[ research report ] 130 march 2007 volume 37 number 3 journal of orthopaedic & sports physical therapy. t Study Design: Repeated-measures experimental

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1 Joel T. Cramer, PhD 1 Terry J. Housh, PhD 2 Glen O. Johnson, PhD 2 Joseph P. Weir, PhD 3 Travis W. Beck, MPE 4 Jared W. Coburn, PhD 5 An Acute Bout of Static Stretching Does Not Affect Maximal Eccentric Isokinetic Peak Torque, the Joint Angle at Peak Torque, Mean Power, Electromyography, or Mechanomyography Static stretching is commonly performed before exercise and athletic events 3 because it is believed that increasing flexibility (joint range of motion) will promote better performance 42,45 and reduce the risk of injury during strenuous exercise. 18,43 Previous studies used muscle stretching techniques to examine passive force production, 29 stress relaxation characteristics of muscle, 35 neuromuscular reflex patterns, 24 factors contributing to muscle t Study Design: Repeated-measures experimental design. t Objective: To examine the acute effects of static stretching on peak torque, the joint angle at peak torque, mean power output, and electromyographic and mechanomyographic amplitudes and mean power frequency of the vastus lateralis and rectus femoris muscles during maximal eccentric isokinetic muscle actions. t Background: A bout of static stretching may impair muscle strength during isometric and concentric muscle actions, but it is unclear how static stretching may affect eccentric force production. t Methods and Measures: Fifteen men (mean 6 SD age, years) performed maximal eccentric isokinetic muscle actions of the dominant and nondominant knee extensor muscles at 60 s 1 and 180 s 1 on an isokinetic dynamometer, while electromyographic and mechanomyographic amplitudes (root-mean-square) and mean power frequency were calculated for the vastus lateralis and rectus femoris muscles. Peak torque (Nm), the joint angle at peak torque ( ), and mean power output (W) values were recorded by the dynamometer. Subsequently, the dominant lower extremity knee extensors underwent static stretching exercises, then the assessments were repeated. t Results: There were no stretching-related changes in peak torque, the joint angle at peak torque, mean power output, electromyographic or mechanomyographic amplitude, or mean power frequency (P..05). However, there were expected velocity-related, limb-related, and muscle-related differences (P<.05) that were unrelated to the stretching intervention. t Conclusion: These results suggest that static stretching does not affect maximal eccentric isokinetic torque or power production, nor does it change muscle activation. J Orthop Sports Phys Ther 2007;37(3): doi: / jospt t Key Words: EMG, muscle activation, muscle stiffness, stretching-induced force deficit damage, 28 and mechanisms of increase in musculotendinous flexibility. 50 Until recently, few studies examined the acute effects of stretching on performance measures. 16 Recent evidence has suggested that pre-exercise stretching may compromise a muscle s ability to produce maximal force. 7,20,39,53 Two primary alternatives that have been proposed to explain the stretching-induced force deficit are (1) mechanical factors such as changes in muscle stiffness 21,39 and (2) neural factors such as altered motor control strategies or reflex sensitivity. 1,7 The simultaneous measurements of mechanomyography (MMG) and electromyography (EMG) can provide unique information about the mechanical and neural properties associated with the motor control strategies used during various types of muscle actions. The MMG signal records and quantifies the low-frequency lateral oscillations of active skeletal muscle fibers and provides a noninvasive method to examine muscle function. 40 Gordon and Holbourn 23 proposed that the lateral oscillations produced by contracting muscles reflect the mechanical counterpart of the motor unit electrical activity as measured by EMG. In fact, it has been suggested that MMG amplitude 1 Assistant Professor, Department of Health and Exercise Science, University of Oklahoma, Norman, OK. 2 Professor, Department of Nutrition & Health Science, University of Nebraska Lincoln, Lincoln, NE. 3 Professor, Department of Physical Therapy, Des Moines University Osteopathic Medical Center, Des Moines, IA. 4 Graduate Assistant, Department of Nutrition & Health Science, University of Nebraska Lincoln, Lincoln, NE. 5 Associate Professor, Department of Kinesiology, California State University, Fullerton, Fullerton, CA. This study was funded in part by the National Strength and Conditioning Association Student Grant Program. This study was approved by the University of Nebraska Lincoln Institutional Review Board for Human Subjects ( FB) under the auspices of Research Compliance Services, 103 Whittier Building, 2255 West Street, PO Box , Lincoln, NE Address correspondence to Dr Joel T. Cramer, Department of Health and Exercise Science, University of Oklahoma, 1401 Asp Avenue, Room 104, Norman, OK jcramer@ou.edu 130 march 2007 volume 37 number 3 journal of orthopaedic & sports physical therapy

