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The Effects of Hamstring Delayed Onset Muscle Soreness on Functional Knee Joint Stability


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THE EFFECTS OF HAMSTRING DELAYED ONSET MUSCLE SORENESS ON FUNCTIONAL KNEE JOINT STABILITY By KYLE ANDREW SMINK A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE IN EXERCISE AND SPORT SCIENCES UNIVERSITY OF FLORIDA 2003

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Copyright 2003 by Kyle Smink

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ACKNOWLEDGMENTS A project such as this could not be completed without the support of numerous others. For that, I would like to express a sincere thank you to the following people who have been there for me throughout the completion of this project. First of all, I would like to thank my family and friends for the love, support and understanding they provided me along this journey. Although I believe none of my family truly understands what I have been doing for the past two years, they have supported me one hundred percent. It has been a struggle at times to stay motivated, but I always had those close to me to keep me on course. Without these people, I do not think I would have made it through this project. I would like to thank Dr. Mike Powers for his knowledge and guidance that allowed me to take my raw ideas and formulate them into a feasible research project. He is an excellent mentor and teacher from whom I have learned so much about research. He was instrumental in assisting me with the conception and design of this study, data collection and analysis, and also helping me fabricate and validate the perturbation device. I would like to express a special thank you to my committee chair, Dr. Mark Tillman. He accepted this burden late in the process, and was an incredible help to me throughout. I cannot say enough to thank him for the amount of time and effort he provided me so I could complete this project on time. His insight and ideas were instrumental in finalizing this paper. iii

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Dr. MaryBeth Horodyski has been helpful throughout the entire process. She was able to provide clarity to certain issues I had during my initial drafts of this project. She was also able to provide me with helpful feedback on potential flaws that may have been overlooked by those of us dealing with it on a daily basis. I would like to thank her for being an integral part of my committee who helped me along the road to the successful completion of this project. I would like to thank Dr. Stephen Dodd immensely for accepting my offer to join my committee at such a late time. His expertise and knowledge in the field of exercise physiology has helped greatly with the successful completion of this research. Finally, I would like to thank the zoo full of friends I have made while in Gainesville, for those are the ones that made sure I got away when I needed to get away, but also made sure I stayed in when I needed to stay in. Many fun times and memories took place while working on this project, none of which I hope to forget, and some that I still cannot remember. iv

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TABLE OF CONTENTS Page ACKNOWLEDGMENTS.................................................................................................iii LIST OF TABLES...........................................................................................................viii LIST OF FIGURES.............................................................................................................x ABSTRACT.......................................................................................................................xi CHAPTER 1 INTRODUCTION........................................................................................................1 Statement of the Problem..............................................................................................2 Research Hypotheses....................................................................................................3 Definition of Terms......................................................................................................3 Assumptions.................................................................................................................4 Limitations....................................................................................................................4 Significance..................................................................................................................5 2 REVIEW OF LITERATURE.......................................................................................6 Introduction...................................................................................................................6 Anatomy and Biomechanics of the Knee.....................................................................6 Articulations..........................................................................................................6 Ligaments..............................................................................................................7 Muscles..................................................................................................................8 Mechanoreceptors................................................................................................10 Mechanism of Injury for ACL Rupture......................................................................11 Delayed Onset Muscle Soreness (DOMS).................................................................11 Electromyography (EMG)..........................................................................................13 Measures of Dynamic Stability..................................................................................14 Summary.....................................................................................................................16 3 METHODS.................................................................................................................17 Subjects.......................................................................................................................17 Instrumentation...........................................................................................................17 Perturbation Device.............................................................................................17 Electromyography...............................................................................................18 v

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Triaxial Force Platform.......................................................................................18 Inclinometer.........................................................................................................18 Measurements.............................................................................................................19 Hamstring Flexibility...........................................................................................19 Pain Measurement...............................................................................................19 Muscle Latency...................................................................................................20 Time to Stabilization...........................................................................................21 Procedures...................................................................................................................22 Statistical Analysis......................................................................................................23 4 RESULTS...................................................................................................................29 DOMS Measures........................................................................................................29 Measurement of Active Range of Motion...........................................................29 Passive Range of Motion Pain Threshold...........................................................30 Pressure Pain Threshold......................................................................................31 Muscle latency............................................................................................................32 Internal Rotation Perturbation.............................................................................32 External Rotation Perturbation............................................................................32 Time to Stabilization...................................................................................................33 Vertical Ground Reaction Force (Fz)..................................................................33 Medial/Lateral Ground Reaction Moment (Mx).................................................33 Anterior/Posterior Ground Reaction Moment (My)............................................34 5 DISCUSSION AND CONCLUSIONS......................................................................35 Discussion...................................................................................................................35 DOMS Measurements................................................................................................36 Muscle Latency...........................................................................................................37 Time to Stabilization...................................................................................................40 Conclusions.................................................................................................................42 Suggestions for Future Research................................................................................42 APPENDIX A LETTER OF INFORMED CONSENT......................................................................46 B INCLUSION QUESTIONNAIRE..............................................................................50 C DECRIPTIVE INFORMATION AND HAMSTRING FLEXIBILITY....................51 D VISUAL ANALOGUE PAIN SCALE......................................................................52 E RAW DATA...............................................................................................................53 F ANOVA SUMMARY TABLES................................................................................62 vi

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LIST OF REFERENCES...................................................................................................65 BIOGRAPHICAL SKETCH.............................................................................................70 vii

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LIST OF TABLES Table page 4-1. Active hamstring range of motion ( SD)...............................................................30 4-2. Pain quotient as measured on a visual analog pain scale for passive range of motion pain threshold (PQ SD).............................................................................31 4-3. Pain quotient as measured on a visual analog pain scale for Pressure Pain Threshold (PQ SD)................................................................................................31 4-4. Internal rotation muscle latency (msec SD)...........................................................32 4-5. External rotation muscle latency (msec SD)..........................................................33 4-6. Vertical TTS based on Fz (msec SD).....................................................................33 4-7. Medial/Lateral TTS based on Mx (msec SD)........................................................34 4-8. Anterior/Posterior TTS based on My (msec SD)...................................................34 E-1. Subject demographic raw data..................................................................................53 E-2. Active range of motion (AROM) raw data (degrees)...............................................54 E-3. Passive range of motion pain threshold (PROMPT) raw data (PQ = 0 100).........55 E-4. Pressure pain threshold (PPT) raw data (PQ = 0 100)...........................................56 E-5. IROT hamstring muscle latency raw data (msec).....................................................57 E-6. EROT hamstring muscle latency raw data (msec)....................................................58 E-7. Time to stabilization based on vertical ground reaction force (Fz) raw data (msec)...............................................................................................................59 E-8. Time to stabilization based on medial/lateral ground reaction force (Mx) raw data (msec).......................................................................................................................60 E-9. Time to stabilization based on anterior/posterior ground reaction force (My) raw data (msec)...............................................................................................................61 viii

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F-1. Active range of motion (ANOVA)............................................................................62 F-2. Passive range of motion pain threshold (ANOVA)...................................................62 F-3. Pressure pain threshold (ANOVA)............................................................................62 F-4. Internal rotation hamstring muscle latency (ANOVA).............................................63 F-5. External rotation hamstring muscle latency (ANOVA)............................................63 F-6. Fz (ANOVA).............................................................................................................64 F-7. Mx (ANOVA)...........................................................................................................64 F-8. My (ANOVA)...........................................................................................................64 ix

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LIST OF FIGURES Figure page 3-1. Lower extremity perturbation device........................................................................24 3-2. Load cell....................................................................................................................24 3-3. Height adjustable release mechanism and trigger switch..........................................24 3-4. Bertec triaxial force platform....................................................................................25 3-5. Inclinometer...............................................................................................................25 3-6. Subject positioning for ROM measure. A) start and B) end....................................25 3-7. Specially designed PVC device used for measuring hamstring range of motion......26 3-8. Nicholas Manual Muscle Tester. This device is a handheld dynamometer used to measure force output................................................................................................26 3-9. Algometer used for measuring the amount of pressure applied to the muscle..........27 3-10. Vertec vertical jump device.....................................................................................27 3-11. Time to stabilization jump landing sequence. A) starting position, B) mid-flight, and C) landing phase................................................................................................28 5-1. Active hamstring range of motion.............................................................................44 5-2. Passive range of motion pain threshold.....................................................................44 5-3. Pressure pain threshold..............................................................................................45 x

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Abstract of Thesis Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science in Exercise and Sport Sciences THE EFFECTS OF HAMSTRING DELAYED ONSET MUSCLE SORENESS ON FUNCTIONAL KNEE JOINT STABILITY By Kyle Andrew Smink August 2003 Chair: Mark D. Tillman, PhD Major Department: Exercise and Sport Sciences Dynamic joint stability is an essential component of athletic performance. If deficits in dynamic stability exist, the athlete may be unable to perform at previous levels of competition and may also be prone to injury. Delayed onset muscle soreness (DOMS) is a response to unaccustomed bouts of strenuous exercise that results in certain physical and physiological markers being present in the local tissue. The purpose of this investigation was to determine the effects of hamstring DOMS on functional knee joint stability. Thirty subjects (18 females, 12 males) with no previous knee injuries participated in this investigation. Subjects were assigned to one of two groups (DOMS, Control). Baseline measures of hamstring flexibility, pressure pain threshold (PPT), passive range of motion pain threshold (PROMPT), hamstring latency, and time to stabilization (TTS) were measured. Subjects in the experimental group then performed 6 sets of 10 eccentric xi

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hamstring contractions using a prone leg curl machine. All subjects returned for reevaluation of all baseline measures 48 and 96 hours following the initial session. Separate analyses of variance were performed for each dependent variable. Tukey HSD post hoc analyses were performed to determine where significance existed among the levels of each factor. A probability level of P < 0.05 was expected to designate statistical significance. DOMS was adequately induced in the experimental group. Active hamstring range of motion in the DOMS subjects significantly decreased after 48 and 96 hours post exercise. PROMPT and PPT increased significantly 48 and 96 hours after the initial session for the DOMS group. Hamstring muscle latency in the medial hamstring had a slower response time to the external rotation perturbation. A significantly faster response time was also present at the 48h and 96h posttest sessions compared to the baseline measures. Time to stabilization for the vertical ground reaction force curve was faster during the 96h posttest session compared to the pretest and posttest 48h sessions, respectively. Based on the results of the present study, it was concluded that DOMS has little to no effect on the functional outcome of dynamic joint stability as measured using a standing rotational perturbation or a jump landing procedure. Future research should investigate the effects of hamstring DOMS on other aspects of proprioception, including active and passive joint repositioning and also threshold to detection of passive movement. Additionally, research should be conducted to examine the effects of a functional fatigue protocol on the entire lower extremity to establish whether or not functional joint stability would be affected if the entire kinetic chain were involved. xii

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CHAPTER 1 INTRODUCTION Knee injuries, particularly those involving the anterior cruciate ligament (ACL), are a common occurrence in athletics. The ACL is the primary stabilizing ligament of the knee and athletes who participate in sports involving high-speed change of direction, pivoting, jumping and landing, and deceleration maneuvers are at an increased risk for ACL injury. Damage to the ACL results in decreased stability of the knee joint and is typically associated with a feeling of giving way. The prevalence of injury in sports such as football, basketball, and soccer are relatively high because they involve some or all of the predisposing components stated above.1 In many cases the injury occurs when there is no apparent contact involved. These non-contact injuries account for approximately 70% of all ACL injuries.1, 2 The incidence of ACL injury in sports is a continuing dilemma. In 2002, during three weeks of NCAA spring practices and one weekend of NFL mini camps, six players were diagnosed with having suffered season ending knee injuries, all involving the anterior cruciate ligament.3, 4, 5 Of those six cases, four of the injuries involved no contact with an opposing player, which is in close agreement with the percentages reported earlier for non-contact ACL injuries. Because contact injuries cannot be controlled, non-contact incidences such as these have researchers probing for answers in an attempt to recognize predisposing factors related to ACL injury. The hamstrings help to dynamically stabilize the knee during athletic movements that may predispose an athlete to ligament injury. DOMS is characterized by pain, 1

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2 decreased strength, decreased range of motion, and swelling of the affected muscles. All of these characteristics can lead to altered responses from the hamstrings, whether it is a decrease in force generation or an increase in muscle reaction time. With a diminished response from these dynamic restraints, functional knee stability could be compromised, resulting in ACL disruption. Statement of the Problem Functional joint stability is a collection of anatomical and physiological components that are present in order to maintain a relatively homeostatic environment of the joint during active bodily movements.6 These components are characterized as either static or dynamic in nature. Static components represent the structural aspect of the joint: ligament, capsule, cartilage, bony congruity, and friction, whereas the dynamic component corresponds to the functional aspect, primarily made up of the muscles that cross the joint. Biological control systems associated with dynamic stabilization are the feedforward or anticipatory and feedback or reactive mechanisms. Impulses from afferent stimuli through somatosensory, visual, and vestibular input allow these control mechanisms to function properly.6, 7 The muscles reactive response to a perturbation plays a major role in dynamic joint stability. The timing of this response is commonly referred to as muscle latency. The hamstrings work synergistically with the ACL as stabilizers of the knee joint, providing resistance to anterior shear forces as well as rotational forces around the knee. The ACL provides a passive resistance, while the hamstrings actively stabilize the knee. An increased latency period of the hamstrings could increase the likelihood of a functionally unstable joint. This could further predispose an athlete to potential ligament injury due to the inhibition of the dynamic components of the sensorimotor system.

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3 DOMS is a physiological response to unaccustomed physical activity that results in pain, decreased strength, decreased range of motion, and swelling of the affected muscles. There is limited research indicating an increase in muscle latency associated with muscular fatigue8 and decreased strength,9 with none having directly studied DOMS to determine if similar effects would be noted. Therefore, the purpose of this study was to assess functional knee joint stability after DOMS has been induced in the hamstring muscles. Functional joint stability will be assessed by measuring time to stabilization of the affected lower extremity and muscle latency of the hamstrings. Research Hypotheses 1. Active hamstring range of motion will significantly decrease after the inducement of DOMS. 2. Passive range of motion pain threshold will significantly increase after the inducement of DOMS. 3. Pressure pain threshold measurement will significantly increase after the inducement of DOMS. 4. Hamstring muscle latency following knee perturbation will significantly increase after the inducement of DOMS. 5. Time to stabilization following a jump landing will significantly increase after the inducement of DOMS. Definition of Terms 1. Eccentric contraction is the lengthening of a muscle when a force/load applied to that muscle is greater than the force production of the muscle. 2. Electromyography is the study of muscle function through the detection of electrical impulses emanating from the muscle itself. 3. Goniometry is a standardized technique of measuring joint motion. 4. Homeostasis is the maintenance of a stable internal environment of the body. 5. Kinesthesia is the ability to perceive extent, direction, or weight of movement.

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4 6. Muscle latency is the time required for a muscle to respond following an induced perturbation. 7. Perturbation is a disruption in homeostasis. 8. Proprioception is the awareness of posture, movement, and changes in equilibrium and the knowledge of position, weight, and resistance of objects in relation to the body. 9. Range of motion (ROM) is the amount of movement of a particular joint measured in degrees by goniometry. 10. Time to Stabilization (TTS) is a measurement tool, calculated in milliseconds, used to assess the length of time needed for one to maintain dynamic stability following a standardized jump for distance and height to a single leg balance position. Assumptions Two assumptions were made for the purpose of this investigation 1. Subjects will be honest in filling out prescreening questionnaire. 2. Subjects will exert full effort when reacting to knee perturbations and performing time to stabilization techniques. Limitations Five limitations were identified for this investigation 1. A sufficient predetermined level of DOMS must be induced in the hamstring muscles; however, the level will vary across subjects. 2. Only hamstring flexibility and muscle soreness will be used as indicators of DOMS. 3. Only subjects who have not performed lower extremity resistance training during the previous six months will be used in the investigation. 4. Functional knee stability will only be assessed 48 and 96 hours after DOMS has been induced. 5. Only healthy subjects free from any acute knee injuries or lower extremity muscle strains will be used for this study.

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5 Significance Injuries to the anterior cruciate ligament continue to be a primary concern to all members of the sports medicine team. The exact cause of ligament failure is unknown, but many assumptions can be made. No study to date has assessed hamstring latency when DOMS has been induced. Determining whether DOMS affects the latency period of the hamstrings could identify a predisposing risk factor to ACL failure in athletics.

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CHAPTER 2 REVIEW OF LITERATURE Introduction Dynamic joint stability is an essential component of athletic performance. This type of stability also helps to protect the joint from injury. If deficits in dynamic stability exist, the athlete may be unable to perform at previous levels of competition and may also be prone to injury. Likewise, athletes who have been previously injured may develop deficits in dynamic stability. The microtrauma that occurs during resistance and other types of exercise, generally referred to as DOMS, induces changes in the local tissue similar to those seen following macrotrauma. Thus, it is possible that this type of trauma would affect dynamic stability. However, at this time the effects of DOMS on dynamic stability have not been investigated. This review of literature will focus on the anatomy and biomechanics of the knee, mechanism of injury for the anterior cruciate ligament, delayed onset muscle soreness, and measures of dynamic stability. Anatomy and Biomechanics of the Knee Articulations The knee joint is composed of two bony articulations, the tibio-femoral joint and the patellofemoral joint. The tibio-femoral (knee) joint, comprised of the femur and the weight-bearing tibia, is a modified hinge synovial joint that allows a great amount of ROM through movements of flexion and extension, but is limited with internal and external rotation.10 The patellofemoral joint is made up of the patella and the femur. The patella, a large sesmoid type bone, is embedded within the patellar tendon and rests in the 6

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7 trochlear groove of the femur.11 The patellas primary function is as a fulcrum for the quadriceps muscles to increase the lever arm during active extension movements at the knee.12 Ligaments Configured in and around the knee are four key ligaments that enable the joint to maintain passive stability during weight bearing activities. These ligaments can be divided into two groups, collaterals and cruciates, whose function is based on their arrangement at the knee. The collaterals are comprised of the lateral collateral ligament (LCL) and the medial collateral ligament (MCL), whereas the cruciates consist of the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL). The orientation and biomechanics of the cruciate ligaments will be provided to allow a better understanding of their role in knee joint stability. The ACL is an important stabilizing ligament in the knee joint and one that, if ruptured, typically requires surgery.13 The ACL functions to reduce anterior shear force as well as control some varus, valgus and rotational forces of the tibia on the femur. Approximately 86% of the primary restraint of anterior tibial translation is provided by the ACL.14 Damage to the ACL creates joint laxity and may lead to episodes of instability in the knee.15 The ACL originates on the medial aspect of the lateral femoral condyle and inserts on the anterior tibial plateau.16 Generally, the ACL is addressed as a single banded ligament that connects the tibia to the femur; however, that is not entirely the case. The ACL is divided into two separate bundles of fibers, an anteromedial and a posterolateral bundle, each offering passive resistance to different stresses placed on the tibio-femoral joint. When the knee is in a fully extended position (zero degrees), the anteromedial bundle is most taut, while the posterolateral bundle is taut in flexion.16

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8 Movements through the range of motion are accommodated by a combination of the two bundles working synchronously. The posterior cruciate ligament serves as the antagonist to the ACL, in that its orientation in the knee runs from the lateral wall of the medial femoral condyle to the posterior tibial shelf.17, 18 The PCL serves to prevent straight posterior displacement of the tibia relative to the femur.19, 20 The PCL, like the ACL, consists of two so-called bands of fibers. During knee flexion movements, the anterolateral portion is tightened while the posteromedial portion is lax. Conversely, in knee extension, the anterolateral bundle is lax, whereas the posteromedial bundle is tight.17, 18 Muscles An extensive knowledge of the musculature that crosses the knee joint is critical in order to understand the proper structure and function of the knee joint and how this relates to overall functional joint stability. There are 12 muscles that cross the knee joint. The primary muscles associated with knee joint movement are the four quadriceps and three hamstring muscles. The remaining muscles, which consist of the gastrocnemius, plantaris, and popliteus in the lower leg, and the sartorius and gracilis of the upper leg, are secondary type muscles that assist movement of the joint, but are not considered prime movers. The quadriceps group is collectively made up of four muscles (Rectus Femoris, Vastus Intermedius, Vastus Lateralis, and Vastus Medialis) that act to extend the knee. Because the Rectus Femoris attaches on the pelvis, this allows it to also function as a hip flexor. The Vastus Medialis and Lateralis originate on the linea aspera on the posterior femur on their respective sides, and the Vastus Intermedius originates on the anterior and

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9 lateral femoral shaft. All four muscles have a common insertion site into the tibial tuberosity via the patellar tendon.21 The hamstrings are the primary muscle group that makes up the posterior thigh, which consists of three separate muscles (Biceps Femoris, Semitendinosus, Semimembranosus) thats main functions are to flex the knee and extend the hip. The hamstrings have a common origin on the ischial tuberosity of the pelvis, though the biceps femoris has an additional origin on the linea aspera of the posterior femur. As a group, they travel down the posterior aspect of the upper leg with individually different insertions. The biceps femoris, semimembranosus, and semitendinosus insert into the head of the fibula, posterior medial tibial condyle, and anterior proximal tibial shaft, respectively.21 Besides providing joint motion, the hamstring muscles also function as joint stabilizers and secondary restraints to anterior tibial translation.22,23 Some research suggests that there is an anterior cruciate ligament hamstring reflex that allows this to happen. However, there has been much controversy over this neuromuscular response. In human and animal studies, researchers have investigated the relationship between anterior tibial displacement and the ACL hamstring reflex with mixed results.1, 13, 15, 24, 25, 26 Boden et al.1 suggest that the hamstrings provide this protective effect when the hip is flexed because it allows the hamstrings to become tighter, allowing less anterior shear of the knee. This protective effect may be diminished with increased hamstring flexibility.1 Their findings suggested that athletes who sustained an ACL injury had greater hamstring flexibility than a control group of subjects.

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10 Mechanoreceptors One of the most important components of motor control is our ability to utilize the numerous mechanoreceptors found throughout the human body. The importance lies in that mechanoreceptors provide afferent input to the central nervous system making them valuable contributors to proprioceptive feedback. The most commonly described mechanoreceptors, muscle spindles and Golgi tendon organs (GTO), are located in muscle and tendon tissue.27, 28 Others that are equally important are those located in the ligaments and joint capsules, particularly Ruffini endings and Pacinian corpuscles.6, 28 Muscle spindles are located in skeletal muscle and are responsible for detecting changes in length of the associated muscle, whereas Golgi tendon organs monitor active force and tension in the muscle through its location in the myotendinous junction. These two mechanoreceptors function via a monosynaptic reflex pathway and are considered to have a slow adaptation rate to their respective responses.6, 7, 28 The Ruffini endings and Pacinian corpuscles respond through the same reflex pathway as mentioned earlier. Like the muscle spindles and Golgi tendon organs, Ruffini endings are slow adaptive and have a low threshold for stimulation. They are primarily located in the joint capsule and ligaments and are responsible for detecting changes in joint pressure. Pacinian corpuscles are also low threshold receptors, but adapt quickly to the stresses placed upon them. They function to sense high frequency vibrations within the joint capsule. This quick adaptive response classifies them as only dynamic receptors, meaning they are inactive when a constant stimulus is placed on the joint.6, 7, 28 The mechanoreceptors described here have independent responsibilities for maintaining dynamic joint stability. However, in order for the joint to function properly, they must work in unison, dependent on each other for maximum proprioceptive feedback.

