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A COMPARISON OF DIFFERENT METHODS FOR IMPROVING HAMSTRING FLEXIBILITY by Kenric Lai A Thesis Submitted to the Faculty of The College of Education in Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, Florida December 2003 A COMPARISON OF DIFFERENT METHODS FOR IMPROVING HAMSTRING FLEXffiiLITY by Kenric Lai This thesis was prepared under the direction of the candidate's thesis advisor, Dr. Joseph A. O'Kroy, Department of Exercise Science and Health Promotion, and has been approved by the members of his supervisory committee. It was submitted to the faculty of the College of Education and was accepted in partial fulfillment of the requirements for the degree of Master of Science. SUPERVISORY COMMITTEE: cJziiL~ £)&-----~ f1,~~J Chairperson, Department of Exercise Science and Health Promotir to/Jy(oJ Date 1 ii 1 ABSTRACT Author: Kenric Lai Title: A Comparison of Different Methods for Improving Hamstring Flexibility Institution: Florida Atlantic University Thesis Advisor: Dr. Joseph A. O'Kroy Degree: Master of Science Year: 2003 Active-isolated (AI=ll) stretching was compared to static stretching (SS=8), proprioceptive neuromuscular facilitation stretching (PNF= 10), and a control group (C=9) at improving hamstring flexibility. Pre- and post-assessments of flexibility were performed with a goniometer on the right leg. All subjects performed a warm-up on an ergometer; after which, subjects in the stretching groups performed mode-specific stretching of both hamstrings 4 days per week for 4 weeks. A significant increase was found in flexibility after training for all stretching groups (p<0.05). However, there were no significant differences in flexibility between groups (ANOV A: p>0.05). It is possible the small number of subjects may have contributed to this finding. iii Table of Contents List of Tables .................................................................................................. v List of Figures ................................................................................................ vi CHAPTER 1 INTRODUCTION .......................................................................................... 1 CHAPTER2 REVIEW OF LITERATURE ......................................................................... 3 CHAPTER3 METHODOLOGY ........................................................................................ 13 Subjects ....................................................................................................... 13 Study paradigm .............................................................................................. 13 Data analysis ................................................................................................. 16 CHAPTER4 RESULTS ...................................................................................................... 17 CHAPTERS DISCUSSION ................................................................................................ 19 References ...................................................................................................... 30 iv List of Tables Table 1: Subject demographics ...................................................................... 23 v List of Figures Figure 1: Flexibility of the hamstrings before and after training .................. 24 Figure 2: Flexibility of the hamstrings before and after training ................... 25 Figure 3: AI subjects' initial flexibility versus changes in flexibility ........... 26 Figure 4: PNF subjects' initial flexibility versus changes in flexibility ........ 27 Figure 5: SS subjects' initial flexibility versus changes in flexibility ........... 28 Figure 6: C subjects' initial flexibility versus changes in flexibility ............. 29 CHAPTER! INTRODUCTION Flexibility is defined as a range of motion about a joint affected by bones, tendons, muscles, and ligaments (3, 12, 15, 16). Other factors may influence flexibility including age, gender, temperature, and type of activity performed (3). For reasons unknown, flexibility has not been researched as thoroughly as other fitness aspects, such as cardiovascular function and muscular strength even though flexibility is also a health-related factor of fitness. James Agre (1) was one of many researchers who have studied hamstring injuries. He concluded that a lack of flexibility, in addition to the lack of strength and warm-up, could lead to injuries. Many authors have agreed that injuries, such as muscle strains, and lack of flexibility were closely related (3, 5, 6, 14, 24, 28, 32). Regardless of the evidence illustrating the effectiveness of flexibility training, one group of researchers disagreed with the notion that pre-exercise stretching decreased injury risk (25). The flexibility/injury relationship is especially important for athletes who usually require a greater range of motion than the average person (1 0). Unlike athletes, however, naturally hyper-mobile individuals and pregnant females should