2 is inversely proportional to the stiffness of an active muscle. 4 Evetovich et al 20 reported stretching-induced increases in MMG amplitude for the biceps brachii muscle; however, other studies 11,15,32 have shown no changes in MMG amplitude after stretching. Surface EMG amplitude may provide insight regarding motor unit activation. 36 Several studies 7,15,21 reported stretching-induced decreases in EMG amplitude, but again at least 1 study 20 reported no changes in EMG amplitude after stretching. Furthermore, the frequency domains of the EMG and MMG signals may be able to track changes in muscle action potential conduction velocity 2 and motor unit firing rates, 5 respectively. Avela et al 1 reported stretching-induced decreases in motor unit firing rates recorded using fine-wire EMG and speculated that a supraspinal fatigue mechanism may be responsible for decreases in muscle strength and activation after a bout of stretching. Therefore, incorporating EMG and MMG amplitude and mean power frequency (MPF) measurements of the stretched and unstretched (contralateral) limbs before and after the static stretching protocol may provide useful information regarding the neural and mechanical changes that have been proposed to explain the stretching-induced force deficit. In a recent study that examined the effects of stretching on explosive force production, Young and Elliott 53 attributed the stretching-induced decreases in drop jump performance to (1) decreases in eccentric strength as a result of a decrease in musculotendinous stiffness and (2) decreases in motor unit activation. However, Wilson et al 52 suggested that there is a direct relationship between musculotendinous stiffness and concentric and isometric strength, but this relationship does not exist for eccentric strength. It has been suggested that static stretching may decrease musculotendinous stiffness by increasing the resting length of sarcomeres, which in turn may alter the shape of the length-tension relationship. 14,39 In support of this hypothesis, researchers reported stretching-induced changes in isometric strength that are joint angle dependent 21,38 and alterations in the characteristics of the isokinetic angle-torque curve. 11 Because previous studies 9,34 used the isokinetic angletorque relationship as a global indicator of the length-tension relationship, variables such as peak torque (PT), the joint angle at PT (APT), and the timeaveraged area under the curve (mean power output [MP]) of the isokinetic angle-torque curve may provide insight regarding the effects of static stretching on the length-tension relationship during eccentric muscle actions. However, the relationship between stretching-induced changes in muscle strength and the length-tension relationship is speculative and requires further exploration. Recent reviews questioned whether stretching would reduce the risk of injury when completed before performance. 22,49 Two reviews suggested that stretching before strenuous exercises may increase the risk of injury. 44,51 Based on the suggestion by Mair and colleagues 30 that a muscle s ability to absorb eccentric energy is critical to avoid injury, Shrier 44 hypothesized that, if stretching reduced eccentric muscle strength, the muscle may be predisposed to strain-related injuries because it would not be able to prevent excessive sarcomere lengthening. To our knowledge, only 1 previous study 12 tested this hypothesis, and the authors concluded that static stretching did not affect eccentric torque production in women. Although it is difficult to extrapolate these findings to explain how stretching may or may not reduce the risk of injury to the musculotendinous unit during eccentric loading conditions, it may be appropriate to test in men the hypothesis by Shrier that stretching reduces eccentric muscle strength. Previous studies examined the effects of stretching on maximal strength, 7,21,39 explosive force production, 53 vertical jump performance, 53 concentric isokinetic PT, 14,20,39 and isometric force production at different joint angles. 7,21,38 Only 1 previous study 21 (to our knowledge) estimated the relative contributions of the mechanical and electrical mechanisms underlying the strength deficit after stretching; however, the authors stated that The duration of stretch performed in this experiment is more similar to prolonged stretch procedures employed in animal experimental models and, therefore, may have limited application to sport stretching performed in conjunction with athletic performance. 21 Thus, limited data are available regarding the mechanical and electrical components of the strength deficit as a result of traditional static stretching. As far as we know, no previous studies investigated how stretching may affect maximal eccentric isokinetic muscle actions of the stretched and unstretched knee extensor muscles in men. If the stretch-induced force deficit is mediated by a central nervous system mechanism, it is possible that the unstretched limb may also be affected. Therefore, the objectives of this study were to examine the acute effects of static stretching on PT, MP, APT, EMG amplitude, EMG MPF, MMG amplitude, and MMG MPF of the vastus lateralis (VL) and rectus femoris (RF) muscles during maximal eccentric isokinetic knee extension at 60 s 1 and 180 s 1 for the stretched and unstretched knee extensors in men. This study was designed (1) to test the hypothesis by Young and Elliott 53 that decreases in drop jump performance as a result of static stretching are due to decreases in eccentric muscle strength; (2) to examine whether static stretching alters the characteristics of the eccentric isokinetic angle-torque relationship by including PT, APT, and MP; and (3) to incorporate surface EMG and MMG signals from the stretched and unstretched knee extensor muscles to examine the neural 7,21 and mechanical 21,39 factors underlying any potential decreases in muscle force production as a result of stretching. journal of orthopaedic & sports physical therapy volume 37 number 3 march

