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Effects of Two Modes of Static Stretching on Muscle Strength and Stiffness

HERDA, TRENT J.1; COSTA, PABLO B.2; WALTER, ASHLEY A.3; RYAN, ERIC D.4; HOGE, KATHERINE M.3; KERKSICK, CHAD M.3; STOUT, JEFFREY R.3; CRAMER, JOEL T.3

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Medicine & Science in Sports & Exercise: September 2011 - Volume 43 - Issue 9 - p 1777-1784
doi: 10.1249/MSS.0b013e318215cda9
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Abstract

Clinically, stretching has been shown to increase the range of motion (ROM) in individuals with leg and foot disorders, such as Achilles tendinitis (17) and plantar fasciitis (29), and limited ankle ROM stroke survivors (40,41). In addition, stretching is regarded as an integral part of fitness and is applied to a diverse population; it is very important to accurately define and prescribe the types of stretching modalities that are most effective for achieving the common goals of increased flexibility and decreased musculotendinous stiffness (MTS). There is little debate over the clear boundaries that separate static, proprioceptive neuromuscular facilitation, ballistic, and dynamic stretching. However, static stretching, for the most commonly recommended modality (33), is loosely defined, and the studies that support its use are difficult to comparatively interpret. For example, the term "static" implies that there is no change in joint angle during the duration of the stretch, and there are numerous studies that have examined changes in flexibility and viscoelastic properties of the musculotendinous unit (MTU) during these constant-angle (CA) stretches (10,24,38). Stretches held at a CA displays a time-dependent property that is called "stress relaxation." Stress relaxation is the result of decreasing resistance (force or torque) in the MTU when the stretch is held at a constant muscle length (CA). There is also a large body of literature suggesting that constant-torque (CT) stretching improves flexibility and decreases MTS (15,31), but although CT stretching is technically not static and there is some joint angle movement during the stretch (i.e., viscoelastic creep), it often falls under the category of static stretching. Viscoelastic creep is the resulting increase in the joint angle caused by the constant pressure being applied to the MTU. Because this disparity exists between CA and CT stretching, there is a need to experimentally compare these two types of static stretching so that appropriate recommendations can be made.

The passive mechanical properties of muscle are typically expressed as stiffness, which is the relationship between passive resistive torque and joint displacement (i.e., angle-torque curve). The resistance produced by the passive mechanical properties is thought to be influenced by several factors, such as stable cross-links between the actin and myosin filaments, resistance from the actin and myosin filaments directly (series elastic component), noncontractile proteins of the endosarcomeric and exosarcomeric cytoskeletons (series elastic component), and deformation of the connective tissues located within and surrounding the muscle belly (parallel elastic component) (11). The MTS measurement is the most common method for assessing the passive mechanical properties of the muscle. The MTS measurement is calculated as the slope of the tangent to the angle-torque curve at a specified joint angle, and therefore, the assessment takes into account the shape of the angle-torque curve. In most static stretching studies, CA stretching will evoke a stress relaxation response that is characterized by a gradual decrease in passive torque from the stretched MTU when held at a CA (35). During CT stretching, a constant force or torque is applied, and the MTU will gradually elongate, resulting in a viscoelastic creep (32,39). Ryan et al. (31) hypothesized that because CT stretching performs more work on the MTU, it may also elicit greater changes in stiffness. In the only known studies to compare CA versus CT stretching, Yeh et al. (40,41) supported this hypothesis and reported greater improvements in ROM and viscoelastic properties from CT than CA stretching in stroke patients after 30 min of stretching of the plantar flexors. The Yeh et al. (40,41) stretching protocols included 30 min of continuous CT stretching, which the subjects expressed as uncomfortable compared with CA stretching. In addition, the researchers planned on modifying "the integrated treatment/assessment device such that it is capable of performing cyclic stretching with CT." Furthermore, Yeh et al. (40,41) did not test the acute effects of stretching on muscle strength and did not hypothesize about how a healthy population might respond to CA and CT stretching. Thus, to make sound recommendations for static stretching to improve flexibility and stiffness while minimizing any potential performance deficits, studies are needed to compare the effects of cyclic CA and CT stretching protocols not only on ROM and MTS but also on muscle strength in healthy populations.