not be allowed to stretch excessively due to their increased risk of injury (9). Hyper-mobile individuals can easily overstretch because of the natural laxity of their connective tissue. Pregnant females can also overstretch as an increase in the hormone called relaxant increases the laxity of their joints (9). Results of studies focusing on flexibility have been inconsistent, but the understanding of its importance has grown extensively (2, 3, 5, 6, 7, 8, 10, 19, 27, 29). Regardless of the strength of the muscular system and efficiency of the cardiovascular system, movement would not occur without flexibility. Flexibility can be improved and maintained by stretching. The main types of stretching include static (SS), ballistic, proprioceptive neuromuscular facilitation (PNF), and a more contemporary flexibility training called active-isolated stretching (AI). Ballistic stretching has fallen out of favor due to the associated high injury rate (5, 12, 30). SS, however, is easily taught and is relatively safe. PNF has also been found to be quite effective, but is more complex and requires more instruction. The AI stretching method, like PNF, includes muscle contraction, but tries to prevent the activation of the stretch reflex. This study hypothesized AI would be more effective than the other stretching methods in increasing the flexibility of the hamstrings. 2 CHAPTER2 REVIEW OF LITERATURE The understanding of the mechanics of flexibility is severely lacking. The literature regarding flexibility is sparse compared to cardiovascular research. Flexibility research also yields inconsistent results (2, 3, 5, 6, 7, 8, 10, 19, 27, 29). In addition, only several theories are related to flexibility. The theory of muscular relaxation and muscular elongation both attempt to explain how flexibility operates. Nevertheless, before exploring the theories of flexibility, it is necessary to understand the fundamental structures that are involved in flexibility. The basic muscle fiber is composed of myofibrils. Myofibrils, in turn, are composed of sarcomeres. A sarcomere can be described as a functional unit of a muscle. The sarcomere has a boundary called a Z-line at each end. Within the sarcomere lies the actin (thin filament) and the myosin (thick filament) (2). The actin and myosin are the focus of the two-filament model, which is used to explain muscle contraction and relaxation. The two-filament model has since given way to a three-filament model. The third filament, called titin, had generally been ignored until the early 1990's because its role in muscle function was unknown. Titin is now understood to attach the myosin filament to the actin filament (18). Together, the titin filaments, actin filaments, and!bridges make up the 1-band and contribute to the striated appearance of muscle. The 1band, also known as the isotropic band, appears as a lighter section of a sarcomere and is so named because light passes through at the same velocity in all directions. 3 Additionally, the A-band, also known as the anisotropic band, is a darker section of the sarcomere and is composed of the myosin and actin filament overlap. The A-band is so named because light does not pass through at the same velocity in all directions. The H-zone is at the center of the A-band and appears as a lighter portion ofthe sarcomere because it is found between the ends of the filaments. TheM-line is at the center of the H-zone and, due to the parallel arrangement ofM-bridges, is a darker portion of the sarcomere (2). As mentioned previously, titin connects the myosin to the actin. Although the existence oftitin has been suspected since the 1950's, it was not significantly incorporated into the two-filament model because the function oftitin was unclear (18). Currently, titin has two known functions, it produces resting tension for a muscle at its relaxed length, and titin may also aid in centering the myosin to the middle of the sarcomere (11 ). In addition, titin is flexible because it extends along with the sarcomere when stretched. Thus, extensibility is not the exclusive domain of the actin-myosin crossbridges. It has been proposed that, within a sarcomere, titin must be folded in some manner. When a stretch is initiated, the portion oftitin between the Z-line and the myosin unfolds and becomes a major contributor to the lengthening of a sarcomere (2). The muscle' s ability to stretch lies in its viscoelastic properties. Taylor et al. (30) explored the viscoelastic characteristics of the muscle-tendon unit. Since muscle behaves viscoelastically, it has both viscous and elastic properties. Viscous properties are described as having time and rate-changing characteristics. In other words, the relative amount of deformation is directly proportional to utilized forces. Elastic properties can be described as a change in length directly proportional to utilized forces. 