3 METHODS Participants Fifteen men (mean 6 SD age, years; mean 6 SD body mass, kg; and mean 6 SD stature, cm) volunteered to participate in the investigation. None of the participants were competitive athletes, but they were recreationally active college students, which was defined as completing 1 to 5 hours of regular exercise per week. All of the participants were healthy because there were no reports of any diseases, regular medication use, or injuries to the lower body within the past 2 years. This study was approved by the University of Nebraska Lincoln Institutional Review Board for Human Subjects, and all participants completed a health history questionnaire and signed written informed consent before testing. Isokinetic Testing Procedure Five to 7 days before the experimental trial, each participant completed a familiarization trial. For familiarization, the participants warmed up on a cycle ergometer and practiced submaximal and maximal isometric and eccentric isokinetic muscle actions of the knee extensors at 60 s 1 and 180 s 1 until they were comfortable with the protocol. For the experimental trial, each participant completed a 5-minute warm-up on a stationary cycle ergometer with the resistance set to 50 W and a pedaling cadence of 60 to 70 rpm before the initial isokinetic testing. Before the prestretching isokinetic assessments, each participant completed two 4-second isometric maximal voluntary contraction (MVC) trials of the knee extensors at a joint angle of 60 below the horizontal plane. Before (prestretching) and after (poststretching) the static stretching exercises, maximal eccentric isokinetic PTs for the knee extensors of the dominant (based on kicking preference) and nondominant lower extremities were measured separately using a calibrated Cybex 6000 dynamometer (CYBEX Division of LUMEX, Inc, Ronkonkoma, NY) at randomly ordered velocities of 60 s 1 and 180 s 1. Slow (60 s 1 ) and fast (180 s 1 ) angular velocities were chosen based on the conclusion by Nelson et al 39 that the effects of static stretching were velocity specific. For testing, the participants were in a seated position with a restraining strap over the pelvis and trunk in accord with the manufacturer s protocol. The input axis of the dynamometer was aligned with the axis of the knee, while the contralateral leg was braced against the limb stabilization bar. The investigator manually lifted the lever arm and leg to the starting position at full knee extension (without assistance from the participant) between each eccentric muscle action. Three submaximal warm-up trials preceded 3 maximal muscle actions at each velocity. The rest period allowed between consecutive muscle actions at each velocity was equal to the time required to bring the lever arm to full extension (ie, 1-2 seconds). A 2-minute rest was allowed between testing at each velocity, and a minimum of 5 minutes was allowed between testing for each limb. The mean 6 SD ranges of motion for the eccentric muscle actions of the knee extensors were for the right limb and for Figure 1. Example of the initial unassisted stretching exercise. the left limb (0 equals full knee extension). The gravity-corrected values for PT (Nm), APT ( ), and MP (W) were derived using the Cybex 6000 software for the repetition yielding the highest total work at both angular velocities. Static Stretching Exercises Immediately following the prestretching isokinetic tests, each participant underwent 4 static stretching exercises designed to stretch the knee extensor muscles of the dominant limb only according to the procedures by Cramer et al 15 and by Nelson et al. 39 Four repetitions of each stretching exercise were held for 30 seconds at a point of mild discomfort but not pain as acknowledged by the participant. Between each stretch repetition, the knee was returned to a neutral position for a 20-second rest period. The total mean 6 SD stretching time from start to finish was minutes. Each participant performed an unassisted stretching exercise (Figure 1), followed by 3 assisted stretching exercises (Figures 2, 3, and 4). For the unassisted stretching exercise, the participant stood upright with 1 hand against a wall for balance. The participant then flexed the knee joint to 90. The ankle of the flexed knee was grasped by the ipsilateral hand, and the foot was raised so that the heel of the dominant foot approached the buttocks (Figure 1). Following the unassisted stretching exercise, the remaining stretching exercises were completed with the assistance of the primary investigator (J.T.C.). Figure 2. Example of the first assisted stretching exercise. 132 march 2007 volume 37 number 3 journal of orthopaedic & sports physical therapy