Despite some conflicting evidence (8,37), many studies have reported transient decreases in muscle strength, strength endurance, power, and balance after an acute bout of static stretching (1,2,4-6,9,10,13,15,26,42). We are aware of no studies showing improvements in performance immediately after static stretching. Therefore, to fully understand the application of CA and CT stretching, it is also important to examine how both types of stretching affect muscle strength and activation as well as flexibility and the viscoelastic properties of the MTU. Therefore, the purpose of the present study was to examine the acute effects of CA versus CT static stretching of the leg flexors muscles on peak torque (PT), EMG amplitude (EMGRMS) at PT, passive ROM (PROM), passive torque (PASTQ), and MTS.

METHODS

Seventeen healthy men (mean ± SD: age = 21.4 ± 2.4 yr, height = 174.2 cm ± 7.2 cm, weight = 81.2 kg ± 10.2 kg) volunteered for this investigation. None of the participants reported any current or ongoing neuromuscular diseases or musculoskeletal injuries specific to the ankle, knee, or hip joints. Each participant completed a preexercise health questionnaire and signed a written informed consent document. Of the 17 participants, 11 reported engaging in 1-10 h·wk−1 of aerobic exercise, 9 reported engaging in 2-7 h·wk−1 of resistance exercise, and 8 reported engaging in 2-8 h·wk−1 of recreational sports. None of the participants were competitive athletes. Therefore, these individuals might be best classified as normal moderately active recreationally trained participants. This study was approved by the university's institutional review board for human subjects research.

This study used a randomized repeated-measures crossover design to examine the acute effects of CA and CT stretching of the leg flexors on PT, EMGRMS, PROM, PASTQ, and MTS. Each participant visited the laboratory three times, separated by 3-5 d. The first visit was a familiarization trial, and the next two visits were experimental trials, in which the subjects were randomly assigned to either the CA or the CT stretching treatment before the first experimental trial and then performed the other treatment on the second experimental trial. During each experimental trial, the participants underwent the prestretching tests (PROM assessments followed by maximal voluntary contraction (MVC) assessments), the stretching intervention, and the poststretching assessments that occurred immediately after the stretching. All experimental trials were performed at the same time of day (±2 h).

Three to five days before the experimental trials, each participant practiced the PT and PROM measurements and experienced the CA and CT stretching protocols to ensure that they were comfortable with the procedures and to minimize any potential learning effects. In addition, the maximum tolerable torque threshold was determined for each individual as the point of discomfort but not pain as verbally acknowledged by the subject during a series of passive stretches of the leg flexors. This predetermined torque threshold was then used for the passive stretching during the CT experimental trial.

To determine PT, each participant performed two 5-s isometric MVC of the right leg flexor muscles before and after the stretching. PT was measured using a Biodex System 3 isokinetic dynamometer (Biodex Medical Systems, Inc., Shirley, NY) at a knee joint angle of 80° below full leg extension. The participants were seated with restraining straps over the pelvis, trunk, and contralateral thigh, and the lateral condyle of the femur was aligned with the input axis of the dynamometer in accordance with the Biodex User's Guide (Biodex Pro Manual, Applications/Operations; Biodex Medical Systems, Inc.). Subjects were seated for approximately 10 min before testing to allow for placement of the EMG and reference electrode. PT was determined as the higher of two consecutive MVC trials separated by 1 min. All isometric PT assessments were performed with a 60° angle between the thigh and the torso. The participants were told to relax their foot in a plantarflexion position during the MVC tests.

The PROM of the leg flexors was determined for each subject during the pre- and poststretching assessments using the isokinetic dynamometer programmed in passive mode, which extended the leg at an angular velocity of 5°·s−1. PROM was the higher of two consecutive PROM trials separated by 1 min. The maximal ROM was determined for each subject as the point of discomfort but not pain, as verbally acknowledged by the subject during the PROM of the leg flexors. All PROM assessments were performed with a 60° angle between the thigh and the torso, the knee joint angle starting at 100° below full extension, and the foot relaxed in a plantarflexion position.

MTS of the leg flexors was quantified using a fourth-order polynomial regression model that was fitted to the passive angle-torque curves for each subject according to the procedure described by Nordez et al. (27). The fourth-order polynomial model was chosen over other models (i.e., second-order polynomial and Sten-Knudson) on the basis of the comparative recommendation of Nordez et al. (27) and because the fourth-order polynomial is clinically used in the literature to assess in vivo MTS (14,15,21,23,30). MTS quantifies the joint angle-specific stiffness of the MTU on the basis of the passive angle-torque relationship. MTS (N·m·°−1) was calculated for each degree increment in the passive angle-torque relationship. MTS was determined at every fifth degree during the final common 16° of the pre- and poststretching PROM assessments for each subject (5°, 10°, and 15°). Therefore, the second to the last common joint angle among the pre- and poststretching assessments (15°) was selected and termed "joint angle 3." Joint angles 1 and 2 were 10° and 5° before joint angle 3, respectively. MTS values were calculated with the following equation (27), where θ represents the joint angle and m, n, o, p, and q were coefficients in the fourth-order polynomial regression model that was fit to the passive angle-torque relationship:

MTS was subsequently calculated with the following equation (27):

MTS was calculated offline using a custom-written software (LabVIEW 8.5; National Instruments, Austin, TX), which included a gravity correction of the limb.

