The NS protocol consisted of substituting step 2 of the stretching protocol with a 3- to 5-minute rest period. The LVPNFS protocol included 2 sets of each stretch. Each subject was immediately stretched to a position of moderate tension and then isometrically contracted the agonist muscles against resistance applied by the investigator at 75% of perceived maximal effort for 5 seconds. A 10-second relaxation period was followed by 10 seconds of passive static stretching to a point of moderate tension. The HVPNFS protocol included 5 sets of each stretch, completed in the same manner as the LVPNFS protocol. The LVSS protocol consisted of 2 sets of each stretch, in which the investigator stretched each subject to a position of moderate tension and held it for 20 seconds. The HVSS protocol included 5 sets of the same stretches, but each was held for 30 seconds.
Subjects first performed the overhead triceps partner stretch. Each stretch was performed in succession alternating to opposite sides of the body. After the overhead triceps stretch was completed, the chest/shoulder partner stretch was performed. A 1-minute rest interval was required between each set of stretching.
A 1-way analysis of variance (ANOVA) with repeated measures was used to determine mean differences between the 5 stretching interventions and for determining the effect of testing order (test day 1 vs. test day 2 vs. test day 3 vs. test day 4 vs. test day 5). In addition, effect size estimates were calculated using Partial Eta Squared. SPSS (version 16.1, SPSS Inc, Chicago, IL) was used for all statistical analyses. An alpha level of p ≤ 0.05 was used to establish significance.
The principal finding of this study was that stretching method and volume had no significant effect on 1RM bench press performance in resistance trained collegiate football players. These findings agree with other studies in which it was reported that there was no effect of stretching on muscular strength or power (7,17,18,30). In contrast, numerous authors have reported an acute decrease in muscular strength or power after stretching (3-6,8-14,19-23,25,35,34).
The results of the study did not support our hypothesis that both HVPNFS and HVSS would have a significant negative effect on 1RM bench press performance. Although there was a nonsignificant difference in the average weight lifted between stretching protocols, it is curious that the HVPNFS and HVSS had the lowest average 1RM bench press values. It is possible that a larger volume or higher intensity of stretching may have produced significant differences in 1RM bench press performance across the stretching interventions. Indeed it has been reported (33) that explosive jump force capabilities are significantly impaired as stretching duration is increased; however, when stretching intensity is reduced (with volume held constant), there was no significant impairment of explosive force production. Thus, it appears that there is a critical combination of stretching volume and intensity that is needed to impair muscular performance.
Two hypotheses have been developed to account for the stretching-induced decrease in muscular-force production capacity: (a) mechanical factors such as reduced stiffness of the musculotendinous unit and (b) neural factors such as altered motor control strategies or greater autogenic inhibition. Wilson et al. (32) found that stiffness of the musculotendinous unit is significantly related to isometric and concentric performance. Similarly, Evetovich et al. (12) reported that increased mechanomyography amplitude in stretched muscles indicated that acute static stretching may reduce muscular stiffness and result in a lower peak torque during concentric isokinetic muscle actions. Three mechanisms have been proposed to explain this phenomenon. The first 2 relate to a stiffer musculotendinous unit that allows for more effective force production from the contractile component because of improved length and velocity conditions. The third relates to the concept that the stiffness of the musculotendinous unit will determine the effectiveness of initial force development. At a given magnitude of contraction, a stiffer musculotendinous unit should in theory, result in a greater length of the contractile component and a reduced contractile component shortening velocity.
Neural factors have also been hypothesized to be responsible for stretch-induced decreases in muscular-force production because of decreased motor unit activation, firing frequency, or altered reflex sensitivity (2,5,10,14,25). This hypothesis is based on studies that have reported a decrease in muscle activation and excitability during stretching as measured by the Hoffman reflex (2,12,15,29,31). Through the use of surface (5,10,14,25) and fine-wire (2) electromyography in addition to twitch interpolation techniques (5,14,25), stretch-induced decreases in muscle activation have been demonstrated.
In the present study, we did not find a decrement in performance regardless of stretching type or volume. Our findings may have been due, in part, to the length of the rest interval after the completion of the stretching interventions to the initial 1RM attempt. This time interval exceeded 5 minutes, which may have been sufficient time to mitigate the effects of the stretching protocol on muscular performance. This is consistent with the findings reported by Torres et al. (30) that acute static, dynamic, and combined dynamic and static stretching had no effect on upper body performance measures in collegiate track throwers with 5 minutes of rest after the stretching interventions. Further, both studies included trained collegiate athletes that performed regular stretching as part of the training warm-up protocol. This raises the possibility that trained athletes that incorporate regular stretching into a warm-up routine may be capable of recovering from altered visceoelastic properties of the musculotendinous unit within 5 minutes of completion of a stretching routine. Because previous research has consistently reported a decrement in performance after lower body stretching, the results of these studies also suggest that the upper body musculature may respond differently to acute stretching than the lower body.
Alternatively, the methods of stretching examined in this study and the angles that the stretches were applied may not have targeted the elastic component of the chest motor units that were recruited during the 1RM bench press test. In addition, a limited stretch shortening cycle may exist when performing the 1RM bench press and thus may account for the absence of a performance effect as a result of the stretching interventions. More research is needed to determine the effect of upper vs. lower body stretching and program variables such as stretching volume, method, and rest intervals on muscular performance across varying age, gender, fitness level, competitive experience, and sport modalities.
The results of this investigation indicate that stretching immediately before maximal isotonic muscular performance has no significant effect on the upper body force producing capabilities of the stretched muscles in resistance-trained collegiate football athletes. Our findings suggest that resistance-trained athletes can include either (a) a dynamic warm-up with no stretching or (b) a dynamic warm-up in concert with low- or high-volume static or PNF flexibility exercises before maximal upper body isotonic resistance training lifts, if adequate rest is allowed before performance.
We wish to thank Barbara Engebretsen for her thoughtful editorial comments and suggestions to improve this manuscript.
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