4 Figure 3. Example of the second assisted stretching exercise. The first assisted stretching exercise was performed with the participant lying prone on a padded table with the knees fully extended (Figure 2). The knee of the dominant lower extremity was flexed and slowly pressed down so that the participant s heel approached the buttocks. If the heel was able to contact the buttocks, the knee was gently lifted off the supporting surface, causing a slight extension at the hip joint, to complete the stretch. To perform the second assisted stretching exercise, the participant stood with his back to a table and rested the dorsal surface of his foot on the table by flexing the knee (Figure 3). From this position, the knee extensors were stretched by gently pushing back on the flexed knee and the corresponding shoulder. The final assisted stretching exercise began with the participant lying supine along the edge of the padded table with the dominant lower extremity hanging off of the table (Figure 4). The dominant knee was flexed, and the hip was slightly extended by gently pressing down on the knee. Immediately after the stretching exercises, each participant sat quietly for a mean 6 SD of minutes before performing the poststretching isokinetic tests for the dominant (stretched) limb and for a mean 6 SD of minutes before testing the nondominant (unstretched) limb. Because the primary objective of this study was to examine the effects of stretching on the stretched limb, the isokinetic testing was always performed on the dominant limb first. Figure 4. Example of the final assisted stretching exercise. EMG Measurements Bipolar (7.62-cm center to center) surface electrode (Quinton Quick-Prep electrodes with 1-cm silver-silver chloride disks; Quinton Instruments Co, Bothell, WA) arrangements were placed along the longitudinal axes of the VL and RF muscles of the dominant and nondominant thighs. 15 The VL and RF muscles were chosen to represent a monoarticular muscle (VL) and a biarticular muscle (RF). The interelectrode distances were selected to accommodate placing the MMG sensors between the EMG electrodes. 6 The electrodes for the VL were placed over the lateral portion of the muscle at approximately the midpoint between the head of the greater trochanter and lateral condyle of the femur. For the RF, the electrodes were placed at 50% of the distance between the inguinal crease and the superior border of the patella. For all EMG measurements, the reference electrodes were placed over the iliac crests. The electrodes remained on the skin throughout the static stretching exercises. Interelectrode impedance for each muscle was kept below 2000 by shaving the area and carefully abrading the skin. The EMG signals (recorded in microvolts) were differentially amplified (gain equals 1000 ) with a bandwidth of direct current 500 Hz, input impedance of 2 M (differential), common-mode rejection ratio of 110 db, and maximum input voltage of 610 V (EMG100C; Biopac Systems Inc, Santa Barbara, CA). MMG Measurements The MMG signals were detected using piezoelectric crystal contact sensors (Hewlett-Packard 21050A, bandwidth of Hz; Hewlett-Packard, Avondale, PA). For each muscle (VL and RF), a sensor was placed between the active EMG electrodes. A stabilizing ring, double-sided foam tape, and microporous tape were used to ensure consistent contact pressure of the MMG sensor. 8 The MMG sensors were removed after the prestretching assessments in preparation for the stretching protocol. The skin was marked where the MMG sensors were placed, so that the sensors could be replaced in the same position after static stretching. Signal Processing The raw EMG and MMG signals were collected using commercially available software (AcqKnowledge III; Biopac Systems Inc, Santa Barbara, CA) and were stored on a personal computer (Macintosh 7100/80 AV Power PC; Apple Inc, Cupertino, CA). The sampling frequency was 1000 Hz for all signals. The EMG and MMG signals were bandpass filtered (zero-phase, fourth-order Butterworth filter) at 10 to 500 Hz and 5 to 100 Hz, respectively. Root-mean-square (rms) amplitude and MPF (Hz) values for the EMG and MMG signals were calculated for a period that corresponded to a 90 range of motion from approximately full knee extension to 90 of flexion at the knee. For example, at 60 s 1, 1.5 seconds of the EMG and MMG signals were analyzed, while at 180 s 1, 0.5 seconds were analyzed. 13 This allowed for comparisons between the velocities that were based on a standardized 90 range of motion. The values calculated from the EMG and MMG signals were synchronized to the isokinetic data using the onset of the EMG signal (ie, 2 SDs above baseline) as the onset of eccentric torque production and the resultant contraction time; therefore, the representative isokinetic values corresponded to EMG and MMG values. journal of orthopaedic & sports physical therapy volume 37 number 3 march