Surface EMG signals were recorded from bipolar preamplified electrodes (EL254S; BIOPAC Systems, Santa Barbara, CA) with a fixed center-to-center interelectrode distance of 20 mm and a gain of 350 placed over the biceps femoris muscle at 66% of the distance between the ischial tuberosity and the lateral epicondyle of the tibia, on the basis of the recommendations of Hermens et al. (16). To reduce interelectrode impedance, the skin was shaved and cleaned with isopropyl alcohol before electrode placement. A single pregelled disposable electrode (Ag-AgCl, Quinton Quick Prep; Quinton Instruments Co., Bothell, WA) was placed on the spinous process of the seventh cervical vertebrae to serve as a reference electrode.

The torque (N·m), angle (°), and EMG (μV) signals were sampled simultaneously at 1 kHz with a BIOPAC data acquisition system (MP150WSW; BIOPAC Systems) during each PROM and MVC. All signals were stored on a personal computer (Dell Inspiron 8200; Dell, Inc., Round Rock, TX) to be processed offline using a custom-written software (LabVIEW 8.5; National Instruments). All EMG signals were filtered with a passband of 10-500 Hz using a zero-phase shift fourth-order Butterworth filter. Amplitude of the EMG signal was calculated using a root mean squared (RMS) function applied to the filtered signals. PT from an MVC was determined as the highest consecutive 500-ms epoch with the corresponding EMGRMS being calculated from that same epoch. To ensure all PROM assessments were passive, EMG was also collected during the PROM measurements. These EMGRMS values were quantified with 200-ms epochs corresponding to the same joint angles used to quantify MTS. EMGRMS baseline noise values were subtracted from the EMGRMS values recorded during the passive movements. The corrected passive EMG values were then normalized to the EMGRMS values recorded during the isometric MVC (i.e., %MVC). PROM measurements were excluded if normalized EMGRMS activity was >5% of the MVC in accordance with Gajdosik et al. (12).

The repeated passive stretching of the right leg flexor muscles was performed using the isokinetic dynamometer in "passive" mode. The dynamometer passively extended the leg at 5°·s−1 until the maximal tolerable torque threshold (CT) (determined during familiarization) was met or until the subject verbally acknowledged discomfort but not pain by saying "stop." The latter procedure was used for the CA stretching treatment. Stretches in both treatments were performed for 30-s bouts with a 20-s rest between bouts, in which the leg was returned to the resting flexed position. Each subject underwent sixteen 30-s bouts of stretching, totaling 8 min of time under stretch and lasting approximately 20 min total. All subjects experienced both stretching treatments in a random order.

Three separate three-way repeated-measures ANOVA (time (pre- vs poststretching) × treatment (CT vs CA) × joint angle (1 vs 2 vs 3)) were used to determine differences between stretching treatments for MTS, PASTQ, and EMGRMS during the PROM assessment. In addition, three separate two-way repeated-measures ANOVA (time (pre- vs poststretching) × treatment (CT vs CA)) were used to determine differences between stretching treatments for PROM, PT, and EMGRMS at PT. When appropriate, follow-up analyses were performed using one-way repeated-measures ANOVA and dependent-samples t-tests with Bonferroni corrections. The level of significance was set at P ≤ 0.05, and all statistical analyses were performed using SPSS v. 16.0 (SPSS, Inc., Chicago, IL). Partial eta squared (ηp2) values are also reported below to reflect the magnitude of the change after each treatment.

RESULTS

For MTS, there was a significant three-way interaction (treatment × time × angle, F2,32 = 8.373, P = 0.001, ηp2 = 0.344). MTS decreased from before to after treatment at all three joint angles for the CT treatment (angle 1: F1,16 = 11.172, P = 0.004, ηp2 = 0.411; angle 2: F1,16 = 9.069, P = 0.008, ηp2 = 0.362; angle 3: F1,16 = 6.869, P = 0.019, ηp2 = 0.300), but MTS did not change for any joint angles during the CA treatment (P > 0.05) (Fig. 1).

