glucocorticoid levels increase or are given exogenously. Cortisol decreases the absorption
of Ca+* and inhibits bone formation (Raisz et al., 1993). This could also increase the bone
loss in post-menopausal women or in people given glucocorticoids. Another
pathophysiological condition which can cause a large decrease in bone mass is organ
transplantation (Braith et al., 1996). These patients are supplemented with corticosteroids
and cyclosporin which can cause precipitous decreases in bone formation. These patients
are also usually sedentary and the lack of physical activity can decrease bone mass.
Bone formation can be impacted by environmental or pathophysiological factors.
It has been observed that there are seasonal alterations in bone metabolism. During the
winter the elderly or immobile do not go outside. VitD must either be consumed in the
diet or obtained through exposure to sunlight (Seino et al., 1993). If the person is not
exposed to sunlight and this is combined with inadequate VitD intake, then Ca**
absorption and serum levels will be impaired. Under these circumstances, a more
collagenous, soft bone will be deposited due to the lack of Ca” and P04-(Seino et al.,
1993) Winter conditions can also lead to decreased physical activity. Physical activity has
been shown to be a determinant of bone mineral density (BMD). Physical activity such as
strength training and running which cause skeletal loading can increase BMD. The
osteoclasts and lining cells of the bone contain mechanoreceptors. These receptors
respond to increased mechanical or electrical stimulation (Rubin and Lanyon, 1984).

23
These physical stimuli are translated into biochemical messages. When this occurs an
increase in 2nd messenger activity is observed in the osteoblasts. Within 10 seconds of
mechanical loading, mRNA levels within the osteoclast increase. In the osteoblast, two
second messenger systems are activated First, adenylate cyclase is activated and cAMP
levels rise. Second, the inositol triphosphate system is activated causing an increase is
inositol diphosphate, protein kinase C, phospholipase A which increase arachidonic acid
entry and formation which leads to the production of PGE2. PGE2 also increases cAMP
(Raisz et al., 1993). The increase in cAMP and PGE2 causes an increase in IGF-I
production and therefore increased bone formation.
Resistance Exercise and Bone Mineral Density
Osteoporosis is a degenerative disease that is characterized by a decrease in bone
mineral density (BMD). This loss makes the bones more susceptible to fractures.
Research has indicated that bone formation can be stimulated by placing a strain on the
bone as is found during resistive exercise (Rubin and Lanyon, 1984). Hamdy et al.(1994)
reported higher BMD in the upper arm in people that weight trained when compared to
runners, but that there was no difference for lower body BMD between the two groups.
Karlsson et al.(1993) reported that active and retired weightlifters had higher BMD for
the spine, hip, tibia, and forearm when compared to controls.
Kohrt et al. (1997) examined the effect of either exercise involving ground reaction
forces (GRF) or joint reaction forces (JRF) on bone mineral density in women aged 60-74
years. Both groups trained for 11 months with the GRF group performing walking,
jogging, and stair climbing while the JRF group performed resistance training and rowing.

24
The resistance training regimen consisted of 8 exercises performed for 2-3 sets, for 8-12
repetitions two times per week. The results indicated significant and similar increases in
BMD for the whole body, lumbar spine, and Ward’s triangle region of the proximal femur
for both groups. Only the GRP group exhibited a significant increase in femoral neck
BMD
Braith et al. (1996) examined the effects of 6 months of resistance exercise on
BMD following heart transplant surgery. Typically, BMD decreases during the post¬
operative period as a consequence of glucocorticoid therapy. The group that performed
strength training was able to return their lumbar, total body, and femoral neck BMD to
near baseline levels while the control group’s BMD remained depressed. Isolated
strength training of the lumbar muscles has also been shown to increase lumbar BMD.
Pollock et al. (1992) showed that 6 months of isolated lumbar training improved lumbar
BMD compared to controls in men and women 60 to 79 years of age.
Menkes et al. (1993) reported a significant increase in femoral neck BMD in
middle-aged to older men following 16 weeks of strength training. The mechanism for
how resistance exercise effects BMD has yet to be determined. It is thought that the strain
placed on bone by loading results in a piezoelectric current which causes an increase in
bone formation. Resistance exercise can also have a significant effect on biochemical
markers of bone metabolism. Menkes et al (1993) reported significant increases in
osteocalcin and skeletal alkaline phosphatase isoenzyme (markers of bone formation) and
a significant decrease in tartrate-resistant acid phosphatase following 16 weeks of training.
However, the results of this study were not replicated in another 16 week study by the

25
same group (Ryan et al., 1994). It is possible that the duration of training was not
adequate to elicit a consistent alteration in the levels of these markers.
Oxidative Stress and Free Radical Production
Free Radicals and Aging
It has been proposed that aging is a consequence of macromolecular disturbances
mediated by oxidative stress (free radical generation)(Harman, 1956, Ji, 1993,and Nohl,
1993, ). Free radicals can be produced in the mitochondria, or in any system that utilizes
oxygen(Yu, 1994). Sites of radical generation are the electron transport chain
(Ubiquinone, Coenzyme Q) and cytochrome P450 in the nucleus as well as other
locations. It has been shown that the mitochondria are prime sites of free radical
production and that damage to DNA is 16 times higher in the mitochondria than in the
nucleus (Yu, 1994). It has also been shown that the mitochondria of aged animals shows
more superoxide (02-) leakage than that of younger animals(Nohl, 1993). Also, free
radicals are produced by xanthine oxidase (XO). During exercise, ATP is converted to
adenosine. At the same time, Xanthine dehydrogenase is converted to XO by the increase
in intracellular calcium seen during exercise. XO acts on the adenosine byproducts to form
uric acid (a free radical) (Yu, 1994).
Oxidative stress is defined as an imbalance between free radical production and the
forces that oppose their production (Jenkins, 1988). Free radicals are also called reactive
oxygen species (ROS). The various forms of free radicals produced are superoxide (02-),
hydroxide (OH), and hydrogen peroxide (H202). These radicals can then take electrons
from other substances and form other radicals and cause damage to biological systems.

26
Common sites for damage are molecules containing sulfhydryl groups (proteins, gates,
DNA), double bonds (Polyunsaturated Fatty Acids, PUFA in membranes), and
carbohydrates (Reid, 1996, and Yu, 1994). The primary defense against this type of
damage includes the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX)
and catalase (CAT). SOD is an enzyme located in the mitochondrial membrane, cytosol,
and plasma (Jenkins, 1988). It scavenges superoxide radicals and converts them to H202.
Although this is still a ROS, it is less reactive than superoxide. H202 can be rendered
harmless by two other enzymes. The first is GPX which uses glutathione to accept the
extra electron and converts the H202 to H20. The glutathione is then regenerated by
glutathione reductase with the help ofNADPH from the pentose phosphate pathway.
H202 can also react with CAT. CAT also converts H202 to H20. One postulated reason
for having the two enzymes is that GPX is active at lower levels of H202 and CAT
becomes active with higher levels.
Superoxide can also be scavenged by dietary antioxidants such as vitamin E, beta
carotene, and vitamin C. Typically, vitamin E is used to squelch superoxide or to insert
itself into the membrane to inhibit the propagation of membrane disruption. Free radicals
will use the double bond site of PUF As in the cell membrane as a place to steal an
electron. This can cause disruption in the membrane because that fatty acid tries to steal
an electron from a neighboring fatty acid. Propagation can result in holes in the cell
membrane. These holes can disrupt the ionic balance of the cell, as well as, allow the
entry of calcium which can activate proteases and cause cellular damage. Vitamin E and
beta carotene are lipid soluble and have long hydrophobic tails. The head of the vitamin E
can accept the free radical and prevent the free radicals from continuing to disrupt the cell

27
membrane. Vitamin E is then recycled through the action of vitamin C and lipoic acid or
through GPX. Although vitamin C is a good antioxidant, it does have a limitation in that
at high levels it can act as a pro-oxidant and promote free radical damage. Lipoic acid
does not scavenge radicals by itself, but rather it serves a supportive function by aiding in
the recycling of vitamin E. Glutathione is the primary thiol scavenger in the antioxidant
defense system. Other minor antioxidants are bilirubin and carbohydrates.
Free radicals and ROS have been implicated as major contributors to the aging
process (Harman, 1956). Aging has been defined as a decreased ability for the cells to
proliferate. This decreased proliferation may be the result of an internal timer within the
cell that when expired, will not allow the cell to survive. It may also be due to impaired
codon transcription (Nohl, 1993, and Yu, 1994), as ROS cross-links proteins. If this
occurred in DNA, then the strand would not be readable. Cross-linking mRNA results in
failure of transcription of the genetic message. Therefore, ROS may be responsible for the
inability to correctly translate the messages found in DNA (Jenkins, 1988, Nohl, 1993, and
Yu, 1994). Ultimately, this could inhibit the cell from proliferating or from correctly
functioning.
Aging is associated with a decrease in muscle mass and strength (sarcopenia). One
cause of a decrease in mass is a loss in muscle fiber number, likely due to a loss of motor
neuron innervation. It has been shown that ROS can negatively impact nerves and either
cause their inactivation or their degeneration (Lou Gehrig’s Disease, Parkinson’s
disease)(Sohal and Orr, 1992). Therefore, ROS are a potential source of denervation and
sarcopenia with aging. ROS can damage the SR and inhibit the release and uptake of
Ca' , leading to decreased contractile force. It has been shown in skinned fiber

28
preparations that the integrity of the contractile element in the muscle fiber remains intact
with aging and does not decrease in force capability (Powers et al., 1994). What does
show impairment is the excitation-contraction coupling (Reid, 1996). ROS have also been
implicated in type I and II diabetes (Yu, 1994). It has been shown that ROS can attack
and deactivate the beta cells in the pancreas which stimulate the release of insulin. It has
also been shown that SOD activity is lower in persons with diabetes. Diabetes is a risk
factor for cardiovascular disease (Yu, 1994).
According to Evans (1995), elderly people experience exacerbated muscle damage
compared to young people as a consequence of exercise. This may be due to several
factors. First, when damage occurs (typically from eccentric contractions) in young,
healthy muscle, neutrophils and lysozymes infiltrate the area and release free radicals as a
means of breaking down damaged tissue. Satellite cells which decrease with age are non
differentiated cells that are next to muscle fibers (Carlson, 1995). They help to repair the
fiber, or can even form new ones. In younger mammals, damaged fibers are replaced with
contractile elements, where in older mammals, contractile elements are replaced with non-
contractile elements like collagen. This would decrease the muscles integrity leaving it
more susceptible to damage.
It has also been shown that tissue levels of vitamin E decrease with age (Yu,
1994). This could be from decreased intake or increased utilization. As mentioned
earlier, aging is associated with increased free radical production. It may also be
associated with or the result of an accumulation of damage incurred by ROS over time. Ji
(1993) showed that with aging, skeletal muscle antioxidant enzyme (AOE) activity
increases. Since AOE activities increase as a result of ROS production the increase in

29
AOE must result from accumulated oxidative stress. This stress may accumulate with
time and cause damage that is outwardly seen as the aging process. Several investigators
have shown that increased metabolic activity has been associated with a shorter life span.
The results have been most clearly demonstrated in fruit flies. When allowed to fly and
mate, their life span decreases compared to those that were kept from flying or
sequestered from the opposite sex.
Exercise and Oxidative Stress
During the aging process, the rate of free radical formation increases (Ji et al.,
1990). This stimulus increases antioxidant enzyme levels that act as defense against this
oxidative stress (Ji, 1993). Increased free radical generation is a signal for an increase in
antioxidant enzyme activity (Jenkins, 1988). Numerous investigations have shown that
acute and chronic exercise can result in an increase in antioxidant enzyme activity
(Hammeren et al., 1992, Ji, 1993, Ji et al., 1991, and Tullson et al., 1994). Aerobic
endurance exercise, particularly intense endurance exercise results in an increase in free
radical generation which also results in increased antioxidant enzyme activities (Tullson et
al., 1994). It has been shown that increasing the metabolic rate or flux of oxygen through
the electron transport system (ETS) promotes ROS generation (Ji, 1993, Powers et al.,
1994, and Reid et al., 1993). As oxygen consumption increases, the possibility ofROS
generation increases. Reid et al. (1993) demonstrated that excessive ROS generation was
related to decreased force production. It has also been shown that ROS can interact with
the sulfhydryl groups on the gates on the sarcoplasmic reticulum and either inhibit the
release or the uptake of Ca” (Reid, 1996). This results in disruption of the force

30
producing capabilities of the muscle and interferes with excitation-contraction coupling
(Reid, 1996). As mentioned earlier, ROS can also cause membrane disruption in the
cellular membrane which would also cause a breakdown in the ionic gradient necessary for
contractions.
Numerous investigators have shown that SOD and GPX levels increase in
response to exercise training (Ji, 1993, Leeuwenburgh et al., 1994, and Powers et al.,
1994). The effects of exercise on CAT activity is not as clear. Therefore, it seems that
ROS generation causes some adaptation which increases antioxidant enzyme (AOE)
activity. This can occur either through promoting the transcription of more enzymes or
through the allosteric modification of existing enzymes allowing them to be more active.
Free radical production can also result from ischemia followed by reperfusion (Das
et al., 1993). During systole, blood flow to the ventricles is momentarily occluded
(ischemia). During diastole, blood flow is restored (reperfiision). During exercise, the
period of diastole and therefore reperfiision is decreased. This type of cycle has been
shown to increase ROS generation and can cause damage to the myocardium or to the
vasculature (Yu, 1994). A similar ischemia/ reperfusion cycle may be present in skeletal
muscle during resistance exercise. Muscular contractions greater than 40% of the maximal
voluntary contraction (MVC) as performed during resistance exercise result in transient
blood flow occlusion in the exercising muscle (Donald et al., 1967). This form of
ischemia/reperfusion could possibly increase antioxidant enzyme activities that leading to
improved defense against oxidative stress. Recently, McBride et al. (1998) demonstrated
that intense resistance exercise causes an increase in free radical production. Subjects
performed 10 repetitions for 3 sets with 1 minute rest periods between sets for 8 exercises.

31
The results showed an increase in malondialdehyde (MDA) levels which indicates an
increase in free radical production. A recent investigation has also demonstrated that
intermittent sprint cycling performed three times per week for 6 weeks followed by a
seventh week with five sessions resulted in an increase in antioxidant enzyme activity
(Hellsten et al., 1996). The subjects performed fifteen 10 second maximal sprints with a
50 second rest period between each sprint during each training session(Hellsten et al.,
1996). Resistance exercise induces a metabolic stress similar to that seen during sprint
exercise. Therefore, resistance exercise may elicit similar increases in antioxidant enzyme
activity observed during sprint exercise.
The same exercise-induced increases in free radical production and elevations in
antioxidant enzyme activities have been shown in senescent animals (Ji, 1993,
Leeuwenburgh et al., 1994, and Powers et al., 1994). As a consequence of endurance
exercise, AOE activities were upregulated to the same extent as in younger animals.
Exercise Prescription for Older Adults
The American College of Sports Medicine (ACSM) currently recommends that
resistance exercise be incorporated as a component of a well-rounded exercise program
for all healthy adults (ACSM,1990). The ACSM recommends 1 set of 8-12 repetitions for
younger adults and 10-15 repetitions for adults over 50-60yr., using 8-10 exercises,
performed 2-3days per week (ACSM, 1990, 1998). The greater repetitions for older
adults is used to decrease the risk of orthopedic injuries which may result from lifting
increased loads associated with low volume higher intensity efforts, while the range in age
reflects individual differences towards weakness or frailty. When initiating an exercise

32
regimen for older adults, it is recommended that the initial resistance used should be 30-
40% of their one repetition maximum (1-RM) for that exercise(Pollock et al., 1994). If a
1-RM is not available, start with a low resistance and progress slowly allowing time for
muscle and soft tissue adaptation. The current intensity recommendation for older adults
corresponds to an RPE of 12-13 (somewhat hard) initially (first 4-6 wk) and then progress
to 14 to 16 (hard) on the RPE scale (Pollock et al., 1994). The intensity should be
perceived as hard by the participant, but should not be to voluntary failure as is
recommended for younger adults until approximately 12 weeks (ACSM, 1990). This time
period should be taken as an estimate, the 12 weeks could be lengthened or shortened
depending on the health status or level of fitness of the individual. Once older adults adapt
to their resistance training regimen, most will be capable of progressing to 10-15RM.

