Stretching can be defined as the act of applying a tensile force to lengthen muscle and connective tissue (30). It is commonly included as an integral part of the warm-up routine for competitive athletes and recreational fitness participants with the principal intent to prevent injury and improve muscular performance. However, recent research (5,9,10,12,14,19,21,23,26,27,28,34) suggests that acute stretching before maximal muscular performance activities may impede the ability of a muscle to produce force. Two primary theories have been proposed to explain the stretching-induced decrease in muscular strength: (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 (2,5,9,10,12,14,17,19,21,22-24,34).
Although the aforementioned theoretical mechanisms may indeed explain most of the reduction in muscular performance reported to accompany acute stretching, program variables such as stretching volume, rest interval, and stretching method may modify these mechanisms and, therefore, could be important determinants of a stretching-induced performance deficit. Previous research has generally focused on examining the effects of relatively high-volume stretching routines on muscular performance in nonathletic populations; however, few studies have directly compared the effects of low- and high-volume stretching on maximal muscular-force production in highly trained athletic populations. Young et al. (35) examined the effects of static stretching volume and intensity on plantar flexor explosive force production and range of motion in 20 college-aged men and women and reported that impairment of explosive jump force capabilities was significantly increased as the duration of stretching increased from 1 to 4 minutes, supporting the notion of a volume effect. This suggests that stretching volume can have a significant effect on the development of maximal muscular force.
In addition, research examining the effects of stretching on upper body performance is limited and has reported conflicting findings. Evetovich et al. (12) reported that static stretching impaired force production of the biceps brachii in untrained college-aged women during fast (270°·s−1) and slow (30°·s−1) isokinetic forearm flexion. In contrast, Torres et al. (30) reported that static, dynamic, and combined static and dynamic stretching had no effect on a variety of upper body performance activities to include 30% 1-repetition maximum (1RM) bench throw, isometric bench press, and overhead medicine ball throw. The authors suggested that acute stretching may have varying effects on upper vs. lower body performance and sufficient rest after acute stretching may mitigate potential negative effects on performance.
Stretching method may also be an important variable in evaluating the effects of stretching on performance. Fagenbaum et al. (13) have shown that static stretching impedes performance in long jump, vertical jump, and shuttle run performance, whereas dynamic stretching significantly enhances performance in the same activities in children. Further, research has shown that proprioceptive neuromuscular facilitation (PNF) stretching may either have no effect (34) or result in a decrement (20) in muscular performance. Thus, more research is needed to evaluate the effects of various types of stretching on muscular performance, particularly in upper body activities.
Therefore, the purpose of this study was to determine the effects of both low- and high-volume PNF and static stretching on acute muscular strength assessed using 1RM bench press performance in resistance trained football athletes. Each stretching intervention was evaluated to determine a combination of stretching type and volume that may elicit the optimal effect on muscular strength.
Experimental Approach to the Problem
To evaluate the experimental hypotheses, a within-subject randomized repeated measures design was used. The investigators proposed that the high-volume static stretching (HVSS) and high-volume PNF stretching (HVPNFS) protocols would have a significant detrimental effect on 1RM bench press because of repeated high-volume stretch placed on the muscle. In this study, our principal objective was to determine the effect of varying the volume of PNF and static stretching on acute muscular strength. Fifteen athletes completed 5 different stretching protocols integrated with a 1RM dynamic warm-up routine followed by 1RM bench press testing in randomly assigned order. The protocols included (a) nonstretching (NS), (b) low-volume PNF stretching (LVPNFS), (c) HVPNFS, (d) low-volume static stretching (LVSS), and (e) HVSS.
Fifteen trained male collegiate football players (Table 1) volunteered to participate in the study. Subjects were informed of the experimental risks and signed an informed consent document before the investigation. The study was approved by the Institutional Review Board for the use of human subjects. All subjects were free from injury and able to perform stretching exercises and 1RM bench press without pain or limitations in the range of motion. None of the subjects had taken creatine or other performance-enhancing substances within the past 90 days. Subjects refrained from vigorous upper body exercise for 48 hours before each testing session. Testing was completed during the winter off-season conditioning program. The athletes were involved in a regular off-season resistance-training program that included the bench press exercise and regular periodic testing using 1RM measurements. In addition, the athletes were involved in a regular flexibility program that targeted the major muscle groups of the body during the competitive football season and the off-season conditioning program.