FIGURE 1
FIGURE 1:
Pre- (shaded squares) and posttreatment (open squares) MTS values (N·m·°−1) for CA and CT treatments at each joint angle (1, 2, and 3). *Significant differences from before to after treatment (P < 0.05). †Significant difference for angle 3 before CA versus angle 3 before CT (P = 0.013). Values are means ± SE. For before CA: angle 1 < angle 2 (P < 0.001) and angle 3 (P = 0.014); for after CA: angle 1 < angle 2 (P < 0.001) and angle 3 (P < 0.001), angle 2 < angle 3 (P < 0.001); for before CT: angle 1 < angle 2 (P < 0.001) and angle 3 (P < 0.001), angle 2 < angle 3 (P < 0.001); for after CT: angle 1 < angle 2 (P < 0.001) and angle 3 (P < 0.001), angle 2 < angle 3 (P < 0.001).

There was no order effect for days (day 1 vs 2) for the prestretching PT (F1,16 = 1.962, P = 0.142, ηp2 = 0.130) or prestretching PROM (F1,16 = 0.247, P = 0.626, ηp2 = 0.015) values. Table 1 contains mean ± SE values for pre- and poststretching MVC PT, EMGRMS at PT, and PROM, whereas MTS and PASTQ values are shown in Table 2.

TABLE 1
TABLE 1:
Mean ± SE values for before and after stretching for MVC PT, MVC EMGRMS, and PROM.
TABLE 2
TABLE 2:
Mean ± SE values for angles 1, 2, and 3 for before and after stretching for MTS and passive torque (PASTQ) values.

For PT, there were no significant two-way interaction (treatment × time, F1,16 = 1.962, P = 0.180, ηp2 = 0.109) and no main effect for treatment (F1,16 = 0.201, P = 0.654, ηp2 = 0.013), but there was a main effect for time (F1,16 = 11.515, P = 0.004, ηp2 = 0.418). PT decreased from before to after stretching (collapsed across CA and CT treatments) by a mean ± SE of 6.41% ± 3.15%.

For EMGRMS at PT, there were no significant two-way interaction (time × treatment, F1,16 = 0.210, P = 0.653, ηp2 = 0.013) and no main effects for time (F1,16 = 0.840, P = 0.373, ηp2 = 0.050) or treatment (F1,16 = 0.143, P = 0.710, ηp2 < 0.001).

For PROM, there were no significant two-way interaction (treatment × time, F1,16 = 0.657, P = 0.429, ηp2 = 0.039) and no main effect for treatment (F1,16 = 2.244, P = 0.154, ηp2 = 0.123), but there was a main effect for time (F1,16 = 19.996, P < 0.001, ηp2 = 0.556). PROM increased by 3.86% ± 1.12% from before to after stretching for both the CA and CT treatments.

For PASTQ, there were no significant three-way interaction (treatment × time × angle, F2,32 = 0.700, P = 0.504, ηp2 = 0.042) and no treatment × angle interaction (F2,32 = 0.330, P = 0.721, ηp2 = 0.020), but there was a time × angle interaction (F2,32 = 8.203, P = 0.001, ηp2 = 0.339). PASTQ decreased from before to after treatment at all angles (collapsed across CA and CT treatments) (Fig. 2).

FIGURE 2
FIGURE 2:
Pre- (shaded squares) and posttreatment (open squares) passive torque (N·m) values during the PROM for CA and CT treatments at each joint angle (1, 2, and 3). *Significant differences from before to after treatment (P < 0.05) collapsed across CA and CT stretching treatments. Values are means ± SE. For before (collapsed across treatments): angle 1 < angle 2 (P < 0.001) and angle 3 (P < 0.001), angle 2 < angle 3 (P < 0.001); for after (collapsed across treatments): angle 1 < angle 2 (P < 0.001) and angle 3 (P < 0.001), angle 2 < angle 3 (P < 0.001).

For EMGRMS during the PROM assessments, there were no significant three-way interaction (treatment × time × angle, F2,32 = 0.660, P = 0.524, ηp2 = 0.362), no significant two-way interactions (treatment × angle, F2,32 = 0.713, P = 0.498, ηp2 = 0.043; time × angle, F2,32 = 0.158, P = 0.854, ηp2 = 0.010; treatment × time, F2,16 = 0.195, P = 0.665, ηp2 = 0.012), and no main effects for angle (F2,16 = 0.235, P = 0.792, ηp2 = 0.014), time (F1,16 = 1.462, P = 0.244, ηp2 = 0.084), or treatment (F1,16 = 0.038, P = 0.848 ηp2 = 0.002).