CHAPTER 3
METHODS
Subjects
The participants for this study were apparently healthy adults between the ages of
60 and 85 years. Eighty-six participants were entered into the study and sixty-two
completed the protocol. Participants were recruited from the Gainesville, Florida and the
surrounding areas. All participants had not participated in in regular resistance training for
at least one year, but may have been engaged in low-intensity aerobic training equal to or
less than 3 times per week.
Subject Eligibility
Inclusion Criteria
Subjects were considered eligible for participation if they were:
• aged 60-85 years
• not participating in regular resistance exercise for at least one year
• free from any orthopedic or cardiovascular problems that would limit exercise
33

34
Exclusion Criteria
Subjects were excluded from study participation if they:
• Participated in regular resistance exercise during the last year or regular moderate
to high intensity aerobic training.
• had known orthopedic, cardiovascular or non-cardiovascular abnormalities that
would preclude participation in exercise.
• Had any abnormalities identified by the American College of Sports Medicine
(ACSM) as absolute or relative criteria for discontinuing exercise as revealed during a
symptom limited graded exercise test (SL-GXT) (3)
Study Design
This investigation was conducted at the Center for Exercise Science located in the
Florida Gym at the University of Florida. Participants were matched and randomly
assigned to 1 of the following three groups:
low-intensity resistance exercise (LEX)
high-intensity resistance exercise (HEX)
wait list control (CON)
Subjects were matched using a composite strength score calculated by adding the chest
press and leg press one-repetition maximum (1RM) values. Three subjects were matched
using the composite strength score when their pre-testing visits were completed and were
then randomly assigned to one of the three groups. Randomization was performed using a
random numbers table. Muscle strength and endurance, bone metabolism, serum lipid

35
peroxidation, and physical function were measured before and after the 6 month training
period.
Participants were scheduled for seven visits prior to the start of the training period.
Visit 1: Participants read and signed an informed consent, and were given an explanation
of the study. They also received an orientation to the resistance exercise machines and the
treadmill protocol that was used during the graded exercise test. Visit 2: Participants
were given an SL-GXT (Naughton protocol) whereby blood pressure, heart rate, ECG,
and symptoms were monitored by a physician. The GXT was terminated upon volitional
fatigue of the subject and/or according to the guidelines established by the American
College of Sports Medicine (3). A blood sample was also collected before and after the
GXT to measure biochemical markers of bone turnover and antioxidant enzyme capacity.
Visit 3: Participants had their maximum strength measured by determining the maximum
load that they could lift for 1 repetition (1-RM) on the leg press, chest press, leg curl, and
biceps curl. Visit 4: Participants had their muscular endurance measured on the leg press
and chest press. They were asked to perform as many repetitions as possible without
assistance while maintaining proper form using 60% of their previously determined 1-RM.
Visit 5: Each subject had their total body and regional bone mineral density measured
using dual-energy X-ray absorptiometry (DXA), Visit 6: Participants were asked to
ascend one flight of stairs as quickly as possible. Two trials were performed. Maximal
isometric strength for the lumbar extensor muscles was measured using a seven angle
lumbar extension test. Visit 7: Body composition was determined using a seven site
skinfold technique. Participants had their maximum strength measured by determining the

maximum load that they could lift for 1 repetition (1-RM) on the seated row, overhead
press, triceps dip, and knee extension.
36
Experimental Protocol
Visit 1. Screening / Orientation
All potential participants were recruited from Gainesville and the surrounding area.
Those volunteers who had no contraindications (see exclusion criteria) were asked to
participate in the study. All participants received a comprehensive explanation of the
proposed study, its benefits, inherent risks, and expected commitments with regard to
time. Following the explanation of the proposed study, all participants were allowed a
period of questioning. Those participants who were willing to participate were required to
read and sign an informed consent document, complete a self-reported activity, medical
history, and dietary questionnaires. Participants were then given an orientation to the
resistance exercise machines and equipment used during the GXT by trained personnel.
The resistance exercise equipment for this investigation was MedX resistance machines
(MedX Corp., Ocala, FL). These machines were selected because their design allows for
proper positioning and weight increases for frail or diseased populations. The smallest
increment of load increase is 2 ft-pounds as opposed to 5 or 10 pounds found with other
such exercise equipment. Participants were instructed as to the proper positioning and
exercise form for each machine. Participants performed 10-15 repetitions on each
machine using a light load (20 ft-lb). The machines used for this study were abdominal
crunch, leg press, leg extension, leg curl, calf press, seated row, chest press, overhead
press, biceps curl, seated dip, leg abduction, leg adduction, and lumbar extensions. The

37
participants were then allowed to walk on the treadmill and practice breathing through the
headgear which was used to collect expired air used for the determination of VO2pe.1t
during the GXT. The subjects walked on the treadmill at 2.0 m.p.h. at a 0% grade for 3
minutes followed by 2 minutes at 2.0 m.p.h. at a 3% grade.
Visit 2. Treadmill Graded Exercise Test and Blood Sample Collection
On visit 2, participants reported to the Center for Exercise after a three hour fast.
Upon arrival participants were seated in a quiet room for 15 minutes where after resting
heart rate (HR), and blood pressure (BP) were obtained using standard auscultation
procedures and a Trimline mercury sphygmomanometer (Pymah Co., Somerville, N.J.). A
medical examination was performed by a physician specializing in geriatric medicine. A 30
ml blood sample was collected via venipuncture of an antecubital vein and used for
measuring bone metabolism and lipid peroxidation. The sample was allowed to clot at
room temperature for 10-20 minutes and then centrifuged for 15 minutes at 0°C. The
serum was then pipetted into polystyrene tubes and stored at minus 80°C for later analysis.
Samples were analyzed for osteocalcin, skeletal alkaline phosphate isoenzyme, and
pyridinoline crosslinks. Osteocalcin and skeletal alkaline phosphate are markers of bone
formation while pyridiniline crosslinks is a marker of bone resorption. All three
biochemical markers have been shown to be valid indicators of bone turnover and sensitive
to changes with exercise (Menkes et al., 1993, Thorsen et al., 1996). The samples were
collected before the test and repeated within 10 minutes following the conclusion of the
GXT.
a

38
The subject performed a walking SL-GXT using an incremental treadmill exercise
protocol (Naughton) to determine peak oxygen consumption (V02peak) The initial
workload was 2.0 m.p.h. at 0% grade and was progressed every two minutes by
increasing the grade 3.5%. Once the test time reached 12 minutes, the treadmill speed
increased to 3.0 m.p.h. and the incline decreased to a 12% grade. From this point, the
grade again increased 3.5% every 2 minutes until the subject reached voluntary maximal
exertion or became symptomatic with positive hemodynamic or medical indices (3). The
following criteria recommended by the ACSM were used for termination of the SL-GXT
(3).
• Fatigue
• Failure of monitoring equipment
• Light-headedness, confusion, ataxia, cyanosis, dyspnea, nausea or any peripheral
• circulatory insufficiency
• Onset of grade II/III angina pectoris (moderate to severe) with exercise
• Mild angina pectoris with 2 mm of ST segment depression
• Symptomatic supraventricular tachycardia
• ST displacement 4 mm or greater in the absence of angina pectoris
• Ventricular tachycardia (3 or more consecutive PVC’s)
• Exercise induced left bundle branch block
• Onset of second and/or third degree A-V block
• R on T PVC’s (one)
• Frequent multifocal PVC’s (30% of the complexes)

39
• Excessive hypotension (greater than 20mmhg drop in systolic BP during
exercise)
• Excessive BP rise: systolic BP greater or equal to 240 or diastolic BP greater
or equal to 110 mm Hg)
• Inappropriate bradycardia (drop in HR greater than 10 beats/min) with an
increase or no change in workload.
During the test, expired gases were collected through a low-resistance one-way
valve (Hans Rudolph). Breath by breath analysis of expired gases was performed
continuously throughout the test using a Medical Graphics Corporation Metabolic Cart
(CPS/Max Medical Graphics TM, St. Paul, MN). The oxygen and carbon dioxide
analyzers were calibrated daily and immediately before and after each test using a known
gas mixture of 12.0% 02 and 5% C02. Ventilatory responses (tidal volume and
frequency of breathing) were measured with a pneumotachograph. Volume calibration was
performed with a 3-liter calibration syringe. Twelve lead electrocardiograms (ECG) were
recorded throughout the test using standard lead placement with a Quinton Q 2000 system
(Quinton Instruments, Seattle, WA). Blood pressure measurements were taken every
other minute using a standard sphygmomanometer and RPE was obtained at the end of
each minute throughout the test using Borg’s RPE 6-20 point scale.
Visit 3. Muscular Strength Assessment
During visit 3, dynamic muscular strength was measured using four resistance
exercises which included: chest press, leg press, leg curl, and biceps curl. For each
dynamic exercise, a one repetition maximum (1-RM) was determined. Participants were

40
properly positioned in the machine and performed a dynamic warm-up using a light
weight. The participant began the test by lifting a light weight and then incremental
increases of 5-10 pounds were made according to the difficulty with which the participant
executed the previous lift. Difficulty was measured by having the participant rate his/her
exertion level using the RPE scale. Two to three minutes rest were given between trials to
prevent premature fatigue. The investigator continued to increase the weight lifted until
reaching the maximum weight that could be lifted in one repetition. This was usually
determined in 5 to 6 trials. Maximal strength was defined as the maximum weight that
could be lifted through a full range of motion with proper form.
Visit 4. Muscular Endurance
During visit 4, assessment of muscular endurance was performed on the chest
press and leg press resistance machines. The participants were properly positioned in the
appropriate machine and allowed a dynamic warm-up with a light weight. The subject
then performed as many repetitions as possible with proper form using 60% of their
previously determined 1-RM. The endurance test for the leg press was always performed
first.
Visit 5: Bone Mineral Density
Bone mineral density (BMD) was assessed using dual energy x-ray absorptiometry
(DXA) (DXA model DPX-L, Lunar Radiation Corp., Madison, WI). DXA is a non-
invasive radiologic projection technique which uses both low and higher energy x-ray
tubes as an energy source. However, radiation exposure is minimal (approximately 1/60

41
of the dose of a chest x-ray). DXA also provides body composition information. During
a DXA scan, the subject was positioned either in a supine or lateral position while the x-
ray scanner performed a series of transverse scans, measured at 1-cm intervals from the
top to the bottom of the region. Four separate skeletal regions were scanned: 1)
anterior/posterior (AP) view of the total body; 2) AP view of the lumbar spine; 3) AP
view of the hips; and 4) lateral view of the lumbar spine.
Visit 6, Balance. Stair Climbing, and Isometric Lumbar Extension Strength
On visit 6, participants were assessed for time to walk up one flight of stairs, and
isolated lumbar extension strength. The participants were asked to walk up a flight of
stairs consisting of 23 steps as quickly as possible. The stairs were 6.5 in. high and 11.5
in. wide. After 14 steps the participants made a left-hand wrap-around turn and then
completed the remaining 9 steps. The participants were not allowed to use the handrails.
The time to complete this task was recorded to the nearest hundredth of a second using a
hand held stopwatch. Participants were required step on all of the steps, taking 2 steps at
a time was not allowed. This test was repeated following a 2-3 minute rest period and the
fastest of the two trials was used for data analysis.
Isometric lumbar extension strength was also tested. Prior to the test, participants
performed a series of stretching exercises and a dynamic variable resistance exercise
session designed to stretch and warm-up the low back, hamstrings, and abdominal areas.
For the dynamic exercise, participants were seated in the MedX isolated lumbar extension
machine (MedX, Ocala, FL) and secured in place by restraints positioned under the feet,
anterior thigh, and posterior pelvis. These restraints restrict movement of the pelvis,
I

42
which facilitates isolation of the lumbar extensor muscles. The participants then moved
from flexion to extension through a full range ROM. Men warmed-up with 40 pounds and
women with 20 pounds for 10 repetitions. This series of stretching and dynamic exercises
lasted approximately 10 minutes. Following the dynamic exercise session participants
completed an isometric test of lumbar extensor muscle strength. Seven testing points (0,
12, 24, 36, 48, 60, and 72 degrees of lumbar flexion) were measured for participants who
had a full range of lumbar motion. The specific angles were modified for those
participants with limited ROM. A maximum isometric contraction was generated at each
o
of these angles beginning with 72 of flexion. Participants were instructed to extend back
slowly building up tension over a 2 to 3 second period. Once maximal tension had been
developed, participants were encouraged to maintain maximal force for an additional 1 to
2 seconds, then slowly relax. Following each isometric contraction was a 10 second rest
period while the next position was set. In this manner a force curve was generated
throughout the ROM for each subject. Participants were given verbal encouragement
during the lifts to ensure a maximal effort.
Visit 7, Body Composition and Muscular Strength Assessment
On visit 7, the participant had their body composition assessed using skinfolds and
1RM muscular strength was determined for the seated row, overhead press, triceps dip,
and knee extension. The procedure for 1RM determination was the same as for visit 3.
Skinfold measurements were taken to the nearest 0.5 mm on the right side of the body
using a Lange caliper (Cambridge Scientific Industries, Cambridge, MD). Seven sites were
measured: chest, axilla, triceps, subscapular, abdomen, suprailiac, and anterior thigh. The

43
landmarks and techniques of Pollock and Wilmore (35) were used for the skinfold
measurements:
Chest fold: The skinfold thickness of the chest was measured as an oblique fold one half
the distance between the anterior axillary line and the nipple for men and one third of the
distance from the anterior axillary line and the equivalent position for women.
Axilla fold: The axilla skinfold was measured as a vertical fold on the midaxillary line at
the level of the xiphoid process of the sternum.
Triceps fold: The triceps fold was measured as a vertical fold midway between the
olecranon and acromium process on the posterior of the brachium with the elbow relaxed
and extended.
Subscapular fold: The subscapular fold was taken on a diagonal line coming from the
vertebral border to 1-2 cm from the inferior angle of the scapula.
Abdominal fold: The subject stood erect with body weight evenly distributed on both feet.
The abdominal skinfold was measured as a vertical fold taken 2 cm lateral to and at the
level of the umbilicus.
Suprailiac fold: The suprailiac skinfold was measured from a diagonal fold at the anterior
axillary line immediately above the crest of the ilium.
Anterior thigh fold: A thigh skinfold was be taken with the subject standing with his/her
weight on the left foot, with a relaxed and slightly flexed right leg. The measurement was
made as a vertical fold located on the midline of the anterior aspect of the thigh midway
between the inguinal crease and the proximal border of the patella.

44
Training Period: Six Months of Dynamic Resistance Exercise
Participants in both the high- and low-intensity training groups were asked to
report to the CES three times per week for 6 months to perform dynamic variable
resistance exercise under the supervision of trained personnel for all machines except the
isolated lumbar extension exercise. Isolated lumbar extensions were performed once per
week under the supervision of personnel certified for the use of MedX rehabilitation
equipment. Each subject received appropriate instruction concerning warm-up and cool¬
down techniques, as well as how to monitor the intensity of the exercise using the RPE
scale. Each subject performed one set on each of the following resistance exercise
machines: abdominal crunch, leg press, leg extension, leg curl, calf press, seated row,
chest press, overhead press, biceps curl, seated dip, and lumbar extensions. There was a 2
minute rest period allowed between each machine. Each set consisted of 8 repetitions for
the HEX group and 13 repetitions for the LEX group at the appropriate resistance load.
To examine the effects of training intensity on the outcome variables and criterion
measures, the LEX group trained at an intensity equivalent to 50% of their 1RM, while
the HEX group used loads corresponding 80% of their 1RM. For the LEX and HEX
groups, the load was increased by 5% when their RPE rating dropped below 18. The
rationale for training the lumbar extensor muscles only one day per week is derived from
previous research in this lab showing that 1 set of this exercise once per week is adequate
for improvements in lumbar strength and that training more often does not provide
superior results. Prior to the dynamic exercise, participants performed the series of
stretches. Participants were then secured in the lumbar extension machine Once secure
the subject was instructed to complete a warm-up set of dynamic variable resistance

45
lumbar extension exercise using 50 percent of their current training weight. Participants
began the dynamic exercise in the fully flexed position (72°), extending their trunk back
against the back pad lifting the weightload over a 2-3 second count. After pausing briefly
in the fully extended position (0°), the subject was instructed to slowly flex their trunk
forward to the starting position over a 4 second count. The combined movement of
extension, brief pause, and flexion constitutes one repetition. The HEX group performed
10 repetitions, while the LEX group performed 15 repetitions.
Biochemical Assays
Markers of Bone Metabolism
Alkaline Phosphatase-B
The bone-specific alkaline phosphatase isoform (BAP) was measured in serum
using an Alkphase-B(r) enzymatic immunoassay kit (EIA) (Metra Biosystems, Mountain
View, CA, USA). The assay is highly specific for BAP, cross-reacting <=8% with liver
AP and not significantly with other AP isoenzymes. The Alkphase-B kit or EIA used
microtiter stripwell format utilizing a monoclonal anti-BAP antibody and the catalytic
activity of the captured enzyme itself to measure BAP activity in serum. BAP in the
sample binds to antibody coated on the stripwell and the reaction is detected with the
substrate, p-nitrophenyl phosphate (pNPP). Color developed during the incubation of
captured BAP and substrate is measured at 405 nm in a microtiter plate reader. BAP
values of unknown specimens are calculated from a calibration curve fit with a quadratic
equation. Values are expressed in U/L; each unit represents one mole of pNPP

46
hydrolyzed per minute at 25°C in 2-amino-2-methyl-l-propanol buffer. 20 pL of serum
per well (assayed in duplicate) was required for determination of BAP.
Osteocalcin
Osteocalcin (OC) also known as bone gla protein was measured with a
NovoCalcin(r) EIA kit (Metra Biosystems, Mountain View, CA, USA), a microtiter
stripwell format utilizing a murine monoclonal anti-OC antibody. [4] OC in the sample
competes for antibody binding sites with OC coated on the stripwell. A rabbit anti-mouse
IgG antibody conjugated to alkaline phosphatase is added and the reaction is detected with
the substrate, p-nitrophenyl phosphate. Color developed during the incubation of
captured enzyme conjugate and substrate is measured at 405 nm in a microtiter plate
reader. OC values of unknown specimens are calculated from a calibration curve fit with a
4-parameter logistic equation. Values are expressed in ng/mL. 25 pL of serum per well
(assayed in duplicate) is required for determination of OC.
Pvridinoline Crosslinks
Serum pyridinoline crosslinks were measured with Serum Pyd(r) EIA kit
purchased from Metra Biosystems (Mountain View, CA, USA). The EIA kit uses a
microtiter stripwell format utilizing a rabbit monoclonal anti-PYD antibody. PYD in the
sample competes for antibody binding sites with PYD coated on the stripwell. A goat
anti-rabbit IgG antibody conjugated to alkaline phosphatase is added and the reaction is
detected with the substrate, p-nitrophenyl phosphate. Color developed during the
incubation of captured enzyme conjugate and substrate is measured at 405 nm in a

47
microtiter plate reader. PYD values of unknown specimens are calculated from a
calibration curve fit with a 4-parameter logistic equation. Values are expressed in nmol/L.
25 |iL of serum per well (assayed in duplicate) is required for determination of serum
PYD.
Biochemical Indicators of Oxidative Stress
Lipid Peroxidation Measurements
Malondialdehyde levels were determined spectrophotometrically using the
thiobarbituric acid-reactive substances (TBARS) method previously described (Uchiyama
and Mihara, 1978). The agent 1,1,3,3-tetraethoxypropane was used as the standard for
this assay. Samples were performed in duplicate.
Lipid hydroperoxides were quantified using the ferrous oxidation/xylenol orange
technique previously reported (Hermes-Lima et al. 1995). Cumene hydroperoxide was
used as the standard for this assay. All samples were performed in triplicate. In our
laboratory, the coefficients of variation for the TBARS and lipid hydroperoxide assays are
-3 and 4 percent, respectively.
Oxidative Challenges in vitro
To investigate the relationship between obesity and myocardial antioxidant
capacity, the serum was subjected to a series of several different ROS-generating systems.
Serum aliquots were incubated at a concentration of 7 mg protein/ml in the presence of an
ROS generating system. Following each challenge, the aliquots were analyzed for lipid
peroxidation using the technique of Uchiyama and Mihara (1978).