4 by its own receptors. A muscle receives both excitatory and inhibitory impulses when stretched. If a stretch is held for a longer period of time, the inhibitory impulses sent from the GTOs eventually override the excitatory impulses causing relaxation. The muscle spindles cause the initial reactions of the stretch reflex, but the GTOs' impulses eventually dominate the weaker impulses sent by the muscle spindles. This protection mechanism may prevent injury from reflex contractions that are caused by excessive stretching (26). On the other hand, reciprocal inhibition occurs when a stretch of the agonist muscle causes the relaxation of the antagonist muscle. The antagonist muscles' motomeurons are inhibited by afferent signals when the agonist muscles' motomeurons receive excitatory signals (26). To clarify, autogenic inhibition and reciprocal inhibition constantly receive both excitatory and inhibitory signals from the afferent nerves. The ratio of the two types of signals determine whether motomeurons will be excited or inhibited (26). With knowledge of basic structures and functions of musculature, theories of flexibility can now be explored. Currently, several theories attempt to elucidate the function of flexibility. The theory of muscular relaxation states that muscles will relax when there are no longer any nerve impulses being received. Physically, the passive occurrence of relaxation is the restoration of the elastic components of muscle that returns the myofibrils to their initial lengths. However, chemical explanations of muscular relaxation are not completely understood. It is hypothesized that during relaxation, the calcium ions are returned to the sarcoplasmic reticulum as the calcium-troponin 7 Another concept pertaining to the flexibility properties of muscle-tendon units included stress relaxation. Stress relaxation, also known as autogenic inhibition, occurs when the force or stress declines in a viscoelastic substance that is stretched (30) and held, such as that which occurs during SS. Stress relaxation occurs with the aid of stretch receptors. Stretch receptors include muscle spindles and Golgi tendon organs (GTO). Muscle spindles are located in the tendons and muscles and are considered to be the primary stretch receptors. Muscle spindles are found in particularly high concentrations in muscles that require fine motor control. The two types of muscle spindles are intrafusal and extrafusal fibers. Intrafusal fibers are located within muscle fibers while extrafusal fibers are located along the outside of the muscle fibers. Intrafusal fibers can be further distinguished as nuclear bag and nuclear chain fibers. Nuclear bag fibers are located near the center of the intrafusal fibers and have many nuclei bundled together. Striated contractile filaments are located near the ends of the nuclear bag fibers. Nuclear chain fibers are shorter than nuclear bag fibers and only have one row of nuclei laid out in series. The ends of the nuclear chain fibers are also made of striated contractile filaments, and all fibers insert into both ends of the connective tissue (2). The innervation of muscle spindles is a complicated process. There are group Ia afferent, called primary endings, and group II afferent, called secondary endings. In this instance, afferent refers to the transduction of a signal from the spindles to the central nervous system. Group Ia fibers, sensitive to stretch and rate, are branched into spiralshapes that connect nuclear bag and nuclear chain fibers. Group II fibers, sensitive mainly to stretch, resemble small branch-like arms that mainly contact nuclear chain fibers. The motor supply to muscle spindles consists of several types of y-motor axons. 5 Nuclear bag fibers have plate endings from dynamic y-motor axons while nuclear chain fibers have plate endings from static y -motor axons (4). GTOs are another type of stretch receptor. GTOs are almost always found in the muscle-tendon (aponeuroses) junctions, and, in mammals, GTOs are encapsulated possibly to increase sensitivity to stimuli (20). GTOs are arranged in series with muscle fibers as opposed to the parallel orientation of the muscle spindles. Muscle spindles have been studied more extensively than GTOs; hence, our greater understanding of the former. Nevertheless, it is now understood that GTOs are more responsive to muscular contraction forces rather than passively generated forces (20). Both the muscle spindles and GTOs work together when a muscle is stretched. Stretching causes a muscle to increase the frequency of impulses transmitted from the muscle spindles to the spinal cord. The transmission causes the muscle spindles to increase the frequency of motor impulses returning to that same muscle causing a reflexive resistance to the stretch (26). Muscle spindles function by detecting a stretch as muscles contract. The stretch causes the spindles to depolarize creating a generator potential. Stronger generator potentials are produced with greater stretch. An action potential results if the depolarization reaches threshold, which allows the amount and rate of stretch to be detected (2). On the