DISCUSSION

The primary finding of the present study was that only the CT stretching decreased muscle stiffness, whereas both types of stretching (CT and CA) improved the ROM. Specifically, 8 min of CA and CT stretching increased PROM and decreased PASTQ at all joint angles; however, MTS only decreased after the CT stretching and was unchanged after CA stretching. Previous studies have examined the effects of a 30-min bout of CA and CT stretching in stroke patients with ankle hypertonia (40,41). The authors reported greater increases in ROM and decreases in the viscoelastic properties of the muscle for the CT stretching treatment compared with the CA stretching treatment. Yeh et al. (40) hypothesized that the greater decreases in stiffness reported with the CT stretching protocol may have been due to "muscle creep" during the stretch. The muscle creep results in slight increases in the ROM during the stretch and, in theory, would result in greater changes to PROM and stiffness because of the constant pressure and energy placed on the viscoelastic properties of the muscle throughout the stretch. Ryan et al. (31) suggested that CT stretching protocols may place more tension and/or apply more work on the MTU, which would result in greater changes in the viscoelastic properties of the muscle when compared with holding a stretch at a constant joint angle. However, unlike Yeh et al. (40,41), the CT stretching in the present study did not result in greater PROM or passive torque changes compared with the CA stretching. Therefore, in the present study, the muscle creep during the CT stretching did not result in greater changes in PROM and passive torque compared with the CA stretching with the stress relaxation response of the muscle. The different dosages of stretching may have accounted for the inconsistencies between Yeh et al. (40,41) and the present study on PROM and passive torque. Yeh et al. (40,41) applied the stretches continuously for 30 min, whereas in the present study, the stretching was performed cyclically for a total time under stretch of 9 min. Nevertheless, the results of the current study do support the hypotheses and suggest that CT stretching is superior to CA stretching for decreasing muscle stiffness.

Despite no differences in PROM and PASTQ between the CT and CA stretching treatments, an interesting finding of the present study was the disassociation between muscle stiffness and joint ROM, which has been suggested previously (20,22). There were decreases in MTS after the CT but not the CA stretching. However, PASTQ decreased and PROM increased after the CA and CT stretching treatments. This finding emphasizes two important factors: (a) simple ROM measurements do not fully describe how the MTU changes during a stretch and (b) MTS is more complex than simple decreases in the passive resistance to stretching (i.e., PASTQ). In addition, Magnusson (20) suggests that it still remains unclear what determines the end point for ROM, and it is typically never accounted for. In the present study, MTS was calculated as the slope of the tangent to the angle-torque curve at the specified joint angle (θ). Therefore, not only does the passive torque (PASTQ) need to decrease but also the shape of the angle-torque curve must change to see the decreases in MTS. Changes in the shape of the angle-torque curve may reflect changes in the viscoelastic properties of the MTU. For example, Gajdosik (11) reported that stretching at a CA affects the viscosity of the muscle-tendon structures but not the elasticity. Thus, it is possible that the decreases in MTS after the CT stretching (slopes of the tangents to the angle-torque curve) in the present study may have reflected the changes in elasticity of the MTU caused by the CT stretching treatment, which may have been why MTS was unaffected by the CA stretching. It is possible that the greater work performed by the CT stretching was enough to affect the viscosity and elasticity of the MTU, which resulted in the morphological change in the angle-torque curve and subsequent decrease in MTS. On the other hand, the CA stretching may have affected only the viscosity but not the elasticity as suggested by Gajdosik (11). Future studies are needed to elucidate the mechanisms underlying the changes in muscle stiffness after CT and CA stretching.