48
Xanthine-Xanthine Oxidase System (Superoxide Generator-),
Superoxide radicals were generated by the reactions involved in a xanthine-
xanthine oxidase system similar to the technique described by Reid et al. (1992). One ml
of 1 mM xanthine and 0.1IU xanthine oxidase were added to a 1 ml aliquot of serum and
incubated at 37°C for 15 min.
Hydrogen Peroxide System
One ml of hydrogen peroxide (100 mM) was added directly to a one ml aliquot of
serum and incubated at 37°C for 15 min according to the method of Scott et al. (1987).
Ferric Chloride System ('Hydroxyl Generator!
Hydroxyl radicals were produced in the serum by adding 0.1 mM ferric chloride
(FeCy. The choice of these particular concentrations is based on the work of Bernier et
al. (1986).
Statistical Analyses
Statistical analyses were performed using the Statistical Package for the Social
Sciences (SPSS) software (version 9.0). Experimental analysis was performed with a3 x 2
repeated-measures analysis of variance (ANOVA) model to determine differences within
and between groups over time. If a significant (group x time) interaction was found, the
appropriate post-hoc procedures were applied. The post-hoc procedure used for this
investigation was a one-way ANOVA with a Scheffé post-hoc test to determine if and

49
where there was a difference between the group means. Although no statistical differences
were observed between groups at study entry, an analysis of covariance (ANCOVA) was
performed on outcome variables at conclusion of the study. When the ANCOVA revealed
that the covariate significantly contributed to the outcome, then the predicted means
generated by the ANCOVA were analyzed with a one-way ANOVA and a Scheffé post-
hoc test. Pearson bivariate correlations were performed to examine the degree of
association between variables. A-priori alpha levels were set at 0.05.

CHAPTER 4
RESULTS
Throughout the results section PRE will refer to testing completed prior to the six
month training or control period, and POST will refer to testing completed after the six
month training or control period. In all tables and figures, the values presented are means
plus and minus standard deviation. At study entry, there were no significant differences
between any of the experimental groups. As a further precaution against the influence of
any pre-training differences, ANCOVAs were performed on all outcome variables.
Subject Characteristics
The characteristics for the participants in this study are presented in Table 4.1.
The groups did not significantly differ with respect to any of the variables listed (p>0.05).
Correlation between pre-training percent body fat measured by skinfold and DXA was
0.86 (p<0.01) with no significant difference between methods. Correlation between post¬
training percent body fat measured by skinfold and DXA was 0.91 (p<0.01) with no
significant difference between methods.
50

51
Table 4.1. Subject Characteristics
VARIABLES
CON (n=16)
LEX (n=24)
HEX (n=22)
PRE
POST
PRE
POST
PRE
POST
AGE
(yrs.)
71.014.7
67.616.3
66.616.7
HEIGHT
(cm)
169.9110
167.2111.5
167.119.7
WEIGHT
(kg)
73.1113.8
71.0114.3
77.4119.3
74.4116.5
74.1114.8
74.8115
SKINFOLD
%FAT
30.317.5
28.917.4
30.916.0
29.015.1
32.017.8
29.917.8
DXA %FAT
33.517.4
34.417.2
34.118.9
34.118.4
35.918.6
36.219.0
FAT FREE
MASS (kg)
46.5110.5
46.0110.6
50.5114.6
48.7113.3
47.7112
47.9112
Values are mean 1 SD. CON = control group, LEX = low-intensity group, HEX = high-
intensity group. DXA = dual energy x-ray absorptiometry

52
Aerobic Endurance
Oxygen Consumption
Values for peak oxygen consumption (V02pe»k) are presented in Table 4.2. The
absolute and percent changes for V02peakare shown in Figures 1 and 2, respectively. As
shown in Figure 1, both the LEX and HEX groups significantly increased V02pcak during
the six months of resistance exercise (p<0.05). However, the CON group did not change
during the control period. Peak oxygen consumption increased 23.5% and 20.1% for the
LEX and FIEX groups, respectively (Figure2.), which was significantly greater than the
percent change for the CON group (p<0.05).
Treadmill Time to Exhaustion
Treadmill time to exhaustion during the graded exercise test is presented in Table
4.2 and figures 3 and 4. The CON, LEX, and HEX groups increased treadmill time by
6.2%, 26.4% and 23.3%, respectively. However, only the LEX and HEX groups
significantly increased their treadmill time from PRE to POST (p<0.05).
Time to Ascend One Flight of Stairs
The stairs used for this test consisted of 22 steps which had to be completed by
touching every step and not holding the railing. Climb data can be found in Table 4.4, and
Figures 4 and 5. Both the LEX and HEX groups significantly decreased the time
necessary to ascend one flight of stairs following training (p<0.05). The LEX and FIEX
groups decreased stair time by 7.3 and 5.8 percent, respectively. However, only the

53
Table 4.2. Comparison of Peak Oxygen Consumption and Treadmill Time to Exhaustion
for the CON, LEX, and HEX groups During a Graded Exercise Test
VARIABLES
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
VOipeak
(ml.kg'.mm‘)
22.6±3.4
22.413.4
20.214.3
24.714.8*
20.916.1
24.415.8*
V02p^
(%Change)
-0.4112.0
23.5114.1**
20.1123.7**
TREADMILL
(min)
11.512.5
12.112.5
11.212.3
14.013.1*
12.213.4
15.014.9* +
TREADMILL
(%Change)
6.2111.4
26.4123.7**
23.3123.1
Values are mean ± SD. *p<0.05 vs PRE, **p<0.05 vs CON. +p<0.05 vs. CON (ANCOVA)
CON = control group, LEX = low-intensity group, HEX = high-intensity group. TREADMILL =
treadmill time to exhaustion during GXT.

54
percent change from pre- to post-training in the LEX group was significantly different
than the CON group (p<0.05).
Changes in Muscular Strength
Chest Press
Muscular strength were determined by determining the maximum amount of
weight that could be lifted for one repetition with good form (1RM). Chest press strength
adaptations to the six months of training are displayed in Table 4.3. The absolute 1EM
values, 1RM normalized for fat free mass (relative), and percent changes in 1RM strength
from pre- to post-training are shown in Figures 7, 8, and 9, respectively. Both the LEX
and HEX groups, but not CON, increased absolute and relative 1RM strength significantly
from pre- to post-training (p<0.05).
Leg Press
Leg press strength adaptations to the six months of training are displayed in Table
4.3 and Figures 10,11, and 12. Both the LEX and HEX groups, but not CON, increased
absolute and relative 1RM strength significantly from PRE to POST-training (p<0.05).
Leg Curl
Leg curl strength adaptations to the six months of training are displayed in Table
4.3 and Figures 13, 14 and 15. Both the LEX and F1EX groups, but not CON, increased
absolute and relative 1RM strength significantly from pre- to post-training (p<0.05).

55
Biceps Curl
Biceps curl strength adaptations to the six months of training are displayed in
Table 4.3 and Figures 16, 17, and 18. Both the LEX and HEX groups, but not CON,
increased absolute and relative 1RM strength significantly from pre- to post-training
(p<0.05).
Seated Row
Seated row strength adaptations to the six months of training are displayed in
Table 4.3 and Figures 19, 20, and 21. Both the LEX and HEX groups, but not CON,
increased absolute and relative 1RM strength significantly from pre- to post-training
(p<0.05).
Overhead Press
Overhead press strength adaptations to the six months of training are displayed in
Table 4.3 and Figures 22, 23, and 24. Both the LEX and HEX groups increased absolute
and relative 1RM strength significantly from pre- to post-training (p<0.05).
Triceps Dip
Triceps dip strength adaptations to the six months of training are displayed in
Table 4.3 and Figures 25, 26, and 27. Both the LEX and HEX groups, but not CON,
increased absolute and relative 1RM strength significantly from pre- to post-training
(p<0.05).

56
Table 4.3. Comparison of Changes in Muscular Strength for the CON, LEX, and HEX
Groups Following Six Months of Resistance Training.
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
CP 1RM
191.7192.3
184.9190.0
223.71116.2
258.81129.8*+
254.31141
287.71157.3*+
CP REL
4.111.1
3.911.2
4.111.4
4.911.3*
5.011.6
5.611.7* ••+
CP %A
-1.2119.9
17.5113.5**
16.0116.6**
LP 1RM
329.1178.4
329.2182.3
401.01120.1
469.11158.6* *•+
375.41171
469.11196.6*
LP REL
7.011.1
7.212.2
7.912.2
9.312.0* *• +
7.711.7
9.7Í2.35 •*+
LP %A
1.5122.3
15.7115.9
27.6118.3**
LC 1RM
180.3155.2
179.2159.2
174.5159.4
217.1173.8*
209.5183.4
246.81108.7*
LC REL
3.810.6
3.810.7
3.510.7
4.410.4*+
4.311
5.011.1* •• +
LC %A
-0.7110
25.3113.4**
17.319.5**
BC 1RM
113.8148.3
107.1144.6
118.4149.8
138.8158.2*
114.4144.9
143.9165.8*
BC REL
2.310.7
2.310.6
2.210.6
2.710.5*
2.410.5
3.010.7* ••+
BC %A
-3.8116.2
17.819.8**
24.6114.3**
SR 1RM
252.6192.9
268.01101.4
318.91125.5
276.21136.9*+
228.81109
376.51140*+
SR REL
5.411.0
5.811.1
5.911.3
7.211.1* **+
6.311.0
7.611.2* **+
SR %A
6.5116.4
19.2111.4**
22.1115.9**
OP 1RM
176.1173.9
169.5178.5
215.3198.4
251.61110.6*
220.51113
257.11135.4*
OP REL
3.711.0
3.611.1
3.911.1
4.811.0*+
4.511.3
5.211.5* **+
OP %A
-3.6118.0
18.8111.7**
16.6110.0**
TO 1RM
219.8169.4
217.7167.7
263.2195.7
310.51111* *•+
265.2199.9
307.91123* **
TO REL
4.710.6
4.810.6
4.810.9
5.910.8* *•+
5.411.0
6.211.2* **+
TO %A
-0.715.8
18.519**
16.1110.0**
LE1RM
234.0175.4
222.9174.7
276.21102
305.61114*
298.11123
347.11167*
LEREL
5.011.0
4.910.9
5.311.0
5.811.0*
5.911.3
6.8ÍÍ.95 ••+
LE%A
-4.618
10.817.3**
14.6111.8**
TS 1RM
16971537
16781535
17191696
20291818*
19091850
226311078*
TS REL
36.014.4
36.016.6
32.219.2
38.518.8*
38.518.9
45.3112.0*+
TS %A
-1.116.3
17.219.7**
17.817.8**
Values are mean ± SD. »p<0.05 vs PRE, *»p<0.05 vs CON. +p<0.05 vs CON (ANCOVA)CON
= control group, LEX = low-intensity group, HEX - high-intensity group. CP = chest press, LP =
leg press, LC = leg curl, BC = biceps curl, SR - seated row, OP = overhead press, TD - triceps
dip, LE = leg extension. TS = total strength. 1RM= one repetition maximum. REL = relative
change (Nm/kg FFM), %A - percent change from PRE to POST.

57
Leg Extension
Leg extension strength adaptations to the six months of training are displayed in
Table 4.3 and Figures 28, 29, and 30. Both the LEX and HEX groups, but not CON,
increased absolute 1RM strength significantly from pre- to post-training (p<0.05).
Total Strength
The result for total strength was computed by summing the 1RM values for the
chest press, leg press, leg curl, biceps curl, seated row, overhead press, triceps dip, and leg
extension. The means and standard deviations for total strength for each of the three
experimental groups can be found in Table 4.3. The results for total strength expressed in
absolute numbers (Nm), relative to fat free mass (Nm/kg FFM), and as percent change
from pre- to post-training are shown in Figures 31, 32, and 33, respectively. Both the
LEX and HEX groups, but not CON, significantly increased absolute and relative force
output from pre to post-training (p<0.05).
Muscular Endurance
Chest Press
Chest press endurance data can be found in Table 4.4. The results for number of
repetitions and percent change from pre- to post-training for chest press endurance are
shown in Figures 34 and 35, respectively. Both the LEX and HEX groups, but not CON,
significantly increased the number of repetitions performed from pre- to post-training
(p<0.05).

58
Lee Press
Leg press endurance data can be found in Table 4.4. The results for number of
repetitions and percent change from pre- to post-training for chest press endurance are
shown in Figures 36 and 37, respectively. Both the LEX and HEX groups, but not CON,
significantly increased the number of repetitions performed from pre- to post-training
(p<0.05).
Table 4.4. Comparison of Stair Climbing Time, Chest Press and Leg Press Endurance for
the CON, LEX, and HEX Groups Following Six Months of Resistance Training
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
STAIRS (s)
9.1±1.2
9.011.0
9.411.7
8.6911.4*
8.2311.8
7.7711.7*+
STAIRS
%A
-0.5816.7
-7.3116.4*
-5.7917.56
CHEST
(reps)
17.615.8
16.915.3
16.914.5
28.617.6* **+
17.118.7
27.4112* **+
CHEST
%A
-0.05132
75.5147.4**
68.0135.2**
LEG (reps)
32.2116.3
29.4118
26.319.4
45.0120*+
25.1113.4
48.3124.5*+
LEG %A
-5.0143.7
79.2180.6**
105194.3**
Values are mean ± SD. *p<0.05 vs PRE, **p<0.05 vs CON. +p<0.05 vs CON (ANCOVA)
CON = control group, LEX = low-intensity group, HEX = high-intensity group. STAIRS = time to
ascend one flight of stairs. CHEST = chest press endurance. LEG = leg press endurance.

59
Lumbar Extension Strength
Lumbar extension strength was measured isometrically at 7 different angles of
lumbar flexion and is expressed in Newton meters (Nm). The seven angles used for this
test were 0, 12, 24, 36, 48, 60, and 72 degrees of lumbar flexion.
0° of Lumbar Flexion
Lumbar extension strength values at 0° of lumbar flexion can be found in Table 4.5
and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly
increased both absolute and relative force output from pre- to post-training (p<0.05).
12° of Lumbar Flexion
Lumbar extension strength values at 12° of lumbar flexion can be found in Table
4.5 and Figures 38, 39, and 40. Both the LEX and HEX groups, but not CON,
significantly increased both absolute and relative force output from pre- to post-training
(p<0.05).
24° of Lumbar Flexion
Lumbar extension strength values at 24° of lumbar flexion can be found in Table
4.5 and Figures 38, 39, and40. Both the LEX and FIEX groups, but not CON,
significantly increased both absolute and relative force output from pre- to post-training
(p<0.05).

60
36° of Lumbar Flexion
Lumbar extension strength data at 36° of lumbar flexion can be found in Table 4.5
and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly
increased both absolute and relative force output from pre- to post-training (p<0.05).
48° of Lumbar Flexion
Lumbar extension strength data at 48° of lumbar flexion can be found in Table 4.5
and Figures 38, 39, and 40. Both the LEX and HEX groups, but not CON, significantly
increased both absolute and relative force output from pre- to post-training (p<0.05).
60° of Lumbar Flexion
Lumbar extension strength data at 60° of lumbar flexion can be found in Table 4.5
and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly
increased both absolute and relative force output from pre- to post-training (p<0.05).
72° of Lumbar Flexion
Lumbar extension strength data at 72° of lumbar flexion can be found in Table 4.5
and Figures 38, 39, and40. Both the LEX and HEX groups, but not CON, significantly
increased both absolute and relative force output from pre to post-training (p<0.05).