other hand, excessive tension within the muscle activates the GTOs whose sensory impulses are carried back to the spinal cord. The impulses from the GTOs have an inhibitory effect on the motor impulses returning to the muscle, thus causing the muscle to relax (26). The concept of autogenic inhibition is based on the function of the muscle spindles and GTOs. Autogenic inhibition occurs when a muscle contraction is inhibited 6 structures separate. This results in the detachment of the actin-myosin structures, which allows the fibers to return to their resting lengths (2). A second theory, the theory of muscular elongation, states muscle fibers are unable to stretch by themselves. Muscle fibers rely on outside forces such as the force of antagonist muscles, movement, gravity, or a force provided by some other part of the body or by another person to be stretched. Theoretically, the length to which a muscle can be stretched can be determined by the extent the sarcomeres can be stretched. The maximum length a sarcomere can be stretched without rupturing was found to be about 3.5 J..UD. A 50% or greater increase in length may occur from resting state since the resting length of a sarcomere is 2.3 j..lm (2). The stretching portions of SS and PNF may be explained by either of the two aforementioned theories. However, in-depth hypotheses for the function ofPNF are few. Several methods of PNF exist, but all of its incarnations include contraction and relaxation of certain muscles preceding a stretch. PNF encompasses additional techniques that aid in stretching, such as facilitatory and inhibitory techniques. Each technique cannot exist without the other because as an antagonist muscle is relaxing, an agonist muscle is facilitated. Facilitatory techniques are intended to increase motomeuron excitability and recruitment. Inhibitory techniques, on the other hand, commence hyperpolarization of motomeurons; in other words, fewer motomeurons are actively discharged (26). Although it may not be as simple as reciprocal inhibition, an additional hypothesis exists about how a stretch is achieved utilizing PNF. Moore and Hutton (21) concluded the discomfort associated with the stretch of a muscle might be masked by the contraction of the agonist muscle. In other words, the subjects did not 8 associate stretching discomfort with the hamstrings, but rather the quadriceps; thereby, allowing subjects to increase the rate of stretch. Even fewer explanations exist for the function of AI. Surprisingly, only one published study investigating AI stretching was found. This study, by Mattes (19), simply chronicled the different methods of flexibility and touted the advantages of AI. For reasons unknown, AI has found more acceptance in the popular press and the commercial fitness centers than in academia. The main difference between AI and the other more established stretching techniques is the length of time a stretch is held. The creator of this technique believed a stretch should only be held for 2 seconds; as opposed to the 20-30 second hold for the other techniques, in order to bypass the stretch reflex (19). The stretch reflex is a protective mechanism governed by the central nervous system. First, the stretch is received by the muscle spindles and golgi tendon organs. Intemeurons, connecting the motomeurons with the sensory neurons, integrate the signals in the spinal cord. The signals then proceed back to the muscles causing them to contract to prevent overstretching. This is the primary reason why ballistic stretching is no longer recommended. The stretch reflex can prevent a good stretch from occurring and cause injury (4); however, it is unknown if the stretch reflex can be bypassed if the stretch is only held for 2 seconds. Static stretching has been the hallmark of flexibility training, but even this method yields contrary results when studied. The following studies chronicle both the benefits and the drawbacks ofSS. Two studies by DePino, Webright, and Arnold (6) and Worrell, Smith, and Winegardner (33), explored the effectiveness of static stretching, but 9 they required that subjects lack 20 degrees of full extension in the hamstrings. The limitation was imposed to ensure participants would respond well to their stretching program. One group of investigators (6) consequently discovered SS was indeed effective. However, the researchers also stated if an athlete waited more than three minutes to begin the event, their gains in flexibility would be lost. Other studies questioned the efficacy of flexibility to reduce injuries. Pope et al. (25) showed static stretching did not reduce the risk of injury in new army recruits. Magnusson et al. (17) utilized an isokinetic dynamometer to train subjects on hamstring flexibility. Their intent was to investigate the long-term (three weeks) effects of stretching on human tissue properties. The research group concluded the increased stretch tolerance allowed for the increases in flexibility, but found no permanent changes in the