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11 Mechanism of Injury for ACL Rupture There are typically two types of mechanisms associated with ACL injuries, contact and non-contact. Contact injuries are those that take place when a direct blow is made to either side of the knee or to the anterior aspect of the knee, forcing it into a varus, valgus, or hyperextended position, respectively. There are numerous non-contact mechanisms that result in injury to the ACL, but the majority occurring in sports participation is while the athletes foot is fixed or planted with either a rotational or varus/valgus force placed on the knee, such as cutting, planting, or pivoting to change direction.8, 29 Injuries are also prevalent in athletic maneuvers that involve a sudden deceleration during or just before a change of direction or landing awkwardly from a jump.1, 2, 23, 29 Research has provided evidence that non-contact ACL injuries are more common than contact mechanisms, accounting for approximately 70 78% of all ACL injuries.1, 2, 22, 23, 30 Delayed Onset Muscle Soreness (DOMS) When healthy people take part in unaccustomed bouts of strenuous exercise, the phenomenon of DOMS typically follows. Delayed onset muscle soreness is commonly noticed after exercise that is relatively intense, of long duration, and/or eccentric in nature. The onset of symptoms begins approximately 8 24 hours post exercise with intensity peaking at 24 48 hours,31, 32 and symptoms lasting up to 7 days. Common physical and physiological markers associated with DOMS are soreness and pain,31, 33 37 decreased strength,33-37 increased plasma creatine kinase (CK) levels,34 39 decreased range of motion,34, 35, 40 and swelling.31, 34, 35 Most recently, Nosaka et al.35 noted a decrease in mean maximal isometric force after one bout of eccentric exercise of the biceps brachii muscle. Range of motion decreased immediately post to 3 days post

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12 exercise. Along with range of motion decrease, there was a significant increase in circumference of the upper arm immediately post exercise, followed by a further increase in swelling at 2 days post exercise. Muscle soreness developed 1 day after exercise and peaked at 2-3 days after, then gradually attenuated. A significant increase was noted in CK after a single bout of exercise, peaking at 3-5 days post exercise.35 Exercise training can have a significant effect on the outcome and subsequent events associated with exercise induced muscle damage. It is widely accepted that a second bout of exercise done at the same intensity as the initial bout will provide somewhat of a protective effect on the muscle, where there may be no increases in muscle damage markers and the recovery time may be decreased.34, 35, 39 41 This phenomenon is called the repeated bout effect. The time frame involved in the repeated bout effect is unclear. Some researchers have also investigated training prior to the first bout of eccentric exercise attempting to determine how it affects delayed onset muscle soreness and the markers involved.36,38 Ebbeling and Clarkson40 studied the effects of performing a second bout of exercise prior to full muscle recovery. They reported that symptoms were not exacerbated, significantly smaller changes in muscle damage indicators were found, and the recovery time was faster following a second bout of eccentric exercise of the elbow flexor muscles,40 however, Nosaka and Clarkson34 concluded that a second and third bout of high force eccentric exercise performed 3 and 6 days following the initial exercise session had neither increased the markers of damage to the tissue nor caused a change in recovery time.34 When a bout of eccentric exercise was repeated 48 hours after an initial bout, there were no beneficial or detrimental effects on the time-course and/or intensity of DOMS, CK, or 1 repetition max strength.39 Schwane,

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13 et al.36 suggested that progressive, short-term training could reduce the effects of delayed onset muscle soreness. They trained subjects with either uphill or downhill treadmill running for 1 and 2 weeks respectively. This was followed by the experimental test, which consisted of 45 minutes of intermittent downhill running at 80%VO2Max. The researchers reported that subjects who performed the downhill running training for 2 weeks displayed less DOMS markers than those subjects who trained downhill for 1 week and also showed less DOMS symptoms/markers than the control and uphill training groups.36 In trained individuals, a smaller metabolic response was reported after performing one bout of high intensity eccentric exercise. Significantly higher CK levels were seen in untrained subjects compared to subjects who took part in a regular training regimen.38 A training effect can be seen from up to 6 weeks to as long as 6 months, but there has been no effect noticed after 6 months.35,41 Electromyography (EMG) Elecromyography techniques are used to determine the electrical activity associated with muscular contraction and nerve function. It can be used to define the onset and intensity of muscle activation. From this, latency periods in muscle can be determined from EMG readings. Muscle latency is used to assess the time from joint movement to the initial onset of muscle activity. Co-contraction of the muscles surrounding the knee joint is thought to provide a protective mechanism against ligamentous injury. Colby et al.22 assessed the activation times of muscular contraction while subjects performed four types of athletic movements (sidestep cutting, cross-cutting, stopping, and landing) typically associated with ACL injuries. They reported that in all trials the quadriceps were activated at higher intensities than the hamstrings leading up to, at foot contact, and at the propulsion phase of the

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14 maneuver the subject was performing.22 These findings might suggest that because the quadriceps are creating more force, more often that this would produce an undesirable anterior shear force of the tibia resulting in increased stress on the ACL. Beard et al.25 and Jennings et al.24 compared reflex hamstring contraction latency in ACL deficient knees to normal knees using a specially designed weight-bearing apparatus. Patients were positioned standing inside the rig with their thigh to be tested resting against a pad. The placement of the pad did not allow any movement of the femur anteriorly. An accelerometer was then placed on the tibial tuberosity. Finally there was a compressed air piston mechanism pressed against the posterior tibia. The perturbation was initiated when the piston was released and an anterior shear force was applied to the tibia. This study was designed to investigate function and instability of the knee joint.24,25 Some skepticism arises when function is mentioned with this maneuver, when there is no functional task addressed. Measures of Dynamic Stability A more accurate assessment of dynamic joint stability would be to use a maneuver that incorporates a functional task. Recent research has addressed this issue. Colby et al.42 and Ross et al.43 integrated this for measurement of time to stabilization. Colby and colleagues42 required subjects to perform a 1-legged step down onto a force plate and a 1-legged hop onto the force plate. The step down measure was from a set height of 19 cm and the hop test was performed at a distance equal to the subjects leg length.42 The design used by Ross et al.43 was similar in theory. Subjects were asked to jump from a two-foot stance a distance of 70cm landing on one foot on a force plate. Included in this design was a standardized protocol for measuring jump height needed for the measure to be consistent. Subjects needed to achieve 50% of their maximum vertical jump height

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15 while covering the 70cm distance. Upon landing, subjects had to remain in the single leg stance position for 20 seconds. A majority of areas typically used to assess dynamic joint stability are represented with these procedures.43 A more functional way to assess hamstring latency was designed by Schultz et al.44 The researchers used a weight-bearing perturbation device designed to induce a forward moment with either an internal or external rotation of the trunk and femur relative to the tibia. Similar to the concept used by Colby22, this device was designed to simulate a typical mechanism associated with ACL injury. Unlike the previous research, Schultzs design allowed the presence of a silent period of the hamstrings before the perturbation was initiated. This maneuver was thus deemed a valid and reliable measure when assessing hamstring latency. Using time to stabilization and hamstring latency as measures of dynamic stability will allow this research to evaluate DOMS as a potential factor affecting neuromuscular control. Speculation can be made that when the signs and symptoms associated with DOMS are exacerbated, an athletes neuromuscular control could be diminished, further leading to injury. Lephart et al.45 have assessed a functional stability paradigm where proprioceptive deficits can lead to decreased neuromuscular control, which in turn can lead to functional instability, finally leading to ligament injury. This paradigm is considered cyclical, meaning that if any of the previously mentioned steps are present, the progression of functional instability will continue. Athletes with diminished time to stabilization could have difficulty achieving the proper balance needed while performing athletic maneuvers such as landing from a jump. When those muscles are negatively affected by DOMS, this could predispose the athlete

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16 to episodes of instability where the only means for joint protection is the passive restraints of that joint (ligaments, cartilage, joint capsule, etc). Similar consideration can also be taken when assessing hamstring latency. The diminished ability of the muscles to fire at the proper time and rate could lead to instability, resulting in joint injury. Therefore, without adequate input from the dynamic control system, the athlete can become vulnerable to joint damage. Summary The exact cause for anterior cruciate ligament injury is unclear. However, a number of predisposing factors are commonly noted in the literature. At this time there is no research to confirm or refute delayed onset muscle soreness as one of those predisposing factors. The microtrauma associated with DOMS presents with specific physiological markers that may affect dynamic joint stability. Strength deficits and an increase in pain perception could cause changes in joint mechanics and muscle firing patterns. A lower force production of the hamstrings during athletic maneuvers could increase the percent of quadriceps to hamstring muscle activation, as noted by Colby et al.,22 resulting in increased anterior shear forces of the tibia. This would diminish the effects the hamstrings provide in protecting the knee during dynamic movements. This overall weaker hamstring response could reduce functional knee stability, ultimately leading to a predisposition to ligament damage. Thus, determining joint stability using functional tasks is the goal of this research.

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CHAPTER 3 METHODS Subjects Thirty healthy, college age subjects were recruited from the University of Florida student population. The first twenty subjects participated in both measures, while the final 10 exclusively took part in the TTS procedure. Prior to participation in the study, all subjects read and signed an informed consent form approved by the university institutional review board (Appendix A). Subjects were evaluated for previous knee injuries using a history questionnaire (Appendix B) and were excluded if prior knee injuries were present. Subjects were also excluded if they were suffering from a previous hamstring injury or any other injury or condition that might have affected dynamic stability or balance. Finally, subjects who have performed lower extremity weightlifting exercises within the previous six months were excluded from this study to eliminate a training effect. Instrumentation Perturbation Device The perturbations were performed with a lower extremity perturbation device (LEPD) (Figure 3-1) designed similarly to those used in previous research. 44, 46, 47 The LEPD produces an unexpected forward perturbation with either an internal or external rotation of the trunk and femur in relation to the fixated foot and tibia. Subjects were wearing a waist harness with hooks attached to each side while being restrained at the hips using cables attached to a release mechanism. To standardize the procedures, a load 17

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18 cell (Transducer Techniques, Inc, Temecula, CA) (Figure 3-2) was attached in the middle of each cable. The height adjustable release mechanism was mounted to the wall and consisted of a .64-cm universal push-to-connect coupling system (Porter-Cable Corporation, Jackson, TN) and a trigger switch to detect when the perturbation was initiated (Figure 3-3). Electromyography A 16 channel Myopac EMG system (Run Technologies, Laguna Hills, CA) interfaced with a laptop-type personal computer was used to record raw EMG signals for the onset times of the lower extremity musculature following a weight-bearing perturbation procedure. The specifications for the electromyography unit included an amplifier gain of 1-mV/V, frequency bandwidth of 10 1000 HZ, CMRR 110 dB, input resistance of 1 M, and a sampling rate of 2000 Hz. Upon completion of data sampling, an analog to digital conversion of the EMG data was performed and stored on the PC using DATAPAC 2000 (Run Technologies, Laguna Hills, CA) software. Triaxial Force Platform Performance of the TTS procedure was assessed using a triaxial force platform (Bertec Corporation, Columbus, OH) (Figure 3-4). The raw signal was acquired at a frequency of 2000 Hz and stored on the same laptop-type computer using the DATAPAC 2000 (Run Technologies, Laguna Hills, CA) software. Inclinometer Hamstring flexibility was assessed using an inclinometer (Figure 3-5). The inclinometer resembles a flat goniometer with 360 marked in single degree increments on the circumference. A freely rotating arm fixed at the center of the inclinometer is used to determine the angular position as it aligns with the degree markings on the

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19 circumference. Because the arm can move without restriction, gravity maintains it in the downward position. Thus, during limb movement the arm remains in the downward position, indicating limb position. Measurements Hamstring Flexibility Subjects were positioned supine with their involved hip actively flexed to 90 and the contralateral lower extremity flat on the table (Figure 3-6). A specially designed apparatus made of PVC pipe was used to ensure the subjects hip remained at this angle through the entire measurement (Figure 3-7). The subject was then instructed to actively extend their knee as far as possible and hold that position for 3 seconds. A Velcro strap was used to secure the inclinometer just above the ankle. Three trials were performed and the average ROM obtained from the three trials was used as the measure of hamstring flexibility (Appendix C). Pain Measurement Subjects were assessed for the level of perceived pain as pressure and passive stretch were applied separately to the hamstring muscles. Both tests were performed with the subjects in the same supine position used for flexibility testing. To assess the perceived pain during a passive stretch, the knee was passively extended to the end range as the examiner applied 6.0-kg of force. A Nicholas Manual Muscle Tester (MMT) (Model 01160, Lafayette Instrument, Lafayette, IN) (Figure 3-8) was used to control the amount of pressure applied. When 6.0-kg of force had been achieved, the subjects were instructed to mark on a visual analogue pain scale (Appendix D) the amount of pain they felt at that moment. They were asked to make a vertical slash across a 10-cm long line between the limits of no pain felt (left end of line) and unbearable pain (right end of line).

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20 The subjects were then assessed for pressure-pain threshold using an algometer (Ametek, Chatillon, NY) (Figure 3-9). The subjects were again passively stretched to end range while an examiner applied 9-kg of pressure with the algometer directly to the belly of the medial hamstrings. The subjects were again asked to mark a vertical slash representing the amount of perceived pain on a separate visual analogue pain scale. The distance of the mark in millimeters from the left end of the line was used as the measure of perceived pain for each visual analogue scale. Muscle Latency Muscle latency following knee perturbation was assessed using EMG. To prepare the subjects for this, the skin overlying the medial and lateral hamstring muscles (MH and LH), and the vastus medialis and lateralis (VM and VL) was shaven and cleaned with isopropyl alcohol to reduce skin impedance. Bipolar 1-mm x 10-mm Ag/AgCl surface electrodes were then placed over the muscles with an interdetection surface distance of 1.5-cm between electrodes. Manual muscle testing was performed to confirm correct electrode placement using real time oscilloscope displays. The waist harness was fitted snugly to the subject and the release mechanism was adjusted to a height level with the subjects anterior superior iliac spine (ASIS) while the subject was standing on the force platform in the flexed knee position. Having the subject focus on the computer screen directly in front of them aided to control visual feedback. The position of the subject was standardized prior to the perturbation using the load cells and a predetermined voltage formula. The voltage formula consisted of a y-intercept equation in which the unknown variable was determined by inserting 5% of the subjects body weight. The product of the formula was then multiplied by 0.10 and this was the final number inserted into the computer. The subjects were instructed to lean into the cables until the voltage reached

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21 the determined level. Three trials of internal and external rotation perturbations were provided for the subjects to become accustomed with the device followed by ten random perturbations (5 IR, 5 ER) while allowing subjects 30s rest time between trials. The acquired raw signals were digitally processed using a symmetric root mean square (RMS) algorithm with a 10-msec time constant. Muscle latency was measured as the time between the initiation of perturbation and the onset of muscle activity, which was determined by calculating a threshold voltage (Vo) for each muscle. The Vo required for muscle onset was determined when the EMG activity exceeded 30% of the muscles peak amplitude for that trial, which was calculated from the following equation: Vo = Max 0.30.48 The onset of muscle activity was determined by comparing discrete data points in a point-by-point fashion to the Vo. The muscle was considered active (or a reflex event to have occurred) when the Vo was exceeded for a minimum of 10-msec. The average MRT of the five trials was calculated and used for statistical comparison. Time to Stabilization Subjects were evaluated for TTS in the medial/lateral, anterior/posterior and vertical planes following a single leg landing from a jump height equivalent to 50% of their maximum vertical jump height, which was assessed prior to the TTS measure. Subjects were positioned under the VertecTM vertical jump device (Figure 3-10) and while standing on their toes, their reach height was determined. Subjects were then asked to jump as high as possible from a stationary stance, touching as many vanes as possible. Maximum vertical jump height was determined based on the number of vanes touched. This procedure was performed a total of three times, with the highest score being used. TTS was then assessed as the subjects jumped from a two-footed stationary stance to a one footed stabilization position onto a force platform 70-cm away (Figure 3-11a-c).

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22 After landing on the platform, subjects were instructed to balance on a single leg for 5-sec. Subjects were allowed three practice trials to become accustomed to the task and then needed to perform this procedure for a total of 3 successful trials. TTS was determined as the time in msec necessary for the sequential average of the data points to fall within 0.25 standard deviations of the mean of the first 3-sec following landing. Procedures After successfully meeting the criteria for inclusion into this study, subjects were asked to report to the Athletic Training/Sports Medicine Research Laboratory for measures of hamstring flexibility, pressure-pain threshold (PPT), passive range of motion pain threshold (PROMPT), time to stabilization (TTS), and hamstring muscle latency. Baseline measures of hamstring flexibility for each subject were taken prior to experimentation. Perturbations and stabilization procedures along with the lower extremity to be tested were randomly assigned as to eliminate any potential threats to validity. Following the baseline measures of muscle latency and TTS, subjects were randomly assigned to either an experimental or control group. Subjects assigned to the experimental group performed 6 sets of 10 eccentric contractions of the hamstrings using a prone lying leg curl machine. Subjects were assessed for single leg 1 repetition max strength concentrically, with 100% of that 1RM being used as the exercise intensity for the subject. Subjects were instructed to lower the weight from a fully flexed knee to a fully extended knee. This movement was standardized using a metronome and lasted for 10 seconds and subjects were given a 10 second rest between each repetition. Subjects were given 1.5 minutes to rest between sets. Participants were asked to return for reevaluation of TTS and muscle latency 48 and 96 hours after the initial testing date. Upon return, subjects had their hamstring flexibility reevaluated, as well as each measure

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23 of pain threshold using the visual analog pain scale used to assess the level of DOMS achieved. Hamstring flexibility, pain threshold, TTS, and perturbation procedures were performed identical to the pretest trials. Statistical Analysis The design of this study was a pretest posttest design. Statistical analysis for the DOMS measure was done using separate two-way mixed design analyses of variance for each dependent measure (AROM, PROMPT, PPT). To determine statistical significance for the muscle latency measure, separate three-way mixed design analyses of variance were used with the independent variables consisting of muscle (MH, LH), time (pretest, 48-hr post, 96-hr post), and physiological state of the hamstrings (DOMS induced, control). Three separate two-way analyses of variance with repeated measures on the factors of time and group were used for the TTS procedure (Fz, Mx, My). If statistical significance was noted, a Tukey HSD post hoc analysis was performed to establish where the significance lies. A probability level of P < .05 was expected to designate statistical significance.

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24 Figure 3-1. Lower extremity perturbation device Figure 3-2. Load cell Figure 3-3. Height adjustable release mechanism and trigger switch

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25 Figure 3-4. Bertec triaxial force platform Figure 3-5. Inclinometer A B Figure 3-6. Subject positioning for ROM measure. A) start and B) end

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26 Figure 3-7. Specially designed PVC device used for measuring hamstring range of motion Figure 3-8. Nicholas Manual Muscle Tester. This device is a handheld dynamometer used to measure force output.

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27 Figure 3-9. Algometer used for measuring the amount of pressure applied to the muscle. Figure 3-10. Vertec vertical jump device.

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28 C B A Figure 3-11. Time to stabilization jump landing sequence. A) starting position, B) mid-flight, and C) landing phase.

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CHAPTER 4 RESULTS Statistical analysis for the DOMS measures was conducted using separate 2-way mixed design ANOVA for each dependent variable (active range of motion, passive range of motion pain threshold, and pressure pain threshold). Two 3-way mixed design ANOVA were used to analyze the muscle latency times for internal and external rotation perturbations. Finally, three separate 2-way mixed design ANOVA were performed for the three TTS measures (based on Fz, Mx, and My) analyzed during the jump landing procedure. Tukeys HSD post hoc analysis was conducted when significance was established. The alpha level was set at 0.05 for all statistical tests. DOMS Measures Measurement of Active Range of Motion Significant main effects for time (F2, 56 = 19.08, P < 0.001) and group (F1, 28 = 11.22, P = 0.002) were observed for the active range of motion measures. Subjects showed significant deficits in hamstring AROM at 48h and 96h posttreatment. A significant recovery of AROM was noticed between the second and third test sessions. Overall, hamstring flexibility was significantly less in the DOMS subjects compared to the control subjects. A significant time x group interaction (F2, 56 = 19.98, P < 0.001) was also noted. Data presented in Table 4.1 indicate that subjects in the DOMS group displayed marked decreases in hamstring flexibility over the 48h and 96h test periods when compared to the pretest measures. A significant decrease from baseline to 48h post exercise was observed. Subjects began to regain significant flexibility between the 29

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30 second and third test session, although significant decreases at 96h posttest were still present compared to baseline. No differences were noted among the three trials for the control groups, but significant decreases were seen comparing between control and DOMS groups at 48h posttest and 96h posttest, respectively. Table 4-1. Active hamstring range of motion ( SD) Group Pretest Post 48h Post 96h Total DOMS 65 14 43 24* 51 18* 53 21 Control 71 13 71 13 72 12 71 13 Total 68 14 57 24* 62 19* Significantly less than pretest group (P < 0.05) Significantly less than control group at same posttest time (P < 0.05) Significantly greater than posttest 48h (P < 0.05) Passive Range of Motion Pain Threshold Significant main effects for time (F2, 56 = 11.97, P < 0.001) and group (F1, 28 = 4.58, P = 0.041) were present for the PROMPT measure. Data presented in Table 4.2 indicate that there was a significant increase in pain perception due to passive stretch of the hamstring muscles in the DOMS group. Overall, subjects also noted significantly higher levels of pain 48 and 96h after exercise. Muscle soreness peaked by the third session, but was only slightly higher than the 48h session. Additionally, a significant time x group interaction (F2, 56 = 10.58, P < 0.001) was identified. A significant increase in pain perception was noted when comparing each posttest DOMS measure to the pretest DOMS measure. No significant changes were present among the control groups, although significant differences were seen when comparing the 48h control group to the 48h posttest DOMS group and the 96h posttest control group to the 96h posttest DOMS group.