61
Table 4.5. Comparison of Changes in Lumbar Extension Strength for the CON, LEX, and
HEX Groups Following Six Months of Resistance Training.
ANGLES
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
0°ABS
137±76
104191
103169
165175*
93174
1721107*
0°REL
2.611.11
1.8411.3
2.211.6
3.611.2* **+
1.811.1
3.411.3* **+
0° % A
-33.3139
141.41184**
130.31114**
12° ABS
185183
1601102
135171
207179*
1381106
2291118*
12° REL
3.711
3.111.3
2.711.4
4.411.2*+
2.711.5
4.611.4* **+
12°% A
-13.9140
87187**
1121110**
24° ABS
2171104
191188
146185
238184*
1871115
2541125*
24° REL
4.311.1
3.811
2.911.6
5.011.0* **+
3.811.6
5.211.3* **+
24°% A
-10124
1361213**
57166
36° ABS
2351108
2181104
1751102
259194*
2071114
2701125*
36° REL
4.611.1
4.311.1
3.411.6
5.311.0*+
4.211.5
5.511.3* **+
36°% A
-5.8120
76.5164**
40.4132**
48° ABS
2371100
2261107
2011103
274192*
2331134
2731134*
48° REL
4.711
4.511.1
3.711.5
5.510.8*+
4.711.7
5.511.4*+
48°% A
-5.7116
53141**
27134
60° ABS
240184
2591113
201199
267187*
2491138
2781134*
60° REL
4.810.9
5.211.2
3.911.5
5.610.8*
5.111.6
5.711.3*
60°% A
7.0119
48137**{
18122
72° ABS
241175
249196
197189
262183*
2541125
2891138*
72° REL
4.911.9
5.112.4
4.211.7
5.711.0*
5.311.3
6.011.2*
72°% A
-7.1140
45.3138** J
17117
TSLB ABS
13421400
12451550
11001494
16131495*
13641796
17721887*
TSLB REL
28.214.7
25.816.3
22.319.2
34.316.3*+
27.519.7
35.918.8* **+
TSLB % A
-8.0123
62.6144**
39.5130.3**
Values are mean ± SD. *p<0.05 vs PRE, **p<0.05 vs CON. Jp<0.05 vs HEX. +p<0.05 vs. CON
(ANCOVA). CON = control group, LEX = low-intensity group, HEX = high-intensity group.
TSLB = total lumbar strength. REL = relative change (Nm/kg FFM), %A = percent change from
PRE to POST. ABS= absolute value (Nm)

62
Total Lumbar Extension Strength
The result for total lumbar extension strength was computed by summing the peak
force generated for each of the seven angles tested. Total lumbar strength data for each of
the three experimental groups can be found in Table 4.5 and Figures 41, 42, and 43. Both
the LEX and HEX groups, but not CON, significantly increased absolute and relative
force output from pre to post-training (p<0.05).
Bone Mineral Density
Total Body Bone Mineral Density
The means and standard deviations for total body bone mineral density (BMD) are
shown in Table 4.6. The results for absolute BMD and percent change from pre to post¬
training can be found in Figures 44 and 45, respectively. There were no significant
differences either between groups or from pre to post-training (p>0.05).
Femoral Neck Bone Mineral Density
Femoral neck bone mineral density data are shown in Table 4.6 and Figures 46 and
47. The HEX group significantly increased BMD of the Femur Neck from pre to post¬
training (p<0.05).
Anterior/Posterior Lumbar Spine Bone Mineral Density
The means and standard deviations for anterior/posterior (AP) lumbar spine bone
mineral density are shown in Table 4.6 and Figures 48 and 49. There were no significant

63
differences between groups at study entry and AP BMD did not change (p>0.05) after 6
months of training or control period.
Lateral Lumbar Spine Bone Mineral Density
Lateral lumbar spine bone mineral density data are shown in Table 4.6 and Figures
50 and 51. There were no significant differences between groups at study entry and lateral
lumbar spine BMD did not change (p>0.05) after 6 months of training or control period.
Ward’s Triangle Bone Mineral Density
Ward’s triangle bone mineral density data are shown in Table 4.6 and Figures 52
and 53. There were no significant differences between groups at study entry and Ward’s
triangle BMD did not change (p>0.05) after 6 months of training or control period.
Correlations Between Physiological Performance Variables and Muscular Strength
Correlation coefficients relating V02|*»k, stair climbing time (STAIRS), and
treadmill time to exhaustion (TREADMILL) to leg press 1RM (LP 1RM), leg press
endurance (LP END), leg curl 1RM (LC 1RM), leg extension (LE 1RM), total strength
(TOTAL STR.), and training volume (TRAINING VOL) can be found in Tables 4.7 and
4.8. Training volume was calculated by multiplying the training weights for each of the
exercises performed on the last day of training times the number of repetitions performed.

64
VO^k
The correlation coefficients for absolute and percent changes in VC^pak
to changes in muscular strength and endurance can be found in Tables 4.7 and 4.8,
respectively. As shown in Table 4.7, absolute VO^k is significantly correlated (p<0.05)
to all muscular strength variables listed except for LP END (p<0.05). This indicates that
resistance training is related to, and can lead to increases in VOipejt. The results from
Table 4.8 show that percent changes in muscular strength are not related to percent
changes in V02pc,k . This indicates that the magnitude of change for the two variables may
not be related. In other words, a 25% increase in leg press 1RM may not correspond to a
25% increase in VOipt.k. However, it is important to note that increased strength is
associated with increased aerobic capacity.
Treadmill Time to Exhaustion
The correlation coefficients for absolute and percent changes in treadmill time to
exhaustion during the GXT and changes in muscular strength and endurance can be found
in Tables 4.7 and 4.8, respectively. As shown in Table 4.7, absolute TREADMILL is
significantly (p<0.05) correlated to all muscular strength variables except for LP 1RM and
TRAINING VOL. (p<0.05). These results indicate that resistance training can increase
TREADMILL during a GXT in the absence of endurance training. It is interesting to
notethat LE was the most highly correlated strength variable to treadmill time, while LP
1RM was not significantly correlated at all, even though both are quadriceps exercises.

65
Table 4.6. Changes in Bone Mineral Density for the CON, LEX, and HEX Groups
Following Six Months of Resistance Training or Control Period.
SITE
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
TOTAL BMD
(g/cm2)
1.19610.1
1.187±0.1
1.19510.1
1.18910.1
1.19210.1
1.18210.1
TOTAL %A
-0.7311.9
-0.4212.1
-0.2111.6
FEMNK
(g/cm2)
0.863±0.1
0.848±0.1
0.89310.2
0.910.18
0.85210.1
0.86910.1*
FEMNK %A
-1.59±4.89
0.6815.57
1.9613.33
APSPINE
(g/cm2)
1.228±0.2
1.222±0.2
1.18610.2
1.18210.2
1.19710.2
1.18810.2
APSPINE %A
-.0251±4.1
-0.46413
-0.95813.5
LTSPN
(g/cm2)
0.64510.2
0.651±0.2
0.71510.3
0.7210.2
0.69410.3
0.67410.2
LATSPINE
%A
0.644113.1
3.22116.9
1.117115.6
WARD’S
(g/cm2)
0.69±0.1
0.67610.2
0.74310.2
0.73310.2
0.67710.1
0.67610.1
WARD’S %A
-1.9418.3
-0.7416.4
-0.1716.7
Values are mean ± SD. *p<0.05 vs PRE. CON = control group, LEX = low-intensity
group, HEX = high-intensity group. TOTAL = total body. FEMNK = femoral neck.
APSPINE = anterior/posterior spine. LTSPN = lateral spine. WARD’S = Ward’s triangle.
%A = percent change from PRE to POST.

Table 4.7. Correlations Between Absolute VCLp^k, Treadmill Time, and Stair Time and
Select Strength Measures, r Values are Shown Followed by Significance Value in
Parentheses
66
vo^
STAIRS
TREADMILL
vo2p^
1.0(0.00)**
-0.53(0.00)**
0.72(0.00)*
STAIRS
-0.53(0.00)**
1.0(0.00)**
-0.34(0.02)*
TREADMILL
0.72(0.00)*
-0.34(0.02)*
1.0(0.00)**
LP 1RM
0.45(0.00)**
-0.73(0.00)**
0.28(0.07)
LP END
0.03(0.85)
-0.09(0.6)
0.37(0.014)*
LC 1RM
0.42(0.01)**
-0.67(0.00)**
0.29(0.054)
LE 1RM
0.54(0.00)**
-0.78(0.00)**
0.43(0.01)**
TOTAL STR.
0.40(0.01)**
-0.64(0.00)**
0.31(0.04)*
TRAINING VOL.
0.46(0.01)**
-0.54(0.00)**
0.24(0.19)
* correlation significant at p<0.05, ‘‘correlation significant at p<0.01. VO^ = maximal
oxygen consumption guring graded exercise test (GXT). TREADMILL = time to
exhaustion during GXT. STAIRS = time to ascend one flight of stairs. LP 1RM = leg
press 1RM. LP END = leg press endurance. LC 1RM = leg curl 1RM. LE 1RM = leg
extension 1RM. TOTAL STR. = total strength. TRAINING VOL. = training volume.

67
Table 4.8. Correlations Between Percent Changes in VC^.k, Treadmill Time, and Stair
Time and Select Strength Measures, r Values are Shown Followed by Significance Value
in Parentheses
vo^
STAIRS
TREADMILL
vo2p^
1.0(0.00)**
-0.19(0.22)
0.26(0.09)
STAIRS
-0.19(0.22)
1.0(0.00)**
-0.17(0.24)
TREADMILL
0.26(0.09)
-0.17(0.24)
1.0(0.00)**
LP 1RM
0.21(0.20)
-0.20(0.18)
0.01(0.93)
LP END
0.13(0.41)
-0.31(0.03)*
0.25(0.11)
LC 1RM
0.36(0.02)*
-0.21(0.15)
0.21(0.17)
LE 1RM
0.06(0.72)
-0.54(0.00)**
0.25(0.12)
TOTAL STR
0.23(0.14)
-0.40(0.00)**
0.17(0.25)
* correlation significant at p<0.05, """correlation significant at p<0.01. VChpck = maximal
oxygen consumption guring graded exercise test (GXT). TREADMILL = time to
exhaustion during GXT. STAIRS = time to ascend one flight of stairs. LP 1RM = leg
press 1RM. LP END = leg press endurance. LC 1RM = leg curl 1RM. LE 1RM = leg
extension 1RM. TOTAL STR. = total strength.

68
Stair Climbing Time
The correlation coefficients for absolute and percent changes in STAIRS to
changes in muscular strength and endurance can be found in Tables 4.7 and 4.8,
respectively. As shown in Table 4.7, absolute STAIRS is significantly (p<0.05) correlated
to all strength variables except for LP END (p>0.05). The correlations are negative
values indicating an inverse correlation. This indicates that as muscular strength increases,
the time necessary to ascend one flight of stairs decreases. STAIRS was also significantly
correlated to the other physiological performance variables of TREADMILL and V02prak.
Percent change in STAIRSjs significantly (p<0.05) correlated to all muscular strength
variables except for LC 1RM (p>0.05). These correlations are also inverse indicators that
the percent increase in muscular strength and endurance is related to a percent decrease in
stair climbing time.
Correlations Between Physiological Performance Variables and Bone Mineral Density
Correlation coefficients relating total body (TOTAL), femoral neck (FEMNK),
Ward’s triangle (WARD’S), anterior/posterior lumbar spine (AP SPINE), and lateral
lumbar spine (LAT SPINE) to leg press 1RM (LP 1RM), overhead press (OP 1RM), total
strength (TOTAL STR ), and total lumbar extension strength (TOTAL LMB) can be
found in Tables 4.9 and 4.10.
Total Body
The correlation coefficients for absolute and percent changes in TOTAL to
changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As shown

69
in Table 4.9, absolute TOTAL was significantly (p<0.05) correlated to all strength
variables. This indicates that greater muscular strength is associated with greater TOTAL
bone mineral density.
Femoral Neck
The correlation coefficients for absolute and percent changes in FEMNK
to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As
shown in Table 4.9, absolute FEMNK was significantly (p<0.05) correlated to all strength
variables except TOTAL LMB. The lack of a correlation between TOTAL LMB and
FEMNK was not surprising because the MedX lumbar extension machine is designed to
isolate the lumbar spine and not involve any other musculature.
Ward’s Triangle
The correlation coefficients for absolute and percent changes in WARD’S
to changes in muscular strength can be found in Tables 4.9 and 4 10, respectively. As
shown in Table 4.9, absolute WARD’S was not significantly correlated to any of the
strength variables (p>0.05). This indicates that greater muscular strength is not associated
with greater WARD’S bone mineral density.
Anterior/Posterior Lumbar Spine
The correlation coefficients for absolute and percent changes in AP SPINE
to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As
shown in Table 4.9, absolute AP SPINE was significantly (p<0.05) correlated to all

70
strength variables. This indicates that greater muscular strength is associated with greater
AP SPINE bone mineral density,
Lateral Lumbar Spine
The correlation coefficients for absolute and percent changes in LAT SPINE
to changes in muscular strength can be found in Tables 4.9 and 4.10, respectively. As
shown in Table 4.9, absolute LAT SPINE was significantly (p<0.05) correlated to all
strength variables. This indicates that greater muscular strength is associated with greater
LAT SPINE bone mineral density.
Table 4.9. Correlations Between Absolute Changes in Bone Mineral Density and Select
Strength Measures, r Values are Shown Followed by Significance Value in Parentheses
SITE
TOTAL STR
TOTAL LMB
LP 1RM
OP 1RM
TOTAL
0.58(0.00)**
0.48(0.00)**
0.60(0.00)**
0.57(0.00)**
FEMNK
0.29(0.04)*
0.18(0.28)
0.29(0.05)*
0.30(0.03)*
WARD’S
.07(0.61)
0.05(0.78)
0.22(0.13)
0.16(0.26)
AP SPINE
0.38(0.01)**
0.33(0.05)*
0.43(0.00)**
0.41(0.00)**
LAT SPINE
0.60(0.00)**
0.44(0.01)**
0.61(0.00)**
0.63(0.00)**
* correlation significant at p<0.05, **correlation significant at p<0.01. LP 1RM = leg
press 1RM. OP 1RM = overhead press 1RM. TOTAL LMB = total lumbar strength.
TOTAL STR. = total strength. TOTAL = total body. FEMNK = femoral neck.
WARD’S = Ward’s triangle. AP SPINE = anterior/posterior spine. LAT SPINE = lateral
spine.

71
Biochemical Analyses
TBARS
Thiobarbituric acid-reactive substances (TBARS) data are shown in Table 4.11.
The results for absolute TBARS and percent change from pre to post-training can be
found in Figures 62 and 63, respectively. The level of peak exercise TBARS, and
therefore lipid peroxidation was lower in the LEX group compared to the CON group
following the post-training GXT (p<0.05). Also, the percent change from pre- to post-
GXT for the LEX group following the training period was significantly lower than those
of the HEX and CON groups (p<0.05). These results suggest that the exercise training
imparted some measure of protection from oxidative stress on the people in the LEX
group. The results for the in vitro oxidative stress challenges are presented in Table 4.11.
The results indicate that the post-training FeCL TBARS response of the HEX group was
significantly greater than those of the LEX and CON groups (p<0.05). However, the
TBARS response following the H202 challenge was lower for the LEX group compared
to the CON group (p<0.05).
Lipid Hydroperoxides
Lipid hydroperoxides values can be found in Table 4.11. The results for lipid
hydroperoxides are shown in figure 64. All groups (CON,LEX, FIEX) significantly
increased lipid hydroperoxide levels at peak exercise at study entry (p<0.05). Following
the training or control period, only the CON group showed a significant increase in lipid
hydroperoxides and the the levels for the LEX and FIEX groups were significantly lower

72
than that of the CON group (p<0.05). The percent increase in lipid hydroperoxides
aimmediately following the post-training GXT was significantly lower for the LEX group
compared to the CON and HEX groups (p<0.05).
Serum Osteocalcin
Serum osteocalcin values are shown in Table 4.12 and Figures 65 and 66. Both the
LEX and HEX groups, but not CON, significantly increased osteocalcin levels from pre to
post-training (p<0.05).
Serum Bone-Specific Alkaline Phosphatase
Serum bone-specific alkaline phosphatase (BAP) data are shown in Table 4.12 and
Figures 67 and 68. The HEX group significantly increased BAP levels from pre to post¬
training (p<0.05).
Serum Pvridinoline Crosslinks
Serum pyridinoline crosslinks (PYD) values are shown in Table 4.12 and Figures 69
and 70. None of the groups significantly changed PYD from pre- to post-training
(p<0.05).

Table 4.10. Correlations Between Percent Changes in Bone Mineral Density and Select
Strength Measures, r Values are Shown Followed by Significance Value in Parentheses
SITE
TOTAL STR
TOTAL LMB
LP 1RM
OP 1RM
TOTAL
0.13(0.36)
0.04(0.81)
-0.11(0.45)
0.04(0.80)
FEMNK
0.33(0.02)*
-0.09(0.61)
0.25(0.09)
0.23(0.11)
WARD’S
0.15(0.28)
0.28(0.09)
0.01(0.94)
0.18(0.22)
AP SPINE
0.01(0.94)**
0.13(0.45)
-0.11(0.47)
-0.02(0.87)
LAT SPINE
0.10(0.48)
0.31(0.06)
0.18(0.23)
0.15(0.29)
* correlation significant at p<0.05, “correlation significant at p<0.01. LP 1RM = leg
press 1RM. OP 1RM = overhead press 1RM. TOTAL LMB = total lumbar strength.
TOTAL STR. = total strength. TOTAL = total body. FEMNK = femoral neck.
WARD’S = Ward’s triangle. AP SPINE = anterior/posterior spine. LAT SPINE = lateral
spine.