viscoelastic properties of human tissue. Additionally, Magnusson and another research team (16) suggested static stretching caused no short-term effects on the viscoelastic properties of the hamstring muscle group. Kubo et al. (14), however, declared static stretching increased elasticity and decreases the viscosity of the muscles even though they did not study the time in which gains in flexibility were maintained. The research group also concluded this effect decreased the chance for injuries in athletes. Shellock and Prentice (28) listed injury prevention as an effect of static stretching. They stated static stretching was indeed effective based on previous research although they were unsure about the optimal amount of time a static stretch should be held. PNF has found many proponents. Sady, Wortman, and Blanke (27) found that PNF was superior when compared to the other types of flexibility training, including static and ballistic stretching. Nevertheless, they were unsure about the optimal amount 10 of time and sets necessary to obtain the best results. Although they only compared the ballistic method against PNF, a Swedish research group confirmed these findings (31 ). In terms offrequency, Wallin et al. (31) found stretching only once a week was enough to maintain flexibility, while stretching more frequently increased flexibility. In addition, Osternig et al. (23) revealed the Stretch-Relax method ofPNF was safer than the other methods ofPNF even though it resulted in 3-6% less gains. Osternig et al. (1990) conducted another study that observed the variances between the different methods of PNF (24). Although they discovered the Agonist-Contract-Relax method increased flexibility the most, they also stated that different athletic populations might benefit more from the other PNF techniques. In addition, Moore and Kukulka (22) supported PNF' s effectiveness, but stated it should be done quickly since post-contraction inhibition ceased quickly. Moreover, Holt, Travis, and Okita (1 0) conducted a much earlier investigation revealing the isometric contraction of the agonist soon followed with a contraction of the antagonist (IA-CA), another method ofPNF, produced more significant gains in flexibility than either ballistic or static stretching. Later, IA-CA PNF came to be known as Contract-Relax-Antagonist-Contract (CRAC-PNF) and was studied by Etnyre and Abraham (7). The researchers stated the CRAC method was the most effective for increasing ankle dorsiflexion. Correspondingly, Etnyre and Lee (8) agreed the CRAC-PNF method was more effective in increasing shoulder extension and hip flexion than both the static and contract-relax method ofPNF. A few studies manifested results contrary to most flexibility studies. One of these studies found static, dynamic, and PNF stretching could all produce significant increases 11 of flexibility in the hamstring-gastrocnemeus muscles (15). However, a later study conducted with only the static and PNF methods manifested no significant improvements in hamstring flexibility (33). More surprisingly, another group of researchers (29) concluded pelvic positioning (anterior) was more important than either the static or PNF stretching method. Hence, the various studies mentioned had just as many varied results. This proposed study investigated the effectiveness of AI stretching against those of SS, PNF stretching, and a control group. 12 placed vertically at the hips. The vertical PVC apparatus was used to guide the subject in maintaining a vertical thigh position 90 degrees of flexion at the hip throughout the flexibility measurement testing. The pretest flexibility measurement was then conducted by taping a goniometer to the lateral side of the right knee. Subjects were instructed to extend the right leg at the knee three times, to ascertain the greatest initial hamstring flexibility. The left leg remained straight and flat on the mat throughout the assessment. Subjects who qualified during the pretest were randomly assigned, using a random number table, to one of the four following groups: control (C), static stretch (SS), proprioceptive neuromuscular facilitation (PNF), and active-isolated stretch (AI). All subjects were instructed to warm-up on a cycle ergometer for five minutes at 25 watts prior to all stretching sessions. Additionally, all subjects were informed that no more than 2 missed stretching days were allowed for the duration of the study to maintain flexibility. Subjects assigned to the control group were instructed not to perform any of the following methods of stretching. However, if subjects in the control group were stretching prior to participating in the study, they were instructed to maintain their stretching program. Control subjects went to the testing lab 4 times per week for 4 weeks to perform the cycle ergometer warm up only. Those assigned to the SS group (n=8) were taught to stretch in a standing position with the right leg extended. The heel of the right foot was positioned on the edge of a