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31 Table 4-2. Pain quotient as measured on a visual analog pain scale for passive range of motion pain threshold (PQ SD) Group Pretest Post 48h Post 96h Total DOMS 18.1 20.6 46.6 27.6* 47.1 28.8* 37.3 28.8 Control 19.3 21.0 20.7 24.1 19.8 25.4 19.9 23.1 Total 18.7 20.4 33.6 28.7* 33.4 30.1* Significantly greater than pretest group (P < 0.05) Significantly greater than control group at same posttest time (P < 0.05) Pressure Pain Threshold A significant main effect for time (F2, 56 = 7.23, P = 0.002) was identified for the PPT measure (Table 4.3). Pain perception peaked at 48h but began to diminish by the 96h post exercise session. A significant group x time interaction (F2, 56 = 6.91, P = 0.002) was also present. Subjects in the DOMS group reported significantly greater levels of perceived pain at the 48h and 96h post exercise sessions compared to the first session. No significant changes were seen across the trials for the control subjects, but a significant difference was present between the posttest 48h control group and the posttest 48h DOMS group. No significant group main effect (F1, 28 = 1.09, P = 0.304) was present for this measure. Table 4-3. Pain quotient as measured on a visual analog pain scale for Pressure Pain Threshold (PQ SD) Group Pretest Post 48h Post 96h Total DOMS 43.9 17.8 63.1 21.8* 58.5 24.2* 55.2 22.5 Control 45.6 27.7 45.0 28.6 47.6 29.8 46.1 28.1 Total 44.7 22.9 54.1 26.6* 53.1 27.2* Significantly greater than pretest group (P < 0.05) Significantly greater than control group at posttest 48h (P < 0.05)

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32 Muscle latency Internal Rotation Perturbation No significant main effects were detected for muscle (F1, 18 = 0.043, P = 0.838) or group (F1, 18 = 2.01, P = 0.173); however, a trend was observed for time (F2, 36 = 2.77, P = 0.076) main effect with the internal rotation lower extremity perturbation (Table 4.4). No significant 2-way interactions were detected for time x group (F2, 36 = 0.35, P = 0.705), muscle x group (F1, 18 = 0.408, P = 0.531), or time x muscle (F2, 36 = 1.03, P = 0.368). Comparison of the 3-way interaction for time x muscle x group also detected no significant results (F2, 36 = 1.80, P = 0.180). Table 4-4. Internal rotation muscle latency (msec SD) Muscle Group Pretest Post 48h Post 96h Total DOMS 97 24 72 23 81 23 MH Control 106 15 99 23 96 33 92 26 DOMS 101 33 106 122 64 23 LH Control 120 34 83 29 87 34 94 58 Total 106 28 90 64 82 30 External Rotation Perturbation Significant main effects were observed for time (F2, 36 = 8.60, P = 0.001) and muscle (F1,18 = 4.97, P = 0.039) for the latent muscle reaction times of the hamstrings (Table 4.5). Subjects recorded significantly quicker response times during the 48h (19 msec) and 96h (16 msec) posttest trials as compared to the pretest measure. Medial hamstring activation times (86 25 msec) were significantly faster than lateral hamstring response times (99 31 msec). No significant interactions were detected, however a trend was noted for the time by group interaction (F2, 36 = 3.05, P = 0.060). No

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33 significant main effect was observed between the DOMS and control groups (F1, 18 = 545.50, P = 0.668) Table 4-5. External rotation muscle latency (msec SD) Muscle Group Pretest Post 48h Post 96h Total DOMS 104 27 81 25 79 18 MH Control 85 20 84 31 84 25 86 25 DOMS 114 26 79 23 86 26 LH Control 113 43 96 32 103 18 99 31 Total 104 31 85 28* 88 23* Significantly less than pretest group (P < 0.05) Significantly faster response than lateral hamstring (P < 0.05) Time to Stabilization Vertical Ground Reaction Force (Fz) A significant time main effect (F2, 54 = 5.04, P = 0.010) for TTS based on Fz was present. Data presented in Table 4.6 indicate that subjects displayed significant improvement of TTS during the 96h posttest session (1515 572 msec) compared to the baseline (1868 514 msec) and posttest 48h session (1839 605 msec). Neither the group main effect (F1, 27 = 1.44, P = 0.240) nor the time x group interaction (F2, 54 = 0.71, P = 0.497) were observed to be significant. Table 4-6. Vertical TTS based on Fz (msec SD) Group Pretest Post 48h Post 96h Total DOMS 1905 404 1911 606 1696 453 1830 643 Control 1834 612 1772 617 1346 634 1635 749 Total 1868 514* 1839 605* 1515 572 Significantly greater than posttest 96h group (P < 0.05) Medial/Lateral Ground Reaction Moment (Mx) No significant time (F2, 54 = 1.49, P = 0.234) or group (F 1, 27 = 1.14, P = 0.294) main effects for TTS based on Mx were present. Similarly, no significant changes were

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34 observed for the time x group interactions (F2, 54 = 0.82, P = 0.448). Data are presented in Table 4.7. Table 4-7. Medial/Lateral TTS based on Mx (msec SD) Group Pretest Post 48h Post 96h Total DOMS 1789 343 1640 203 1582 419 1670 529 Control 1579 290 1641 425 1506 377 1575 564 Total 1680 329 16401 331 1542 392 Anterior/Posterior Ground Reaction Moment (My) Analysis of TTS based on My revealed no significant main effects for time (F2, 54 = 0.22, P = 0.806) or group (F 1, 27 = 2.86, P = 0.102). Additionally, no significant differences were detected for the time x group interaction (F2, 54 = 0.72, P = 0.492). Data appear in Table 4.8. Table 4-8. Anterior/Posterior TTS based on My (msec SD) Group Pretest Post 48h Post 96h Total DOMS 1606 288 1618 334 1657 346 1627 538 Control 1599 268 1494 319 1453 315 1516 558 Total 1603 273 1554 327 1552 341

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CHAPTER 5 DISCUSSION AND CONCLUSIONS Discussion Neuromuscular control testing continues to be a thoroughly studied topic among researchers in the sports medicine field. The majority of research in this area has focused on the dynamic measurement of joint stability and postural control. Current research uses the TTS measure defined in the present study. The most recent research has investigated whether ground reaction forces differ between a static single limb stance and a dynamic single limb stance. Results indicate that greater GRFs exist in the A/P and M/L planes for dynamic single limb stance compared to static single limb stance. It was concluded that the static measure might be a better indicator of stable posture.49 Shultz and colleagues continue to incorporate the use of the LEPD in the examination of hamstring muscle activation. In fact, she is currently investigating how the menstrual cycle of healthy females affects latent muscle reaction times of the lower extremity. Bell et al.50 have investigated the effects of trunk position on muscle reaction times of the lower extremity using the LEPD. They concluded that trunk position does not affect muscle reflex onset based on where center of pressure is in relation to the foot, but that reflex amplitude is affected. Several quantitative physiological markers of DOMS have been used to confirm the presence of this condition. Although these physiological measures were not used in this study, successful completion of the work hinged on the ability to effectively induce 35

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36 DOMS. Alternatively, subjective (PROMPT and PPT) and objective (AROM) outcome measures associated with DOMS were utilized. The purpose of this investigation was to determine if hamstring DOMS had any deleterious effects on functional joint stability at the knee. More specifically, it was hypothesized that measures of DOMS would be significantly changed after the exercise protocol for the experimental group. It was further hypothesized that subjects in the experimental group would present with significantly slower reaction times in relation to both latent muscle response times of the hamstrings and TTS following a jump landing procedure. DOMS Measurements Based on the results presented, I am confident that DOMS was adequately induced. Certain markers that were discussed in Chapter 2, such as range of motion and perceived pain, were significantly different after the exercise protocol. Active range of motion in the experimental group showed the greatest decrease approximately 48h after the exercise session (Figure 5.1). Subjects began to regain motion at 96h post exercise, but were still not fully recovered from the muscle tightness. Peak levels of perceived pain were noted at 48 96h post exercise for the PROMPT measure (Figure 5.2). Similar results were observed with the PPT measures, noting that levels of perceived pain peaked at 48 96h post exercise (Figure 5.3). All measures are similar to previous literature related to the time course and intensity of DOMS.31, 32, 34, 51 Typically, symptoms are noticed approximately 8 24h after exercise, with symptoms reported peaking at 48 72h. Symptoms begin to diminish after this time and will subside within 5 7 days. Previous research has used other means of determining DOMS

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37 markers,32, 34, 35 37, 51, 52, 53 however, our markers were deemed more relevant with respect to this study. This may create limitations when assessing the level of DOMS that was induced when making comparisons to previous research. For this study, only three measures associated with assessment of DOMS markers were used, however these measures were all confirmed to have significant changes. Other measures such as muscular strength, plasma creatine kinase levels, and muscular swelling were not included. We chose to use the AROM, PROMPT, and PPT as the measures of DOMS inducement due to their ease of measurement as well as to eliminate any invasive measures such as with the CK tests. No correlation analyses have been performed specifically to determine whether differences exist among the multiple DOMS markers. All the procedures are independently considered valid and reliable measures to assess DOMS.36, 38, 39, 51 Muscle Latency When assessing joint stability with EMG, multiple models have been used8, 24, 25, 44, 54 57 A review of the relevant research revealed no data published to assess temporal patterns of a dynamic protocol. To avoid learning effects in previous studies, researchers allowed multiple practice trials before the actual recording of the data. This was also done in the present study, but because of the number of test trials over time, it seems that there may be a greater training effect associated with the LEPD. Following two sessions, pretest and posttest 48h, it appears that subjects may have begun to develop a learning pattern relative to the perturbation. This was evidenced by their reduced latency times. Although only significantly different during the EROT perturbation, there was a similar trend observed with the IROT perturbation. It is difficult to explain this faster response time. Measurements from pretest to both posttests were performed

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38 identically. Subjects may have become accustomed to the device and learned to anticipate the rotational perturbation, which would allow them to respond sooner. On the other hand, when the subjects were leaning forward, they may have been required to utilize predominantly their quadriceps to maintain stability in the upright posture. Therefore, when the perturbation was initiated, some level of reciprocal inhibition of the hamstrings may have existed, causing them to be recruited far slower than in previous studies. Previous research assessed muscle latency in the hamstrings using both weight-bearing15, 24 26, 44, 46, 47 and non weight-bearing perturbations.54 The assessment of non weight-bearing perturbations cannot be directly related to this research because the proprioceptive feedback is more likely to come from joint receptors being stimulated as opposed to the muscle spindles that would be activated with a weight-bearing task. When non-weight bearing, the muscles are not loaded and would require a larger amount of joint movement to stimulate the muscle spindle. The more obvious receptors that would be activated during this type of perturbation would be the receptors located in the joint as well as the capsule and ligaments.54 Weight-bearing perturbations require somewhat of a preactivation of the muscle, which allows the muscle spindles to respond to changes in muscle length earlier than other receptors. Shultz et al.44 described the same activation patterns of the medial and lateral hamstrings in response to both IROT and EROT as were seen in the present study. It was noted that the medial hamstrings respond faster to both perturbations. This makes sense for EROT, because the afferent response from the muscle spindle would cause a reflex contraction of the medial hamstring to prevent the trunk and femur from further

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39 externally rotating. For the muscles to respond to the IROT perturbation similarly is not as easily understandable when the same muscle spindle theory is applied. In this instance, the lateral hamstring should respond quicker due to the stretch reflex associated with that muscle. Shultz et al.44 stated that the possibility for this faster response from the medial hamstrings could be due to the innervation of the muscle. The semitendinosus and semimembranosus are supplied by the tibial nerve, whereas the biceps femoris is supplied by both the tibial (long head) and common peroneal (short head) nerves.21 Based on this reasoning, a second theory was identified. Therefore, this theory implies that if the tibial nerve and common peroneal nerve are not stimulated by the perturbation, or that the recording area of the biceps femoris was over the peroneal nerve, differing times could be recorded. The researchers further identified factors in their study to support this theory. When the medial hamstrings were compared to the medial and lateral gastrocnemius muscles, which are all innervated by the tibial nerve, there were no significant differences.44 Although the results of Shultz et al.44 are consistent with our findings based on the firing patterns of the hamstrings, we noticed a much longer latency when compared to their findings. A long latency response time for the medial hamstring ranged from 58 60 msec and 70 77 msec for the lateral hamstring. Our results ranged from approximately 86 92 msec for medial hamstring and 94 99 msec for the lateral hamstrings. It is difficult to make a direct assessment relative to other research because the methods of this study are not entirely the same as others. Shultz et al.44 used a similar perturbation device that required their subjects to maintain their center of mass over the midfoot. In this investigation, subjects were asked to lean into the cables using load cells

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40 as the standardization protocol. Although the subjects position was consistent across the trials, center of mass location could not be assessed. A possible flaw with this setup is that it does not mimic the typical injury model for most ligament injuries in sports. Most frequently a deceleration or sudden change of direction results in ligament damage. With a deceleration or change of direction, the athletes center of mass should remain within or posterior to the base of support. Upon further assessment of this model, it would appear that the center of mass of the subject would lie outside the base of support. Bell et al.50 concluded no change in hamstring response time relative to where the center of pressure lies, whether it is over the heel, midfoot, or toes. Their study, however, could not assess the possibility of the subjects center of mass falling outside that base of support. Subjects may have also been able to incorporate the use of their hips to become more adept at responding to the perturbations. Because the hip is a triaxial joint, able to move in all three of the cardinal planes, there is the possibility that the subjects were responding to the perturbation by utilizing their ability to rotate the pelvic girdle relative to the femur and limit the internal and external rotation at the knee joint. Time to Stabilization Static and dynamic procedures have been utilized to investigate stability of the lower extremity. Various static measurements for the lower extremity have been used in previous research. These static measures either incorporate the use of a single leg balance test,8, 58 center of pressure velocity (COPV),59, 60 or postural sway.61 To date, very few studies have used a functional task to assess joint stability. Colby et al.42 and Ross et al.43 have attempted to study stability of the lower extremity using a functional task. A potential limitation with these studies is that they only made comparisons between injured populations to uninjured populations. No research has been performed

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41 to validate whether a jump landing is different in healthy subjects with an intervention protocol or whether there is a change in results over time. Colby et al.42 concluded that subjects with ACL reconstructed knees showed significantly slower stabilization times based on the vertical force component compared to healthy subjects during a step down maneuver. Our results also noted differences in the vertical component, however these results showed faster stabilization times over multiple sessions while performing a jump landing technique. Figure 5.1 indicates that a learning effect may have taken place based on the Fz for the TTS measure. Subjects appeared to improve their ability to stick the landing after two sessions. This may have occurred because the subjects were more familiar with the task after multiple trials during multiple sessions. The jump landing task takes a great deal of coordination to complete successfully. Subjects were asked to focus on three main criteria in order for the jump landing to be considered successful (reach 50% of their max vertical jump height, cover a distance of 70cm, and land in the center of the force plate on one foot). Subjects who could not focus on all three criteria simultaneously seemed to be unable to complete the task consistently. This inconsistency was evident in the fact that, although all subjects completed the trials successfully, there was variability among subjects based on the number of total trials attempted to complete three successfully. It appears that subjects need to be adequately familiarized with the jump landing procedure in order to remain consistent over time. It is difficult to compare the results of the present study with those of previous research. Different methods were used to assess TTS and different subject populations were used. Collection frequency could be a limitation of previous research as well. The current investigation used a sampling frequency of 2000Hz to collect data, while other

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42 researchers have been collecting at much lower sampling rates, some as low as 180Hz for the TTS procedure.62 In previous studies using the jump landing procedure with low sampling frequencies, researchers would have included fewer data points in the analysis, which could have resulted in altered outcomes. Based on the results of this procedure, it is likely that DOMS has little or no effect on a subjects ability to stabilize after a functional task, such as a jump landing maneuver. Because of the dynamic nature of the task, subjects would have to incorporate the use of not only the hamstring muscles, but would also need to rely on the entire kinetic chain of the lower extremity to stabilize themselves. It would appear that function of the lower extremity as a whole to control dynamic posture is too great to be significantly affected by limiting one muscle group. Conclusions The exercise procedure conducted to induce DOMS can be considered a valid protocol for this type of research. Subjects presented with marked changes across time for each measure. The change in the associated markers is consistent with past literature. The results of the present study suggest that functional joint stability, as measured by the combination of hamstring muscle latency and TTS after a jump landing, is not affected by DOMS. When subjects return to activity while affected by DOMS, the physiological and physical markers of muscle damage are still present. It is difficult to speculate why no effect is present. Apparently these markers are not influential enough to change the performance of the affected muscles. The protective effect the hamstrings provide at the knee joint to assist with dynamic stability does not appear to be influenced by DOMS. Suggestions for Future Research Future research should continue to build upon the present work as well as previous literature utilizing the jump landing procedure. An area that needs to be addressed is the

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43 reliability of testing subjects over multiple days to determine if a learning response exists. Additionally, the development of a standardized TTS protocol to establish baseline criteria for functional task procedures is also necessary. The task suggested here is an effective model, but something more appropriate would be to develop criteria to standardize both jump height and jump distance. The incorporation of a standardized jump distance based on a percentage of the standing broad jump for each subject would produce a consistent trajectory from take off to landing. This would create a reliable pattern among subjects that to date has not been identified. Utilizing a functional task to determine if hamstring DOMS affected knee joint stability was the goal of this research. Further research should examine the effects of hamstring DOMS on other aspects of proprioception. Some areas that should be investigated include active and passive joint repositioning in addition to threshold to detection of passive movement. Because the hamstrings play a major role in joint movement at both the hip and knee, it would seem sensible to study each independently.

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44 020406080100PretestPosttest 48h*Posttest 96h*Group (day)Range of motion (degrees) DOMS Control Figure 5-1. Active hamstring range of motion 020406080100PretestPosttest 48h*Posttest 96h*Group (day)Perceived pain (PQ) DOMS Control Figure 5-2. Passive range of motion pain threshold

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45 0102030405060708090100PretestPosttest 48h*Posttest 96h*Group (day)Perceived pain (PQ) DOMS Control Figure 5-3. Pressure pain threshold

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APPENDIX A LETTER OF INFORMED CONSENT Informed Consent Agreement Project Title: The effects of hamstring delayed onset muscle soreness on functional knee joint stability. Investigators: Kyle A Smink, ATC, Graduate Student, Department of Exercise and Sport Sciences & Michael E. Powers, PhD., ATC, CSCS, Assisstant Professor, Department of Exercise and Sport Sciences. Purpose of the study: The purpose of this study is to determine if the occurrence of delayed onset muscle soreness in the hamstring group can affect functional knee joint stability. Delayed onset muscle soreness is a physiological response that occurs when individuals take part in unaccustomed bouts of rigorous exercise and is typically noticed 24 48 hours after the initial activity. At this time, no study has been published investigating the occurrence of delayed onset muscle soreness and its effects on functional joint stability. We are performing this research in order to help gain knowledge and further understand this subject as it relates to the sports medicine field. Please read this consent carefully before you decide to participate in this study. What will you do in this study? You will be excluded from participating in this study if you have had any leg injuries, either muscular or ligament, that required a doctor visit within the past six months. You will also be excluded from this study if you have taken part in any rigorous weight training for your leg muscles in the past six months. Upon arrival to the Athletic Training/Sports Medicine Research Lab (FLG 105D), you will be asked to complete a medical history questionnaire to determine if you are eligible to participate in this study. If eligible, we will measure your hamstring (muscles in the back of your thigh) flexibility, pressure-pain threshold, and passive (relaxed) range of motion pain threshold. We will ask you to lie on your back with your non-dominant (the leg you would not kick a ball with) leg flexed at the hip. The opposite leg will remain flat on the table. A specially designed device made of PVC pipe will be used to make sure your hip remains at this angle through the entire measurement. You will then be asked to straighten your knee as far as possible. As you do this we will measure how far in degrees you can straighten your knee. While remaining is this position, an 46

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47 examiner will stretch your hamstring muscles (by straightening your knee) to the maximum range of motion. You will be asked to make a pencil mark on a visual analog pain scale representing the amount of pain you feel during the stretch. This scale consists of a 10-centimeter line with the left end representing no pain at all and the right end representing the most unbearable pain imaginable. After you make the pencil mark, your hamstrings will be stretched again. This time, pressure will be applied to the hamstring muscles using an algometer (a device about the size of a pencil with a rubber tip used to apply a standard amount of pressure). You will again be asked to make a pencil mark in a visual analogue scale representing the amount of pain you feel while the pressure is applied. Following the baseline measures for hamstring flexibility and pain threshold, you will be measured for muscle latency and time to stabilization. First, small areas of your skin will be shaven and cleaned with isopropyl alcohol. Self-adhesive surface electrodes will then be placed on the skin overlying the medial and lateral hamstrings (rear thigh), medial and lateral quadriceps (front thigh), and medial and lateral gastrocnemius (calf) muscles. These electrodes will detect electrical impulses of the muscle, however, you will not feel these impulses and no electrical current will enter the body. A device called a goniometer (a device that measures joint angles) will be placed over the outside of your knee to assess how far your knee is bent. You will then be asked to perform the knee perturbation and time to stabilization measures in a random order determined by a random numbers chart. For the knee perturbation, you will be fitted with a harness applied snugly around your waist. Two cables connected to two separate release mechanisms affixed to a wall will be attached to the harness. You will be asked to stand on a force plate and assume a single leg stance on the test leg. You will then be asked to lean forward so that your knee is flexed to approximately 30 and your weight is supported by the cables attached to the wall. You will be able to view a computer screen, which will allow you to monitor the position of your weight. You will be wearing headphones to avoid hearing sounds that may allow anticipation reflexes to occur. At random times one of the two cables will be released. This will cause your hips and upper body to move forward and rotate causing the knee to naturally rotate and flex. Three trials of each cable release (left and right side) will be performed so you may become accustomed with the device. Immediately following, ten random perturbations (5 left and 5 right) will be performed while allowing a 30 second rest time between trials. When all 10 trials are successfully completed, we will perform the same procedures for the opposite leg. For the time to stabilization measurement, your maximum vertical leap (how high you can jump) will be determined. To do this, we will first measure how high you can reach while standing on your toes. You will then be asked to jump as high as possible and touch markers supported on a stand. Based on the number of markers you touch, the height of your jump is determined. We will have you repeat this two more times to ensure that we get an accurate measure. We will then measure how long it takes you to balance after jumping onto a platform. You will be asked to jump so that you reach a height equivalent to half of your maximum jump height and land on a platform about 27 away. We will ask that you land on the test leg only and balance yourself while your hands remain on your hips for a period of 5 seconds. After the 5-second period you will be asked to return to the starting position and repeat the measurement. This will be done

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48 two more times for a total of three trials for each leg. Following the baseline measures of muscle latency and time to stabilization, you will perform 6 sets of 10 negative (muscle lengthens while it contracts, otherwise known as a eccentric) contractions of the hamstrings using a leg curl machine. First, we will determine your 1 repetition maximum strength, which will be used as your exercise intensity. When the three sets are completed the session will be over. You will be asked to return for reevaluation of time to stabilization and muscle latency 48 and 96 hours after the initial testing date. Upon return, you will have your hamstring flexibility and pain threshold reevaluated which will be used to assess the level of DOMS achieved. All evaluation procedures will be performed identical to the pretest trials, However no resistance exercise (leg curls) will be performed. Time required: Three sessions requiring approximately 90 minutes each. Risks: Discomfort and soreness in the hamstring muscles will be experienced following the bout of eccentric exercise. You may also experience some discomfort with the pressure threshold measure, but this discomfort will only last a few seconds while the measure is being taken. As with any type of resistance exercise, there is a slight risk of musculoskeletal injury. A certified athletic trainer will be present to evaluate and treat any such injuries that may occur. If you are still suffering from soreness in the hamstring muscles after the 96-hour posttest measure, the certified athletic trainer will instruct you on ways to decrease the soreness. No stretching may take place prior to this time. Benefits/Compensation: There are no direct benefits to you for participating. Confidentiality: Data will be kept confidential to the extent provided by the law. Your information will be assigned a code number. The list connecting your name to this number will be kept in a locked file. When the study is completed and the data have been analyzed, the list will be destroyed. Your name will not be used in any report. Voluntary Participation: Your participation is completely voluntary. There is no penalty for not participating. Right to withdraw from the study: You have the right to withdraw from the study at anytime without penalty.