74
Table 4.11. Comparison of Changes in Markers of Oxidative Stress for the CON, LEX,
and HEX Groups Following Six Months of Resistance Training.
MARKER
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
TBARS
PRE-GXT
f nmol/ml)
0.23410.05
0.22210.05
0.21110.04
0.20710.03
0.2401.0.07
0.21110.03
%A
-4.85111.2
-0.12116.1
-7.81121.6
TBARS
POST-
GXT
0.25110.06
0.25410.07
0.22210.06
0.21010.04**
0.28510.12
0.2311.06
%A
1.85111.5
-2.52117.1
-11.6128.2
%A PRE-/
POST-
GXT
7.1116.4
15.9124.8
5.1113.7
2.4*14.4** t
20.3141.5
9.9121.8
FECL3
(nmol/ml)
0.28310.04
0.27910.05
0.29110.06
0.28810.05
0.31710.04
0.34±0.04**{
XO
(nmol/ml)
0.22510.06
0.25910.11
0.25310.11
0.26610.11
0.27110.12
0.23510.04
H202
(nmol/ml)
0.55410.36
0.71110.37
0.43310.28
0.46910.25**
0.57910.46
0.67810.37
LPD-HPX
PRE-GXT
2.3310.62
2.5210.56
2.7710.78
2.5510.72
2.2610.64
2.32±0.60**í
%A
12.8130.3
-1.91138.8
2.83140.4
LPD-HPX
POST-
GXT
2.9111.16*
3.4110.51*
3.3010.90*
2.9210.76**
3.0210.77*
2.8710.5**
%A PRE-/
POST-
GXI
22.5117.0
39.2127.1
20.4121.0
16.9±18.9**í
34.2140.4
33.4130.1
Values are mean ± SD. *p<0.05 vs PRE-GXT. **p<0.05 vs. CON (ANCOVA). Jp<0.05
HEX vs. LEX (ANCOVA). CON = control group, LEX = low-intensity group, HEX =
high-intensity group.FECL3 = ferric chloride. XO = hypothanine/xanthine oxidase. H202
= hydrogen peroxide. LPD-HPX = lipid hydroperoxides. PRE-GXT = before graded
exercise test.. POST-GXT = post-graded exercise test. %A = percent change from PRE to
POST-training. TBARS = thiobarbituric acid-reactive substances

75
Table 4.12. Comparison of Changes in Markers of Bone Metabolism for the CON, LEX,
and HEX Groups Following Six Months of Resistance Training.
MARKER
CON
LEX
HEX
PRE
POST
PRE
POST
PRE
POST
OSCAL
(ng/ml)
12.32±5.4
13.23±5.2
10.7414.0
13.5817.2*
11.9415.0
15.5717.4*
%A
6.6±31.7
25.1136.8
39.0144.6
ALKPHOS
(U/L)
21.14110.4
18.8814.6
16.6215.6
17.5415.7
17.8616.6
19.1517.5*
%A
3.0115.9
7.8120.7
7.1113.3
PYD
(nmol/L)
1.8210.8
1.7210.6
1.5010.7
1.5110.6
1.5310.7
1.4510.6
%A
-1.3134.5
11.3152.7
-9.9166.4
Values are mean ± SD. *p<0.05 vs PRE. CON = control group, LEX = low-intensity
group, HEX = high-intensity group. OSCAL = serum osteocalcin. ALKPHOS = bone-
specific alkaline phosphatase. PYD = serum pyridinoline crosslinks. %A = percent change
from PRE to POST-training.

o
>
15.0
10.0
5.0
0.0
PRE
POST
ÃœCON
â–  LEX
0 HEX
Figure 1. Absolute peak oxygen consumption (V02peak) measured
during a graded exercise test before (PRE) and after (POST) six
months of resistance training.
*p<0.05 vs PRE

% Change
77
Figure 2. Percent change in peak oxygen consumption (V02eak) after
six months of resistance training.
+p<0.05 vs CON

Minutes
78
20.0
18.0
16.0
14.0
12.0
10.0
8.0
6.0
4.0
2.0
0.0
PRE
POST
Figure 3. Absolute treadmill time during a graded exercise test
measured before (PRE) and after (POST) six months of resistance
training.
*p<0.05 vs PRE

% Change
79
50.0
45.0 -
40.0 -
35.0 -
30.0 -
25.0 -
20.0 -
15.0 -
10.0 -
0.0
CON LEX HEX
Figure 4. Percent change in treadmill time during a graded exercise
test after six months of resistance training.
+p<0.05 vs CON

Seconds
80
12.0
10.0 -
PRE POST
Figure 5. Absolute stair climbing time measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE

% Change
81
CON LEX
0.0 -r
-2.0 -
-4.0 -
-6.0 -
-8.0 -
-10.0 -
-12.0 -
-14.0 -
-16.0 -
HEX
Figure 6. Percent change in stair climbing time after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
82
450.0 -i
400.0 -
350.0 -
300.0 -
250.0 -
200.0 -
150.0 -
100.0 -
50.0 -
0.0 -
*
PRE
POST
â–  CON
â–  LEX
Q HEX
Figure 7. Absolute chest press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs PRE

83
7 -
6 -
5 -
3 -
2 -
1 -
O
PRE
*+
Figure 8. Relative chest press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON

% Change
84
40.0
30.0 -
-10.0 -
-20.0 -
-30.0 J
Figure 9. Percent change in chest press 1RM after six months of
resistance training.
+p<0.05 vs CON

(tubOlMHl
85
700.0
600.0 -
PRE
Figure 10. Absolute leg press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs PRE
+p<0.05 vs. CON

86
14
12 -
10 -
PRE POST
EICON
â–  LEX
a HEX
Figure 11. Relative leg press 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE

% Change
87
60.0 i
50.0 -
40.0 -
30.0 -
20.0 -
10.0 -
0.0
CON LEX
+
HEX
Figure 12. Percent change in leg press 1RM after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
88
350.0
*
Figure 13. Absolute leg curl 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0 05 vs PRE

89
7 -i
* **
+
5 -
4 -
3
2 -
1 -
O
â–  CON
â–  LEX
â–¡ HEX
PRE
POST
Figure 14. Relative leg curl 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON
**p<0.05 vs. LEX

% Change
90
Figure 15. Percent change in leg curl 1RM after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
91
200.0 -i
180.0 -
*
160.0
140.0
120.0
100.0
80.0
60.0
40.0
20.0
0.0
â–  CON
â–  LEX
Q HEX
POST
Figure 16. Absolute biceps curl 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE

Nm/kg FFM
92
4 i
3.5 -
3 -
2.5 -
PRE
POST
Figure 17. Relative biceps curl 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs. PRE

% Change
93
50.0
40.0
30.0 -
-10.0 -
-20.0 -
-30.0 J
Figure 18. Percent change in biceps curl 1RM after six months of
resistance training.
+p<0.05 vs PRE

1RM (Nm)
94
500.0 n
450.0 -
400.0 -
350.0
PRE
POST
â–  CON
â–  LEX
Q HEX
Figure 19. Absolute seated row 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE

95
8
7 -
PRE
POST
â–  CON
â–  LEX
â–¡ HEX
Figure 20. Relative seated row 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.o5 vs. CON

% Change
96
40.0 -i
+
35.0 -
+
30.0
25.0 -
20.0 -
15.0 -
10.0 -
LEX
Figure 21. Percent change in seated row 1RM after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
97
PRE
POST
Figure 22. Absolute overhead press 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE

98
Figure 23. Relative overhead press 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON

% Change
99
40.0
30.0 -
20.0 -
-10.0 -
-20.0 -
-30.0 J
Figure 24. Percent change in overhead press 1RM after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
100
450.0 -|
PRE POST
Figure 25. Absolute triceps dip 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs PRE
+p<0.05 vs. CON

101
5 -
3 -
2 -
1 -
0
PRE
*+
*
POST
HCON
â–  LEX
QHEX
Figure 26. Relative triceps dip 1RM measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON

% Change
102
Figure 27. Percent change in triceps dip 1RM after six months of
resistance training.
+p<0.05 vs CON

1RM (Nm)
103
500.0
»+
450.0 -
PRE
POST
Figure 28. Absolute leg extension 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON

104
Figure 29. Relative leg extension 1RM measured before (PRE) and
after (POST) six months of resistance training.
*p<0.05 vs. PRE
+p<0.05 vs. CON

% Change
105
25.0
+
+
20.0
15.0 -
-10.0 -
-15.0 J
Figure 30. Percent change in leg extension 1RM after six months of
resistance exercise.
+p<0.05 vs CON

106
3500 i
*
Pre
Post
Figure 31. Absolute total strength measured before (PRE) and after
(POST) sue months of resistance training.
*p<0.05 vs. PRE

60
50
40
30
20
10
0
107
*
PRE
POST
â–¡ COK
â–  LEX
â–¡ HEX
Figure 32. Relative total strength measured before (PRE) and after
(POST) six months of resistance training.
*p<0.05 vs. PRE

% Change
108
30.0
25.0
20.0 -
15.0 -
10.0 -
5.0 -
-10.0 -
-15.0
Figure 33. Percent change in total strength after six months of
resistance training.
+p<0.05 vs CON

Repetitions
109
Figure 34. Absolute Chest Press Endurance measured before (PRE)
and after (POST) six months of resistance exercise.
* p<0.05 vs PRE
+p< 0.05 vs CON

% Change
110
140.0 -i
120.0 -
100.0 -
80.0 -
60.0 -
40.0 -
20.0 -
0.0 -
-20.0 -
-40.0 -
-60.0 -
Figure 35. Percent change in chest press endurance measured after six
months of resistance exercise.
+p< 0.05 vs CON

Repetitions
111
80.0
70.0 -
60.0 -
50.0 -
40.0 -
PRE
POST
Figure 36. Absolute change in leg press endurance measured before
(PRE) and after (POST) six months of resistance exercise.
+p<0.05 vs PRE

% Change
112
Figure 37. Percent change in leg press endurance after six months of
resistance exercise.
+p<0.05 vs CON.

Nm
113
350.0
300.0 -
250.0 -
200.0 -
150.0 -
100.0
50.0
0.0
*
1 1 1 1 1 1 1
0 12 24 36 48 60 72
Degrees of Lumbar Flexion
Figure 38. Absolute lumbar extension strength measured before
(PRE) and after (POST) six months of resistance exercise.
*p<0.05 vs. PRE for both LEX and HEX groups

114
6 -
5 -
4 -
fe
oo
3 -
2 -
1 -
0 12 24 36 48 60 72
Degrees of Lumbar Flexion
Figure 39. Relative lumbar extension strength measured before
(PRE) and after (POST) six months of resistance training.
*p<0.05 vs. PRE for both LEX and HEX groups

% Change
115
250.0
200.0
150.0
100.0
-50.0
-100.0
50.0
II
36
II
48
Degrees of Lumbar Flexion
â–  CON
a LEX
(a HEX
+ +
** **
Figure 40. Percent change in lumbar extension strength after six
months of resistance training.
+ p<0.05 vs CON
** p<0.05 vs HEX

Nm
116
3000.0
2500.0
*
Figure 41. Absolute total lumbar extension strength measured before
(PRE) and after (POST) six months of resistance training.
*p<0.05 vs PRE

117
Figure 42. Relative total lumbar extension strength measured before
(PRE) and after (POST) six months of resistance training.
*p<0.05 vs. PRE

118
Figure 43. Percent change in total lumbar strength after six months of
resistance taming.
* p<0.05 vs PRE

119
1.225
1.200 -
â– Bb
1.175 -
ÃœCON
â–  LEX
â–¡ HEX
1.150
Figure 44. Absolute total body bone mineral density measured before
(PRE) and after (POST) six months of resistance training.

% Change
120
CON
LEX
HEX
Figure 45. Percent change in total body bone mineral density after six
months of resistance training.

g/cm2
121
0.940
0.920
0.900
0.880
0.860
0.840
0.820
0.800
EICON
â–  LEX
Q HEX
Figure 46. Absolute femoral neck bone mineral density
measured before (PRE) and after (POST) six months of
resistance training.
*p<0.05 vs. PRE

122
8 n
6 -
O
v?
O'
-2 -
-6
-8
Figure 47. Percent change in femoral neck bone mineral density after
six months of resistance training.

g/cm2
123
1.300
1.280
1.260
1.240
1.220
1.200
1.180
1.160
1.140
1.120
1.100
PRE
POST
EICON
â–  LEX
H HEX
Figure 48. Absolute anterior/posterior lumbar spine bone mineral
density measured before (PRE) and after (POST) six months of
resistance training.

% Change
124
CON
-0.4 -
-0.6 -
-0.8 -
-1 -
-1.2 -
-1.4 -
-1.6 -
-1.8 -
LEX
HEX
-2 J
Figure 49. Percent change in anterior/posterior lumbar spine bone
mineral density after six months of resistance training.

g/cm2
125
0.780
0.760
0.740 -
0.720 -
0.700 -
0.680 -
0.660 -
0.640 -
0.620
0.600
PRE
POST
HCON
â–  LEX
â–¡ HEX
Figure 50. Absolute lateral lumbar spine bone mineral density
measured before (PRE) and after (POST) six months of resistance
training.

126
CON LEX HEX
8 1
6 -
-4
-6
Figure 51. Percent change in lateral lumbar spine bone density after
six months of resistance training.

g/cm2
127
0.790 i
0.770
0.750
0.730 -
0.710 -
0.690 -
0.670 -
0.650
PRE
POST
CD CON
â–  LEX
â–¡ HEX
Figure 52. Absolute Ward's triangle bone mineral density measured
before (PRE) and after (POST) six months of resistance training.

% Change
128
CON
LEX
HEX
Figure 53. Percent change in Ward's triangle bone mineral density
after six months of resistance training.

129
Nm
Figure 54. Relationship of V02peak to total strength measured before
and after six months of resistance training.

130
10 -
5 -
0 -I —i 1 r 1 1 1
0 100 200 300 400 500 600
Nm
Figure 55. Relationship between V02peak and leg press 1RM
measured before and after six months of resistance exercise.
700

Time (min.)
131
Figure 56. Relationship of GXT treadmill time to total strength
measured before and after six months of resistance training.
6000

Time (min.)
132
25.00
0.00 +-
0
-i i •—i 1 1 r—
100 200 300 400 500 600
Nm
Figure 57. Relationship between leg press 1RM and treadmill time
during a GXT measured before and after six months of resistance
training.
700

V02peak Percent Change
133
Total Strength % Change
Figure 58. Relationship of percent change in V02peak to percent
change in total strength after six months of resistance training.

% Change in V02peak
134
Figure 59. Relatioship of percent change in V02peak to percent
change in leg press 1RM measured before (PRE) and after(POST) six
months of resistance training.

% Change in Treadmill Time
135
80.00
70.00
♦
60.00
• ♦
*50.00
♦
♦
40.00
♦
30.00
0
R2 = 0.0298
♦
♦
♦
♦ ♦ —'
♦ ♦ ^
20.00 «
♦
*0.00
• *.
♦
r * 0*06-
*■■ ♦ T ,
-20.00 -10.00 0.
)0 10.00 « 20.00 30.00 40.00 50.00
-10.00
♦
♦
-20.00 -
% Change in Total Strength
Figure 60. Relationship of Percent Change in Total Strength to
Percent Change in Treadmill Time after six months of resistance
training.

Treadmill Time (% change)
136
Figure 61. Relationship between percent change in treadmill time
during a GXT and percent change in leg press 1RM measured before
and after six months of resistance exercise.

nmol/ml
137
O PRE-TR A
â–  PRE-TRB
HPOST-TR A
BPOST-TRB
Groups
Figure 62 TBARS Measured Before and After Training, and Before
and After GXT.
PRE-TR A = pre-training before GXT
PRE-TR B = pre-training after GXT
POST-TR A = post-training before GXT
POST-TR B = post-training after GXT
*p<0.05 vs. CON POST-TR B

138
45
40 -
35 -
30 -
POST-TR
â–¡ COK
â–  LEX
Q HEX
Figure 63. Percent Change inTBARS Following a GXT, Pre-Post
Training
*p<0.05 vs CON and HEX - ANCOVA

nmol/ml
139
â–¡ CON PRE-GXT
â–  CON POST-GXT
B LEX PRE-GXT
â–¡ LEX POST-GXT
â–¡ HEX PRE-GXT
â–¡ HEX POST-GXT
Figure 64. Lipid Hydroperoxides Pre- and Post-GXT, Before and
After 6 months of training or Control
*p<0.05 vs PRE-GXT
**p<0.05 vs. CON (ANCOVA)
+p<0.05 vs. LEX (ANCOVA)

140
PRE
POST
Figure 65. Serum osteocalcin levels before (PRE) and after (POST)
six months of resistance exercise or control period.
*p<0.05 vs. PRE.

141
80 -i
70 -
60 -
50 -
CON LEX
Figure 66. Percent change in serum osteocalcin levelsd after six
months of resistance exercise.

142
30
25 -
20 -
15 -
10 -
0
PRE POST
Figure 67. Serum bone-specific alkaline phosphatase measured before
(PRE) and after (POST) six months of resistance exercise.
*p<0.05 vs. PRE
EICON
â–  LEX
â–¡ HEX

143
30
25 -
20 -
CON LEX
â–¡ CON
â–  LEX
QHEX
HEX
Figure 68. Percent change in serum bone-specific alkaline phosphatase
measured before (PRE) and after (POST) six months of resistance
exercise.

nmol/L
144
3 n
2.5 -
PRE POST
â–¡ CON
â–  LEX
â–¡ HEX
Figure 69. Serum Pyridiniline Crosslinks measured before (PRE) and
after (POST) six months of resistance exercise.

145
â–¡ CON
â–  LEX
â–¡ HEX
Figure 70. Percent change in serum pyridinoline crosslinks measured
after six months of resistance exercise.