table with approximately 90 degrees of hip flexion. Subjects then bent at the waist until they felt a stretch in the hamstrings with a slight level of discomfort, but no pain. 14 Subjects performed 4 repetitions of 20 seconds duration for each stretch, with 5 seconds rest between stretches. This procedure was performed 4 days per week for 4 weeks. Subjects assigned to the PNF group were also taught to stretch in a standing position with the right heel extended on the edge of a table with approximately 90 degrees of hip flexion. These subjects maximally contracted their right hamstring isometrically for 5 seconds. They then relaxed for 5 seconds after which they contracted their right quadriceps isometrically for 5 seconds. Afterwards, they bent at the waist until they felt a stretch in the hamstring, but no pain, for 20 seconds. Subjects performed 4 repetitions of the above sequence. This procedure was performed 4 days per week for 4 weeks. The AI group was instructed to lay supine on a stretching table with the left leg bent at the knee and foot flat on the table. AI stretching was performed as instructed in reference #19. During exhalation, the right leg was then raised as high as possible by contracting the quadriceps muscles. The principal investigator (PI) assisted in the maintenance of the extension of the right leg by placing one hand just above the patella and the other behind the heel without assisting in elevating the leg. Each stretch lasted 2 seconds, after which the leg was returned to rest, flat on the table after each stretch. Four sets often contractions with five second' s rest between sets were performed. The frequency of stretching sessions was also 4 days per week for 4 weeks. In order to observe changes in flexibility, a post-test was conducted in the same manner as the pretest after the 4-week duration of flexibility training for all subjects in all groups. Pre- and post-test measurements for flexibility were taken only on the right leg even though the stretch training was conducted on both legs. Stretching the left leg was 15 an additional benefit for the subjects. In addition to the pre- and post-test measurements, height, weight, age, gender, and activity level were recorded. Data Analysis After collecting the data from both pre- and post-testing, a repeated-measures ANOV A (p>0.05) was utilized to observe for changes in flexibility of the hamstrings. Significant differences were further analyzed using a dependent t-test to determine group pre- and post-test differences. Further analyses were completed to observe correlations between initial flexibility and changes in flexibility. All data were mean± standard deviation (SD). 16 CHAPTER4 RESULTS A total of 38 subjects qualified and were randomly assigned to one of 4 groups (AI=11; SS=8; PNF=10; C=9). Twenty-four subjects did not qualify for the study due to their hamstrings being too flexible and six subjects were dropped due to excessive absences. The subjects who were dropped missed more than two stretching sessions and could not continue in the study due to lack of consistent stretching. The data indicated a significant increase in flexibility for all stretching groups after training (see Figure 1). The following results are the changes in flexibility of the hamstrings for all groups after their 4-week training sessions utilizing a paired T-test. Before stretching, the PNF group's pre-test results were 144.5°±7.9. However, after their stretch training, their posttest results showed an increase to 157.9°±12.5, P=0.0007. Similarly, the AI group' s initial flexibility measurements were 149.3°±8.7; while their post-test results showed a small increase to 156.4°±7.6, P=0.0123. Correspondingly, the initial flexibility of the SS group was 146.0°±8.8. This group showed an increase of flexibility to 156.6°±15.0, P=0.0397. Finally, the control group's initial flexibility was 151.5°±3.9. The group's changes of 154.3°±6.9, P=0.1710 were small. There was, however, no significant difference between each of the flexibility training groups (see Figures 1 and 2). Likewise, there were no significant differences in initial flexibility between groups 17 quadricep muscles caused a relaxation of the hamstrings which could have aided their gains in flexibility (26). Nevertheless, the fact that SS and PNF groups required subjects to stand and place their heels on the edge of a table may have been a disadvantage. A few subjects were so inflexible that the position made it difficult for them to acquire the anterior pelvic tilt position. Sullivan, DeJulia, and Worrell (29) stated the anterior pelvic tilt position was more important than the actual stretching method, but the effect of anterior pelvic tilt position was not taken into account in the current study. Moore and Hutton (21) discovered subjects in the PNF-CRAC group achieved the greatest flexibility when compared toSS and another PNF group that only utilized the contraction and relaxation portion of the technique. Their study, however, included