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49 Who to contact if you have questions about the study: Kyle A Smink, BS, ATC Mike Powers, Ph.D., ATC, CSCS University of Florida University of Florida Graduate Assistant Athletic Trainer Director of Athletic Training Education Department of Exercise and Sport Sciences Assistant Professor 2700 SW Archer Road, Apt. A-22 Department of Exercise and Sport Sciences Gainesville, FL 32608 148 Florida Gym Home#: 373-9250 PO Box 118205 Cellular#: (352) 281-3534 Gainesville, FL 32611-8205 E-mail: ksmink1@ufl.edu (352) 392-0584, ext. 1332 Fax: (352) 392-5262 E-mail: mpowers@hhp.ufl.edu Who to contact about your rights in the study: UFIRB Office Box 112250, University of Florida Gainesville FL 32611-2250 (352) 392-0433. Agreement: I have read the procedure described above. I voluntarily agree to participate in the procedure and I have received a copy of this description. Participant:______________________________ Date:__________ Principal Investigator:___________________________ Date:__________

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APPENDIX B INCLUSION QUESTIONNAIRE History questionnaire Subject #: 1. Have you visited a physician for any knee injuries in the past 6 months? YES NO 2. Have you had any giving way episodes with your knee in the past 6 months? YES NO 3. Have you had any locking or clicking episodes with your knee in the past 6 months? YES NO 4. Have you had any knee pain walking up or down stairs in the past 6 months? YES NO 5. Have you visited a physician for any hamstring muscle injuries in the past six months? YES NO 6. Have you participated in any strenuous lower extremity weight training within the past six months? YES NO 50

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APPENDIX C DECRIPTIVE INFORMATION AND HAMSTRING FLEXIBILITY Descriptive Information Subject #: Gender: Age: Height: Weight: Standing max reach: Vertical jump height: Hamstring Flexibility Pretest: Right Left Trial 1: Trial 2: Trial 3: Post-test 48h: Right Left Trial 1: Trial 2: Trial 3: Post-test 96h: Right Left Trial 1: Trial 2: Trial 3: 51

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APPENDIX D VISUAL ANALOGUE PAIN SCALE Subject # Pre / Post Date: Session # Range of Motion No Pain ________________________________________________Unbearable Pain Pressure Medial Hamstring No Pain ________________________________________________Unbearable Pain 52

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APPENDIX E RAW DATA Table E-1. Subject demographic raw data Subject Age (y) Height (cm) Mass (kg) ks001 22 170 60.0 ks002 21 163 60.0 ks003 23 170 64.0 ks004 21 157 60.0 ks005 22 177 76.0 ks006 21 170 55.0 ks007 20 163 57.0 ks008 21 170 71.0 ks009 21 170 63.5 ks010 23 170 67.5 ks011 22 160 70.0 ks012 24 183 76.5 ks013 23 170 63.5 ks014 21 173 68.5 ks015 20 154 57.5 ks016 27 180 65.5 ks017 24 178 77.0 ks018 21 173 84.5 ks019 20 188 74.0 ks020 22 170 59.5 ks021 22 166 62.0 ks022 22 178 74.0 ks023 20 165 59.0 ks024 20 160 47.5 ks025 21 170 84.5 ks026 22 188 85.0 ks027 22 178 83.0 ks028 22 170 68.5 ks029 22 185 70.5 ks030 21 175 59.0 53

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54 Table E-2. Active range of motion (AROM) raw data (degrees) Subject Pretest Post-test 48h Post-test 96h Group ks001 78 65 71 DOMS ks003 62 24 33 DOMS ks005 67 48 67 DOMS ks006 68 28 48 DOMS ks008 85 53 75 DOMS ks009 86 72 67 DOMS ks011 70 70 63 DOMS ks017 82 85 77 DOMS ks018 62 23 27 DOMS ks019 43 19 30 DOMS ks002 78 83 80 Control ks004 80 84 85 Control ks007 85 84 87 Control ks010 90 90 90 Control ks012 80 71 78 Control ks013 73 73 72 Control ks014 78 76 78 Control ks015 66 64 64 Control ks016 61 64 52 Control ks020 76 82 84 Control

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55 Table E-3. Passive range of motion pain threshold (PROMPT) raw data (PQ = 0 100) Subject Pretest Post-test 48h Post-test 96h Group ks001 72.5 61 77 DOMS ks003 5 22 16.5 DOMS ks005 7 23 6 DOMS ks006 10 55.5 68 DOMS ks008 0 64.5 42 DOMS ks009 36 73.5 98.5 DOMS ks011 32 54 62 DOMS ks017 0 8 59.5 DOMS ks018 2 83.5 71 DOMS ks019 0 14.5 0 DOMS ks022 4 84 60.5 DOMS ks024 16.5 45 32 DOMS ks026 22 27 20.5 DOMS ks027 21.5 7 28 DOMS ks028 43 76.5 65 DOMS ks002 0 0 0 Control ks004 39 48 52 Control ks007 0 0 0 Control ks010 49 49 57 Control ks012 0 0 0 Control ks013 14.5 12.5 15.5 Control ks014 54 47 63 Control ks015 7 9 8.5 Control ks016 40.5 40 18 Control ks020 15 12 11 Control ks021 52 74.5 65 Control ks023 7 1 0 Control ks025 2 1 1.5 Control ks029 8 9.5 3 Control ks030 2 7 2 Control

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56 Table E-4. Pressure pain threshold (PPT) raw data (PQ = 0 100) Subject Pretest Post-test 48h Post-test 96h Group ks001 58 64 55.5 DOMS ks003 39 53 43 DOMS ks005 37 36 18.5 DOMS ks006 37 74.5 73 DOMS ks008 64.5 79 85 DOMS ks009 47 92.5 100 DOMS ks011 43 71 56.5 DOMS ks017 22 41 68.5 DOMS ks018 43 100 82 DOMS ks019 0 21.5 13.5 DOMS ks022 64 43 53 DOMS ks024 46.5 72 62 DOMS ks026 70 82 75.5 DOMS ks027 34 53.5 32.5 DOMS ks028 53.5 63.5 59 DOMS ks002 5 6 0 Control ks004 54 61 67 Control ks007 63.5 38 47 Control ks010 46.5 59 56 Control ks012 13.5 4 22 Control ks013 61 72 75 Control ks014 88 85 90 Control ks015 11 14 13.5 Control ks016 74 66.5 70 Control ks020 0 12 10.5 Control ks021 63 59 77 Control ks023 22.5 8.5 5 Control ks025 62.5 62.5 63 Control ks029 56 77.5 70.5 Control ks030 63 50 47.5 Control

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57 Table E-5. IROT hamstring muscle latency raw data (msec) Subject Pre MH Post48 MH Post 96 MH Pre LH Post 48 LH Post 96 LH Group ks001 91 30 87 139 30 95 DOMS ks003 90 62 30 108 30 DOMS ks005 135 94 95 117 52 65 DOMS ks006 76 82 64 100 47 33 DOMS ks008 92 86 91 71 68 80 DOMS ks009 99 85 88 115 76 88 DOMS ks011 60 60 70 56 76 72 DOMS ks017 107 87 119 151 107 78 DOMS ks018 138 96 84 101 75 66 DOMS ks019 89 38 82 55 81 37 DOMS ks002 101 77 65 131 63 38 Control ks004 123 99 58 89 83 62 Control ks007 124 69 96 167 30 44 Control ks010 98 98 90 157 107 133 Control ks012 123 88 101 123 94 109 Control ks013 108 128 87 89 88 73 Control ks014 97 90 105 94 108 109 Control ks015 83 144 102 83 46 73 Control ks016 117 110 180 165 121 107 Control ks020 87 87 80 99 94 125 Control

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58 Table E-6. EROT hamstring muscle latency raw data (msec) Subject Pre MH Post48 MH Post 96 MH Pre LH Post 48 LH Post 96 LH Group ks001 93 30 65 124 30 99 DOMS ks003 102 72 70 81 64 66 DOMS ks005 127 99 64 133 77 77 DOMS ks006 70 77 78 84 82 60 DOMS ks008 73 94 58 116 101 113 DOMS ks009 90 92 93 128 98 106 DOMS ks011 97 46 77 91 87 88 DOMS ks017 110 101 123 148 102 100 DOMS ks018 116 99 81 93 93 37 DOMS ks019 161 103 79 147 60 115 DOMS ks002 77 35 46 103 89 90 Control ks004 76 76 77 73 74 76 Control ks007 60 68 55 188 144 96 Control ks010 114 95 100 95 58 88 Control ks012 104 116 103 109 111 100 Control ks013 84 94 87 161 131 124 Control ks014 76 100 99 113 108 132 Control ks015 59 35 59 34 41 95 Control ks016 114 97 123 138 107 110 Control ks020 86 127 88 111 95 120 Control

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59 Table E-7. Time to stabilization based on vertical ground reaction force (Fz) raw data (msec) Subject Pretest Post48 Post96 Group ks03 2175 1908 1295 DOMS ks05 2645 1714 1848 DOMS ks06 1979 2622 1674 DOMS ks08 1158 1342 1426 DOMS ks09 2290 2120 1640 DOMS ks11 1839 2550 2322 DOMS ks17 1847 2631 2130 DOMS ks18 2155 2587 1943 DOMS ks19 1184 1024 847 DOMS ks22 2128 1355 968 DOMS ks24 1897 1699 1422 DOMS ks26 2059 2571 1990 DOMS ks27 1696 1638 2161 DOMS ks28 1617 997 2070 DOMS ks02 1085 2633 2322 Control ks04 2717 1372 2206 Control ks07 2187 1206 979 Control ks10 2359 1500 1203 Control ks12 953 1636 2004 Control ks13 1125 1732 809 Control ks14 838 1098 544 Control ks15 1721 1599 1054 Control ks16 2169 2833 839 Control ks20 2135 2723 1461 Control ks21 1645 1023 912 Control ks23 2543 1960 1182 Control ks25 2387 2387 2536 Control ks29 2112 1827 1441 Control ks30 1539 1053 704 Control

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60 Table E-8. Time to stabilization based on medial/lateral ground reaction force (Mx) raw data (msec) Subject Pretest Post48 Post96 Group ks03 1373 1541 1771 DOMS ks05 2016 1667 2139 DOMS ks06 1966 1973 1747 DOMS ks08 1484 1689 1435 DOMS ks09 1868 1795 2387 DOMS ks11 1575 1299 1246 DOMS ks17 1996 1216 968 DOMS ks18 2214 1711 1466 DOMS ks19 1851 1609 1444 DOMS ks22 2125 1620 2166 DOMS ks24 2218 1611 1179 DOMS ks26 1851 1910 1586 DOMS ks27 1141 1726 1132 DOMS ks28 1366 1600 1470 DOMS ks02 1869 1616 1320 Control ks04 1318 2043 1727 Control ks07 1516 964 898 Control ks10 1561 1256 1240 Control ks12 1511 1323 2107 Control ks13 1099 1672 1658 Control ks14 1469 1198 1387 Control ks15 1801 2279 1540 Control ks16 1834 2375 1552 Control ks20 1404 1157 1724 Control ks21 2134 1573 859 Control ks23 1513 1928 1419 Control ks25 1875 1606 1652 Control ks29 1675 2074 2222 Control ks30 1111 1555 1283 Control

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61 Table E-9. Time to stabilization based on anterior/posterior ground reaction force (My) raw data (msec) Subject Pretest Post48 Post96 Group ks03 1891 1232 1513 DOMS ks05 1108 1113 1900 DOMS ks06 1945 1733 1348 DOMS ks08 1768 1379 1932 DOMS ks09 1641 1875 1787 DOMS ks11 1662 1483 1498 DOMS ks17 1465 1017 1453 DOMS ks18 1669 1820 1289 DOMS ks19 1541 2012 2057 DOMS ks22 2103 1856 1634 DOMS ks24 1288 1705 1798 DOMS ks26 1324 1811 1533 DOMS ks27 1277 2090 1067 DOMS ks28 1807 1530 2393 DOMS ks02 1633 1640 1129 Control ks04 1622 1624 1404 Control ks07 1442 812 1370 Control ks10 1783 1142 1894 Control ks12 1805 1296 1257 Control ks13 1920 1671 1479 Control ks14 1390 1139 1347 Control ks15 2025 1498 1254 Control ks16 1329 1324 1572 Control ks20 1246 1478 Control ks21 1251 1852 1629 Control ks23 1799 1792 1319 Control ks25 1571 1982 1319 Control ks29 1258 1811 1941 Control ks30 1914 1351 2021 Control 863

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APPENDIX F ANOVA SUMMARY TABLES Table F-1. Active range of motion (ANOVA) Source SS DF MS F Significance Group 7902.346 1 7902.346 11.222 0.002 Error 19717.827 28 704.208 Time 1823.262 2 911.631 19.082 0.000 Time x Group 1909.306 2 954.653 19.983 0.000 Error 2675.358 56 47.774 Table F-2. Passive range of motion pain threshold (ANOVA) Source SS DF MS F Significance Group 6760.000 1 6760.000 4.583 0.041 Error 41303.433 28 1475.123 Time 4396.317 2 2198.158 11.967 0.000 Time x Group 3885.817 2 1942.908 10.577 0.000 Error 10286.533 56 183.688 Table F-3. Pressure pain threshold (ANOVA) Source SS DF MS F Significance Group 1867.778 1 1867.778 1.095 0.304 Error 47775.278 28 1706.260 Time 1569.672 2 784.836 7.228 0.002 Time x Group 1501.206 2 750.603 6.913 0.002 Error 6080.456 56 108.580 62

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63 Table F-4. Internal rotation hamstring muscle latency (ANOVA) Source SS DF MS F Significance Group 4039.120 1 4039.120 2.014 0.173 Error 36093.463 18 2005.192 Time 11917.994 2 5958.997 2.767 0.076 Time x Group 1552.550 2 761.275 0.353 0.705 Error (Time) 77537.708 36 2153.825 Muscle 88.714 1 88.714 0.043 0.838 Muscle x Group 847.063 1 847.063 0.408 0.531 Error (Muscle) 37341.163 18 2074.509 Time x Muscle 3244.221 2 1622.111 1.027 0.368 Time x Muscle x Group 5682.575 2 2841.288 1.799 0.180 Error (Time x Muscle) 56859.445 36 1579.429 Table F-5. External rotation hamstring muscle latency (ANOVA) Source SS DF MS F Significance Group 355.782 1 355.782 0.190 0.668 Error 33749.259 18 1874.959 Time 82299.626 2 4114.83 8.601 0.001 Time x Group 2918.814 2 1459.407 3.051 0.060 Error (Time) 17222.554 36 478.404 Muscle 4666.586 1 4666.586 4.969 0.039 Muscle x Group 1507.157 1 1507.157 1.605 0.221 Error (Muscle) 16905.978 18 939.221 Time x Muscle 1019.349 2 509.675 1.833 0.174 Time x Muscle x Group 31.005 2 15.503 0.056 0.946 Error (Time x Muscle) 10007.553 36 277.988

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64 Table F-6. Fz (ANOVA) Source SS DF MS F Significance Group 754142.407 1 754142.407 1.442 0.240 Error 14118967.75 27 522924.731 Time 2174292.874 2 1087146.437 5.044 0.010 Time x Group 305274.461 2 152637.231 0.708 0.497 Error 11638461.88 54 215527.072 Table F-7. Mx (ANOVA) Source SS DF MS F Significance Group 194639.022 1 194639.022 1.143 0.294 Error 4597459.284 27 170276.270 Time 300364.828 2 150182.414 1.491 0.234 Time x Group 164279.966 2 82139.983 0.816 0.448 Error 5437986.165 54 100703.447 Table F-8. My (ANOVA) Source SS DF MS F Significance Group 270936.707 1 270936.707 2.858 0.102 Error 2559315.561 27 94789.465 Time 42795.786 2 21397.893 .216 0.806 Time x Group 142122.692 2 71061.346 0.718 0.492 Error 5345552.934 54 98991.721

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66 13. Fujita I, Nishikawa T, Kambic HE, Andrish JT, Grabiner MD. Characterization of hamstring reflexes during anterior cruciate ligament disruption: In vivo results from a goat model. J Orthop Res. 2000; 18(2): 183-189. 14. Seto JL, Orofino AS, Morrisey MC, Medeiros JM, Mason WJ. Assessment of quadriceps/ hamstring strength, knee ligament stability, functional and sports activity levels five years after anterior cruciate ligament reconstruction. Am J Sports Med. 1988; 16: 170-180. 15. Di Fabio RP, Graf B, Badke MB, Breunig A, Jensen K. Effect of knee joint laxity on long-loop postural reflexes: evidence for a human capsular-hamstring reflex. Exp Brain Res. 1992; 90(1): 189-200. 16. Smith BA, Livesay GA, Woo SL. Biology and biomechanics of the anterior cruciate ligament. Clinics in Sports Med. 1993; 12(4): 637-670. 17. Covey DC, Sapega AA. Anatomy and function of the posterior cruciate ligament. Clinics in Sports Med. 1994; 13(3): 509-518. 18. Girgis FG, Marshall JL, Al Monajem ARS. The cruciate ligaments of the knee joint. Anatomical, functional and experimental analysis. Clin Orthop. 1975; 106: 216-231. 19. Butler DL, Noyes FR, Grood ES. Ligamentous restraints to anterior-posterior drawer in the human knee. A biomechanical study. J Bone Joint Surg. 1980; 62: 259-270. 20. Gollehon DL, Torzilli PA, Warren RF. The role of the posterolateral and cruciate ligaments in the stability of the human knee. A biomechanical study. J Bone Joint Surg. 1987; 69: 233-242. 21. Sieg KW, Adams SP. Illustrated Essentials of Musculoskeletal Anatomy, 2nd ed. Gainesville, FL: Megabooks; 1985. 22. Colby S, Francisco A, Yu B, Kirkendall D, Finch M, Garrett W. Electromyographic and kinematic analysis of cutting maneuvers: implications for anterior cruciate ligament injury. Am J Sports Med. 2000; 28(2): 234-240. 23. Arendt EA, Agel J, Dick R. Anterior cruciate ligament injury patterns among collegiate men and women. J Athl Train. 1999; 34(2); 86-92. 24. Jennings AG, Seedhom BB: Proprioception in the knee and reflex hamstring contraction latency. J Bone Joint Surg. 1994 ; 768: 491-494. 25. Beard DJ, Kyberd PJ, Fergusson CM, Dodd CA. Proprioception after rupture of the anterior cruciate ligament. An objective indication of the need for surgery? J Bone Joint Surg Br 1993;75(2):311-5

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67 26. Beard DJ, Kyberd PJ, O'Connor JJ, et al: Reflex hamstring contraction latency in anterior cruciate ligament deficiency. J Orthop Res 1994; 12(2): 219-228. 27. Powers, Scott K., and Edward T. Howley. Exercise Physiology. 3rd ed. Boston: McGraw-Hill, 1997. 28. Lephart SM, Pincivero DM, Giraldo JL, Fu FH. The role of proprioception in the management and rehabilitation of athletic injuries. Am J Sports Med. 1997; 25(1): 130-137. 29. Feagin JA, Lambert KL. Mechanism of injury and pathology of anterior cruciate ligament injuries. Orthop Clin North Am. 1985; 16: 41-45. 30. Noyes F, Mooar PA, Matthews DS, Butler DL. The symptomatic anterior cruciate-deficient knee, I: the long term functional disability in athletically active individuals. J Bone Joint Surg Am. 1983; 65: 154-162. 31. Bobbert MF, Hollander PA, Huijing PA. Factors in delayed onset muscle soreness of man. Med Sci Sports Exerc. 1986; 18(1): 75-81. 32. Isabell WK, Durrant E, Myrer W, Anderson S. The effects of ice massage, ice massage with exercise, and exercise in treatment of delayed onset muscle soreness. J Ath Train. 1992; 27(3): 208-217. 33. Friden J, Sjostrom M, Eklblom B. Myofibrilar damage following intense eccentric exercise in man. Int J Sports Med. 1983; 4: 170-176 34. Nosaka K, Clarkson PM. Muscle damage following repeated bouts of high force eccentric exercise. Med Sci Sport Exerc. 1995; 27(9): 1263-1269. 35. Nosaka K, Sakamoto K, Newton M, Sacco P. How long does the protective effect on eccentric exercise-induced muscle damage last? Med Sci Sports Exerc. 2001; 33: 1490-1495. 36. Schwane JA, Williams JS, Sloan JH. Effects of training on delayed muscle soreness and serum creatine kinase activity after running. Med Sci Sports Exerc. 1987; 19(6): 584-590. 37. Tiidus PM, Ianuzzo CD. Effects of intensity and duration of muscular exercise on delayed soreness and serum enzyme activities. Med Sci Sports Exerc. 1983; 15: 461-465. 38. Evans WJ, Meredith CN, Cannon JG, Dinarello CA, Frontera WR, Hughes VA, Jones BH, and Knuttgen HG. Metabolic changes following eccentric exercise in trained and untrained men. J Appl Physiol. 1986; 61(5): 1864-1868. 39. Smith LL. Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Med Sci Sports Exerc. 1991; 23(5): 542-551.

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68 40. Ebbeling CB, Clarkson PM. Muscle adaptation prior to recovery following eccentric exercise. Eur J Appl Physiol. 1990; 60: 26-31. 41. Byrnes WC, Clarkson PM, Spencer-white J, Hseih SS, Frykman PB, Maughan RJ. Delayed onset muscle soreness following repeated bouts of downhill running. J Appl Physiol. 1985; 59: 710-715. 42. Colby S, Hintermeister R, Torry M, Steadman R. Lower limb stability with ACL impairment. J Orthopaedic Sports Physical Therapy 1999; 29(2): 444-451. 43. Ross S, Guskiewicz K, Yu B. Comparison of time to stabilization measures in functionally unstable versus stable ankles. J Ath Train 2001; 36(2); S-76. 44. Shultz SJ, Perrin DH, Adams JM, Arnold BL, Gansneder BM, Granata KP. Assessment of neuromuscular response characteristics at the knee following a functional perturbation. J Electromyogr Kinesiol 2000;10 (3):159-170. 45. Lephart SM, Henry TJ. The physiological basis for open and closed kinetic chain rehabilitation for the upper extremity. J Sport Rehab 1996; 5(1): 71-87. 46. Rose HM, Shultz SJ, Arnold BL, Gansneder BM, Perrin DH. Acute orthotic intervention does not affect muscular response times and activation patterns at the knee. J Ath Train. 2002; 37(2): 133-140. 47. Shultz SJ, Perrin DH, Carcia CR, Gansneder BM. Lower extremity alignment affects muscle activation patterns at the knee following a weight-bearing perturbation. J Ath Train 2002; 37(2): S-28. 48. Cauraugh, JH, Sangbum K. Two coupled motor recovery protocols are better than one. Stroke 2002; 33: 1589-1594. 49. Ross SE, Guskiewicz KM. Differences between ground reaction force measures of a static single limb stance and a single limb stance following a jump landing. J Ath Train 2003 38(2)S: S-24. 50. Bell DR, Sander TC, Gansneder BM, Shultz SJ. Posterior trunk position increases reflex amplitude at the knee in response to a perturbation. J Ath Train 2003; 38(2)S: S-103. 51. Nosaka K, Clarkson PM. Changes in indicators of inflammation after eccentric exercise of the elbow flexors. Med Sci Sports Exerc 1996; 28(8): 953-961. 52. Nosaka K, Sakamoto K, Newton M, Sacco P. The repeated bout effect of reduced-load eccentric exercise on elbow flexor muscle damage. Eur J Appl Physiol 2001; 85: 34-40.

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69 53. Smith LL, Fulmer MG, Holbert D, McCammon MR, Houmard JA, Frazer DD, Nsien E, Israel RG. The impact of a repeated bout of eccentric exercise on muscular strength, muscle soreness and creatine kinase. Br J Sp Med 1994; 28(4): 267-271. 54. Solomonow M, Baratta M, Zhou BH, Shoji H, Bose W, Beck C, DAmbrosia R. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med 1987; 15: 207-213. 55. Ebig M, Lephart SM, Burdett RG, Miller MC, Pincivero DM. The effect of suddent inversion stress on EMG activity of peroneal and tibialis anterior muscles in the chronically unstable ankle. J Orthop Sports Phys Therapy 1997; 26(2): 73-77. 56. Isakov E, Mizrahi J, Solzi P, Susak Z, Lotem M. Response of the peroneal muscles to sudden inversion of the ankle during standing. International J Sport Biomech 1986; 2: 100-109. 57. Johnson MB, Johnson CL. Electromyographic response of peroneal muscles in surgical and nonsurgical injured ankles during sudden inversion. J Orthop Sports Phys Therapy 1993; 18(3): 497-501. 58. Hoffman M, Schrader J, Koceja D. An investigation of postural control in postoperative anterior cruciate ligament reconstruction patients. J Ath Train 1999; 34(2): 130-136. 59. Hertel J, Gay MR, Denegar CR. Differences in potural control during single-leg stance among healthy individuals with different foot types. J Ath Train 2002; 37(2): 129-132. 60. Hertel J, Denegar CR, Buckley WE, Sharkey NA, Stokes, WL. Effect of rear-foot orthtics on postural control in healthy subjects. J Sport Rehab 2001; 10: 36-47. 61. Ochsendorf DT, Mattacola CG, Arnold BL. Effect of orthotics on postural sway after fatigue of the plantar flexors and dorsiflexors. J Ath Train 2000; 35(1): 26-30. 62. Ross SE, Guskiewicz KM. Time to stabilization: A method for analyzing dynamic postural control. Ath Therapy Today 2003; 8(3): 37-39.