CHAPTER 5
DISCUSSION
Overview and Principle Findings
This study was the first to investigate the effects of two different intensities of
resistance exercise on muscular strength and endurance, stair climbing ability, aerobic
endurance, bone metabolism, and serum lipid peroxidation in adults aged 60-85 years.
Previous investigations have attempted to address one or two of these variables but did
not comprehensively address multiple outcomes nor have they addressed the issue of
intensity (Pollock and Vincent, 1997). This investigation was designed to examine two
hypotheses. We postulated that (1) resistance exercise would improve muscular strength
and endurance, stair climbing ability, cardiorespiratory endurance, serum markers of bone
metabolism, bone mineral density (BMD) and serum lipid peroxidation, and (2) that there
would be no significant differences in the criterion measures between the high- and low-
intensity training groups due to the equivalent training volumes.
The data clearly support hypothesis #1. Resistance exercise did improve muscular
strength and endurance, stair climb ability, V02peak, treadmill time to exhaustion during a
graded exercise test (GXT), and serum lipid peroxidation. However, BMD of only one
skeletal region improved and there was only a modest effect on serum markers of bone
metabolism.
146

147
Hypothesis #2 is also supported by the results. There were similar improvements
in muscular strength and endurance, physical function, aerobic endurance, bone
metabolism, and serum lipid peroxidation between the two training groups. The two
exercise regimens were designed to achieve equivalent workloads but the means of
achieving those volumes were different. The low-intensity (LEX) group performed 13
repetitions with approximately 50% of their one-repetition maximum (1RM) while the
high-intensity group (HEX) performed 8 repetitions with 80% of their 1RM.
Muscular Strength. Muscular Endurance, and Stair Climbing
Muscular Strength
The results indicate that the regimen used for this study was effective in increasing
muscular strength as evidenced by the improvements in one repetition maximum (1RM)
values each exercise. Muscular strength significantly increased for the chest press (17.5%
LEX, 16.0 % HEX), leg press (15.7% LEX, 27.6 % HEX), leg curl (25.3% LEX, 17.3 %
HEX), biceps curl (17.8% LEX, 24.6 % HEX), seated row (19.2% LEX, 22.1 % HEX),
overhead press (18.8% LEX, 16.6 % HEX), leg extension (10.8% LEX, 14.6 % HEX),
and triceps dip (18.5% LEX, 16.1 % HEX). Total strength significantly increased 17.2
and 17.8% for the LEX and HEX groups respectively. These data are in accord with
those presented by Brown et a], (1990), Fiatarone et al. (1994), Frontera et al. (1988),
Frontera et al. (1990), and Hagberg et al. (1989) who all reported increased strength
following resistance training in older adults. The strength increases in this study (~17%)
are of the same magnitude as those reported in the Hagberg study (~13%). This is most
likely because our study and the Hagberg study used similar one set exercise regimens

148
with a similar repetition range. However, our results are somewhat lower than reported in
Brown, Fiatarone, and Frontera (48-113%) who used multiple set protocols. The greater
volume used in those studies would reasonably be expected to produce greater results.
Although this investigation did not determine the mechanisms for an increase in
strength, several possibilities have been examined by other investigators including
increased muscle cross-sectional area (CSA) and neural adaptations. First, increased
muscle CSA following resistance training in older adults has been reported by Brown et al
(1990), Fiatarone et al. (1994), and Frontera et al. (1990). Muscle CSA was determined
in each study by computerized tomography (CT) scans and increased from 3-17%
following training. Both Frontera and Brown obtained muscle biopsies to determine fiber
type increases in CSA; each reported a significant increase for both the type I and type II
fibers. However, Frontera reported that the increase was similar for both types of fibers,
while Brown reported that type II fibers increased more than type I fibers. Unfortunately,
neither study attempted to examine the relationship between the increase in strength to the
increase in muscle CSA. Second, both Brown et al. (1990) and Hakkinen et al. (1998)
examined electromyographic (EMG) adaptations to resistance exercise in older adults.
Hakkinen reported increased voluntary activation of the agonistic muscles with a
concomitant decrease in antagonistic muscle activation in older (72±3 yr.) adults. The net
result of this type of an adaptation would be an net increase in force production. The
authors also used CT scans to measure muscle CSA. The authors reported a 20-30%
increase in muscular strength with only a 2-6% increase in muscle CSA. The authors
indicated that neural adaptations were more important than increases in CSA for the
development of muscular strength in this population. Another interesting finding was that

149
the authors measured EMG adaptations every two months during the six months of
training and found EMG alterations at each time point. This indicates that neural
adaptations can occur beyond the first 6-10 weeks in contrast to what has been reported
by other investigators (Fleck and Kraemer, 1997). Furthermore, Brown et al. (1990)
reported EMG adaptations (increased half-relaxation time) which allowed maximal force
production at lower motor unit firing rates. Theoretically, this adaptation could lead to
increased resistance to fatigue.
Muscular Endurance
The subjects in this study demonstrated significant improvements in muscular
endurance. Improvements in endurance for the chest press and leg press ranged from 68-
105% for both training groups (p<0.05) compared to the CON group. These results are in
accord with those of Brown et al. (1990) who also reported increased muscular endurance
following 12 weeks of resistance training in older adults (63±3 yr.). The increased
endurance could be the result of several factors. First, since the weight lifted for the
endurance test was the same for the pre- and post-test, the overall increase in strength
would make the load relatively easier during the post-test facilitating the performance of
more repetitions. Second, the adaptations reported by Brown et al. (1990) indicate that
there are neural alterations which could contribute to increased resistance to fatigue.
Finally, it is possible that the increased endurance may be partially the result of increased
concentrations of glycogen, ATP and creatine phosphate which have been documented
with chronic resistance training (Costill et al., 1979, MacDougall et al., 1977).

150
Stair Climbing Ability
Accompanying the training-related increases in strength and endurance was a
significant decrease in the time to ascend one flight of stairs. These data are in agreement
with both Rooks et al. (1997) and Fiatarone et al.(1994) who reported an increase in stair
climbing speed and an increase in stair climbing power post-resistance training,
respectfully. Stair climbing time inversely correlates to leg press, leg curl, and leg
extension 1RM, total strength and training volume with r values ranging from -0.54 to -
0.78 (p<0.01). Since there were no significant changes in body weight and the same set of
stairs was used for both the pre-and post-testing, the improvement in time is not
attributable to a decrease in the work necessary to complete the task. Therefore, the
improvement in stair climbing time can be largely attributed to increased muscular
strength.
Physiological Significance of Strength Data
As previously discussed, decreased strength and muscle mass are associated with
decreased physical function, increased risk of falling, decreased physical independence,
and decreased feelings of self worth. Improving muscular strength can have a beneficial
impact on all of these factors. As a consequence of resistance training, rising from a chair,
climbing stairs, carrying groceries, and housework would become easier. Furthermore,
decreased fear of falling could lead to increased physical activity and lifestyle
independence, a positive cycle that continue to improve functional ability. Participation in
resistance training, and therefore increased strength and endurance could lead to an
improved ability to accomplish the activities of daily living.

151
Aerobic Endurance
VO,„.v
Investigations examining the effects of resistance exercise on aerobic endurance
have produced mixed results (Gettman and Pollock, 1981, Stone et al., 1991). One factor
that influences the disparate results is the style of resistance exercise employed by each
study. For example, traditional circuit weight training (CWT), characterized by high
repetitions and short rest periods, modestly increases VO^t (3-11%, Frontera et al.,
1990, Gettman and Pollock, 1981, Gettman et al., 1982). Conversely, more traditional
programs consisting of multiple sets and longer rest periods (2-4 min.) have reported no
change or sometimes a decrease in V02peak (Goldberg et al., 1994, Hickson et al., 1980,
Nakao et al., 1995). However, Gettman et al. (1978), Hagberg et al. (1989) and Marcinik
et al. (1991) all reported non-significant changes in V02p<»k following 12-26 weeks of
CWT when the values were normalized to body weight. Another confounding factor is
the study length. Training program durations may vary from 8 to 20 weeks making
comparisons between studies difficult. For the remainder of this discussion, only studies
utilizing regimens similar in design and length to the present investigation will be
presented.
In the present study, a 23.5% and 20.1% increase in V02peat was observed for the
LEX and HEX groups, respectively. These values are considerably higher than those
reported by Frontera et al. (1990) and Gettman et al. (1982), both of which found
increases of 5-12% in VOaâ„¢* It is possible that the reason for this is that those studies
trained their subjects for only 12 weeks as compared to 24 weeks in this study. Also, the

152
average age for the subjects in the Gettman study was 35.7 years, considerably younger
than the subjects in this study. The mean age for the subjects in the Frontera study was
not reported, but the authors indicated that the subject’s age ranged from 60 to 72.
However, the Gettman exercise regimen only consisted of leg flexion and extension, while
this study employed a comprehensive training regimen. Wilmore et al. (1978) reported an
11% increase in VC^pok for their female subjects, but no change for their male subjects.
The authors speculated that the increase in the female subjects occurred because they were
less fit than their male counterparts. It is known that less fit subjects commonly
demonstrate greater increases in strength or fitness when compared to fit subjects
(Gettman and Pollock, 1981). This fact may explain why the subjects in the current study
demonstrated a greater increase than is commonly reported. Since these subjects were
sedentary elderly people, their level of fitness was lower than that of the subjects in studies
using younger participants.
The mechanism underlying the increase in VO^k following resistance exercise
training is unclear. It is possible that measurement of true V02pCak in untrained subjects is
prohibited/prevented by inadequate leg strength. Because devices used to measure
VOjpeak place an enormous premium upon leg strength the subject may be unable to reach
their true maximum due to a lack of strength in the lower extremities and not because they
have central cardiovascular limitations/exhaustion. Therefore, training induced increases
in VChpeik may not be due to an increased ability to consume oxygen, but rather it may be
that the person now has the leg strength to approach or to reach central cardiovascular
limitations. In support of this postulate, VOjpeak was significantly correlated to total
strength, leg press, leg curl, and leg extension strength (p<0.01). We also observed that

153
oxygen consumption was significantly correlated with training volume (p<0.01). This
finding is in accord with that reported by Gettman and Ayers (1978a). That study
examined the effects of two different isokinetic resistance training regimens on aerobic
performance. Each of the two groups performed the same number of repetitions, but one
group did more work than the other by moving at a slower speed and against a greater
resistance. They reported that the slow speed group increased V02pe.k 7% more than the
fast group indicating a relationship between resistance training volume and aerobic
capacity improvement.
The possibility exists that the increase in aerobic capacity in the elderly may be in
part due to an increase in oxidative enzyme activities. Frontera et al. (1990) reported a
38% increase in citrate synthase (CS) enzyme activity following 12 weeks of resistance
exercise. They also reported a 15% increase in capillaries per fiber. The Frontera regimen
consisted of 3 sets of 8 repetitions at 80% of 1RM for the knee flexors and extensors.
The authors reported that the increases in CS and capillary density were most likely due to
the resistance exercise and not an increase in daily activity due to their increased strength
because their daily activity logs showed no change from pre- to post-study. Although the
regimen used in that study is different that the one used in the present study, it is
reasonable to conclude that a similar result may have occurred for this population.
Specifically, the subjects in this study trained twice as long and performed more leg
exercises than the Frontera et al.(1990) subjects.

154
Treadmill Time to Exhaustion
Treadmill time to exhaustion during the graded exercise test (GXT) was improved
by 26.4 and a 23.3% in the LEX and HEX groups, respectively. Since this increase was
observed during a maximal exercise bout, it is reasonable to conclude that endurance
performance during a submaximal test would also be improved. This could indicate that
the trained elderly subjects from this study may be better able to perform activities of daily
living that require endurance such as shopping in a mall or mowing the lawn compared to
their untrained counterparts. Treadmill time was significantly correlated to V02pe,k, leg
press endurance, leg extension, and total strength (p<0.05).
Several investigations have reported an increase in endurance performance without
a concomitant increase in VC^t (Ades et al., 1996, Hickson et al., 1980, Marcinik et al.,
1991). Marcinik et al. (1991) reported a 33% increase in cycle time to exhaustion at 75%
ofVOaâ„¢ following 12 weeks of resistance training in young adults. The subjects
performed a CWT regimen consisting of 3 sets of 10 exercises separated by 30s rest
periods. The authors also reported a 12% increase in lactate threshold. The increased
time to exhaustion was significantly (p<0.001) correlated to increased lactate threshold (r
= 0.78) and 1RM leg extension strength (r = 0.89). Ades et al. (1996) reported a 38%
increase in submaximal treadmill walking time following 12 weeks of resistance exercise in
older adults. Hickson et al. (1980) reported increases in stationary cycle (47%) and
treadmill running (12%) time to exhaustion following 10 weeks of resistance training. The
authors also reported that V02p«,k only increased 4% as a consequence of the exercise
training.

155
Although it was not the purpose of this investigation to measure the possible
mechanisms that may have contributed to the increased endurance, it is possible that
improved endurance was the result of increased strength, CS activity, and capillary
density. Increased endurance is also possibly related to increased concentrations of ATP
and creatine phosphate shown to occur with resistance training (Costill et al., 1979,
MacDougall et al., 1977).
Bone Mineral Density and Bone Metabolism
Bone Mineral Density
The exercise regimen used in this study was effective in increasing femoral neck
bone mineral density (BMD) in the HEX group (p<0.05). However, there were no other
significant changes in BMD for any of the groups at the femoral neck, Ward’s triangle,
lateral spine, anterior/posterior spine, or for total body BMD. Previous investigations in
older adults (50-61yr.) have shown that resistance exercise is an effective means for
increasing BMD (Braith et al., 1996, Menkes et al., 1993). However, the subjects in the
Braith et al. (1996) study were organ transplant recipients immunosupressed with
glucocorticoids that had significantly depressed BMD compared to healthy age matched
controls. Also, although the subjects in the Menkes et al. (1993) study improved their
femoral neck and lumbar spine BMD, examination of their data shows that the training
group had lower bone density values as compared to the control group at the start of the
study. It is possible that the significant increases reported in those two studies was a
matter of the training groups regressing toward the mean and approaching normal levels
of BMD.

156
In a follow-up to the Menkes study, the same group tried to replicate their findings
using a bigger sample size and subjects with higher initial BMD (Ryan et al. (1994). Using
the same exact regimen as in the Menkes study, Ryan reported similar increases in total
strength (45 vs 39%) following 16 weeks of resistance exercise. However, Ryan only
found increased BMD for the femoral neck and not for any other site. Our data are in
accord with those presented by Ryan as we observed a significant increase only at the
femoral neck. Ryan postulated that the discrepancy between their study and Menkes was
a consequence of the higher initial BMD values for their subjects as compared to those in
the Menkes study.
Pruitt et al. (1995) examined the effects of 12 months of high- (HI, 80% of 1RM)
versus low-intensity (LI, 40% 1RM) resistance exercise on lumbar spine, femoral neck,
and Ward’s triangle BMD in twenty-six women between the ages of 65 and 79. Strength
increased following the training but BMD did not. The authors attributed the lack of
BMD changes to the fact that the subjects had normal BMD values prior to study
participation. Nichols et al. (1995) examined the effects of 12 months of high-intensity
(80% 1RM) resistance exercise on BMD in older women (67.1± 1.5 yr ). No significant
changes in BMD were observed. Again, the authors concluded that the lack of a training-
induced improvement in BMD was due to the normal pre-training BMD values. The
initial BMD values for the spine, femoral neck, and total body were 96%, 105%, and 98%,
respectively. The authors also noted that none of the women in the study were on
hormone replacement therapy. The subjects in the present study also had normal levels of
BMD prior to study participation. The mean percent of age-matched norms at the start of
the study were 102%, 113%, 115%, 108%, and 102% for femoral neck, anterior/posterior

157
spine, lateral spine, total body, and Ward’s triangle, respectively. It is also noteworthy
that at study entry the women had a significantly higher percentage of normal compared to
the men. Since the values were at or above normal, it is not surprising that BMD did not
increase in response to resistance exercise. It is unclear why femoral neck BMD
significantly increased in the present study while there were no changes observed at the
other sites.
Biochemical Markers of Bone Metabolism
In an attempt to examine the biochemical alterations underlying BMD changes
with resistance training, several serum markers of bone metabolism were measured.
Serum osteocalcin and bone-specific alkaline phosphatase (BAP) were measured as
indices of bone formation while serum pyridinoline (PYD) was measured as a marker of
bone resorption (Calvo et al.,1996). We observed a significant increase in osteocalcin for
both the LEX and the HEX groups, while only the HEX group demonstrated a significant
increase in BAP. These data are in accord with Menkes et al. (1993) who reported
significant increases in osteocalcin and BAP following 16 weeks of resistance training.
However, neither the follow-up to that study (Ryan et al., 1994) or Pruitt et al. (1995)
reported significant increases in either osteocalcin or BAP. The interpretation of these
results is unclear. Possibly, biochemical alterations were observed prior to measurable
changes in the skeletal BMD. It may be that more time would be necessary to observe
measurable alterations in BMD, and that the biochemical markers serve as precursors to
skeletal changes.