5 All time and frequency domain analyses were performed using custom programs written with LabVIEW software, Version (National Instruments, Austin, TX). To determine the center frequency, each EMG and MMG epoch was processed using a Hamming window and the discrete Fourier transform. The discrete Fourier transform was chosen, as opposed to the fast Fourier transform, because the discrete Fourier transform is not constrained to 2 n number of data points. Therefore, discrete Fourier transform analyses were performed without having to truncate the data segments or resort to zero padding. The MPF was selected to represent the power spectrum based on the recommendations by Diemont et al 17 and by Hermens et al 25 and was calculated as described by Kwatny et al. 27 After the absolute EMG and MMG amplitude (μvrms and mvrms, respectively) and MPF (Hz) values were calculated, each participant s data were normalized separately to the rms and MPF values recorded during the prestretching MVC trial that yielded the highest PT value. This was calculated as a percentage (%MVC) of the amplitude and frequency values obtained during the middle 2-second epoch of the 4-second MVC trial. Normalization of the EMG and MMG amplitude and MPF values allowed for comparisons between muscles, limbs, and velocities. 46 Reliability Test-retest reliability was previously recorded in our laboratory during maximal eccentric isokinetic muscle actions at 60 s 1 and 180 s 1 for 8 male participants measured 48 hours apart. The results indicated that the intraclass correlation coefficients for PT, EMG amplitude, EMG MPF, MMG amplitude, and MMG MPF ranged from 0.88 to 0.97, 0.85 to 0.96, 0.82 to 0.90, 0.97 to 0.98, and 0.76 to 0.95, respectively. There were no significant (P..05) differences between mean values for test versus retest at either velocity (60 s 1 or 180 s 1 ). TABLE 1 Prestretching Statistical Analysis Three separate 3-way repeated-measures analyses of variance (ANOVAs) (time [prestretching versus poststretching] by limb [stretched versus unstretched] by velocity [60 s 1 versus 180 s 1 ]) were used to analyze the PT, APT, and MP data. Four separate 4-way repeatedmeasures ANOVAs (time [prestretching versus poststretching] by limb [stretched versus unstretched] by velocity [60 s 1 versus 180 s 1 ] by muscle [VL versus RF]) were used to analyze the normalized EMG amplitude, EMG MPF, MMG amplitude, and MMG MPF data. When appropriate, follow-up analyses included t tests for dependent samples. In addition, the strength of association (effect size) was estimated using the partial eta squared (h 2 ) statistic. 48 An a level of P<.05 was considered statistically significant for all comparisons. SPSS software Version 12.0 (SPSS Inc, Chicago, IL) was used for all statistical analyses. RESULTS Isokinetic Assessments Table 1 gives the mean 6 SD values for the isokinetic variables, including PT, APT, and MP. The 3-way ANOVAs (time by limb by velocity) for PT indicated no 3-way interaction (P =.916, h 2 = 0.001); no 2-way interactions for time by limb (P =.186, h 2 = 0.121), limb 60 s s 1 60 s s 1 Peak torque (Nm) Joint angle at peak torque ( ) Mean power output (W) Poststretching Peak torque (Nm) Joint angle at peak torque ( ) Mean power output (W) * All values are mean 6 SD. Peak Torque, Joint Angle at Peak Torque, and Mean Power Output for Stretched and Unstretched Limbs During Eccentric Muscle Actions* Stretched Limb Unstretched Limb by velocity (P =.459, h 2 = 0.040), or time by velocity (P =.131, h 2 = 0.155); no main effects for time (P =.595, h 2 = 0.021) or limb (P =.328, h 2 = 0.068), but a significant main effect for velocity (P,.001, h 2 = 0.737). Therefore, PT decreased from 60 s 1 (mean 6 SD, Nm) to 180 s 1 (mean 6 SD, Nm); however, there were no changes due to static stretching. The 3-way ANOVA for APT indicated no 3-way interaction (P =.627, h 2 = 0.017); no 2-way interactions for time by limb (P =.181, h 2 = 0.124), limb by velocity (P =.640, h 2 = 0.016), or time by velocity (P =.667, h 2 = 0.014); no main effects for time (P =.661, h 2 = 0.014) or limb (P =.058, h 2 = 0.233), but a significant main effect for velocity (P,.001, h 2 = 0.771). Therefore, as expected, APT was greater at 60 s 1 (mean 6 SD, ) than at 180 s 1 (mean 6 SD, ); however, static stretching did not change the APT (Table 1). For MP (Table 1), there was no significant 3-way interaction (P =.493, h 2 = 0.034); no 2-way interaction for time by limb (P =.135, h 2 = 0.152), limb by velocity (P =.223, h 2 = 0.104), or time by velocity (P =.868, h 2 = 0.002); no main effect for time (P =.706, h 2 = 0.010) or limb (P =.289, h 2 = 0.080), but a significant main effect for velocity (P,.001, h 2 = 0.958). Therefore, as expected, MP was lower at 60 s 1 (mean 6 SD, march 2007 volume 37 number 3 journal of orthopaedic & sports physical therapy

6 TABLE 2 Normalized EMG and MMG Amplitude and Mean Power Frequency Recorded From the Vastus Lateralis and Rectus Femoris Muscles of Stretched and Unstretched Limbs During the Eccentric Muscle Actions* V vastus Lateralis rectus Femoris vastus Lateralis rectus Femoris Prestretching W) than at 180 s 1 (mean 6 SD, W), but there were no changes due to static stretching. Electromyography Table 2 gives the mean 6 SD values for normalized EMG and MMG amplitudes and MPF. For EMG amplitude, there was no 4-way interaction for time by limb by velocity by muscle (P =.990, h 2,0.001); no 3-way interaction for time by limb by velocity (P =.391, h 2 = 0.053), limb by velocity by muscle (P =.279, h 2 = 0.083), or time by velocity by muscle (P =.468, h 2 = 0.038); no 2-way interaction for time by velocity (P =.465, h 2 = 0.039), limb by velocity (P =.640, h 2 = 0.016), or velocity by muscle (P =.388, h 2 = 0.054); but a significant 3-way interaction for time by limb by muscle (P =.049, h 2 = 0.250) and stretched Limb EMG amplitude EMG mean power frequency MMG amplitude