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BIOGRAPHICAL SKETCH I was born on June 11, 1975, to David James and Eve Ann Smink (Rodman) in Shamokin, PA. Shamokin is a small coal-mining town in east central Pennsylvania. This is where I spent my entire youth growing up with my older brother Keith. When I was in fourth grade, I experienced the first tragedy of my young life. My father was taken from us in an automobile accident. This was a difficult time in our lives, but we had friends and family to help us through. My mother has worked hard throughout her life to provide for us and I love her immensely for that. She has been the most supportive person in my life, sacrificing herself to ensure I would not falter on my own. She has taught me much about respect, honesty, and the importance of family. While growing up a stubborn young boy, I did not always adhere to her sound advice, ignorant to the fact she had many similar life experiences to draw from. It was not until she met my stepfather that I truly began to understand what it would take to become a man. He has taught me many life lessons, such as hard work, dedication, and patience. Without this man, I truly do not think I would be where I am today. My education began in the Shamokin area public school system where I graduated from high school in 1993. Since I had not chosen a career goal, I chose to work for a year before attending college. It was during this time that I had an accident while playing basketball that changed my life forever. During the summer of 1993, I tore the anterior cruciate ligament in my left knee, which required surgery to repair. Following the 70

PAGE 83

71 surgery and rehabilitation process, I realized that my career goal was to become a physical therapist so I could help others who were in similar situations. The next two and a half years, I attended the University of Pittsburgh at Bradford studying sports medicine. It was at that point that I realized I no longer had the desire to work in a physical therapy clinic and that I wanted to work as an athletic trainer. I immediately began researching schools in the area with accredited undergraduate programs and came across Lock Haven University. Upon being accepted, I then applied for acceptance into the athletic training education program, which I was denied after my first year. Unaffected, I continued to work hard and study. The following year I reapplied and was accepted to begin classes in the curriculum. The next two years were an exciting time for me. I was assigned to work with the university football, volleyball, and track & field teams as well as with a local high school. While working closely with my program director, I once again had a change of goals I needed to achieve. I wanted to learn more about the research process, but in order to achieve this goal, I would need to continue my education towards a masters degree. I applied to several universities and was thrilled to accept an assistantship position from the University of Florida. I began my graduate education in the fall of 2001. During my first year, I was assigned to work with a local private school, Oak Hall. I thoroughly enjoyed working there and met many wonderful people. The summer between my first and second year in Gainesville is when I realized that I wanted to give back to the students. I assisted teaching a lab section for the undergraduate students and it was at that point I made a decision that I wanted to become an instructor in the athletic training field. Throughout my second year, in which I worked at Gainesville High

PAGE 84

72 School, I continued to teach numerous lab sessions in the AT department. Based on this newfound desire to teach, I decided to apply to several universities in an attempt to continue my education towards my PhD. I am eager to graduate from UF so I may pursue my next aspiration. I will be enrolling at the University of Delaware in the fall of 2003 in the Biomechanics and Movement Science department pursuing my doctoral candidacy. My life has taken many twists and turns over the years, but now I feel I am on track to attain my final goal.


Permanent Link: http://ufdc.ufl.edu/UFE0001500/00001

Material Information

Title: The Effects of Hamstring Delayed Onset Muscle Soreness on Functional Knee Joint Stability
Physical Description: Mixed Material
Copyright Date: 2008

Record Information

Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
System ID: UFE0001500:00001

Permanent Link: http://ufdc.ufl.edu/UFE0001500/00001

Material Information

Title: The Effects of Hamstring Delayed Onset Muscle Soreness on Functional Knee Joint Stability
Physical Description: Mixed Material
Copyright Date: 2008

Record Information

Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
System ID: UFE0001500:00001


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THE EFFECTS OF HAMSTRING DELAYED ONSET MUSCLE SORENESS ON
FUNCTIONAL KNEE JOINT STABILITY


















By

KYLE ANDREW SMINK


A THESIS PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF SCIENCE IN EXERCISE AND SPORT SCIENCES

UNIVERSITY OF FLORIDA


2003

































Copyright 2003

by

Kyle Smink















ACKNOWLEDGMENTS

A project such as this could not be completed without the support of numerous

others. For that, I would like to express a sincere thank you to the following people who

have been there for me throughout the completion of this project.

First of all, I would like to thank my family and friends for the love, support and

understanding they provided me along this journey. Although I believe none of my

family truly understands what I have been doing for the past two years, they have

supported me one hundred percent. It has been a struggle at times to stay motivated, but I

always had those close to me to keep me on course. Without these people, I do not think

I would have made it through this project.

I would like to thank Dr. Mike Powers for his knowledge and guidance that

allowed me to take my raw ideas and formulate them into a feasible research project. He

is an excellent mentor and teacher from whom I have learned so much about research.

He was instrumental in assisting me with the conception and design of this study, data

collection and analysis, and also helping me fabricate and validate the perturbation

device.

I would like to express a special thank you to my committee chair, Dr. Mark

Tillman. He accepted this burden late in the process, and was an incredible help to me

throughout. I cannot say enough to thank him for the amount of time and effort he

provided me so I could complete this project on time. His insight and ideas were

instrumental in finalizing this paper.









Dr. MaryBeth Horodyski has been helpful throughout the entire process. She was

able to provide clarity to certain issues I had during my initial drafts of this project. She

was also able to provide me with helpful feedback on potential flaws that may have been

overlooked by those of us dealing with it on a daily basis. I would like to thank her for

being an integral part of my committee who helped me along the road to the successful

completion of this project.

I would like to thank Dr. Stephen Dodd immensely for accepting my offer to join

my committee at such a late time. His expertise and knowledge in the field of exercise

physiology has helped greatly with the successful completion of this research.

Finally, I would like to thank the zoo full of friends I have made while in

Gainesville, for those are the ones that made sure I got away when I needed to get away,

but also made sure I stayed in when I needed to stay in. Many fun times and memories

took place while working on this project, none of which I hope to forget, and some that I

still cannot remember.
















TABLE OF CONTENTS
Page

A C K N O W L E D G M E N T S ......... .................................................................................... iii

LIST OF TABLES ................................................. ................... viii

LIST OF FIGURES ................................. .. ... ... ................. .x

ABSTRACT .............. ......................................... xi

CHAPTER

1 IN TR OD U CTION ............................................... .. ......................... ..

Statem ent of the P problem ............................................................................. ....... .2
R research H ypotheses .................. ........................................ .. ...... .....3
D definition of T erm s ....................................................... 3
A ssum options ................................................. ............................
L im itatio n s ................................................................................. 4
S ig n ifican ce ....................................................... 5

2 REV IEW O F LITER A TU RE .......................................................................... ....... 6

Introdu action .................................................................................................... 6
Anatomy and Biomechanics of the Knee ........................................... ...............6
A rticu latio n s ....................................................... 6
L ig a m e n ts .............................................................................................................. 7
M u scle s ................................................ 8
M echanoreceptors ................ ............................. .. ...... .................. 10
Mechanism of Injury for ACL Rupture...................................... .....................11
D elayed Onset M uscle Soreness (D OM S) ................................................................11
Electromyography (EMG) .............. ........................................... 13
M measures of Dynamic Stability ................................. ............................ 14
Sum m ary ......................................................................................... ...........16

3 METHODS ......................... ............................ 17

S u b j e c ts ................................................................................................................. 1 7
Instrumentation ............... ......... .......................17
Perturbation Device ............... ......... .................17
E lectro m y o g rap h y ...............................................................................................18


v









T riaxial F orce Platform ............................................... ............................ 18
In c lin o m ete r ................................................................................................... 1 8
M easurem ents ..................19................................................
H am string Flexibility ..................................................................................... 19
Pain M easurem ent ...................... .................. ................... .. ...... 19
M uscle L agency .......................................... .. .. .... ......... ......... 20
T im e to Stabilization ..................... .. ...................... .. .. ...... ........... 2 1
P procedures ....................................................................................................... 22
Statistical A nalysis................................................... 23

4 R E S U L T S .............................................................................2 9

D OM S M measures ........................................29
Measurement of Active Range of Motion ................................................... 29
Passive Range of Motion Pain Threshold ................................................... 30
Pressure Pain Threshold .................................. ....................... .. ........ 31
M uscle latency ....................................................................................................32
Internal Rotation Perturbation ....................... ............ ............. 32
External Rotation Perturbation ................. .......... ........... ......... 32
Tim e to Stabilization.................................................................. .......... 33
Vertical Ground Reaction Force (Fz) ................ ..................................... 33
Medial/Lateral Ground Reaction Moment (Mx)...............................................33
Anterior/Posterior Ground Reaction Moment (My) ............... ............ 34

5 DISCUSSION AND CONCLUSIONS ........................... ....... ...............35

D isc u ssio n ............................................................................................................. 3 5
D OM S M easurem ents .................................. ........................................... 36
M u scle L agency ....................................................................................... . 37
T im e to Stabilization.... ............. .... ..................................... ............... 40
C on clu sion s........... .... .. .................................... .. ........ ............ ............ .. .. 42
Suggestions for Future R research ............................................................. ...............42

APPENDIX

A LETTER OF INFORMED CONSENT ......... ............................. .. ...............46

B INCLUSION QUESTIONNAIRE...................................... ...............50

C DECRIPTIVE INFORMATION AND HAMSTRING FLEXIBILITY ....................51

D VISUAL ANALOGUE PAIN SCALE ............................................ .....................52

E R A W D A T A ....................................................................................................53

F ANOVA SUMMARY TABLES ....................................................62









L IST O F R E F E R E N C E S ...................................... .................................... ....................65

B IO G R A PH IC A L SK E TCH ...................................................................... ..................70
















LIST OF TABLES


Table page

4-1. Active hamstring range of motion (o SD)........_.... ......... ................... 30

4-2. Pain quotient as measured on a visual analog pain scale for passive range of
motion pain threshold (PQ SD)....... ..... ............... ............. ... ............ 31

4-3. Pain quotient as measured on a visual analog pain scale for Pressure Pain
Threshold (PQ SD) ................................... ......... .................. .....31

4-4. Internal rotation muscle latency (m sec + SD) ................................. ............... 32

4-5. External rotation muscle latency (msec SD) .................................. ............... 33

4-6. Vertical TTS based on Fz (msec SD).................................... ...............33

4-7. M edial/Lateral TTS based on M x (msec SD) ................................ ............... 34

4-8. Anterior/Posterior TTS based on My (msec SD) ....................................... 34

E-1. Subject dem graphic raw data ............................................................................ 53

E-2. Active range of motion (AROM) raw data (degrees) .............................................54

E-3. Passive range of motion pain threshold (PROMPT) raw data (PQ = 0 100).........55

E-4. Pressure pain threshold (PPT) raw data (PQ = 0 100).......................................56

E-5. IROT hamstring muscle latency raw data (msec).............................. .............57

E-6. EROT hamstring muscle latency raw data (msec).......................... ..............58

E-7. Time to stabilization based on vertical ground reaction force (Fz) raw
d ata (m se c ) ...............................................................................................................5 9

E-8. Time to stabilization based on medial/lateral ground reaction force (Mx) raw data
(m sec) ..................................... .................. ................. ......... 60

E-9. Time to stabilization based on anterior/posterior ground reaction force (My) raw
d a ta (m se c ) ...............................................................................................................6 1









F-1. Active range of m otion (AN OVA)....................................... ......................... 62

F-2. Passive range of motion pain threshold (ANOVA)................................................62

F-3. Pressure pain threshold (ANOVA)................................ ......................... ........ 62

F-4. Internal rotation hamstring muscle latency (ANOVA)..........................................63

F-5. External rotation hamstring muscle latency (ANOVA)................. ............ .......63

F-6. Fz (ANOVA) .................. ............. ...................... ..........64

F-7. M x (A N O V A ) .......................... ........................... .... ........ ......... 64

F-8. M y (A N O V A ) .......................... ........................... .... ........ ......... 64
















LIST OF FIGURES

Figure page

3-1. Lower extreme ity perturbation device ............................................. ............... 24

3 -2 L o ad c ell ................................................................2 4

3-3. Height adjustable release mechanism and trigger switch........................................24

3-4. Bertec triaxial force platform .............................................................................. 25

3 -5 In clin o m eter .............................................. .. ................ ................ 2 5

3-6. Subject positioning for ROM measure. A) start and B) end .............................. 25

3-7. Specially designed PVC device used for measuring hamstring range of motion......26

3-8. Nicholas Manual Muscle Tester. This device is a handheld dynamometer used to
m measure force output. ........................................... ................... .. .. .... 26

3-9. Algometer used for measuring the amount of pressure applied to the muscle..........27

3-10. V ertec vertical jum p device .................................. ............... ............... 27

3-11. Time to stabilization jump landing sequence. A) starting position, B) mid-flight,
and C ) landing phase. ............................ ........................... .......... ................28

5-1. A ctive ham string range of m otion............................................................ ........... 44

5-2. Passive range of motion pain threshold.................. .................. ...................44

5-3. Pressure pain threshold .......................................... ................... ............... 45















Abstract of Thesis Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Master of Science in Exercise and Sport Sciences

THE EFFECTS OF HAMSTRING DELAYED ONSET MUSCLE SORENESS ON
FUNCTIONAL KNEE JOINT STABILITY

By

Kyle Andrew Smink

August 2003

Chair: Mark D. Tillman, PhD
Major Department: Exercise and Sport Sciences

Dynamic joint stability is an essential component of athletic performance. If

deficits in dynamic stability exist, the athlete may be unable to perform at previous levels

of competition and may also be prone to injury. Delayed onset muscle soreness (DOMS)

is a response to unaccustomed bouts of strenuous exercise that results in certain physical

and physiological markers being present in the local tissue. The purpose of this

investigation was to determine the effects of hamstring DOMS on functional knee joint

stability.

Thirty subjects (18 females, 12 males) with no previous knee injuries participated

in this investigation. Subjects were assigned to one of two groups (DOMS, Control).

Baseline measures of hamstring flexibility, pressure pain threshold (PPT), passive range

of motion pain threshold (PROMPT), hamstring latency, and time to stabilization (TTS)

were measured. Subjects in the experimental group then performed 6 sets of 10 eccentric









hamstring contractions using a prone leg curl machine. All subjects returned for

reevaluation of all baseline measures 48 and 96 hours following the initial session.

Separate analyses of variance were performed for each dependent variable.

Tukey HSD post hoc analyses were performed to determine where significance existed

among the levels of each factor. A probability level ofP < 0.05 was expected to

designate statistical significance.

DOMS was adequately induced in the experimental group. Active hamstring

range of motion in the DOMS subjects significantly decreased after 48 and 96 hours post

exercise. PROMPT and PPT increased significantly 48 and 96 hours after the initial

session for the DOMS group. Hamstring muscle latency in the medial hamstring had a

slower response time to the external rotation perturbation. A significantly faster response

time was also present at the 48h and 96h posttest sessions compared to the baseline

measures. Time to stabilization for the vertical ground reaction force curve was faster

during the 96h posttest session compared to the pretest and posttest 48h sessions,

respectively.

Based on the results of the present study, it was concluded that DOMS has little to

no effect on the functional outcome of dynamic joint stability as measured using a

standing rotational perturbation or a jump landing procedure. Future research should

investigate the effects of hamstring DOMS on other aspects of proprioception, including

active and passive joint repositioning and also threshold to detection of passive

movement. Additionally, research should be conducted to examine the effects of a

functional fatigue protocol on the entire lower extremity to establish whether or not

functional joint stability would be affected if the entire kinetic chain were involved.














CHAPTER 1
INTRODUCTION

Knee injuries, particularly those involving the anterior cruciate ligament (ACL),

are a common occurrence in athletics. The ACL is the primary stabilizing ligament of the

knee and athletes who participate in sports involving high-speed change of direction,

pivoting, jumping and landing, and deceleration maneuvers are at an increased risk for

ACL injury. Damage to the ACL results in decreased stability of the knee joint and is

typically associated with a feeling of "giving way". The prevalence of injury in sports

such as football, basketball, and soccer are relatively high because they involve some or

all of the predisposing components stated above.1 In many cases the injury occurs when

there is no apparent contact involved. These non-contact injuries account for

approximately 70% of all ACL injuries. 1,2

The incidence of ACL injury in sports is a continuing dilemma. In 2002, during

three weeks of NCAA spring practices and one weekend of NFL mini camps, six players

were diagnosed with having suffered season ending knee injuries, all involving the

anterior cruciate ligament.3 4 5 Of those six cases, four of the injuries involved no contact

with an opposing player, which is in close agreement with the percentages reported

earlier for non-contact ACL injuries. Because contact injuries cannot be controlled, non-

contact incidences such as these have researchers probing for answers in an attempt to

recognize predisposing factors related to ACL injury.

The hamstrings help to dynamically stabilize the knee during athletic movements

that may predispose an athlete to ligament injury. DOMS is characterized by pain,









decreased strength, decreased range of motion, and swelling of the affected muscles. All

of these characteristics can lead to altered responses from the hamstrings, whether it is a

decrease in force generation or an increase in muscle reaction time. With a diminished

response from these dynamic restraints, functional knee stability could be compromised,

resulting in ACL disruption.

Statement of the Problem

Functional joint stability is a collection of anatomical and physiological

components that are present in order to maintain a relatively homeostatic environment of

the joint during active bodily movements.6 These components are characterized as either

static or dynamic in nature. Static components represent the structural aspect of the joint:

ligament, capsule, cartilage, bony congruity, and friction, whereas the dynamic

component corresponds to the functional aspect, primarily made up of the muscles that

cross the joint. Biological control systems associated with dynamic stabilization are the

feedforward or anticipatory and feedback or reactive mechanisms. Impulses from

afferent stimuli through somatosensory, visual, and vestibular input allow these control

mechanisms to function properly.6' 7 The muscle's reactive response to a perturbation

plays a major role in dynamic joint stability. The timing of this response is commonly

referred to as muscle latency.

The hamstrings work synergistically with the ACL as stabilizers of the knee joint,

providing resistance to anterior shear forces as well as rotational forces around the knee.

The ACL provides a passive resistance, while the hamstrings actively stabilize the knee.

An increased latency period of the hamstrings could increase the likelihood of a

functionally unstable joint. This could further predispose an athlete to potential ligament

injury due to the inhibition of the dynamic components of the sensorimotor system.









DOMS is a physiological response to unaccustomed physical activity that results

in pain, decreased strength, decreased range of motion, and swelling of the affected

muscles. There is limited research indicating an increase in muscle latency associated

with muscular fatigue8 and decreased strength,9 with none having directly studied DOMS

to determine if similar effects would be noted. Therefore, the purpose of this study was

to assess functional knee joint stability after DOMS has been induced in the hamstring

muscles. Functional joint stability will be assessed by measuring time to stabilization of

the affected lower extremity and muscle latency of the hamstrings.

Research Hypotheses

1. Active hamstring range of motion will significantly decrease after the inducement
of DOMS.

2. Passive range of motion pain threshold will significantly increase after the
inducement of DOMS.

3. Pressure pain threshold measurement will significantly increase after the
inducement of DOMS.

4. Hamstring muscle latency following knee perturbation will significantly increase
after the inducement of DOMS.

5. Time to stabilization following a jump landing will significantly increase after the
inducement of DOMS.

Definition of Terms

1. Eccentric contraction is the lengthening of a muscle when a force/load applied to
that muscle is greater than the force production of the muscle.

2. Electromyography is the study of muscle function through the detection of
electrical impulses emanating from the muscle itself.

3. Goniometry is a standardized technique of measuring joint motion.

4. Homeostasis is the maintenance of a stable internal environment of the body.

5. Kinesthesia is the ability to perceive extent, direction, or weight of movement.









6. Muscle latency is the time required for a muscle to respond following an induced
perturbation.

7. Perturbation is a disruption in homeostasis.

8. Proprioception is the awareness of posture, movement, and changes in equilibrium
and the knowledge of position, weight, and resistance of objects in relation to the
body.

9. Range of motion (ROM) is the amount of movement of a particular joint
measured in degrees by goniometry.

10. Time to Stabilization (TTS) is a measurement tool, calculated in milliseconds,
used to assess the length of time needed for one to maintain dynamic stability
following a standardized jump for distance and height to a single leg balance
position.

Assumptions

Two assumptions were made for the purpose of this investigation

1. Subjects will be honest in filling out prescreening questionnaire.

2. Subjects will exert full effort when reacting to knee perturbations and performing
time to stabilization techniques.

Limitations

Five limitations were identified for this investigation

1. A sufficient predetermined level of DOMS must be induced in the hamstring
muscles; however, the level will vary across subjects.

2. Only hamstring flexibility and muscle soreness will be used as indicators of
DOMS.

3. Only subjects who have not performed lower extremity resistance training during
the previous six months will be used in the investigation.

4. Functional knee stability will only be assessed 48 and 96 hours after DOMS has
been induced.

5. Only healthy subjects free from any acute knee injuries or lower extremity muscle
strains will be used for this study.






5


Significance

Injuries to the anterior cruciate ligament continue to be a primary concern to all

members of the sports medicine team. The exact cause of ligament failure is unknown,

but many assumptions can be made. No study to date has assessed hamstring latency

when DOMS has been induced. Determining whether DOMS affects the latency period

of the hamstrings could identify a predisposing risk factor to ACL failure in athletics.














CHAPTER 2
REVIEW OF LITERATURE

Introduction

Dynamic joint stability is an essential component of athletic performance. This

type of stability also helps to protect the joint from injury. If deficits in dynamic stability

exist, the athlete may be unable to perform at previous levels of competition and may also

be prone to injury. Likewise, athletes who have been previously injured may develop

deficits in dynamic stability. The microtrauma that occurs during resistance and other

types of exercise, generally referred to as DOMS, induces changes in the local tissue

similar to those seen following macrotrauma. Thus, it is possible that this type of trauma

would affect dynamic stability. However, at this time the effects of DOMS on dynamic

stability have not been investigated. This review of literature will focus on the anatomy

and biomechanics of the knee, mechanism of injury for the anterior cruciate ligament,

delayed onset muscle soreness, and measures of dynamic stability.

Anatomy and Biomechanics of the Knee

Articulations

The knee joint is composed of two bony articulations, the tibio-femoral joint and

the patellofemoral joint. The tibio-femoral (knee) joint, comprised of the femur and the

weight-bearing tibia, is a modified hinge synovial joint that allows a great amount of

ROM through movements of flexion and extension, but is limited with internal and

external rotation.10 The patellofemoral joint is made up of the patella and the femur. The

patella, a large sesmoid type bone, is embedded within the patellar tendon and rests in the









trochlear groove of the femur.11 The patella's primary function is as a fulcrum for the

quadriceps muscles to increase the lever arm during active extension movements at the

knee.12

Ligaments

Configured in and around the knee are four key ligaments that enable the joint to

maintain passive stability during weight bearing activities. These ligaments can be

divided into two groups, collaterals and cruciates, whose function is based on their

arrangement at the knee. The collaterals are comprised of the lateral collateral ligament

(LCL) and the medial collateral ligament (MCL), whereas the cruciates consist of the

anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL). The

orientation and biomechanics of the cruciate ligaments will be provided to allow a better

understanding of their role in knee joint stability.