158
Osteocalcin and BAP have been shown to be sensitive to alterations in bone
metabolism following disease, menopause, and hormone replacement therapy (Calvo et al.,
1996, Delams, 1993, Ross and Knowlton, 1998). However, interpretation of the results
can be clouded by the phase of bone metabolism, the stage of the disease being examined,
liver function, and aging therapy (Calvo et al., 1996, Delams, 1993, Ross and Knowlton,
1998). For example, osteocalcin increases at the onset of menopause, but then decreases
back to normal levels within several months. BAP, although a measure of bone formation,
can be associated with rapid bone loss and increased risk for fracture (Delmas, 1993).
Serum pyridinoline cross-links (PYD) are an indicator of bone resorption and theoretically
should increase with increased bone resorption. The assay for serum PYD is new and has
not been used in any published studies in this type of setting. Therefore, comparisons of
the values from this study cannot be made to those of other resistance training studies.
However, urinary PYD has been shown to be a sensitive marker of bone resorption.
Further investigations of a longer duration are necessary to determine if early
biochemical changes are associated with delayed increases in BMD. Another possibility is
that the biochemical markers indicate initial changes in bone metabolism that favor
increased bone mass. However, measurable (by DXA) increases in regional BMD may lag
behind and be undetectable after only 6 months of resistance training. This is an area that
warrants further investigation.
Physiological Significance
Although the exercise regimen used in this study failed to increase BMD at several
sites, it is important to note that one site that was impacted was the femoral neck.

159
According to the National Osteoporosis Foundation (1990), 250,000 hip fractures were
reported in the United States in 1987. These fractures were associated with a cost of 3.9
billion dollars. Osteoporosis is a primary cause of fractures, disability, decreased
independence, and death in the elderly. After experiencing a fall induced hip fracture a
20% increase in mortality has been seen within one year of the fracture. Those who
survive, are forced to decrease their level of activity (National Osteoporosis Foundation,
1990). Therefore, interventions that can prevent the decrease of or increase femoral neck
BMD are extremely important. The results from this study indicate that even in older
adults with normal levels of femoral neck BMD, significant improvements in BMD can be
derived.
Lipid Peroxidation and Resistance to Oxidative Stress
Basal and post-oxidative challenge lipid peroxidation values were measured in all
three groups. Basal serum lipid peroxidation values (TBARS and hydroperoxides) were
not significantly different between the control and two training groups at conclusion of the
study. This finding suggests that neither low- or high-intensity weight training with 1 set
per exercise three times a week was an adequate stimulus to lower the resting lipid
peroxidation values in this population. This finding is not surprising considering that most
reports indicate that long-term high-intensity aerobic training (60-90min/ day) is necessary
to lower resting TBARS or hydroperoxides levels (Ji, 1995). Fligher volumes of resistance
exercise training (i.e., >1 set per exercise) may lower resting lipid peroxidation values; this
idea is testable and warrants further investigation.

160
Physical Challenge in vivo
Both resistance-trained groups had significantly reduced lipid peroxidation
compared to the control group following an oxidative challenge in vivo as indicated by
lower hydroperoxides and TBARS levels. For this study, the in vivo challenge was
defined as the graded exercise test (GXT). This finding suggests that six months of
resistance exercise reduced oxidative stress in response to acute maximal activity.
Furthermore, resistance exercise reduced lipid peroxidation during maximal aerobic
exercise, indicating a type of “cross protection” from one exercise modality to another.
Most research has indicated that chronic (>10-12 weeks) aerobic exercise can protect
tissue against lipid peroxidation induced by an acute physiological stress such as maximal
exercise or ischemia (Ji, 1995). Flowever, these are the first data to indicate that
resistance exercise confers protection against tissue lipid peroxidation and to show that
protection afforded in one exercise modality can be effective following another modality.
There are a few possibilities to explain this finding: (1) the resistance trained groups
generated fewer free radicals during the maximal treadmill test compared to the controls,
(2) the resistance trained groups had a greater antioxidant capacity to scavenge the free
radicals compared to the controls, or (3) a combination of 1 and 2.
First, a possibility exists that trained individuals generate fewer radicals compared
to their control counterparts. Earlier reports indicate that exercise training may increase
the number of mitochondrial proteins and therefore reduce the electron flux through each
electron transport chain. This may reduce the risk for electron leakage and radical
formation (Davies e tal. 1981). In addition, previous reports indicate that up-regulation of
antioxidant defenses may suppress the formation of free radicals in the mitochondria of

161
skeletal muscle (Davies 1981, Ji 1988). Aerobic training reduces skeletal muscle
mitochondrial sulfhydryl oxidation and exercise-induced inactivation of muscle enzymes
following an acute exercise bout (Ji, 1993). These findings are evidence that fewer radical
species are formed in trained subjects. It is unknown whether these same adaptations
occur in resistance trained subjects, therefore, these adaptations may be viable
possibilities.
Second, it has been shown that repeated bouts of ischemia in muscle can lead to
formation of free radicals such as superoxide via a xanthine/ xanthine oxidase pathway
(Yu, 1994). It has been postulated that weight-training movements also produce transient
ishcemia and alterations in calcium homeostasis, processes that may also generate free
radicals (Yu, 1994). Increased oxygen consumption as a consequence of the exercise also
increases the probability of electron leakage in the mitochondria and subsequent formation
of free radicals (Ji, 1995). Recently, Kraemer et al. (1998) demonstrated that serum lipid
peroxidation values increased following an acute bout of resistance exercise. Repeated
exposure of muscle to oxidative species through the xanthine oxidase pathway or
increased oxygen consumption may promote up-regulation of antioxidants such as
glutathione and antioxidant enzymes such as superoxide dismutase, catalase and
glutathione peroxidase (Ji, 1995). It is possible that the chronic resistance exercise training
stimulus in this study was sufficient to up-regulate some of these antioxidants and increase
glutathione stores within the muscle tissue and in the plasma (Robertson et al. 1991). The
physiological consequence of this adaptation in resistance trained persons would be a
reduced level of serum lipid peroxidation following a strenuous bout of activity.

162
Lastly, it is possible that resistance exercise improved the antioxidant defenses and
reduced the formation of free radicals during exercise. Skeletal muscle adaptation to
chronic resistance exercise includes increased synthesis of contractile and oxidative
proteins such as citrate synthase (Frontera et al., 1990). Training-induced elevations in
cellular respiration are likely accompanied by increased mitochondrial enzyme and
antioxidant enzyme synthesis. Together, these adaptations improve V02max and muscle
endurance without the elevations in tissue lipid peroxidation observed in control subjects.
Oxidative Challenges in Vitro
Serum samples were exposed to a series of radical generating systems in vitro,
including xanthine/ xanthine oxidase (superoxide generator), ferric chloride (hydroxyl ion
generator) and hydrogen peroxide. Interestingly, we found that the serum from the HEX
group contained significantly more TBARS following exposure to FeCl3, and the serum
from the LEX group contained fewer TBARS following the H202 challenge compared to
the other two groups. The increase in TBARS values in the HEX group following the
FeCl3 challenge indicates that these elderly subjects are more resistant to oxidative species
that are generated in normal metabolism. A possible mechanism to explain this finding is
that there may be a greater antioxidant capacity of the serum. Specifically, aerobic training
has been shown to increase circulating glutathione (Jenkins, 1988), a potent antioxidant/
reductant, and superoxide dismutase (Ji, 1995), an enzyme which catalyzes the reduction
of superoxide.

163
Physiological Consequence and Significance
What is the physiological consequence of lowered lipid peroxidation in response to
physical stress following resistance exercise? To date, investigators have only been able to
speculate about the role of lipid peroxidation on physical performance and health. It is
unclear whether lipid peroxidation is the cause of tissue dysfunction and cellular injury or
simply a consequence of an oxidative reaction (Ji, 1995). However, decreased lipid
peroxidation has been correlated with reduced muscle fatigue (Vincent et al., 1999),
lowered cardiovascular disease and decreased risk for a cardiac event (Ji, 1993).
Considerable attention has been given to resistance exercise may be able to provide health
benefits to the elderly by lowering the risk for cardiovascular disease.
Major Conclusions
It is well documented that resistance training elicits increases in muscular strength
and endurance. However, this investigation demonstrated that resistance training (RT)
with one set per exercise can also be an effective means of improving \Oi^, treadmill
time to exhaustion, and stair climbing time in healthy older adults. An exciting new
finding from this study was that resistance exercise lowered serum oxidative stress as
evidenced by the decreased lipid peroxidation following a physiological oxidative
challenge in vivo. The mechanisms underlying this adaptation are unclear but warrant
further study. The regimen used in the present study did not increase bone mineral density
at all skeletal regions measured, but the biochemical markers indicate increased bone
turnover. Considering that the subjects had normal bone density values prior to the study,
it is possible that a greater training duration and/or volume were required to elicit

164
physiological changes. Therefore, one set resistance training seems to be a sufficient
stimulus to elicit “health-related” adaptations in older adults. Further, some of the
adaptations found with this study such as increased VChpc.k, increased endurance, and
resistance to oxidative stress are more commonly associated with endurance type exercise,
indicating that resistance exercise is an appropriate exercise modality for improved health
Finally, these data indicate that the low- and high-intensity routines produced very similar
improvements in physiological performance. Therefore, based on these data we would
recommend that older adults perform resistance exercise consisting of 12 to 15 repetitions
per set to decrease the risk of injury that is more likely when using heavier loads and fewer
repetitions.
Physiological Significance
The number of elderly people in America is increasing with each passing year.
Commonly associated with increased age is decreased physical independence. Exercise is
seen as a means for increasing the health and physical independence of older adults. The
results from this study show that resistance exercise can be an effective means for
increasing functional capacity for older people. Increased strength and endurance can give
someone the ability to go shopping independently, travel, do housework, or to maintain an
independent lifestyle without relying on the services of family members or the health care
system. Furthermore, these data indicate that resistance exercise may be an effective
means of decreasing serum oxidative stress. Increased oxidative stress has been
implicated in a host of debilitating age-related diseases; increased lipid peroxidation is

165
associated with tissue dysfunction and compromised performance. Reducing the
susceptibility of tissue to oxidative stress may serve to limit the aging process on tissue, or
the destructive consequences of free radical generation. These data also show that
improved physiological capacity can be obtained with one set of resistance exercise in
older adults. This provides the older population with another viable means for improving
their health and quality of life without having to perform multiple set regimens that may be
too time consuming or high-intensity routines that increase the possibility of injury.
Limitations to the Experiment and Future Directions
It is important to note that this experiment was designed to test what we felt was a
realistic exercise regimen. Specifically, the regimen needed to be one that we could
realistically expect older people to perform, or are currently performing in health club
settings across the country. In so doing, our regimen differs from those used in previous
studies which used a very high training volume. Although high volumes are designed to
guarantee an adaptation, they can not be performed by an older population on a consistent
basis. With this in mind, there are several limitations to the current experiment. First, the
subjects for this study were volunteers recruited from the community through advertising
and word of mouth. This automatically induces a selection bias where only those that
want to or are motivated to exercise will join and the most sedentary segment of the
population will not be reached. Second, we sought to recruit “healthy” older adults who
did not have any complicating health disorders. In so doing, we may have recruited a
population that was too healthy to realize some of the adaptations that we were
anticipating in the time frame of the study. Third, the study was designed to test two

166
different intensity levels (low and high) but with each group performing an equivalent
volume of work. As described in the methods chapter, subjects were matched using a
composite strength score following the pre-testing so that each of the groups started with
a similar absolute strength measure. However, as a consequence of subject drop-outs the
groups did not have equal volumes of work at the study’s conclusion. The HEX group
exercised at 79% of maximum while the low group was at 59%, not 50% as was
proposed. Further analysis revealed that the LEX group trained with 539.5 Nm/kg FFM
while the HEX group used 429.4 Nm/kg FFM. It should be noted that when the subjects
were matched, they were matched for absolute strength, not for relative strength.
Therefore, while the HEX group worked at a significantly higher percentage of 1RM than
the LEX group, the participants in the LEX group performed more relative work when
compared to FFM. Although the issue of volume is a limitation, we felt that using the
RPE scale to make sure that each exercise was performed to the same level of difficulty
was important to ensure that each muscle group was receiving a similar stimulus. If we
had adhered to a strict percentage of 1RM, not every muscle group would have been
worked to the same level of difficulty as shown by Hoeger et al. (1990). They showed
that at the same percent of 1RM, exercises can produce vastly different numbers of
repetitions and levels of difficulty. We also felt that using a strict percentage of 1RM so
that some exercises are easier than others does not appropriately reflect the regimens
utilized by people engaged in resistance exercise.
Future experiments could pursue several possible avenues of investigation. First,
the duration of the present study may not have been long enough with the level of stimulus
provided. If the one set regimen is to elicit adaptations in bone density in healthy people,

167
the study duration may have to be extended to at least one year. Second, the issue of
training volume could be addressed by examining the difference between one and multiple
sets of exercise. It may be that the greater volume may be necessary for healthy people to
see changes in bone intensity in six months. However, the greater volume could
potentially lead to a increased probability of injury. Third, the resistance to oxidative
stress that was observed with this investigation warrants further examination. It is unclear
whether the level of protection provided by this study can impart any systemic benefit or if
greater adaptations can be observed with greater volumes of training. Fourth, the extent
of the bone and antioxidant adaptations consequential to this type of exercise should be
examined in clinical populations such as cardiovascular disease, arthritic, and frail elderly
persons to determine the level of benefit those “high risk” populations can derive from
resistance exercise. Lastly, future studies may need to consider matching subjects for
relative strength, not just absolute strength.

APPENDIX A
A-PRIORI SAMPLE SIZE ESTIMATION AND POWER ANALYSIS
Using the criterion measures to detect a difference in femoral neck bone mineral density
between groups.
Based on DXA data from Menkes et al. (1993).
n = (Zo/2)ig2
E2
Where at a 95% confidence interval, Z = 1.96, and a width of 0.033 g/cm2 where the
variance, a = 0.05 g/cm2
N = (L96)2 0 062 = 8.8 subjects per group
0.0332
Using the criterion measures to detect a difference in serum osteocalcin between groups.
Based on data from Ryan et al (1994).
n = (Za/2Xlg2
E2
Where at a 95% confidence interval, Z = 1.96, and a width of 0.4 pg/L where the
variance, a = 0.8 pg/L
N = (1.96) 2 0.82 = 15.4 subjects per group
0.42
168

APPENDIX B
INFORMED CONSENT TO PARTICIPATE IN RESEARCH
IRB#
Informed Consent to Participate in Research
The University of Florida
Health Science Center
Gainesville, Florida 32610
You are being invited to participate in a research study. This form is designed to provide
you with information about this study. The Principal Investigator or representative will
describe this study to you and answer any of your questions. If you have any questions or
complaints about the informed consent process or the research study, please contact the
Institutional Review Board (IRB), the committee that protects human subjects, at (352)
846-1494.
1. Name of Subject
2. Title of Research Study
The Effects of Low versus High Intensity Resistance Exercise on Antioxidant Enzyme
Activities, Biochemical Markers of Bone Metabolism, and Physical Function in Adults
Aged 60-85 Years.
3. a. Principal Investigator(s) and Telephone Number(s)
Principal Investigator: Randy W. Braith, Ph.D.(352-392-9575)
Co-Investigators: Jeff Bauer, PhD.
Michael N. Fulton, M.D.
David T. Lowenthal, M.D., Ph D.
Jay Mehta, M.D.
Scott K. Powers, Ph D.
Tim Sarac, M.D.
Kevin R. Vincent, M S.
Charles Wood, Ph D
169

170
b. Sponsor of the Study (if any)
none.
4. The Purpose of the Research
As people get older, certain chemical substances (“oxidants”) increase in
the body. These oxidants may be linked to problems of aging such as loss of muscle,
bone, and good physical condition and may even be the cause of aging. A certain type of
exercise (resistance exercise) may keep oxidants from forming. With resistance exercise,
you use different exercise machines to stimulate different muscles by pushing against
weights.
The purpose of this study is to see the effects of resistance exercise on the
bones, muscles, and overall physical condition of people your age. We are asking 80
people from 60 to 85 years of age from Gainesville and the surrounding area to be in this
study.
5. Procedures for This Research
This study will be conducted at the Center for Exercise Science (CES) at the
University of Florida and will last 7 to 8 months. You might be in an exercise group or
you might be in a group that does not exercise. Which group you are in will be decided at
random (like the toss of a coin). If you are not in the exercise group, you will be offered a
free exercise program when the study is completed. A list of all the tests for the study and
a schedule of the exercise program are included at the end of this Consent Form. If you
qualify to be in the study, it will consist of 6 visits over 15 to 19 days for testing that will
take about an hour each visit; 6 months of no exercise or exercise 3 days a week, 30 to 45
minutes each day. After the 6 months of exercise or no exercise, there will be 6 visits for
testing again over 15 to 19 days. Detailed descriptions of the tests and exercises follow:
Screening Visits
To see if you are healthy enough to be in the study, you will first go through an
orientation (explanation of what the study involves) and a series of tests which will occur
over 2 visits as follows:
Visit 1/Day 1 (about 75 minutes)
We will explain everything about the study and tell you about its risks and benefits.
You will be asked to fill out 3 questionnaires about your health, your quality of life, and
your medical history. It is very important that you be completely honest about any leisure
time activity you do or any diseases, sicknesses, or drug prescriptions you have. We will
also give you a form to take home to record exactly what you eat over a three day period.
You will then be given an orientation to the resistance exercise machines that will be used
in the study (Table Bl). You will be shown how to use each machine and then you will