the use of electromyography (EMG) in order to observe the electrical activity that occurred during stretching. It was revealed the PNF-CRAC group had the highest EMG activity; yet, the method of stretching yielded the greatest increases in range-of-motion. A popular notion of stretching is that a muscle has to be relaxed in order to stretch, but Moore and Hutton's study (21) showed increases in flexibility were possible even during high levels of muscle recruitment. Similarly speaking, Magnusson et al. (17) detected no changes in the viscoelastic properties of the hamstring muscles after being stretched for three weeks. A change in tissue properties did not occur, because there was no decrease in force at the same joint angle when measured with an isokinetic machine. The research also suggested the increased range of motion was a result of increased stretch tolerance. However, the 20 (p>0.05). At the inception of the study, it was postulated that the less flexible subjects would show greater increases in flexibility, while the more flexible subjects would show less increase in flexibility. However, none of the groups manifested a significant correlation between the initial hamstring flexibility and the increase in flexibility measured after training (see Fig. 3-6). 18 CHAPTERS DISCUSSION The significant finding of this study was that an increase in the flexibility of the hamstrings was found within each of the stretching groups after training. Although SS and PNF manifested greater increases in flexibility than AI, no between-group differences were indicated. A possibility for the lack of significance was the low number of subjects in each group. The large individual differences in stretch performance also possibly contributed to the lack of significance. An increase in the number of subjects would probably also increase the power of the study. Although the study by Worrell, Smith, and Winegardner (33) did not have the same test procedures, they had the similar results. Utilizing both SS and PNF stretching with each of their 19 subjects, the researchers found no significant increases in flexibility even though there was a trend towards significance. They also acknowledged the small sample size and large subject variation in stretch performance as the main obstacles to reaching significance. In this current study, subjects randomly assigned to either the SS or PNF group generally showed good improvement in their hamstring flexibility. SS takes advantage of autogenic inhibition concept. It is possible the inhibitory impulses from the GTOs caused the motomeurons to reduce their activity affecting relaxation when a stretch was held for an extended period of time. The PNF group also took advantage of autogenic inhibition, but the technique had an additional advantage of employing reciprocal inhibition when subjects contracted their quadricep muscles. The contraction of the 19 source of the altered stretch tolerance remains unknown. The increased flexibility of the hamstrings in this current study may also have been due to an increased stretch tolerance. The effectiveness of increasing hamstring flexibility with AI stretching was minimal in this study. The procedure for stretching the hamstrings utilizing AI was followed as it was written in Mattes' article (19). Another factor that may have limited the efficacy of AI was that the stretch did not utilize the bodyweight of the subject. In both the SS and PNF groups, subjects were instructed to bend at the waist to attain a stretch in the hamstrings. The bending action of the hips allowed the weight of the upper torso to contribute to the stretch. Subjects stretching utilizing AI only had the weight of one leg to contribute to the stretch. Additionally, a type of stretching called Active-Assisted (AA) stretching existed prior to the creation of AI. This type of stretching required that subjects contract their quadriceps until they could no longer raise it further. As the range of motion was achieved, the leg was further stretched by a partner. AA is very similar to AI, and Iashvili' s study ( 13) observed a higher correlation of sports achievement and active flexibility even though active range of motion (ROM) measurements were lower than passive ROM' s. The combination of passive and active ranges of motion makes up the total range of motion. If active stretching is practiced, then active flexibility will be developed. The same reasoning applies to passive stretching. The range in which the subject' s joint can be pushed in a passive stretch is called the zone of passive adequacy. The range in which their joint can no longer be pushed is called the zone of passive inadequacy. Active stretching also has the same zones, but they are called the zones of active adequacy (e.g. 21 how high subjects can lift their leg utilizing their own strength) and active inadequacy (e.g., the area in which subjects can not lift their leg on their own.) The chance for injury increases if there is a great difference between