The ACL is an important stabilizing ligament in the knee joint and one that, if

ruptured, typically requires surgery.13 The ACL functions to reduce anterior shear force

as well as control some varus, valgus and rotational forces of the tibia on the femur.

Approximately 86% of the primary restraint of anterior tibial translation is provided by

the ACL.14 Damage to the ACL creates joint laxity and may lead to episodes of

instability in the knee.15 The ACL originates on the medial aspect of the lateral femoral

condyle and inserts on the anterior tibial plateau.16 Generally, the ACL is addressed as a

single banded ligament that connects the tibia to the femur; however, that is not entirely

the case. The ACL is divided into two separate bundles of fibers, an anteromedial and a

posterolateral bundle, each offering passive resistance to different stresses placed on the

tibio-femoral joint. When the knee is in a fully extended position (zero degrees), the

anteromedial bundle is most taut, while the posterolateral bundle is taut in flexion.16









Movements through the range of motion are accommodated by a combination of the two

bundles working synchronously.

The posterior cruciate ligament serves as the antagonist to the ACL, in that its

orientation in the knee runs from the lateral wall of the medial femoral condyle to the

posterior tibial shelf.17 18 The PCL serves to prevent straight posterior displacement of

the tibia relative to the femur.19,20

The PCL, like the ACL, consists of two so-called bands of fibers. During knee

flexion movements, the anterolateral portion is tightened while the posteromedial portion

is lax. Conversely, in knee extension, the anterolateral bundle is lax, whereas the

posteromedial bundle is tight.17' 18

Muscles

An extensive knowledge of the musculature that crosses the knee joint is critical in

order to understand the proper structure and function of the knee joint and how this

relates to overall functional joint stability. There are 12 muscles that cross the knee joint.

The primary muscles associated with knee joint movement are the four quadriceps and

three hamstring muscles. The remaining muscles, which consist of the gastrocnemius,

plantaris, and popliteus in the lower leg, and the sartorius and gracilis of the upper leg,

are secondary type muscles that assist movement of the joint, but are not considered

prime movers.

The quadriceps group is collectively made up of four muscles (Rectus Femoris,

Vastus Intermedius, Vastus Lateralis, and Vastus Medialis) that act to extend the knee.

Because the Rectus Femoris attaches on the pelvis, this allows it to also function as a hip

flexor. The Vastus Medialis and Lateralis originate on the linea aspera on the posterior

femur on their respective sides, and the Vastus Intermedius originates on the anterior and









lateral femoral shaft. All four muscles have a common insertion site into the tibial

tuberosity via the patellar tendon.21

The hamstrings are the primary muscle group that makes up the posterior thigh,

which consists of three separate muscles (Biceps Femoris, Semitendinosus,

Semimembranosus) that's main functions are to flex the knee and extend the hip. The

hamstrings have a common origin on the ischial tuberosity of the pelvis, though the

biceps femoris has an additional origin on the linea aspera of the posterior femur. As a

group, they travel down the posterior aspect of the upper leg with individually different

insertions. The biceps femoris, semimembranosus, and semitendinosus insert into the

head of the fibula, posterior medial tibial condyle, and anterior proximal tibial shaft,

respectively.21

Besides providing joint motion, the hamstring muscles also function as joint

stabilizers and secondary restraints to anterior tibial translation.22'23 Some research

suggests that there is an anterior cruciate ligament hamstring reflex that allows this to

happen. However, there has been much controversy over this neuromuscular response.

In human and animal studies, researchers have investigated the relationship between

anterior tibial displacement and the ACL hamstring reflex with mixed results." 13, 15,24,

25,26 Boden et al.1 suggest that the hamstrings provide this protective effect when the hip

is flexed because it allows the hamstrings to become tighter, allowing less anterior shear

of the knee. This protective effect may be diminished with increased hamstring

flexibility.1 Their findings suggested that athletes who sustained an ACL injury had

greater hamstring flexibility than a control group of subjects.









Mechanoreceptors

One of the most important components of motor control is our ability to utilize the

numerous mechanoreceptors found throughout the human body. The importance lies in

that mechanoreceptors provide afferent input to the central nervous system making them

valuable contributors to proprioceptive feedback. The most commonly described

mechanoreceptors, muscle spindles and Golgi tendon organs (GTO), are located in

muscle and tendon tissue.27 28 Others that are equally important are those located in the

ligaments and joint capsules, particularly Ruffini endings and Pacinian corpuscles.6' 28

Muscle spindles are located in skeletal muscle and are responsible for detecting changes

in length of the associated muscle, whereas Golgi tendon organs monitor active force and

tension in the muscle through its location in the myotendinous junction. These two

mechanoreceptors function via a monosynaptic reflex pathway and are considered to

have a slow adaptation rate to their respective responses.6' 7, 28 The Ruffini endings and

Pacinian corpuscles respond through the same reflex pathway as mentioned earlier. Like

the muscle spindles and Golgi tendon organs, Ruffini endings are slow adaptive and have

a low threshold for stimulation. They are primarily located in the joint capsule and

ligaments and are responsible for detecting changes in joint pressure. Pacinian

corpuscles are also low threshold receptors, but adapt quickly to the stresses placed upon

them. They function to sense high frequency vibrations within the joint capsule. This

quick adaptive response classifies them as only dynamic receptors, meaning they are

inactive when a constant stimulus is placed on the joint.6' 7,28 The mechanoreceptors

described here have independent responsibilities for maintaining dynamic joint stability.

However, in order for the joint to function properly, they must work in unison, dependent

on each other for maximum proprioceptive feedback.









Mechanism of Injury for ACL Rupture

There are typically two types of mechanisms associated with ACL injuries,

contact and non-contact. Contact injuries are those that take place when a direct blow is

made to either side of the knee or to the anterior aspect of the knee, forcing it into a

varus, valgus, or hyperextended position, respectively. There are numerous non-contact

mechanisms that result in injury to the ACL, but the majority occurring in sports

participation is while the athlete's foot is fixed or planted with either a rotational or

varus/valgus force placed on the knee, such as cutting, planting, or pivoting to change

direction.8, 29 Injuries are also prevalent in athletic maneuvers that involve a sudden

deceleration during or just before a change of direction or landing awkwardly from a

jump., 2' 23, 29 Research has provided evidence that non-contact ACL injuries are more

common than contact mechanisms, accounting for approximately 70- 78% of all ACL

injuries.1' 2, 22, 23, 30

Delayed Onset Muscle Soreness (DOMS)

When healthy people take part in unaccustomed bouts of strenuous exercise, the

phenomenon of DOMS typically follows. Delayed onset muscle soreness is commonly

noticed after exercise that is relatively intense, of long duration, and/or eccentric in

nature. The onset of symptoms begins approximately 8 24 hours post exercise with

intensity peaking at 24 48 hours,31'32 and symptoms lasting up to 7 days. Common

physical and physiological markers associated with DOMS are soreness and pain,31 33 37

decreased strength,33-37 increased plasma creatine kinase (CK) levels,34 39 decreased

range of motion,34' 35,40 and swelling.31 34 35 Most recently, Nosaka et al.35 noted a

decrease in mean maximal isometric force after one bout of eccentric exercise of the

biceps brachii muscle. Range of motion decreased immediately post to 3 days post









exercise. Along with range of motion decrease, there was a significant increase in

circumference of the upper arm immediately post exercise, followed by a further increase

in swelling at 2 days post exercise. Muscle soreness developed 1 day after exercise and

peaked at 2-3 days after, then gradually attenuated. A significant increase was noted in

CK after a single bout of exercise, peaking at 3-5 days post exercise.35

Exercise training can have a significant effect on the outcome and subsequent

events associated with exercise induced muscle damage. It is widely accepted that a

second bout of exercise done at the same intensity as the initial bout will provide

somewhat of a protective effect on the muscle, where there may be no increases in

muscle damage markers and the recovery time may be decreased.34' 35, 39 41 This

phenomenon is called the repeated bout effect. The time frame involved in the repeated

bout effect is unclear. Some researchers have also investigated training prior to the first

bout of eccentric exercise attempting to determine how it affects delayed onset muscle

soreness and the markers involved.36'38 Ebbeling and Clarkson40 studied the effects of

performing a second bout of exercise prior to full muscle recovery. They reported that

symptoms were not exacerbated, significantly smaller changes in muscle damage

indicators were found, and the recovery time was faster following a second bout of

eccentric exercise of the elbow flexor muscles,40 however, Nosaka and Clarkson34

concluded that a second and third bout of high force eccentric exercise performed 3 and 6

days following the initial exercise session had neither increased the markers of damage to

the tissue nor caused a change in recovery time.34 When a bout of eccentric exercise was

repeated 48 hours after an initial bout, there were no beneficial or detrimental effects on

the time-course and/or intensity ofDOMS, CK, or 1 repetition max strength.39 Schwane,









et al.36 suggested that progressive, short-term training could reduce the effects of delayed

onset muscle soreness. They trained subjects with either uphill or downhill treadmill

running for 1 and 2 weeks respectively. This was followed by the experimental test,

which consisted of 45 minutes of intermittent downhill running at 80%VO2Max. The

researchers reported that subjects who performed the downhill running training for 2

weeks displayed less DOMS markers than those subjects who trained downhill for 1

week and also showed less DOMS symptoms/markers than the control and uphill training

groups.36 In trained individuals, a smaller metabolic response was reported after

performing one bout of high intensity eccentric exercise. Significantly higher CK levels

were seen in untrained subjects compared to subjects who took part in a regular training

regimen.38 A training effect can be seen from up to 6 weeks to as long as 6 months, but

there has been no effect noticed after 6 months.35'41

Electromyography (EMG)

Elecromyography techniques are used to determine the electrical activity

associated with muscular contraction and nerve function. It can be used to define the

onset and intensity of muscle activation. From this, latency periods in muscle can be

determined from EMG readings. Muscle latency is used to assess the time from joint

movement to the initial onset of muscle activity.

Co-contraction of the muscles surrounding the knee joint is thought to provide a

protective mechanism against ligamentous injury. Colby et al.22 assessed the activation

times of muscular contraction while subjects performed four types of athletic movements

(sidestep cutting, cross-cutting, stopping, and landing) typically associated with ACL

injuries. They reported that in all trials the quadriceps were activated at higher intensities

than the hamstrings leading up to, at foot contact, and at the propulsion phase of the









maneuver the subject was performing.22 These findings might suggest that because the

quadriceps are creating more force, more often that this would produce an undesirable

anterior shear force of the tibia resulting in increased stress on the ACL.

Beard et al.25 and Jennings et al.24 compared reflex hamstring contraction latency in

ACL deficient knees to normal knees using a specially designed weight-bearing

apparatus. Patients were positioned standing inside the rig with their thigh to be tested

resting against a pad. The placement of the pad did not allow any movement of the femur

anteriorly. An accelerometer was then placed on the tibial tuberosity. Finally there was a

compressed air piston mechanism pressed against the posterior tibia. The perturbation

was initiated when the piston was released and an anterior shear force was applied to the

tibia. This study was designed to investigate function and instability of the knee joint.24'25

Some skepticism arises when function is mentioned with this maneuver, when there is no

functional task addressed.

Measures of Dynamic Stability

A more accurate assessment of dynamic joint stability would be to use a maneuver

that incorporates a functional task. Recent research has addressed this issue. Colby et

al.42 and Ross et al.43 integrated this for measurement of time to stabilization. Colby and

colleagues42 required subjects to perform a 1-legged step down onto a force plate and a 1-

legged hop onto the force plate. The step down measure was from a set height of 19 cm

and the hop test was performed at a distance equal to the subject's leg length.42 The

design used by Ross et al.43 was similar in theory. Subjects were asked to jump from a

two-foot stance a distance of 70cm landing on one foot on a force plate. Included in this

design was a standardized protocol for measuring jump height needed for the measure to

be consistent. Subjects needed to achieve 50% of their maximum vertical jump height









while covering the 70cm distance. Upon landing, subjects had to remain in the single leg

stance position for 20 seconds. A majority of areas typically used to assess dynamic joint

stability are represented with these procedures.43

A more functional way to assess hamstring latency was designed by Schultz et

al.44 The researchers used a weight-bearing perturbation device designed to induce a

forward moment with either an internal or external rotation of the trunk and femur

relative to the tibia. Similar to the concept used by Colby22, this device was designed to

simulate a typical mechanism associated with ACL injury. Unlike the previous research,

Schultz's design allowed the presence of a silent period of the hamstrings before the

perturbation was initiated. This maneuver was thus deemed a valid and reliable measure

when assessing hamstring latency.

Using time to stabilization and hamstring latency as measures of dynamic stability

will allow this research to evaluate DOMS as a potential factor affecting neuromuscular

control. Speculation can be made that when the signs and symptoms associated with

DOMS are exacerbated, an athlete's neuromuscular control could be diminished, further

leading to injury. Lephart et al.45 have assessed a functional stability paradigm where

proprioceptive deficits can lead to decreased neuromuscular control, which in turn can

lead to functional instability, finally leading to ligament injury. This paradigm is

considered cyclical, meaning that if any of the previously mentioned steps are present,

the progression of functional instability will continue.

Athletes with diminished time to stabilization could have difficulty achieving the

proper balance needed while performing athletic maneuvers such as landing from a jump.

When those muscles are negatively affected by DOMS, this could predispose the athlete









to episodes of instability where the only means for joint protection is the passive

restraints of that joint (ligaments, cartilage, joint capsule, etc). Similar consideration can

also be taken when assessing hamstring latency. The diminished ability of the muscles to

fire at the proper time and rate could lead to instability, resulting in joint injury.

Therefore, without adequate input from the dynamic control system, the athlete can

become vulnerable to joint damage.

Summary

The exact cause for anterior cruciate ligament injury is unclear. However, a

number of predisposing factors are commonly noted in the literature. At this time there is

no research to confirm or refute delayed onset muscle soreness as one of those

predisposing factors. The microtrauma associated with DOMS presents with specific

physiological markers that may affect dynamic joint stability. Strength deficits and an

increase in pain perception could cause changes in joint mechanics and muscle firing

patterns. A lower force production of the hamstrings during athletic maneuvers could

increase the percent of quadriceps to hamstring muscle activation, as noted by Colby et

al.,22 resulting in increased anterior shear forces of the tibia. This would diminish the

effects the hamstrings provide in protecting the knee during dynamic movements. This

overall weaker hamstring response could reduce functional knee stability, ultimately

leading to a predisposition to ligament damage. Thus, determining joint stability using

functional tasks is the goal of this research.














CHAPTER 3
METHODS

Subjects

Thirty healthy, college age subjects were recruited from the University of Florida

student population. The first twenty subjects participated in both measures, while the

final 10 exclusively took part in the TTS procedure. Prior to participation in the study, all

subjects read and signed an informed consent form approved by the university

institutional review board (Appendix A). Subjects were evaluated for previous knee

injuries using a history questionnaire (Appendix B) and were excluded if prior knee

injuries were present. Subjects were also excluded if they were suffering from a previous

hamstring injury or any other injury or condition that might have affected dynamic

stability or balance. Finally, subjects who have performed lower extremity weightlifting

exercises within the previous six months were excluded from this study to eliminate a

training effect.

Instrumentation

Perturbation Device

The perturbations were performed with a lower extremity perturbation device

(LEPD) (Figure 3-1) designed similarly to those used in previous research. 44,46,47 The

LEPD produces an unexpected forward perturbation with either an internal or external

rotation of the trunk and femur in relation to the fixated foot and tibia. Subjects were

wearing a waist harness with hooks attached to each side while being restrained at the

hips using cables attached to a release mechanism. To standardize the procedures, a load









cell (Transducer Techniques, Inc, Temecula, CA) (Figure 3-2) was attached in the middle

of each cable. The height adjustable release mechanism was mounted to the wall and

consisted of a .64-cm universal push-to-connect coupling system (Porter-Cable

Corporation, Jackson, TN) and a trigger switch to detect when the perturbation was

initiated (Figure 3-3).

Electromyography

A 16 channel Myopac EMG system (Run Technologies, Laguna Hills, CA)

interfaced with a laptop-type personal computer was used to record raw EMG signals for

the onset times of the lower extremity musculature following a weight-bearing

perturbation procedure. The specifications for the electromyography unit included an

amplifier gain of 1-mV/V, frequency bandwidth of 10 1000 HZ, CMRR 110 dB, input

resistance of 1 MQ, and a sampling rate of 2000 Hz. Upon completion of data sampling,

an analog to digital conversion of the EMG data was performed and stored on the PC

using DATAPAC 2000 (Run Technologies, Laguna Hills, CA) software.

Triaxial Force Platform

Performance of the TTS procedure was assessed using a triaxial force platform

(Bertec Corporation, Columbus, OH) (Figure 3-4). The raw signal was acquired at a

frequency of 2000 Hz and stored on the same laptop-type computer using the DATAPAC

2000 (Run Technologies, Laguna Hills, CA) software.

Inclinometer

Hamstring flexibility was assessed using an inclinometer (Figure 3-5). The

inclinometer resembles a flat goniometer with 3600 marked in single degree increments

on the circumference. A freely rotating arm fixed at the center of the inclinometer is used

to determine the angular position as it aligns with the degree markings on the









circumference. Because the arm can move without restriction, gravity maintains it in the

downward position. Thus, during limb movement the arm remains in the downward

position, indicating limb position.

Measurements

Hamstring Flexibility

Subjects were positioned supine with their involved hip actively flexed to 900 and

the contralateral lower extremity flat on the table (Figure 3-6). A specially designed

apparatus made of PVC pipe was used to ensure the subjects' hip remained at this angle

through the entire measurement (Figure 3-7). The subject was then instructed to actively

extend their knee as far as possible and hold that position for 3 seconds. A VelcroTM

strap was used to secure the inclinometer just above the ankle. Three trials were

performed and the average ROM obtained from the three trials was used as the measure

of hamstring flexibility (Appendix C).

Pain Measurement

Subjects were assessed for the level of perceived pain as pressure and passive

stretch were applied separately to the hamstring muscles. Both tests were performed with

the subjects in the same supine position used for flexibility testing. To assess the

perceived pain during a passive stretch, the knee was passively extended to the end range

as the examiner applied 6.0-kg of force. A Nicholas Manual Muscle Tester (MMT)

(Model 01160, Lafayette Instrument, Lafayette, IN) (Figure 3-8) was used to control the

amount of pressure applied. When 6.0-kg of force had been achieved, the subjects were

instructed to mark on a visual analogue pain scale (Appendix D) the amount of pain they

felt at that moment. They were asked to make a vertical slash across a 10-cm long line

between the limits of no pain felt (left end of line) and unbearable pain (right end of line).









The subjects were then assessed for pressure-pain threshold using an algometer (Ametek,

Chatillon, NY) (Figure 3-9). The subjects were again passively stretched to end range

while an examiner applied 9-kg of pressure with the algometer directly to the belly of the

medial hamstrings. The subjects were again asked to mark a vertical slash representing

the amount of perceived pain on a separate visual analogue pain scale. The distance of

the mark in millimeters from the left end of the line was used as the measure of perceived

pain for each visual analogue scale.

Muscle Latency

Muscle latency following knee perturbation was assessed using EMG. To prepare

the subjects for this, the skin overlying the medial and lateral hamstring muscles (MH

and LH), and the vastus medialis and lateralis (VM and VL) was shaven and cleaned with

isopropyl alcohol to reduce skin impedance. Bipolar 1-mm x 10-mm Ag/AgCl surface

electrodes were then placed over the muscles with an interdetection surface distance of

1.5-cm between electrodes. Manual muscle testing was performed to confirm correct

electrode placement using real time oscilloscope displays. The waist harness was fitted

snugly to the subject and the release mechanism was adjusted to a height level with the

subject's anterior superior iliac spine (ASIS) while the subject was standing on the force

platform in the flexed knee position. Having the subject focus on the computer screen

directly in front of them aided to control visual feedback. The position of the subject was

standardized prior to the perturbation using the load cells and a predetermined voltage

formula. The voltage formula consisted of a y-intercept equation in which the unknown

variable was determined by inserting 5% of the subject's body weight. The product of

the formula was then multiplied by 0.10 and this was the final number inserted into the

computer. The subjects were instructed to lean into the cables until the voltage reached









the determined level. Three trials of internal and external rotation perturbations were

provided for the subjects to become accustomed with the device followed by ten random

perturbations (5 IR, 5 ER) while allowing subjects 30s rest time between trials.

The acquired raw signals were digitally processed using a symmetric root mean

square (RMS) algorithm with a 10-msec time constant. Muscle latency was measured as

the time between the initiation of perturbation and the onset of muscle activity, which

was determined by calculating a threshold voltage (Vo) for each muscle. The Vo required

for muscle onset was determined when the EMG activity exceeded 30% of the muscles

peak amplitude for that trial, which was calculated from the following equation: Vo =

Max 0.30.48 The onset of muscle activity was determined by comparing discrete data

points in a point-by-point fashion to the Vo. The muscle was considered active (or a

reflex event to have occurred) when the Vo was exceeded for a minimum of 10-msec.

The average MRT of the five trials was calculated and used for statistical comparison.

Time to Stabilization

Subjects were evaluated for TTS in the medial/lateral, anterior/posterior and

vertical planes following a single leg landing from a jump height equivalent to 50% of

their maximum vertical jump height, which was assessed prior to the TTS measure.

Subjects were positioned under the VertecTM vertical jump device (Figure 3-10) and

while standing on their toes, their reach height was determined. Subjects were then asked

to jump as high as possible from a stationary stance, touching as many vanes as possible.

Maximum vertical jump height was determined based on the number of vanes touched.

This procedure was performed a total of three times, with the highest score being used.

TTS was then assessed as the subjects jumped from a two-footed stationary stance to a

one footed stabilization position onto a force platform 70-cm away (Figure 3-1 la-c).









After landing on the platform, subjects were instructed to balance on a single leg for 5-

sec. Subjects were allowed three practice trials to become accustomed to the task and

then needed to perform this procedure for a total of 3 successful trials. TTS was

determined as the time in msec necessary for the sequential average of the data points to

fall within 0.25 standard deviations of the mean of the first 3-sec following landing.

Procedures

After successfully meeting the criteria for inclusion into this study, subjects were

asked to report to the Athletic Training/Sports Medicine Research Laboratory for

measures of hamstring flexibility, pressure-pain threshold (PPT), passive range of motion

pain threshold (PROMPT), time to stabilization (TTS), and hamstring muscle latency.

Baseline measures of hamstring flexibility for each subject were taken prior to

experimentation. Perturbations and stabilization procedures along with the lower

extremity to be tested were randomly assigned as to eliminate any potential threats to

validity. Following the baseline measures of muscle latency and TTS, subjects were

randomly assigned to either an experimental or control group. Subjects assigned to the

experimental group performed 6 sets of 10 eccentric contractions of the hamstrings using

a prone lying leg curl machine. Subjects were assessed for single leg 1 repetition max

strength concentrically, with 100% of that 1RM being used as the exercise intensity for

the subject. Subjects were instructed to lower the weight from a fully flexed knee to a

fully extended knee. This movement was standardized using a metronome and lasted for

10 seconds and subjects were given a 10 second rest between each repetition. Subjects

were given 1.5 minutes to rest between sets. Participants were asked to return for

reevaluation of TTS and muscle latency 48 and 96 hours after the initial testing date.

Upon return, subjects had their hamstring flexibility reevaluated, as well as each measure









of pain threshold using the visual analog pain scale used to assess the level of DOMS

achieved. Hamstring flexibility, pain threshold, TTS, and perturbation procedures were

performed identical to the pretest trials.