MMG mean power frequency Poststretching EMG amplitude EMG mean power frequency MMG amplitude MMG mean power frequency Prestretching Unstretched Limb EMG amplitude EMG mean power frequency MMG amplitude MMG mean power frequency Poststretching 60 s -1 EMG amplitude EMG mean power frequency MMG amplitude MMG mean power frequency Abbreviations: EMG, electromyographic; MMG, mechanomyographic; SD, standard deviation * All values are mean 6 SD normalized to percent maximum voluntary contraction (%MVC). a significant main effect for velocity (P =.003, h 2 = 0.477). Results of the t tests for dependent samples on the marginal means for EMG amplitude (collapsed across velocity) indicated no changes from prestretching to poststretching for the VL or RF muscle of the stretched or unstretched limbs (P value range, ; h 2 value range, ). However, there were sporadic differences in EMG amplitudes between the VL and RF muscles and between the stretched and unstretched limbs that had no relation to the stretching. In addition, EMG amplitude was greater at 60 s 1 (mean 6 SD, %MVC) than at 180 s 1 (mean 6 SD, %MVC). For EMG MPF (Table 2), there was no 4-way interaction for time by limb by velocity by muscle (P =.451, h 2 = 0.041); 180 s -1 no 3-way interaction for time by limb by velocity (P =.929, h 2 = 0.001), limb by velocity by muscle (P =.931, h 2 = 0.001), time by velocity by muscle (P =.314, h 2 = 0.072), or time by limb by muscle (P =.201, h 2 = 0.114); no 2-way interaction for time by limb (P =.400, h 2 = 0.051), time by velocity (P =.615, h 2 = 0.019), time by muscle (P =.489, h 2 = 0.035), limb by velocity (P =.092, h 2 = 0.189), limb by muscle (P =.395, h 2 = 0.052), or velocity by muscle (P =.191, h 2 = 0.119); and no main effect for time (P =.618, h 2 = 0.018), limb (P =.850, h 2 = 0.003), or velocity (P =.077, h 2 = 0.206); but a significant main effect for muscle (P =.004, h 2 = 0.460). The EMG MPF was greater for the VL muscle (mean 6 SD, %MVC) than for the RF muscle (mean 6 SD, %MVC), journal of orthopaedic & sports physical therapy volume 37 number 3 march

7 but there were no changes due to static stretching. Mechanomyography For MMG amplitude (Table 2), there was no 4-way interaction for time by limb by velocity by muscle (P =.225, h 2 = 0.103); no 3-way interaction for time by limb by velocity (P =.079, h 2 = 0.204), limb by velocity by muscle (P =.614, h 2 = 0.019), time by velocity by muscle (P =.137, h 2 = 0.151), or time by limb by muscle (P =.679, h 2 = 0.013); no 2-way interaction for time by limb (P =.633, h 2 = 0.017), time by velocity (P =.287, h 2 = 0.081), time by muscle (P =.322, h 2 = 0.070), limb by velocity (P =.990, h 2,.0001), limb by muscle (P =.392, h 2 = 0.053), or velocity by muscle (P =.097, h 2 = 0.184); no main effect for time (P =.761, h 2 = 0.007), limb (P =.598, h 2 = 0.020), or muscle (P =.402, h 2 = 0.051), but a significant main effect for velocity (P,.0001, h 2 = 0.736). The MMG amplitude was lower for 60 s 1 (mean 6 SD, %MVC) compared with that for 180 s 1 (mean 6 SD, %MVC), but there were no changes as a result of static stretching. For MMG MPF (Table 2), there was no 4-way interaction for time by limb by velocity by muscle (P =.169, h 2 = 0.131); no 3-way interaction for time by limb by velocity (P =.151, h 2 = 0.141), limb by velocity by muscle (P =.125, h 2 = 0.160), or time by limb by muscle (P =.897, h 2 = 0.001); and no 2-way interaction for time by velocity (P =.269, h 2 = 0.086), time by limb (P =.397, h 2 = 0.052), time by muscle (P = 0.557, h 2 = 0.025), limb by velocity (P =.335, h 2 = 0.067), or limb by muscle (P =.716, h 2 = 0.010). There was a significant 3-way interaction for time by velocity by muscle (P =.013, h 2 = 0.369) and a significant main effect for limb (P =.044, h 2 = 0.259). There were no changes in MMG MPF as a result of static stretching; however, there were sporadic differences in MMG MPF between muscles, velocities, and limbs that were unrelated to the stretching intervention. DISCUSSION The results of the present study indicate no stretching-induced changes in PT, MP, or EMG or MMG amplitude or frequency for the stretched or unstretched limbs. These results were consistent with the only previous study 12 (to our knowledge) that examined the acute effects of static stretching on maximal eccentric isokinetic muscle actions, which reported no stretching-related changes in eccentric PT or the joint angle at PT in women. However, our findings were not consistent with several previous studies that reported stretching-induced decreases in force production during isolated concentric 39 and isometric 7,21 muscle actions and during multijoint performance measures such as the vertical jump. 10,53 The results of the present study, in conjunction with the findings of previous studies, 7,21,39 suggest that static stretching decreases maximal concentric 14,39 and isometric 7,21 force production but does not affect eccentric PT. 12 It has been suggested that stretchinginduced decreases in force production during concentric and isometric muscle actions may be due to decreases in musculotendinous stiffness that increase the resting length of the sarcomeres, which in turn may alter the length-tension relationship. 