All anthropometric measurements were taken before testing. Measurements included height, weight, and body composition. Height was measured to the nearest tenth of a centimeter using a Seca #220 wall stadiometer. Body weight was assessed to the nearest 10th of a kilogram using a Befour Inc. (Cedarburg, WI, USA) digital scale. Body composition was estimated using an age/gender specific 3-site skinfold equation (chest, abdomen, and thigh) developed by Jackson and Pollock (16).
Strength Testing Protocol
The American College of Sports Medicine guidelines (1) for 1RM lifts were used to determine 1RM bench press. All testing was completed within a 3-week time frame.
In the bench press lift, subjects assumed a supine position on a bench with the feet flat on the ground. The bar was grasped at a width comfortable to the subject, which typically was slightly wider than shoulder width. The weighted bar was lowered to the chest in a smooth and controlled manner and subsequently extended to the maximal upper limb length.
Subjects were randomly assigned, varying order for each of 5 stretching protocols: (a) NS, (b) low-volume PNF, (c) high-volume PNF, (d) low-volume static, and (d) high-volume static before 1RM testing. The experimental protocol was as follows: (a) subjects performed a warm-up of 5-10 repetitions at 40-60% of the perceived maximum; (b) after a 1-minute rest interval, the randomly assigned stretching protocol was performed; (c) this was followed by another set of 3-5 repetitions at 60-80% of perceived 1RM; (d) after 3-5 minutes of rest, a maximal lift was attempted; (e) if the lift was successful, a rest period of 3-5 minutes was provided, and the process continued until a failed attempt occurred; (f) if the lift was unsuccessful, a rest period of 3-5 minutes was provided and another lift was attempted using a weight between the unsuccessful attempt and the last successful lift. The goal was to find the 1RM within 3-5 maximal lift attempts. The 1RM was determined using the weight from the last successful lift.
Two flexibility exercises were used to stretch the upper body. They consisted of the chest/shoulder partner stretch and the overhead triceps partner stretch. The investigator performed each stretch on all subjects to ensure consistency in stretching procedure. The chest/shoulder partner stretch (Figure 1) involved the subject standing in front of the investigator, with the investigator grasping the inside of the elbow joint. The subject abducted the shoulders and extended the arms to a position that was slightly below parallel to the ground. The investigator then pushed the arms together just above the elbow joints to stretch the pectoralis major and anterior deltoid muscles. The overhead triceps partner stretch (Figure 2) consisted of the subject placing 1 arm behind the head and trying to touch the opposite shoulder blade with the hand. The investigator placed a hand on the elbow of the stretched arm and began the stretch pushing the elbow across the subject's body toward the opposite shoulder. The investigator's opposite hand was placed on the subjects opposite shoulder to stabilize the upper body during the stretch.
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.
One-way ANOVA analysis showed that there was no significant effect (p > 0.05, effect size = 0.117) of any of the 5 stretching treatments on 1RM bench press performance to include NS (mean ± SEM; 129.7 ± 3.3 kg), LVPNFS (128.9 ± 3.8 kg), HVPNFS (128.3 ± 3.7 kg), LVSS (129.7 ± 3.7 kg) and HVSS (128.2 ± 3.7 kg). Figure 3 displays individual bench press performance (weight ± SEM, kg) across each stretching intervention. Further, the results of the repeated measures ANOVA revealed no significant (p > 0.05) differences among the testing days, which indicates there was no testing order effect.
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.
Wilson et al. (32) studied 13 trained male subjects using a series of maximal effort eccentric, concentric, and isometric muscular contractions in a bench press-type movement and reported that subjects with stiffer musculotendinous systems had a greater rate of initial power production in a concentric movement than in subjects with more compliant systems. They proposed that a stiffer musculotendinous unit may serve to facilitate the initial transmission of force from the contractile component to the skeletal structures.
Marek et al. (20) conducted a study on the effects of static and PNF stretching on lower body power output and strength and found decreases in both power output and strength with both static and PNF stretching protocols. The difference in the results of this study compared with the present study may be because of differences in the tests used (lower vs. upper body), stretching protocols (varying rest intervals, volume, intensity, and warm-up methods), and subject physical characteristics (male and female nonathletes vs. trained male athletes).
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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