Statistical Analysis

The design of this study was a pretest posttest design. Statistical analysis for the

DOMS measure was done using separate two-way mixed design analyses of variance for

each dependent measure (AROM, PROMPT, PPT). To determine statistical significance

for the muscle latency measure, separate three-way mixed design analyses of variance

were used with the independent variables consisting of muscle (MH, LH), time pretestt,

48-hr post, 96-hr post), and physiological state of the hamstrings (DOMS induced,

control). Three separate two-way analyses of variance with repeated measures on the

factors of time and group were used for the TTS procedure (Fz, Mx, My). If statistical

significance was noted, a Tukey HSD post hoc analysis was performed to establish where

the significance lies. A probability level ofP < .05 was expected to designate statistical

significance.




























Figure 3-1. Lower extremity perturbation device


Figure 3-2. Load cell


Figure 3-3. Height adjustable release mechanism and trigger switch























Figure 3-4. Bertec triaxial force platform


Figure 3-5. Inclinometer


Figure 3-6. Subject positioning for ROM measure. A) start and B) end


Z
























Figure 3-7. Specially designed PVC device used for measuring hamstring range of
motion


Figure 3-8. Nicholas Manual Muscle Tester. This device is a handheld dynamometer
used to measure force output.




























Figure 3-9. Algometer used for measuring the amount of pressure applied to the muscle.


Figure 3-10. Vertec vertical jump device.






























U -B A


Figure 3-11. Time to stabilization jump landing sequence. A) starting position, B) mid-
flight, and C) landing phase.














CHAPTER 4
RESULTS

Statistical analysis for the DOMS measures was conducted using separate 2-way

mixed design ANOVA for each dependent variable (active range of motion, passive

range of motion pain threshold, and pressure pain threshold). Two 3-way mixed design

ANOVA were used to analyze the muscle latency times for internal and external rotation

perturbations. Finally, three separate 2-way mixed design ANOVA were performed for

the three TTS measures (based on Fz, Mx, and My) analyzed during the jump landing

procedure. Tukey's HSD post hoc analysis was conducted when significance was

established. The alpha level was set at 0.05 for all statistical tests.

DOMS Measures

Measurement of Active Range of Motion

Significant main effects for time (F2, 56 = 19.08, P < 0.001) and group (F1, 28 =

11.22, P = 0.002) were observed for the active range of motion measures. Subjects

showed significant deficits in hamstring AROM at 48h and 96h posttreatment. A

significant recovery of AROM was noticed between the second and third test sessions.

Overall, hamstring flexibility was significantly less in the DOMS subjects compared to

the control subjects. A significant time x group interaction (F2, 56 = 19.98, P < 0.001) was

also noted. Data presented in Table 4.1 indicate that subjects in the DOMS group

displayed marked decreases in hamstring flexibility over the 48h and 96h test periods

when compared to the pretest measures. A significant decrease from baseline to 48h post

exercise was observed. Subjects began to regain significant flexibility between the









second and third test session, although significant decreases at 96h posttest were still

present compared to baseline. No differences were noted among the three trials for the

control groups, but significant decreases were seen comparing between control and

DOMS groups at 48h posttest and 96h posttest, respectively.

Table 4-1. Active hamstring range of motion (o + SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 65 14 43 24*t 51 + 18*t 53 21t
Control 71 + 13 71 + 13 72 12 71 + 13
Total 68 14 57 24* 62 19*"
* Significantly less than pretest group (P < 0.05)
f Significantly less than control group at same posttest time (P < 0.05)
1 Significantly greater than posttest 48h (P < 0.05)


Passive Range of Motion Pain Threshold

Significant main effects for time (F2, 56 = 11.97, P < 0.001) and group (Fi, 28 =

4.58, P = 0.041) were present for the PROMPT measure. Data presented in Table 4.2

indicate that there was a significant increase in pain perception due to passive stretch of

the hamstring muscles in the DOMS group. Overall, subjects also noted significantly

higher levels of pain 48 and 96h after exercise. Muscle soreness peaked by the third

session, but was only slightly higher than the 48h session. Additionally, a significant

time x group interaction (F2, 56 = 10.58, P < 0.001) was identified. A significant increase

in pain perception was noted when comparing each posttest DOMS measure to the pretest

DOMS measure. No significant changes were present among the control groups,

although significant differences were seen when comparing the 48h control group to the

48h posttest DOMS group and the 96h posttest control group to the 96h posttest DOMS

group.









Table 4-2. Pain quotient as measured on a visual analog pain scale for passive range of
motion pain threshold (PQ SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 18.1 20.6 46.6 + 27.6*t 47.1 + 28.8*t 37.3 28.8t
Control 19.3 21.0 20.7 24.1 19.8 25.4 19.9 23.1
Total 18.7 20.4 33.6 28.7* 33.4 30.1*
* Significantly greater than pretest group (P < 0.05)
f Significantly greater than control group at same posttest time (P < 0.05)


Pressure Pain Threshold

A significant main effect for time (F2, 56 = 7.23, P = 0.002) was identified for the

PPT measure (Table 4.3). Pain perception peaked at 48h but began to diminish by the

96h post exercise session. A significant group x time interaction (F2, 56 = 6.91, P = 0.002)

was also present. Subjects in the DOMS group reported significantly greater levels of

perceived pain at the 48h and 96h post exercise sessions compared to the first session.

No significant changes were seen across the trials for the control subjects, but a

significant difference was present between the posttest 48h control group and the posttest

48h DOMS group. No significant group main effect (F1, 28 = 1.09, P = 0.304) was

present for this measure.

Table 4-3. Pain quotient as measured on a visual analog pain scale for Pressure Pain
Threshold (PQ SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 43.9 + 17.8 63.1 + 21.8*t 58.5 24.2* 55.2 22.5
Control 45.6 27.7 45.0 + 28.6 47.6 + 29.8 46.1 + 28.1
Total 44.7 + 22.9 54.1 + 26.6* 53.1 + 27.2*
* Significantly greater than pretest group (P < 0.05)
f Significantly greater than control group at posttest 48h (P < 0.05)









Muscle latency

Internal Rotation Perturbation

No significant main effects were detected for muscle (Fi, 18 = 0.043, P = 0.838) or

group (Fi, 18 = 2.01, P = 0.173); however, a trend was observed for time (F2,36 = 2.77, P =

0.076) main effect with the internal rotation lower extremity perturbation (Table 4.4). No

significant 2-way interactions were detected for time x group (F2, 36 = 0.35, P = 0.705),

muscle x group (F1, 18 = 0.408, P = 0.531), or time x muscle (F2, 36 = 1.03, P = 0.368).

Comparison of the 3-way interaction for time x muscle x group also detected no

significant results (F2,36 = 1.80, P = 0.180).

Table 4-4. Internal rotation muscle latency (msec SD)

Muscle Group Pretest Post 48h Post 96h Total
DOMS 97 + 24 72 + 23 81 + 23
MH 92 + 26
Control 106 15 99 23 96 33
DOMS 101 33 106 122 64 23
LH 94 + 58
Control 120 34 83 29 87 34
Total 106 28 90 64 82 30


External Rotation Perturbation

Significant main effects were observed for time (F2,36 = 8.60, P = 0.001) and

muscle (F,8is = 4.97, P = 0.039) for the latent muscle reaction times of the hamstrings

(Table 4.5). Subjects recorded significantly quicker response times during the 48h (19

msec) and 96h (16 msec) posttest trials as compared to the pretest measure. Medial

hamstring activation times (86 25 msec) were significantly faster than lateral hamstring

response times (99 + 31 msec). No significant interactions were detected, however a

trend was noted for the time by group interaction (F2,36 = 3.05, P = 0.060). No









significant main effect was observed between the DOMS and control groups (Fi, 18 =

545.50, P = 0.668)

Table 4-5. External rotation muscle latency (msec SD)

Muscle Group Pretest Post 48h Post 96h Total
DOMS 104 27 81 25 79 18 86
Control 85 20 84 31 84 25
DOMS 114 26 79 23 86 26
LH 99 + 31
Control 113 43 96 32 103 18
Total 104 31 85 28* 88 23*
* Significantly less than pretest group (P < 0.05)
f Significantly faster response than lateral hamstring (P < 0.05)


Time to Stabilization

Vertical Ground Reaction Force (Fz)

A significant time main effect (F2, 54 = 5.04, P = 0.010) for TTS based on Fz was

present. Data presented in Table 4.6 indicate that subjects displayed significant

improvement of TTS during the 96h posttest session (1515 572 msec) compared to the

baseline (1868 + 514 msec) and posttest 48h session (1839 + 605 msec). Neither the

group main effect (Fi, 27 = 1.44, P = 0.240) nor the time x group interaction (F2,54 = 0.71,

P = 0.497) were observed to be significant.

Table 4-6. Vertical TTS based on Fz (msec SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 1905 404 1911 606 1696 453 1830 643
Control 1834 612 1772 617 1346 634 1635 749
Total 1868 514* 1839 605* 1515 572
* Significantly greater than posttest 96h group (P < 0.05)


Medial/Lateral Ground Reaction Moment (Mx)

No significant time (F2, 54 = 1.49, P = 0.234) or group (F 1, 27 = 1.14, P = 0.294)

main effects for TTS based on Mx were present. Similarly, no significant changes were









observed for the time x group interactions (F2, 54 = 0.82, P = 0.448). Data are presented

in Table 4.7.

Table 4-7. Medial/Lateral TTS based on Mx (msec SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 1789 343 1640 203 1582 419 1670 529
Control 1579 290 1641 425 1506 377 1575 564
Total 1680 329 16401 331 1542 392


Anterior/Posterior Ground Reaction Moment (My)

Analysis of TTS based on My revealed no significant main effects for time (F2, 54

= 0.22, P = 0.806) or group (F 1, 27 = 2.86, P = 0.102). Additionally, no significant

differences were detected for the time x group interaction (F2, 54 = 0.72, P = 0.492). Data

appear in Table 4.8.

Table 4-8. Anterior/Posterior TTS based on My (msec SD)

Group Pretest Post 48h Post 96h Total
Group
DOMS 1606 288 1618 334 1657 346 1627 538
Control 1599 268 1494 319 1453 315 1516 558
Total 1603 273 1554 327 1552 341














CHAPTER 5
DISCUSSION AND CONCLUSIONS

Discussion

Neuromuscular control testing continues to be a thoroughly studied topic among

researchers in the sports medicine field. The majority of research in this area has focused

on the dynamic measurement of joint stability and postural control. Current research uses

the TTS measure defined in the present study. The most recent research has investigated

whether ground reaction forces differ between a static single limb stance and a dynamic

single limb stance. Results indicate that greater GRFs exist in the A/P and M/L planes

for dynamic single limb stance compared to static single limb stance. It was concluded

that the static measure might be a better indicator of stable posture.49

Shultz and colleagues continue to incorporate the use of the LEPD in the

examination of hamstring muscle activation. In fact, she is currently investigating how

the menstrual cycle of healthy females affects latent muscle reaction times of the lower

extremity. Bell et al.50 have investigated the effects of trunk position on muscle reaction

times of the lower extremity using the LEPD. They concluded that trunk position does

not affect muscle reflex onset based on where center of pressure is in relation to the foot,

but that reflex amplitude is affected.

Several quantitative physiological markers of DOMS have been used to confirm the

presence of this condition. Although these physiological measures were not used in this

study, successful completion of the work hinged on the ability to effectively induce









DOMS. Alternatively, subjective (PROMPT and PPT) and objective (AROM) outcome

measures associated with DOMS were utilized.

The purpose of this investigation was to determine if hamstring DOMS had any

deleterious effects on functional joint stability at the knee. More specifically, it was

hypothesized that measures of DOMS would be significantly changed after the exercise

protocol for the experimental group. It was further hypothesized that subjects in the

experimental group would present with significantly slower reaction times in relation to

both latent muscle response times of the hamstrings and TTS following a jump landing

procedure.

DOMS Measurements

Based on the results presented, I am confident that DOMS was adequately induced.

Certain markers that were discussed in Chapter 2, such as range of motion and perceived

pain, were significantly different after the exercise protocol. Active range of motion in

the experimental group showed the greatest decrease approximately 48h after the exercise

session (Figure 5.1). Subjects began to regain motion at 96h post exercise, but were still

not fully recovered from the muscle tightness. Peak levels of perceived pain were noted

at 48 96h post exercise for the PROMPT measure (Figure 5.2). Similar results were

observed with the PPT measures, noting that levels of perceived pain peaked at 48 96h

post exercise (Figure 5.3). All measures are similar to previous literature related to the

time course and intensity of DOMS.31 32 34 51 Typically, symptoms are noticed

approximately 8 24h after exercise, with symptoms reported peaking at 48 72h.

Symptoms begin to diminish after this time and will subside within 5 7 days.

Previous research has used other means of determining DOMS









markers,32, 34, 35- 37, 51, 52,53 however, our markers were deemed more relevant with respect

to this study. This may create limitations when assessing the level of DOMS that was

induced when making comparisons to previous research. For this study, only three

measures associated with assessment of DOMS markers were used, however these

measures were all confirmed to have significant changes. Other measures such as

muscular strength, plasma creatine kinase levels, and muscular swelling were not

included. We chose to use the AROM, PROMPT, and PPT as the measures of DOMS

inducement due to their ease of measurement as well as to eliminate any invasive

measures such as with the CK tests. No correlation analyses have been performed

specifically to determine whether differences exist among the multiple DOMS markers.

All the procedures are independently considered valid and reliable measures to assess

DOMS.36, 38, 39, 51

Muscle Latency

When assessing joint stability with EMG, multiple models have been

used8, 24, 25, 44, 54- 57 A review of the relevant research revealed no data published to assess

temporal patterns of a dynamic protocol. To avoid learning effects in previous studies,

researchers allowed multiple practice trials before the actual recording of the data. This

was also done in the present study, but because of the number of test trials over time, it

seems that there may be a greater training effect associated with the LEPD. Following

two sessions, pretest and posttest 48h, it appears that subjects may have begun to develop

a learning pattern relative to the perturbation. This was evidenced by their reduced

latency times. Although only significantly different during the EROT perturbation, there

was a similar trend observed with the IROT perturbation. It is difficult to explain this

faster response time. Measurements from pretest to both posttests were performed









identically. Subjects may have become accustomed to the device and learned to

anticipate the rotational perturbation, which would allow them to respond sooner. On the

other hand, when the subjects were leaning forward, they may have been required to

utilize predominantly their quadriceps to maintain stability in the upright posture.

Therefore, when the perturbation was initiated, some level of reciprocal inhibition of the

hamstrings may have existed, causing them to be recruited far slower than in previous

studies.

Previous research assessed muscle latency in the hamstrings using both weight-

bearing15, 24 26'44,46,47 and non weight-bearing perturbations.54 The assessment of non

weight-bearing perturbations cannot be directly related to this research because the

proprioceptive feedback is more likely to come from joint receptors being stimulated as

opposed to the muscle spindles that would be activated with a weight-bearing task.

When non-weight bearing, the muscles are not loaded and would require a larger amount

of joint movement to stimulate the muscle spindle. The more obvious receptors that

would be activated during this type of perturbation would be the receptors located in the

joint as well as the capsule and ligaments.54 Weight-bearing perturbations require

somewhat of a preactivation of the muscle, which allows the muscle spindles to respond

to changes in muscle length earlier than other receptors.

Shultz et al.44 described the same activation patterns of the medial and lateral

hamstrings in response to both IROT and EROT as were seen in the present study. It was

noted that the medial hamstrings respond faster to both perturbations. This makes sense

for EROT, because the afferent response from the muscle spindle would cause a reflex

contraction of the medial hamstring to prevent the trunk and femur from further









externally rotating. For the muscles to respond to the IROT perturbation similarly is not

as easily understandable when the same muscle spindle theory is applied. In this

instance, the lateral hamstring should respond quicker due to the stretch reflex associated

with that muscle. Shultz et al.44 stated that the possibility for this faster response from the

medial hamstrings could be due to the innervation of the muscle. The semitendinosus

and semimembranosus are supplied by the tibial nerve, whereas the biceps femoris is

supplied by both the tibial (long head) and common peroneal (short head) nerves.21

Based on this reasoning, a second theory was identified. Therefore, this theory implies

that if the tibial nerve and common peroneal nerve are not stimulated by the perturbation,

or that the recording area of the biceps femoris was over the peroneal nerve, differing

times could be recorded. The researchers further identified factors in their study to

support this theory. When the medial hamstrings were compared to the medial and

lateral gastrocnemius muscles, which are all innervated by the tibial nerve, there were no

significant differences.44

Although the results of Shultz et al.44 are consistent with our findings based on the

firing patterns of the hamstrings, we noticed a much longer latency when compared to

their findings. A long latency response time for the medial hamstring ranged from 58 -

60 msec and 70 77 msec for the lateral hamstring. Our results ranged from

approximately 86 92 msec for medial hamstring and 94 99 msec for the lateral

hamstrings. It is difficult to make a direct assessment relative to other research because

the methods of this study are not entirely the same as others. Shultz et al.44 used a similar

perturbation device that required their subjects to maintain their center of mass over the

midfoot. In this investigation, subjects were asked to lean into the cables using load cells









as the standardization protocol. Although the subjects' position was consistent across the

trials, center of mass location could not be assessed. A possible flaw with this setup is

that it does not mimic the typical injury model for most ligament injuries in sports. Most

frequently a deceleration or sudden change of direction results in ligament damage. With

a deceleration or change of direction, the athletes center of mass should remain within or

posterior to the base of support. Upon further assessment of this model, it would appear

that the center of mass of the subject would lie outside the base of support. Bell et al.50

concluded no change in hamstring response time relative to where the center of pressure

lies, whether it is over the heel, midfoot, or toes. Their study, however, could not assess

the possibility of the subjects' center of mass falling outside that base of support.

Subjects may have also been able to incorporate the use of their hips to become more

adept at responding to the perturbations. Because the hip is a triaxial joint, able to move

in all three of the cardinal planes, there is the possibility that the subjects were responding

to the perturbation by utilizing their ability to rotate the pelvic girdle relative to the femur

and limit the internal and external rotation at the knee joint.

Time to Stabilization

Static and dynamic procedures have been utilized to investigate stability of the

lower extremity. Various static measurements for the lower extremity have been used in

previous research. These static measures either incorporate the use of a single leg

balance test,8 58 center of pressure velocity (COPV),59, 60 or postural sway.61 To date,

very few studies have used a functional task to assess joint stability. Colby et al.42 and

Ross et al.43 have attempted to study stability of the lower extremity using a functional

task. A potential limitation with these studies is that they only made comparisons

between injured populations to uninjured populations. No research has been performed









to validate whether a jump landing is different in healthy subjects with an intervention

protocol or whether there is a change in results over time. Colby et al.42 concluded that

subjects with ACL reconstructed knees showed significantly slower stabilization times

based on the vertical force component compared to healthy subjects during a step down

maneuver. Our results also noted differences in the vertical component, however these

results showed faster stabilization times over multiple sessions while performing a jump

landing technique. Figure 5.1 indicates that a learning effect may have taken place based

on the Fz for the TTS measure. Subjects appeared to improve their ability to "stick" the

landing after two sessions. This may have occurred because the subjects were more

familiar with the task after multiple trials during multiple sessions. The jump landing

task takes a great deal of coordination to complete successfully. Subjects were asked to

focus on three main criteria in order for the jump landing to be considered successful

(reach 50% of their max vertical jump height, cover a distance of 70cm, and land in the

center of the force plate on one foot). Subjects who could not focus on all three criteria

simultaneously seemed to be unable to complete the task consistently. This inconsistency

was evident in the fact that, although all subjects completed the trials successfully, there

was variability among subjects based on the number of total trials attempted to complete

three successfully. It appears that subjects need to be adequately familiarized with the

jump landing procedure in order to remain consistent over time.

It is difficult to compare the results of the present study with those of previous

research. Different methods were used to assess TTS and different subject populations

were used. Collection frequency could be a limitation of previous research as well. The

current investigation used a sampling frequency of 2000Hz to collect data, while other









researchers have been collecting at much lower sampling rates, some as low as 180Hz for

the TTS procedure.62 In previous studies using the jump landing procedure with low

sampling frequencies, researchers would have included fewer data points in the analysis,

which could have resulted in altered outcomes. Based on the results of this procedure, it

is likely that DOMS has little or no effect on a subject's ability to stabilize after a

functional task, such as a jump landing maneuver. Because of the dynamic nature of the

task, subjects would have to incorporate the use of not only the hamstring muscles, but

would also need to rely on the entire kinetic chain of the lower extremity to stabilize

themselves. It would appear that function of the lower extremity as a whole to control

dynamic posture is too great to be significantly affected by limiting one muscle group.

Conclusions

The exercise procedure conducted to induce DOMS can be considered a valid

protocol for this type of research. Subjects presented with marked changes across time

for each measure. The change in the associated markers is consistent with past literature.

The results of the present study suggest that functional joint stability, as measured by the

combination of hamstring muscle latency and TTS after a jump landing, is not affected

by DOMS. When subjects return to activity while affected by DOMS, the physiological

and physical markers of muscle damage are still present. It is difficult to speculate why

no effect is present. Apparently these markers are not influential enough to change the

performance of the affected muscles. The protective effect the hamstrings provide at the

knee joint to assist with dynamic stability does not appear to be influenced by DOMS.

Suggestions for Future Research

Future research should continue to build upon the present work as well as previous

literature utilizing the jump landing procedure. An area that needs to be addressed is the









reliability of testing subjects over multiple days to determine if a learning response exists.

Additionally, the development of a standardized TTS protocol to establish baseline

criteria for functional task procedures is also necessary. The task suggested here is an

effective model, but something more appropriate would be to develop criteria to

standardize both jump height and jump distance. The incorporation of a standardized

jump distance based on a percentage of the standing broad jump for each subject would

produce a consistent trajectory from take off to landing. This would create a reliable

pattern among subjects that to date has not been identified.

Utilizing a functional task to determine if hamstring DOMS affected knee joint

stability was the goal of this research. Further research should examine the effects of

hamstring DOMS on other aspects of proprioception. Some areas that should be

investigated include active and passive joint repositioning in addition to threshold to

detection of passive movement. Because the hamstrings play a major role in joint

movement at both the hip and knee, it would seem sensible to study each independently.










100

80

60

40

20-

0


Pretest Posttest 48h*

Group (day)

Figure 5-1. Active hamstring range of motion


Posttest 96h*t


100

80

60

40

20

0


Pretest Posttest 48h*
Group (day)

Figure 5-2. Passive range of motion pain threshold


Posttest 96h*


* DOMS
O Control





















IDOMS
O Control











100
90
80
S70-
6 DOMS
S50 -
40 O Control
30
20
10 -
0
Pretest Posttest 48h* Posttest 96h*

Group (day)


Figure 5-3. Pressure pain threshold














APPENDIX A
LETTER OF INFORMED CONSENT

Informed Consent Agreement
Project Title: The effects of hamstring delayed onset muscle soreness on functional knee
joint stability.

Investigators: Kyle A Smink, ATC, Graduate Student, Department of Exercise and Sport
Sciences & Michael E. Powers, PhD., ATC, CSCS, Assisstant Professor, Department of
Exercise and Sport Sciences.

Purpose of the study:
The purpose of this study is to determine if the occurrence of delayed onset muscle
soreness in the hamstring group can affect functional knee joint stability. Delayed onset
muscle soreness is a physiological response that occurs when individuals take part in
unaccustomed bouts of rigorous exercise and is typically noticed 24 48 hours after the
initial activity.

At this time, no study has been published investigating the occurrence of delayed onset
muscle soreness and its effects on functional joint stability. We are performing this
research in order to help gain knowledge and further understand this subject as it relates
to the sports medicine field.


Please read this consent carefully before you decide to participate in this study.