11,21,39 In support of this hypothesis, Fowles et al 21 suggested that, after 15 minutes of recovery from prolonged passive stretching, most of the decreases in muscle strength were attributable to intrinsic mechanical properties of the musculotendinous unit. Nelson et al 38 reported joint angle-specific decreases in torque production as a result of stretching, while another study 14 found stretching-induced shifts in the joint angle at PT, which indirectly suggested that stretching may alter the length-tension relationship. In a previous study 11 from our laboratory, static stretching decreased isokinetic PT but did not alter work or MP, which suggested that the stretching decreased the peak but did not change the area under the angle-torque relationship. Because the shape and parameters of the isokinetic angle-torque relationship can be used as global indicators of the length-tension relationship, 9,34 there is some evidence to suggest that static stretching may change the shape of the length-tension relationships of active sarcomeres. However, the results of the present study suggest that any decreases in musculotendinous stiffness that may have resulted from static stretching were not manifested through changes in PT or MP during maximal eccentric isokinetic muscle actions. Therefore, these findings are consistent with the hypothesis by Wilson et al 52 that there is no relationship between musculotendinous stiffness and eccentric force production. However, it is possible that the maximal eccentric isokinetic loading in the present study may not reflect the type of eccentric loading that occurs during the stretch-shortening cycle. Future studies should attempt to examine the effect of static stretching on the eccentric loading that occurs during stretch-shortening cycle performance tasks. It has also been suggested that neural factors, such as decreased muscle activation or altered reflex sensitivity, may account for the stretching-induced decreases in force production during concentric and isometric muscle actions. 1,7,21 Previous studies supported this hypothesis by demonstrating stretchinginduced decreases in surface EMG amplitude, 11,15,32 fine-wire EMG, 1 and muscle activation estimated by twitch interpolation. 7,21 Previous studies from our laboratory found stretching-induced decreases in PT 14,15 and EMG amplitude 15 for the stretched and unstretched (contralateral) limbs. We hypothesized that the decreases in strength and muscle activation in the unstretched limb as a result of the stretching could be due to a central nervous system inhibitory mechanism. However, there were no such changes in PT or MP for the stretched or unstretched limbs in the present study. In addition, unlike in previous studies, 7,15,21 the lack of change in EMG amplitude in the present study suggested that there was no 136 march 2007 volume 37 number 3 journal of orthopaedic & sports physical therapy

8 change in muscle activation as a result of static stretching. These findings may reflect the unique motor control strategies used during eccentric muscle actions compared with those used during concentric and isometric muscle actions. 19,47 For example, eccentric muscle actions tend to exhibit greater force-producing capabilities but less muscle activation, 47 which has been attributed to the selective recruitment of fast-twitch motor units 37 or to a unique recruitment of motor units specifically for eccentric muscle actions. 19 Therefore, these findings suggest that static stretching may not affect the motor control strategies that influence eccentric muscle force production. In a recent study, Young and Elliott 53 attributed the stretching-induced decreases in maximal power output measured during the drop jump to (1) decreases in eccentric force-producing capabilities as a result of a decrease in musculotendinous stiffness or (2) decreases in motor unit activation due to an inverse myotatic reflex. However, the results of the present study did not support these hypotheses 53 in that there were no stretching-induced changes in PT or MP (eccentric forceproducing capabilities) or EMG amplitude (muscle activation) during maximal eccentric isokinetic muscle actions. These findings, in conjunction with results from other studies, 26,39 suggest that the stretching-induced decreases in drop jump performance reported by Young and Elliott 53 may be related to the decreases in concentric force-producing capabilities 26,39 or to a stretching-induced decrease in explosive force production that is unrelated to eccentric PT, MP, or muscle activation. Orizio et al 41 reported that, during maximal or near maximal isometric muscle actions, a high level of muscle stiffness may interfere with the capability of muscle fibers to oscillate, which would ultimately suppress MMG amplitude. Therefore, we hypothesized that the stretching-induced decreases in musculotendinous stiffness suggested by Nelson et al 39 may result in an increase in MMG amplitude. This hypothesis is supported by a study by Evetovich et al 20 that demonstrated stretching-induced increases in MMG amplitude for the biceps brachii during concentric muscle actions. However, other studies 11,15,32 have shown no changes in MMG amplitude as a result of stretching. Nelson et al 39 hypothesized that the stretching-induced decreases in PT observed during maximal concentric isokinetic muscle actions were primarily due to the stretching-induced decreases in musculotendinous stiffness. This hypothesis was based on the findings by Wilson et al 52 that musculotendinous stiffness was significantly related to isometric and concentric muscle performance. Specifically, as the stiffness of the musculotendinous unit increased, isometric and concentric performance also increased. The authors reported that, unlike isometric and concentric muscle actions, there was no relationship between musculotendinous stiffness and eccentric force production and During an eccentric movement the musculature lengthens, and thus the mechanisms underlying the relationship between musculotendinous stiffness and isometric and concentric performance do not apply. 