171
use it 10 times in a row with the machine set at an easy level. You will then be shown the
equipment that will be used to see if you are physically able to be in the study. For this
orientation, you will be asked to walk on the treadmill for 5 minutes and to wear the
headgear used to collect your expired air. The exercise test is done on visit 2.
Visit 2/ Day 3 (about 60 minutes)
Graded Exercise Test: Before the test, a physician will ask you questions about
your medical history and will perform a cardiovascular examination. The physician will
watch you during the treadmill test. Also during this test, an electrocardiograph (ECG.
electrical tracing of heartbeats) will be taken. Your heart rate and blood pressure will be
monitored before the test, every 2 minutes during the test, and after the test until you
recover from the test. The test starts with you walking slow on the treadmill and
gradually becomes more difficult because the treadmill is raised every 2 minutes as if you
were climbing a hill You will continue to walk until you are unable to continue because
of fatigue or until the physician stops the test because it is putting too much stress on your
body. If the test shows you are healthy enough to exercise, you can continue with the
study. If you are not able to complete the test it will be stopped immediately and you will
be referred to your personal physician.
Blood Sample: We will ask you not to eat or drink anything after 12:00 a m.
(midnight) the night before this visit. After 15 minutes of quiet sitting, your blood will be
sampled from the inside of your elbow. The sample will be collected using a single
puncture from your arm. The total amount of blood taken will be about 5 tablespoons
which should not affect your daily activities. The blood sample will be done by a trained
technician to ensure your safety. A second sample will be taken 10 minutes after the
completion of the exercise test.
Visit 3/ Day 6 (about 60 minutes)
Muscle Strength: For this we will measure the heaviest weight you can lift with
your legs, chest, and arms. After a period of light warm-up and stretching, you will be
asked to perform a leg press, leg curl, chest press, and biceps (arm) curl. Each exercise,
will begin with a light weight which will be gradually increased by either 5 or 10 pounds,
depending on how difficult each increase is, until you can no longer lift the weight. There
will be a 2-5 minute rest between lifts. This process usually takes 5 to 6 lifts for each type
of exercise.
Visit 4/ Day 9-13 (60 minutes)
Bone Mineral Density: Your body composition and bone mineral density will be
measured by a dual X-ray absorptiometer (DXA), a type of X-ray. You will lie first on
your back and then on your side for a total of 20-30 minutes while the scanner arm of the
machine passes over you and records your total bone mineral, fat, and lean body mass
(muscle) composition. This test will be done by a technician certified to do the test.
Muscular Endurance. Your muscular endurance will be measured on the chest
press and leg press exercises. You will be asked to perform as many repetitions (lifts) as
possible on a chest press and leg press machine using 60% of the greatest weight you

172
lifted on these machines during Visit 3. A 5 minute rest will be allowed between the two
exercises.
Visit 5/ Day 13-16 (about 60 minutes)
Balance. You will place a special insert inside your shoe to measure how your
weight is distributed on your feet. You will be asked to stand as still as possible for 30
seconds. You will then be asked to walk about 11 yards (10 meters), turn around and
walk back to the starting point. This procedure will be done twice.
Time to walk up a flight of stairs. As a test of your physical function, you will be
asked to walk up a flight of stairs, using each step, as fast as possible. You will be asked
to repeat this test after a 5 minute rest.
Low back strength. You will be positioned in a MedX Clinical Lumbar Extension
Machine. Straps will be placed across your lap and legs to keep you stable in the machine.
Measurements of isometric lumbar extension strength will be made at seven different
angles (72, 60, 48, 36, 24, 12, and 0 degrees). To begin the test, you will be positioned
bent forward, with your chest near your lap (72 degrees). You will be instructed to push
against a back pad by slowly building up tension over a 2-3 second period. Once maximal
tension has been developed, you will be encouraged to maintain maximal force for an
additional 1-2 seconds, then slowly relax. This will be done at each of the angles. A 10
second rest will be allowed between each push. It is important that you do not hold your
breath while you are pushing with your low back.
Visit 6/ Day 15-19 (about 60 minutes)
Body composition(amount of body fat: For this test a staff member will measure
how much fat is on your body by pinching and measuring the thickness of your skin and
underlying fat layer with a device called a caliper. Seven measurements will be taken at
standard locations on your body (for example; upper arms, thighs, and hips).
Circumferences (distances around) of the different parts of your body segments will then
be measured using a measuring tape. Height and weight will also be measured.
Muscle Strength: For this we again will measure the heaviest weight you can lift with
your legs, chest, and arms, but using different exercises than on visit 3. After a period of
light warm-up and stretching, you will be asked to perform a leg extension, seated row,
triceps pushdown, and overhead press. Each exercise, will begin with a light weight which
will be gradually increased by either 5 or 10 pounds, depending on how difficult each
increase is, until you can no longer lift the weight. There will be a 2-5 minute rest
between lifts. This process usually takes 5 to 6 lifts for each type of exercise
Exercise Training
At the end of the testing, you will exercise in one of the following 3 groups for 6
months: no resistance exercise, low-intensity resistance exercise, or high-intensity
resistance exercise. A list of the exercises is attached to this consent form (Table B2).
During the 6 months if you are in an exercise group, you will be asked to report to the

173
CES 3 times per week to do the exercises. Each of these sessions will last from 30 to 45
minutes. The difference between the low-intensity and the high-intensity exercise will be
how hard we ask you to exercise: with low-intensity exercise, we will ask you to exercise
somewhat hard to hard, with high-intensity, we will ask you to exercise very hard to
maximal.
Repeat Testing
After the 6 months of exercise or no exercise, all the screening tests performed
before the 6-month training period will be repeated again over 15 to 19 days.
6. Potential Health Risks or Discomforts
If you wish to discuss these or any of the other possible discomforts you may experience,
you may call the Principal Investigator listed in #3 of this form.
Graded Exercise Test (GXT): The GXT is associated with a small risk of cardiovascular
complications. The risk for exercise is about 3-4 non-fatal events in 10,000 GXT’s, and
one fatal event per 25,000 tests in a hospital population. The risk to you will be
minimized in this study because all personnel involved are experienced in exercise testing
and emergency treatment is readily available Some fatigue and shortness of breath can be
expected during testing. Following testing, you may experience some muscle soreness.
This muscle soreness is normal and temporary, and most likely will not interfere with your
daily activities.
Blood Draws: Drawing blood may involve some discomfort at the site, possible bruising
and swelling around the site, and rarely an infection if the site is not kept clean. The
volume of blood taken per visit (2 visits, pre/post) will be equivalent to 10 tablespoons
and should not cause faintness or inhibit you from your normal daily activities. All blood
collection procedures will be performed by a trained technician, and will adhere to the
strictest policies regarding blood sample collection to ensure your safety.
Muscle Strength Tests: You may experience temporary muscle fatigue(tiredness) and
discomfort from these tests. This is normal and is a natural result of your muscles
working. Additionally, your muscles may be sore or stiff for a couple of days after the
testing. This also is normal and should not limit your normal daily activities. With any
form of resistance exercise there is a slight risk of injury to muscles or bone. These risks
are extremely rare and include, but are not limited to: muscle strains, connective tissue
(cartilage) sprains, joint injury, and spinal disk herniations. Previous injury to a joint
increases the risk. The use of the exercise machines and instruction and supervision by
personnel trained in the use of the machines will help to minimize any possible risks.
Resistance Training: As mentioned above, there is the slight possibility of injuries to
muscles or bones during any form of resistance training. You will be instructed on the
proper use of each machine. All sessions will be monitored by instructors trained in the

174
use of this equipment. You may experience muscle soreness, discomfort, fatigue, or
stiffness following the training sessions. This is normal and will disappear within 48-72
hours. The weight used will be light at the start of the study and then slowly increased to
minimize soreness or discomfort.
Bone Mineral Density: The X-ray exposure from the DXA scan is very low. The
radiation dose during the total body scan is 0.5mrem. This exposure is 1/60 of the
average radiation exposure from a front/back chest film (30 mrem). A quality control test
is run every day the machine is used in order to ensure that only low levels of radiation are
emitted.
Body Composition: There is a slight risk of minor bruising from the calipers.
7.Potential Health Benefits to You or to Others
The major health benefit to you is the participation in an exercise
program designed to increase muscular strength and endurance. You will also receive an
evaluation of your body composition, muscle strength and endurance, and bone mineral
density. Increased strength can improve balance and physical function. Resistance
training can also increase muscle mass and bone density. You will also be contributing to
knowledge concerning the effects of resistance exercise on strength and body
composition.
If you are selected to be in the control group, there will be little or no health
benefit, but at the end of the control period you will be given the opportunity to go
through the exercise program at no cost.
8. Potential Financial Risks
There are no financial risks associated with participation in this study.
9. Potential Financial Benefits to You or to Others
There are no financial benefits associated with your participation in this
study.
10. Compensation For Research Related Injury
In the unlikely event of you sustaining a physical or psychological injury which is
approximately caused by this study:
X professional medical; or professional dental; or professional
consultative

175
care received at the University of Florida Health Science Center will be provided without
charge. However, hospital expenses will have to be paid by you or your insurance
provider. You will not have to pay hospital expenses if you are being treated at the
Veterans Administration Medical Center (VAMC) and sustain any physical injury during
participation in VAMC-approved studies.
11. Conflict of Interest
There is no conflict of interest involved with this study beyond the
professional benefit from academic publication or presentation of the results.
12. Alternatives to Participating in this Research Study
You are free not to participate in this study. If you choose to participate,
you are free to withdraw your consent and discontinue participation in this research study
at any time without this decision affecting your medical care. If you have any question
regarding your rights as a subject, you may phone the Institutional Review Board (IRB)
office at (352) 846-1494.
13. Withdrawal From this Research Study
If you wish to stop your participation in this research study for any reason,
you should contact Dr. Randy W. Braith at (352) 392-9575. You may also contact the
Institutional Review Board (IRB) Office at (352) 846-1494.
14. Confidentiality
The University of Florida and the Veterans Administration Medical Center
will protect the confidentiality of your records to the extent provided by Law. The Study
Sponsor, Food and Drug Administration and the Institutional Review Board have the legal
right to review your records.

176
15. Signatures
Subject's Name
The Principal or Co-Principal Investigator or representative has explained the nature and
purpose of the above-described procedure and the benefits and risks that are involved in
this research protocol.
Signature of Principal or Co-Principal Date
Investigator or representative obtaining consent
You have been informed of the above-described procedure with its possible benefits and
risks and you have received a copy of this description. You have given permission for
your participation in this study.
Signature of Subject or Representative Date
If you are not the subject, please print your name and indicate one of the following:
The subject's parent
The subject’s guardian
A surrogate
A durable power of attorney
A proxy
Other, please explain:
Signature of Witness Date
If a representative signs and if appropriate, the subject of this research should indicate
assent by signing below.
Subject's signature
Date

177
Table B1. Testing Schedule at the Beginning of the Study and After 6
Months. Time as Listed is 15-19 Days to Complete All Visits
Visit 1 (duration: 75 minutes)
Orientation to Study
Informed Consent
Medical History Form
Food Record
Orientation to Resistance Machines
Orientation to Graded Exercise Test Equipment
Visit 2 (duration: 60 minutes) scheduled 2 days after visit 1
Graded Exercise Test (Stress Test)
Blood Sample
Visit 3 (duration: 60 minutes) scheduled for 3 days after Visit 2.
Strength Testing By: Leg Press
Leg Curl
Chest Press
Biceps Curl
Visit 4 (duration: 60 minutes) scheduled for 3-7 days after visit 3.
Bone Mineral Density X-ray (Dual Energy X-ray Absorptiometer)
Muscular Endurance By: Leg Press
Chest Press
Visit 5 (duration: 45 minutes) scheduled for 3 days after visit 4
Time to Walk Up a Flight of Stairs
Isometric Lumbar (Back) Extension Test
Visit 6 (duration: 60 minutes) scheduled for 3 days after visit 5
Skinfold Test
Height and Weight Measured
Segment Circumferences
Strength Testing By: Leg Extension
Seated Row
Overhead Press
Triceps Pushdown

Table B2.
Resistance Exercise Training Regimen For Both Groups
Performed Three Times Per Week for 6 Months
Each Session 30-45 Minutes
178
Exercise
Sets
Repetitions
1. Abdominal Crunch
1
11-14
2. Leg Press
1
11-14
3. Leg Extension
1
11-14
4. Leg Curl
1
11-14
5. Seated Row
1
11-14
6. Chest Press
1
11-14
7. Overhead Press
1
11-14
8. Biceps Curl
1
11-14
9. Seated Dip
1
11-14
10. CalfPress
1
11-14
11. Leg Abduction
1
11-14
12. Leg Adduction
1
11-14
13. Isolated Lumbar *
1
11-14
Extension
* Only performed once per week
- 2 minutes rest will be allowed between each set

APPENDIX C
INSTITUTIONAL REVIEW BOARD APPROVAL FORM TO PERFORM RESEARCH
UNIVERSITY OF
FLORIDA
IRB PROJECT II 375-97
EXPIRES 11/14/98
Health Center Institutional Review Board 1*0 Box 1181177
(I.iinesvillr, l:l.3261(1 0173
Principal Investigator: POLLOCK, MICHAEL L. (.352)ftlft-14‘M
Add* css: BOX 100277 Fnx (.152)84(1-1497
THE EFFECTS OF LOW VERSUS HIGH INTENSITY RESISTANCE EXERCISE ON
ANTIOXIDANT ENZYME ACTIVITIES, BIOCHEMICAL MARKERS OF BONE METABOLISM,
AND PHYSICAL FUNCTION IN ADULTS AGED 60-85 YEARS
Congratulations on receiving IRB approval to conduct research at the
University of Florida. Approval of this project was granted on 11/14/97.
Enclosed is the dated, IRB-approved Informed Consent Form that must be
used for enrolling subjects into this project. You have approval for
12 months only.
You are responsible for obtaining renewal of this approval prior to the
expiration date. Reapproval of this project must be granted before the
expiration date or the project will be automatically suspended. If
suspended, new subject accrual must stop. Research interventions must
also stop unless there is a concern for the safety or well-being of the
subjects. Upon completion of the study, you are required to submit a
summary of the project to the IRB office.
The IRB has approved exactly what was submitted and reviewed. Any change
in the research, no matter how minor, may not be initiated without IRB
review and approval except where necessary to eliminate hazards to human
subjects. If a change is required due to a potential hazard, that change
must be promptly reported to the IRB.
Any severe or unanticipated side effects or problems and all protocol
deviations must be reported, in writing, within 5 working days.
Research records must be retained for three years after completion of
the research; it is recommended that they be retained for eight years.
If VAMC patients will be included in this project, or if the project is
to be conducted in part on VA premises or performed by a VA employee
during VA-compensated time, final approval should be obtained by
application to the VA Research Office.
You are responsible for notifying all parties about the approval of this
project, including your co-PIs and Department Chair. If you have any
questions, please feel free to contact Barbara Frentzen, at (352) 846-1494.
R. Peter Iafrate, Pharm.Djf) // . fj U
Ch„lr. IRB• 01 ^
cc: IRB File; Division of Sponsored Research; Rhonda Cooper-DeHoff,
Pharmacy; Edward Block, VA; Sandra Barnawell, CRC
Enclosed: Stamped, dated, IRB-approved Informed Consent. Form
DEPARTMENT OF MEDICINE
GRANTS MANAGEMFNi â– **.*_.,Am.
179

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BIOGRAPHICAL SKETCH
Kevin Robert Vincent completed his undergraduate training at the University of
Connecticut in 1990 with a major in sports medicince/athletic training. He then entered
graduate school at the University of Massachusetts where he received his master’s degree
in exercise science in 1996. While he was at the University of Massachusetts, Dr. Priscilla
M. Clarkson served as his advisor. Also during his career at the University of
Massachusetts, Kevin served as the Assistant Editor for the International Journal of Sport
Nutrition, a teaching assistant, and as an assistant residence director. In the fall of 1996,
he entered the doctoral program at the University of Florida in the Department of Exercise
and Sport Science under the direction of Dr. Michael L. Pollock. After Dr. Pollock’s
passing, Kevin finished his studies under the direction of Dr. Randy W. Braith. Kevin is
currently the Coordinator of Strength and Conditioning for the recreation and fitness
centers at the University of Florida and has served as an adjunct faculty member at Santa
Fe Community College, teaching in the Cardiopulmonary Technology Department.
Kevin’s wife, Heather, also received her Ph D. from the Exercise and Sports Science
Department at the University of Florida. They have a son, Ian. Kevin will be entering
medical school at the University of Florida in August of 1999.
193

I certify that I have read this study and that in my opinion it conforms to acceptable
standards of scholarly presentation and is fully adequate, in scope and quality, as a
dissertation for the degree of Doctor of Philosophy.
''Randv W Braith. Chair
'Randy Wl Braith, Chair
Associate Professor of Exercise
and Sport Science
I certify that I have read this study and that in my opinion it conforms to acceptable
standards of scholarly presentation and is fully adequate, in scope and quality, as a
dissertation for the degree of Doctor of Philosophy.
J^f&eyCA. Bauer
Assistant Professor of Exercise
and Sport Science
I certify that I have read this study and that in my opinion it conforms to acceptable
standards of scholarly presentation and is fully adequate, in scope and quality, as a
dissertation for the degree of Doctor of Philosophy.
Lowénjhal
ifessor of Exercise and Sport
Science
I certify that I have read this study and that in my opinion it conforms to acceptable
standards of scholarly presentation and is fully adequate, in scope and quality, as a
dissertation for the degree of Doctor of Philosophy. // (
Charles E. Wood
Professor of Physiology

This dissertation was submitted to the Graduate Faculty of the College of Health and
Human Performance and to the Graduate School and was accepted as partial fulfillment of
the requirements for the degree of Doctor of Philosophy.
Aui“’'1999 jfí éi
Dean, éollege/of Health and Human
Performance
Dean, Graduate School

LD
1780
1999
y i? 2,
UNIVERSITY OF FLORIDA
3 1262 08556 6890