What will you do in this study?
You will be excluded from participating in this study if you have had any leg
injuries, either muscular or ligament, that required a doctor visit within the past six
months. You will also be excluded from this study if you have taken part in any rigorous
weight training for your leg muscles in the past six months.
Upon arrival to the Athletic Training/Sports Medicine Research Lab (FLG 105D),
you will be asked to complete a medical history questionnaire to determine if you are
eligible to participate in this study. If eligible, we will measure your hamstring (muscles
in the back of your thigh) flexibility, pressure-pain threshold, and passive (relaxed) range
of motion pain threshold. We will ask you to lie on your back with your non-dominant
(the leg you would not kick a ball with) leg flexed at the hip. The opposite leg will
remain flat on the table. A specially designed device made of PVC pipe will be used to
make sure your hip remains at this angle through the entire measurement. You will then
be asked to straighten your knee as far as possible. As you do this we will measure how
far in degrees you can straighten your knee. While remaining is this position, an









examiner will stretch your hamstring muscles (by straightening your knee) to the
maximum range of motion. You will be asked to make a pencil mark on a visual analog
pain scale representing the amount of pain you feel during the stretch. This scale consists
of a 10-centimeter line with the left end representing no pain at all and the right end
representing the most unbearable pain imaginable. After you make the pencil mark, your
hamstrings will be stretched again. This time, pressure will be applied to the hamstring
muscles using an algometer (a device about the size of a pencil with a rubber tip used to
apply a standard amount of pressure). You will again be asked to make a pencil mark in
a visual analogue scale representing the amount of pain you feel while the pressure is
applied.
Following the baseline measures for hamstring flexibility and pain threshold, you
will be measured for muscle latency and time to stabilization. First, small areas of your
skin will be shaven and cleaned with isopropyl alcohol. Self-adhesive surface electrodes
will then be placed on the skin overlying the medial and lateral hamstrings (rear thigh),
medial and lateral quadriceps (front thigh), and medial and lateral gastrocnemius (calf)
muscles. These electrodes will detect electrical impulses of the muscle, however, you
will not feel these impulses and no electrical current will enter the body. A device called
a goniometer (a device that measures joint angles) will be placed over the outside of your
knee to assess how far your knee is bent. You will then be asked to perform the knee
perturbation and time to stabilization measures in a random order determined by a
random numbers chart.
For the knee perturbation, you will be fitted with a harness applied snugly around
your waist. Two cables connected to two separate release mechanisms affixed to a wall
will be attached to the harness. You will be asked to stand on a force plate and assume a
single leg stance on the test leg. You will then be asked to lean forward so that your knee
is flexed to approximately 30 and your weight is supported by the cables attached to the
wall. You will be able to view a computer screen, which will allow you to monitor the
position of your weight. You will be wearing headphones to avoid hearing sounds that
may allow anticipation reflexes to occur. At random times one of the two cables will be
released. This will cause your hips and upper body to move forward and rotate causing
the knee to naturally rotate and flex. Three trials of each cable release (left and right
side) will be performed so you may become accustomed with the device. Immediately
following, ten random perturbations (5 left and 5 right) will be performed while allowing
a 30 second rest time between trials. When all 10 trials are successfully completed, we
will perform the same procedures for the opposite leg.
For the time to stabilization measurement, your maximum vertical leap (how high
you can jump) will be determined. To do this, we will first measure how high you can
reach while standing on your toes. You will then be asked to jump as high as possible
and touch markers supported on a stand. Based on the number of markers you touch, the
height of your jump is determined. We will have you repeat this two more times to
ensure that we get an accurate measure. We will then measure how long it takes you to
balance after jumping onto a platform. You will be asked to jump so that you reach a
height equivalent to half of your maximum jump height and land on a platform about 27"
away. We will ask that you land on the test leg only and balance yourself while your
hands remain on your hips for a period of 5 seconds. After the 5-second period you will
be asked to return to the starting position and repeat the measurement. This will be done









two more times for a total of three trials for each leg.
Following the baseline measures of muscle latency and time to stabilization, you
will perform 6 sets of 10 negative (muscle lengthens while it contracts, otherwise known
as a eccentric) contractions of the hamstrings using a leg curl machine. First, we will
determine your 1 repetition maximum strength, which will be used as your exercise
intensity. When the three sets are completed the session will be over.
You will be asked to return for reevaluation of time to stabilization and muscle
latency 48 and 96 hours after the initial testing date. Upon return, you will have your
hamstring flexibility and pain threshold reevaluated which will be used to assess the level
of DOMS achieved. All evaluation procedures will be performed identical to the pretest
trials, However no resistance exercise (leg curls) will be performed.


Time required:
Three sessions requiring approximately 90 minutes each.


Risks:
Discomfort and soreness in the hamstring muscles will be experienced following the bout
of eccentric exercise. You may also experience some discomfort with the pressure
threshold measure, but this discomfort will only last a few seconds while the measure is
being taken. As with any type of resistance exercise, there is a slight risk of
musculoskeletal injury. A certified athletic trainer will be present to evaluate and treat
any such injuries that may occur. If you are still suffering from soreness in the hamstring
muscles after the 96-hour posttest measure, the certified athletic trainer will instruct you
on ways to decrease the soreness. No stretching may take place prior to this time.


Benefits/Compensation:
There are no direct benefits to you for participating.


Confidentiality:
Data will be kept confidential to the extent provided by the law. Your information will
be assigned a code number. The list connecting your name to this number will be kept in
a locked file. When the study is completed and the data have been analyzed, the list will
be destroyed. Your name will not be used in any report.


Voluntary Participation:
Your participation is completely voluntary. There is no penalty for not participating.


Right to withdraw from the study:
You have the right to withdraw from the study at anytime without penalty.










Who to contact if you have questions about the study:


Kyle A Smink, BS, ATC
University of Florida
Graduate Assistant Athletic Trainer
Department of Exercise and Sport Sciences
2700 SW Archer Road, Apt. A-22
Gainesville, FL 32608
Home#: 373-9250
Cellular#: (352) 281-3534
E-mail: ksminkl@ufl.edu


Mike Powers, Ph.D., ATC, CSCS
University of Florida
Director of Athletic Training Education
Assistant Professor
Department of Exercise and Sport Sciences
148 Florida Gym
PO Box 118205
Gainesville, FL 32611-8205
(352) 392-0584, ext. 1332


Fax: (352) 392-5262
E-mail: mpowers@hhp.ufl.edu


Who to contact about your rights in the study:
UFIRB Office
Box 112250, University of Florida
Gainesville FL 32611-2250
(352) 392-0433.


Agreement:
I have read the procedure described above. I voluntarily agree to participate in the
procedure and I have received a copy of this description.


Participant:


Date:


Principal Investigator:


Date:















APPENDIX B
INCLUSION QUESTIONNAIRE

History questionnaire

Subject #:



1. Have you visited a physician for any knee injuries in the past 6 months?


YES


2. Have you had any "giving way" episodes with your knee in the past 6 months?


YES


NO


3. Have you had any "locking" or "clicking" episodes with your knee in the past 6
months?


YES


4. Have you had any knee pain walking up or down stairs in the past 6 months?


YES


5. Have you visited a physician for any hamstring muscle injuries in the past six
months?


YES


6. Have you participated in any strenuous lower extremity weight training within the
past six months?


YES















APPENDIX C
DECRIPTIVE INFORMATION AND HAMSTRING FLEXIBILITY

Descriptive Information


Subject #:
Gender:
Age:
Height:
Weight:
Standing max reach:

Vertical jump height:

Hamstring Flexibility
Pretest: Right Left

Trial 1:

Trial 2:

Trial 3:

Post-test 48h: Right Left

Trial 1:

Trial 2:

Trial 3:

Post-test 96h: Right Left

Trial 1:

Trial 2:

Trial 3:















APPENDIX D
VISUAL ANALOGUE PAIN SCALE


Pre / Post


Date:


Session #


Unbearable Pain


Unbearable Pain


Subject #


Range of Motion


No Pain


Pressure



Medial Hamstring


No Pain
















APPENDIX E
RAW DATA


Table E-1. Subject demographic raw data


Subject
ks001
ks002
ks003
ks004
ks005
ks006
ks007
ks008
ks009
ks010
ks011
ks012
ks013
ks014
ks015
ks016
ks017
ks018
ks019
ks020
ks021
ks022
ks023
ks024
ks025
ks026
ks027
ks028
ks029
ks030


Age (y)
22
21
23
21
22
21
20
21
21
23
22
24
23
21
20
27
24
21
20
22
22
22
20
20
21
22
22
22
22
21


Height (cm)


Mass (kg)
60.0
60.0
64.0
60.0
76.0
55.0
57.0
71.0
63.5
67.5
70.0
76.5
63.5
68.5
57.5
65.5
77.0
84.5
74.0
59.5
62.0
74.0
59.0
47.5
84.5
85.0
83.0
68.5
70.5
59.0











Table E-2. Active range of motion (AROM) raw data (degrees)


Subject
ks001
ks003
ks005
ks006
ks008
ks009
ks011
ks017
ks018
ks019
ks002
ks004
ks007
ks010
ks012
ks013
ks014
ks015
ks016
ks020


Pretest

78
62
67
68
85
86
70
82
62
43
78
80
85
90
80
73
78
66
61
76


Post-test 48h

65
24
48
28
53
72
70
85
23
19
83
84
84
90
71
73
76
64
64
82


Post-test 96h

71
33
67
48
75
67
63
77
27
30
80
85
87
90
78
72
78
64
52
84


Group
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control











Table E-3. Passive range of motion pain threshold (PROMPT) raw data (PQ = 0 100)


Subject
ks001
ks003
ks005
ks006
ks008
ks009
ks011
ks017
ks018
ks019
ks022
ks024
ks026
ks027
ks028
ks002
ks004
ks007
ks010
ks012
ks013
ks014
ks015
ks016
ks020
ks021
ks023
ks025
ks029
ks030


Pretest

72.5
5
7
10
0
36
32
0
2
0
4
16.5
22
21.5
43
0
39
0
49
0
14.5
54
7
40.5
15
52
7
2
8
2


Post-test 48h

61
22
23
55.5
64.5
73.5
54
8
83.5
14.5
84
45
27
7
76.5
0
48
0
49
0
12.5
47
9
40
12
74.5
1
1
9.5
7


Post-test 96h

77
16.5
6
68
42
98.5
62
59.5
71
0
60.5
32
20.5
28
65
0
52
0
57
0
15.5
63
8.5
18
11
65
0
1.5
3
2


Group
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control











Table E-4. Pressure pain threshold (PPT) raw data (PQ = 0 100)


Subject
ks001
ks003
ks005
ks006
ks008
ks009
ks011
ks017
ks018
ks019
ks022
ks024
ks026
ks027
ks028
ks002
ks004
ks007
ks010
ks012
ks013
ks014
ks015
ks016
ks020
ks021
ks023
ks025
ks029
ks030


Pretest

58
39
37
37
64.5
47
43
22
43
0
64
46.5
70
34
53.5
5
54
63.5
46.5
13.5
61
88
11
74
0
63
22.5
62.5
56
63


Post-test 48h

64
53
36
74.5
79
92.5
71
41
100
21.5
43
72
82
53.5
63.5
6
61
38
59
4
72
85
14
66.5
12
59
8.5
62.5
77.5
50


Post-test 96h

55.5
43
18.5
73
85
100
56.5
68.5
82
13.5
53
62
75.5
32.5
59
0
67
47
56
22
75
90
13.5
70
10.5
77
5
63
70.5
47.5


Group
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control











Table E-5. IROT hamstring muscle latency raw data (msec)


Subject

ks001
ks003
ks005
ks006
ks008
ks009
ks011
ks017
ks018
ks019
ks002
ks004
ks007
ks010
ks012
ks013
ks014
ks015
ks016
ks020


Post48
Pre MH
MH
91 30
90 62
135 94
76 82
92 86
99 85
60 60
107 87
138 96
89 38
101 77
123 99
124 69
98 98
123 88
108 128
97 90
83 144
117 110
87 87


Post 48
Pre LH o
LH
139 30


Post 96
MH
87
30
95
64
91
88
70
119
84
82
65
58
96
90
101
87
105
102
180
80


Post 96
LH
95
30
65
33
80
88
72
78
66
37
38
62
44
133
109
73
109
73
107
125


Group

DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control











Table E-6. EROT hamstring muscle latency raw data (msec)


Subject

ks001
ks003
ks005
ks006
ks008
ks009
ks011
ks017
ks018
ks019
ks002
ks004
ks007
ks010
ks012
ks013
ks014
ks015
ks016
ks020


Post48
Pre MH
MH
93 30
102 72
127 99
70 77
73 94
90 92
97 46
110 101
116 99
161 103
77 35
76 76
60 68
114 95
104 116
84 94
76 100
59 35
114 97
86 127


Post 96
MH
65
70
64
78
58
93
77
123
81
79
46
77
55
100
103
87
99
59
123
88


Post 48
Pre LH o
LH
124 30
81 64
133 77
84 82
116 101
128 98
91 87
148 102
93 93
147 60
103 89
73 74
188 144
95 58
109 111
161 131
113 108
34 41
138 107
111 95


Post 96
LH
99
66
77
60
113
106
88
100
37
115
90
76
96
88
100
124
132
95
110
120


Group

DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
DOMS
Control
Control
Control
Control
Control
Control
Control
Control
Control
Control











Table E-7. Time to stabilization based on vertical ground reaction force (Fz) raw data
(msec)
Subject Pretest Post48 Post96 Group
ks03 2175 1908 1295 DOMS
ks05 2645 1714 1848 DOMS
ks06 1979 2622 1674 DOMS
ks08 1158 1342 1426 DOMS
ks09 2290 2120 1640 DOMS
ks11 1839 2550 2322 DOMS
ks17 1847 2631 2130 DOMS
ks18 2155 2587 1943 DOMS
ks19 1184 1024 847 DOMS
ks22 2128 1355 968 DOMS
ks24 1897 1699 1422 DOMS
ks26 2059 2571 1990 DOMS
ks27 1696 1638 2161 DOMS
ks28 1617 997 2070 DOMS
ks02 1085 2633 2322 Control
ks04 2717 1372 2206 Control
ks07 2187 1206 979 Control
ks10 2359 1500 1203 Control
ks12 953 1636 2004 Control
ks13 1125 1732 809 Control
ks14 838 1098 544 Control
ks15 1721 1599 1054 Control
ks16 2169 2833 839 Control
ks20 2135 2723 1461 Control
ks21 1645 1023 912 Control
ks23 2543 1960 1182 Control
ks25 2387 2387 2536 Control
ks29 2112 1827 1441 Control
ks30 1539 1053 704 Control











Table E-8. Time to stabilization based on medial/lateral ground reaction force (Mx) raw
data (msec)

Subject Pretest Post48 Post96 Group
ks03 1373 1541 1771 DOMS
ks05 2016 1667 2139 DOMS
ks06 1966 1973 1747 DOMS
ks08 1484 1689 1435 DOMS
ks09 1868 1795 2387 DOMS
ks11 1575 1299 1246 DOMS
ks17 1996 1216 968 DOMS
ks18 2214 1711 1466 DOMS
ks19 1851 1609 1444 DOMS
ks22 2125 1620 2166 DOMS
ks24 2218 1611 1179 DOMS
ks26 1851 1910 1586 DOMS
ks27 1141 1726 1132 DOMS
ks28 1366 1600 1470 DOMS
ks02 1869 1616 1320 Control
ks04 1318 2043 1727 Control
ks07 1516 964 898 Control
ks10 1561 1256 1240 Control
ks12 1511 1323 2107 Control
ks13 1099 1672 1658 Control
ks14 1469 1198 1387 Control
ks15 1801 2279 1540 Control
ks16 1834 2375 1552 Control
ks20 1404 1157 1724 Control
ks21 2134 1573 859 Control
ks23 1513 1928 1419 Control
ks25 1875 1606 1652 Control
ks29 1675 2074 2222 Control
ks30 1111 1555 1283 Control











Table E-9. Time to stabilization based on anterior/posterior ground reaction force (My)
raw data (msec)

Subject Pretest Post48 Post96 Group
ks03 1891 1232 1513 DOMS
ks05 1108 1113 1900 DOMS
ks06 1945 1733 1348 DOMS
ks08 1768 1379 1932 DOMS
ks09 1641 1875 1787 DOMS
ks11 1662 1483 1498 DOMS
ks17 1465 1017 1453 DOMS
ks18 1669 1820 1289 DOMS
ks19 1541 2012 2057 DOMS
ks22 2103 1856 1634 DOMS
ks24 1288 1705 1798 DOMS
ks26 1324 1811 1533 DOMS
ks27 1277 2090 1067 DOMS
ks28 1807 1530 2393 DOMS
ks02 1633 1640 1129 Control
ks04 1622 1624 1404 Control
ks07 1442 812 1370 Control
ks10 1783 1142 1894 Control
ks12 1805 1296 1257 Control
ks13 1920 1671 1479 Control
ks14 1390 1139 1347 Control
ks15 2025 1498 1254 Control
ks16 1329 1324 1572 Control
ks20 1246 1478 863 Control
ks21 1251 1852 1629 Control
ks23 1799 1792 1319 Control
ks25 1571 1982 1319 Control
ks29 1258 1811 1941 Control
ks30 1914 1351 2021 Control















APPENDIX F
ANOVA SUMMARY TABLES


Table F-1. Active range of motion (ANOVA)
Source SS DF MS F Significance
Group 7902.346 1 7902.346 11.222 0.002
Error 19717.827 28 704.208

Time 1823.262 2 911.631 19.082 0.000
Time x Group 1909.306 2 954.653 19.983 0.000
Error 2675.358 56 47.774






Table F-2. Passive range of motion pain threshold (ANOVA)
Source SS DF MS F Significance
Group 6760.000 1 6760.000 4.583 0.041
Error 41303.433 28 1475.123

Time 4396.317 2 2198.158 11.967 0.000
Time x Group 3885.817 2 1942.908 10.577 0.000
Error 10286.533 56 183.688






Table F-3. Pressure pain threshold (ANOVA)
Source SS DF MS F Significance
Group 1867.778 1 1867.778 1.095 0.304
Error 47775.278 28 1706.260

Time 1569.672 2 784.836 7.228 0.002
Time x Group 1501.206 2 750.603 6.913 0.002
Error 6080.456 56 108.580











Table F-4. Internal rotation hamstring muscle latency (ANOVA)


Source
Group
Error


Time
Time x Group
Error (Time)

Muscle
Muscle x
Group
Error (Muscle)

Time x Muscle
Time x Muscle
x Group
Error (Time x
Muscle)


SS
4039.120
36093.463

11917.994
1552.550
77537.708

88.714
847.063

37341.163

3244.221
5682.575

56859.445


MS
4039.120
2005.192

5958.997
761.275
2153.825

88.714
847.063

2074.509

1622.111
2841.288

1579.429


F
2.014


2.767
0.353


0.043
0.408


1.027
1.799


Significance
0.173


0.076
0.705


0.838
0.531


0.368
0.180


Table F-5. External rotation hamstring muscle latency (ANOVA)


Source
Group
Error


Time
Time x Group
Error (Time)

Muscle
Muscle x
Group
Error (Muscle)

Time x Muscle
Time x Muscle
x Group
Error (Time x
Muscle)


SS
355.782
33749.259

82299.626
2918.814
17222.554

4666.586
1507.157
16905.978

1019.349
31.005

10007.553


MS
355.782
1874.959

4114.83
1459.407
478.404

4666.586
1507.157

939.221

509.675
15.503


F
0.190


8.601
3.051


4.969
1.605


1.833
0.056


Significance
0.668


0.001
0.060


0.039
0.221


0.174
0.946


36 277.988











Table F-6. Fz (ANOVA)
Source SS DF MS F Significance
Group 754142.407 1 754142.407 1.442 0.240
Error 14118967.75 27 522924.731

Time 2174292.874 2 1087146.437 5.044 0.010
Time x Group 305274.461 2 152637.231 0.708 0.497
Error 11638461.88 54 215527.072


Table F-7. Mx (ANOVA)
Source SS DF MS F Significance
Group 194639.022 1 194639.022 1.143 0.294
Error 4597459.284 27 170276.270

Time 300364.828 2 150182.414 1.491 0.234
Time x Group 164279.966 2 82139.983 0.816 0.448
Error 5437986.165 54 100703.447


Table F-8. My (ANOVA)
Source SS DF MS F Significance
Group 270936.707 1 270936.707 2.858 0.102
Error 2559315.561 27 94789.465

Time 42795.786 2 21397.893 .216 0.806
Time x Group 142122.692 2 71061.346 0.718 0.492
Error 5345552.934 54 98991.721















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BIOGRAPHICAL SKETCH

I was born on June 11, 1975, to David James and Eve Ann Smink (Rodman) in

Shamokin, PA. Shamokin is a small coal-mining town in east central Pennsylvania. This

is where I spent my entire youth growing up with my older brother Keith. When I was in

fourth grade, I experienced the first tragedy of my young life. My father was taken from

us in an automobile accident. This was a difficult time in our lives, but we had friends

and family to help us through.

My mother has worked hard throughout her life to provide for us and I love her

immensely for that. She has been the most supportive person in my life, sacrificing

herself to ensure I would not falter on my own. She has taught me much about respect,

honesty, and the importance of family. While growing up a stubborn young boy, I did

not always adhere to her sound advice, ignorant to the fact she had many similar life

experiences to draw from. It was not until she met my stepfather that I truly began to

understand what it would take to become a man. He has taught me many life lessons,

such as hard work, dedication, and patience. Without this man, I truly do not think I

would be where I am today.

My education began in the Shamokin area public school system where I graduated

from high school in 1993. Since I had not chosen a career goal, I chose to work for a

year before attending college. It was during this time that I had an accident while playing

basketball that changed my life forever. During the summer of 1993, I tore the anterior

cruciate ligament in my left knee, which required surgery to repair. Following the









surgery and rehabilitation process, I realized that my career goal was to become a

physical therapist so I could help others who were in similar situations. The next two and

a half years, I attended the University of Pittsburgh at Bradford studying sports medicine.

It was at that point that I realized I no longer had the desire to work in a physical therapy

clinic and that I wanted to work as an athletic trainer. I immediately began researching

schools in the area with accredited undergraduate programs and came across Lock Haven

University. Upon being accepted, I then applied for acceptance into the athletic training

education program, which I was denied after my first year. Unaffected, I continued to

work hard and study. The following year I reapplied and was accepted to begin classes in

the curriculum. The next two years were an exciting time for me. I was assigned to work

with the university football, volleyball, and track & field teams as well as with a local

high school. While working closely with my program director, I once again had a change

of goals I needed to achieve. I wanted to learn more about the research process, but in

order to achieve this goal, I would need to continue my education towards a master's

degree.

I applied to several universities and was thrilled to accept an assistantship position

from the University of Florida. I began my graduate education in the fall of 2001.

During my first year, I was assigned to work with a local private school, Oak Hall. I

thoroughly enjoyed working there and met many wonderful people. The summer

between my first and second year in Gainesville is when I realized that I wanted to give

back to the students. I assisted teaching a lab section for the undergraduate students and

it was at that point I made a decision that I wanted to become an instructor in the athletic

training field. Throughout my second year, in which I worked at Gainesville High






72


School, I continued to teach numerous lab sessions in the AT department. Based on this

newfound desire to teach, I decided to apply to several universities in an attempt to

continue my education towards my PhD.

I am eager to graduate from UF so I may pursue my next aspiration. I will be

enrolling at the University of Delaware in the fall of 2003 in the Biomechanics and

Movement Science department pursuing my doctoral candidacy. My life has taken many

twists and turns over the years, but now I feel I am on track to attain my final goal.