the ranges of passive and active ranges of motion. Strength exercises performed in the active inadequacy zone may aid in the reduction of injuries (13). According to Mattes (19), AI is completely an active stretch so subjects would not get the benefit of an outside force pushing their stretches further. Since overall flexibility can be improved by both passive and active stretches, AI may be more beneficial if a passive component is added. The current study revealed stretching was indeed beneficial if increased flexibility of the hamstrings is desired. However, choosing the most effective stretching method is difficult since there was no difference between groups. At this juncture, AI stretching was not shown to be superior to the other methods of stretching at increasing hamstring flexibility. Nevertheless, stretching may indeed enhance the flexibility of the hamstrings regardless of technique utilized. Moreover, most flexibility studies, including this study, are further complicated by the fact that individual stretching effort cannot be measured. As a result, some subjects in the same stretching group yielded very different results. Future research should investigate methods to gauge individual stretching effort and include a larger number of subjects. 22 Table 1 . Subject demographics Group Gender Age Height Weight Initial Flexibility (years) (em) (kg) (mean ±SO) AI M=4, F=7 23.3 ±3.8 172.5 ±8.6 72.5 ±15.5 7.1 ±7.8 PNF M=5, F=5 25.6±6.9 172.7 ±8.9 77.1±16.1 13.4±8.4 ss M=3, F=5 25.6±6.5 167.1 ±9.7 72.8±14.4 10.6±11.9 c M=5 , F=4 25.6±4.3 172.5 ±6.6 74.2±13.4 2.7±5.5 N w All data are mean ± SO. AI= Active-isolated stretching; PNF= Proprioceptive Neuromuscular Facilitation stretching; SS= Static stretching; C= Control; None of the initial flexibility measures were significantly different between groups (p>0.05). 175 I (B ss • PNF II 170 165 ,....... 160 ell Q) Q) II II &AI II rn c I T ~ 155 j * * * B N ~ ·--·0'>l ,D - 150 I Q) ~ 145 * * * 140 135 I PreTraining PostTraining Figure 1. Flexibility of the hamstrings before and after training. All training groups (*) significantly increased hamstring flexibility post training (p<0.05). The control group was not different post training (p>0.05). There were no significant differences post training. SS= Static stretching; PNF= Proprioceptive Neuromuscular Facilitation stretching; AI= Active-Isolated stretching; C= Control. Figure 2. Flexibility of the hamstrings before and after training. All training groups significantly increased flexibility after training(*; p<0.05). There was no significance between groups after training. PNF= proprioceptive neuromuscular facilitation; C= control; SS= static stretching; AI= active-isolated stretching 165 160 -1 fll 155 Go~ Go~ ~ • ~ • • • ............... • a.. ~ ,e. ....Go~ "CC I 150 ....== r= ,.Q ~ -.....-... Go~ c N 0'1 145 - ~ = ..... • ............... -0.58, P= 0.062 • I • AI subjects' initial flexibility vs. changes in flexibility • I 140 • 135 • 130 -15 -10 -5 0 5 10 15 20 Changes in flexibility (degrees) Figure 3. AI subjects' initial flexibility versus changes in flexibility. Initial flexibility was not correlated to the changes in flexibility with training for the AI group. 170 165 160 • 155 ~ ~ ... ~ 150 .....-... --.... .... ~ N --l ,e. 145 .c 140 ·~ • • • ~ ~ • • • • • ~ ~ 135 ~ .... = ~ 130 r= 0.161 , p= 0.657 • • 125 120 PNF subjects' initial flexibility vs. changes in flexibilitv 115 110 -5 0 5 15 10 Changes in Flexibility (degrees) 20 25 Figure 4. PNF subjects' initial flexibility versus changes in flexibility. Initial flexibility was not correlated to the changes in flexibility with training for the PNF group. 30 170 165 - 160 ~ • • ~ ~ 155 ~ "CC -t> 150 ·-·- 145 ·--" 140 ..·-= 135 ,.Q • ~ ~ N QC • • ~ ;: • • 130 r= 0.022, p= 0.96 • SS subjects' initial flexibility vs. changes in flexibil!!Y_ 125 120 -10 -5 0 5 10 15 20 25 30 35 Changes in Flexibility (degrees) Figure 5. SS subjects' initial flexibility versus changes in flexibility. Initial flexibility was not correlated to the changes in flexibility with training for the SS group. 165 I r= 0.052, p= 0.894 • 160 ' - C subjects' initial flexibility vs . changes in flexibility "'-! • ~ i.... 155 ,e. -........ - j • • I ,.Q ~ ~ N \0 -.....-...== ~ 150 1 • • • • • """' 145 • I 140+-------~--------~------~--------~------~~------~------~ -15 -10 -5 0 5 10 15 Changes in Flexibility (degrees) Figure 6. C subjects' initial flexibility versus changes in flexibility. Initial flexibility was not correlated to the changes in flexibility with training for the C group. 20 References 1. Agre, J. C. Hamstring injuries: Proposed aetiological factors, prevention, and treatment. Sports Med. 2: 21-33, 1985. 2. Alter, M. J. Science ofFlexibility, (2nd ed.) Champaign, IL: Human Kinetics, 1996. 3. Anderson, B. and Burke, E. R. Scientific, medical, and practical aspects of stretching. Clinics Sports Med. 10: 63-86, 1991. 4. Berne, R. M., and Levy, M. N. Physiology, (3rd ed.) 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