The results in the present study indicated that CT stretching should be used for specific patient populations where decreasing MTS is the objective, such as individuals with Achilles tendinitis (17) and plantar fasciitis (29) and stroke survivors (40,41). It has been hypothesized that the stretching-induced decreases in MTS would reduce the amount of strain on the MTU throughout a given ROM, thereby decreasing the risk for muscle strain injuries (7). Taylor et al. (35) demonstrated that 10 cycles of stretching to 50% of the determined failure length in rabbit muscle resulted in greater muscle length before injury. The authors concluded that less force would be placed on the MTU throughout the required ROM after stretching, which would reduce the risk of muscle strains. Although there were differences in MTS between the stretching conditions, because there were similar changes between CA and CT stretching on PROM and passive torque, it is unclear if either form of stretching would be more beneficial in reducing the risk of muscle strains. There is, however, only limited evidence to directly support that acute static stretching does reduce musculotendinous injuries (34,36). Furthermore, in animal models, there is evidence that suggests that muscle damage is more of a function of the muscle fiber strain that occurs during the lengthening of an activated muscle (18,19), and it is unclear what the effects of the stretching protocols in the present study would have on active muscle strains. In addition, Pereles et al. (28) examined a prerun stretching protocol in runners who completed at least 10 miles·wk−1 and reported that there were no differences in injury risk between the prerun stretch and nonstretch run groups. Clearly, future research is needed before stating definitively that the reduction of MTS after CT stretching could result in decreases of muscle strains.

Previous studies have reported stretching-induced decreases in strength. However, no studies have examined strength deficits specifically comparing CA and CT stretching. Some comparisons can be made between studies that used CA or CT stretching. For example, McHugh and Nesse (24) reported that 9 min of CA stretching resulted in a decrease in PT at shorter muscle lengths. Furthermore, Herda et al. (13) also reported a decrease in PT at the shorter muscle lengths after roughly 9 min of static stretching. The stretching protocol in Herda et al. (13) used a combination of assisted partner stretching with a constant pressure being applied by the investigator and unassisted stretching that required the subjects to "reach until the right leg flexors were stretched." It is possible that the unassisted stretching procedure in the study of Herda et al. (13) was not truly a CA stretch with the subject reaching a little further ever so often. In addition, it is unknown if the pressure that was applied by the investigator during the assisted partner stretch was truly a constant pressure throughout the stretching. It is critical that future studies report and monitor the type of static stretching that is being implemented because it would elucidate which type of static stretching would have a greater decrement on performance. Nevertheless, Herda et al. (13) could not make a distinction on which mode of stretching was more detrimental to strength.

In the present study, PT decreased to the same extent after CA and CT stretching, and EMG was unchanged after CA and CT stretching. Ryan et al. (31) examined the effects of shorter durations (≤8 min) of CT stretching of the plantar flexors and reported decreases in strength with no changes in muscle activation. Our results support the findings of Ryan et al. (31) in that there were no changes in muscle activation after 8 min of CA or CT stretching. Furthermore, the results of the present study are consistent with the studies of McHugh and Nesse (24) and Herda et al. (13) who reported decreases in leg flexor strength at shorter muscle lengths (the muscle length tested in the current study is consistent with the shortest muscle length tested in the studies of McHugh and Nesse [24] and Herda et al. [13]) and concluded that stretching may have caused a shift in the length-tension relationship, with decreases in strength at the shorter muscle lengths and possible increases in strength at the longest muscle lengths. Nelson et al. (25) also reported that leg extensor PT decreased at the shortest tested muscle length (knee joint angle at 162°) and was unchanged for all the longer muscle lengths. In addition, stretching resulted in decreases in peak twitch force and rate of force development (3) and an increase in the electromechanical delay (14), which the authors suggested was a result of the decreases in MTS. Therefore, CT stretching may hinder performance tasks that require rapid force generation more so than CA stretching because of the decreases in MTS. In summary, CA and CT stretching negatively affected muscle strength to the same extent, and therefore, it is recommended to incorporate a CT stretching routine before performance to reduce MTS with the understanding that it would not cause any greater decrement in strength compared with CA stretching.

In summary, PASTQ and PROM changed in a similar manner for both treatments; however, MTS decreased after CT but not CA stretching. If the primary goal of the stretching routine is to decrease MTS, these results suggest that a static stretch held with a constant pressure (CT stretching) would be more appropriate than stretching held at a constant muscle length (CA stretching). Practitioners should be aware that despite the greater changes in MTS after CT stretching, there will not be a greater decrement in strength compared with CA stretching. In the present study, the stretching methodology applied is not practical for a stretching routine (16 stretches for 30 s each for one muscle group), and therefore, future research is needed to examine the effects of CA and CT stretching incorporated in a practical stretching routine on MTS in both males and females. In addition, future research is needed to identify a simpler valid method to quantify MTS in a clinical setting.

There was no funding for this project.

The results of the present study do not constitute endorsement by the American College of Sports Medicine.

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Keywords:

MUSCULOTENDINOUS STIFFNESS; PASSIVE RANGE OF MOTION; LEG FLEXORS; EMG

©2011The American College of Sports Medicine