52 Therefore, it is conceivable that any decreases in musculotendinous stiffness that resulted from static stretching in the present study were not detected by MMG amplitude because of the lack of a relationship between musculotendinous stiffness and eccentric force production. At the present time, the effect of musculotendinous stiffness on muscle strength is speculative. Future studies should examine the relationships among experimentally induced changes in muscle strength, MMG amplitude, and musculotendinous stiffness. To our knowledge, no previous studies examined the effects of static stretching on MMG MPF. However, it has been suggested that the frequency domain of the MMG signal reflects the firing rates of the activated motor units 5 and can be used to discriminate between slow-twitch and fast-twitch fibers. For example, Marchetti et al 31 reported higher MMG center frequencies in muscles composed primarily of fast-twitch compared with slow-twitch fibers. The results of the present study indicate that there were no stretchinginduced changes in MMG MPF. Therefore, these results suggest that static stretching does not affect motor unit firing rates during maximal eccentric isokinetic muscle actions. As far as we know, no previous studies evaluated the effects of static stretching on EMG MPF. It has been suggested that the EMG power spectrum reflects muscle fiber action potential conduction velocity, which may provide information about fiber-type recruitment patterns. 2 Specifically, the EMG frequency spectrum tends to be lower during lowthreshold slow motor unit activation than during high-threshold fast motor unit activation. In the present study, there were no changes in EMG MPF as a result of static stretching. These findings suggest that static stretching does not affect motor unit action potential conduction velocity during maximal eccentric isokinetic muscle actions. Masuda et al 33 challenged this hypothesis and suggested that EMG center frequency is not related to action potential conduction velocities during nonfatiguing muscle actions. Therefore, additional research is necessary to clarify the relationships among muscle fiber action potential conduction velocity, EMG MPF, and motor control strategies during nonfatiguing maximal eccentric isokinetic muscle actions. CONCLUSION The primary findings of this study were that static stretching had no effect on PT, MP, EMG amplitude, EMG MPF, MMG amplitude, or MMG MPF for the stretched or unstretched limbs. In conjunction with the findings of previous studies, 7,15,21,39 these results suggest that the acute detrimental effects of static stretching may be mode specific, affecting concentric and isometric strength but not eccentric PT. Because static stretching did not affect PT, MP, or MMG journal of orthopaedic & sports physical therapy volume 37 number 3 march

9 amplitude, our findings suggest that any stretching-induced decreases in musculotendinous stiffness were not manifested through changes in the characteristics of the eccentric isokinetic angle-torque relationship (PT or MP) or indirect measures of muscle stiffness (MMG amplitude), which have been speculated in previous studies 11,14,20 to reduce muscle strength during concentric muscle actions. The fact that static stretching did not affect EMG amplitude, EMG MPF, or MMG MPF in the stretched or unstretched limbs in the present study suggests that static stretching may not influence the unique motor control strategies used for eccentric muscle actions, 19 despite previous studies that found stretchinginduced decreases in muscle activation for concentric 11,15 and isometric 7,21 muscle actions. Overall, these findings suggest that any stretching-induced decreases in performance observed during activities with concentric and eccentric components (eg, drop jump and vertical jump) may not be due to decreases in eccentric force production but rather may be due to decreases in the concentric component. The results of this study do not support the hypothesis by Shrier 44 that stretching before athletic activities increases the risk of injury due to decreases in eccentric force capabilities as a result of stretching, because the maintenance of eccentric muscle strength may be necessary to resist the high deceleration forces often associated with musculotendinous strains that occur under heavy eccentric loading conditions. t REFERENCES 1. Avela J, Kyrolainen H, Komi PV. Altered reflex sensitivity after repeated and prolonged passive muscle stretching. J Appl Physiol. 1999;86: Basmajian JV, De Luca CJ. Muscles Alive: Their Functions Revealed by Electromyography. 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