Surface electromyography (sEMG) is a popular research tool in sport and rehabilitation sciences. Common study designs include the comparison of sEMG amplitudes collected from different muscles as participants perform various exercises and techniques under different loads. Based on such comparisons, researchers attempt to draw conclusions concerning the neuro- and electrophysiological underpinning of force production and hypothesize about possible longitudinal adaptations, such as strength and hypertrophy. However, such conclusions are frequently unsubstantiated and unwarranted. Hence, the goal of this review is to discuss what can and cannot be inferred from comparative research designs as it pertains to both the acute and longitudinal outcomes. General methodological recommendations are made, gaps in the literature are identified, and lines for future research to help improve the applicability of sEMG are suggested.

Resistance training is the most effective method to increase muscle mass. It has also been shown to promote many health benefits. Although it is deemed safe and of clinical relevance for treating and preventing a vast number of diseases, a time-efficient and minimal dose of exercise has been the focus of a great number of research studies. Similarly, an inverted U-shaped relationship between training dose/volume and physiological response has been hypothesized to exist. However, the majority of available evidence supports a clear dose-response relationship between resistance training volume and physiological responses, such as muscle hypertrophy and health outcomes. Additionally, there is a paucity of data to support the inverted U-shaped response. Although it may indeed exist, it appears to be much more plastic than previously thought. The overarching principle argued herein is that volume is the most easily modifiable variable that has the most evidenced-based response with important repercussions, be these muscle hypertrophy or health-related outcomes.

The purpose of the present study was to examine the possible inhibitory effect of passive plantar flexor muscle stretching on the motoneuron facilitatory system. Achilles tendon vibration (70 Hz) and triceps surae electrical stimulation (20 Hz) were imposed simultaneously in 11 subjects to elicit contraction through reflexive pathways in two experiments. In experiment 1, a vibration-stimulation protocol was implemented with the ankle joint plantar flexed (+10°), neutral (0°), and dorsiflexed (-10°). In experiment 2, the vibration-stimulation protocol was performed twice before (control), then immediately, 5, 10, and 15 min after a 5-min intermittent muscle stretch protocol. Plantar flexor torque and medial and lateral gastrocnemius and soleus (EMGSol) EMG amplitudes measured during and after (i.e., self-sustained motor unit firing) the vibration protocol were used as an indicator of this facilitatory pathway. In experiment 1, vibration torque, self-sustained torque and EMGSol were higher with the ankle at -10° compared with 0° and +10°, suggesting that this method is valid to assess motoneuronal facilitation. In experiment 2, torque during vibration was reduced by ∼ 60% immediately after stretch and remained depressed by ∼ 35% at 5 min after stretch (P< 0.05). Self-sustained torque was also reduced by ∼ 65% immediately after stretch (P < 0.05) but recovered by 5 min. Similarly, medial gastrocnemius EMG during vibration was reduced by ∼ 40% immediately after stretch (P < 0.05), and EMGSol during the self-sustained torque period was reduced by 44% immediately after stretch (P < 0.05). In conclusion, passive stretch negatively affected the motoneuronal amplification for at least 5 min, suggesting that motoneuron disfacilitation is a possible mechanism influencing the stretch-induced torque loss.

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The purpose of the present research was to identify the contribution of central vs. peripheral factors to the force loss after passive muscle stretching. Thirteen men randomly performed both a 5-min constant-torque stretch of the plantar flexors on an isokinetic dynamometer and a resting condition on 2 separate days. The triceps surae electromyogram (EMG) was recorded simultaneously with plantar flexor isometric torque. Measures of central drive, including the EMG amplitude normalized to the muscle compound action potential amplitude (EMG/M), percent voluntary activation and first volitional wave amplitude, and measures of peripheral function, including the twitch peak torque, 20-to-80-Hz tetanic torque ratio and torque during 20-Hz stimulation preceded by a doublet, were taken before and immediately and 15 min after each condition. Peak torque (-15.7%), EMG/M (-8.2%), and both twitch (-9.4%) and 20-Hz peak torques (-11.5%) were reduced immediately after stretch but recovered by 15 min. There were strong correlations between the torque loss and the reductions in central drive parameters (r = 0.65-0.93). Torque recovery was also strongly correlated with the recovery in EMG/M and percent voluntary activation (r = 0.77-0.81). The moderate decreases in measures of peripheral function were not related to the torque loss or recovery. These results suggest that 1) central factors were strongly related to the torque reduction immediately after stretch and during torque recovery; and 2) the muscle's contractile capacity was moderately reduced, although these changes were not associated with the torque reduction, and changes in excitation-contraction coupling efficiency were not observed.

It is well known that prolonged passive muscle stretch reduces maximal muscle force production. There is a growing body of evidence suggesting that adaptations occurring within the nervous system play a major role in this stretch-induced force reduction. This article reviews the existing literature, and some new evidence, regarding acute neurophysiological changes in response to passive muscle stretching. We discuss the possible contribution of supra-spinal and spinal structures to the force reduction after passive muscle stretch. In summary, based on the recent evidence reviewed we propose a new hypothesis that a disfacilitation occurring at the motoneuronal level after passive muscle stretch is a major factor affecting the neural efferent drive to the muscle and, subsequently, its ability to produce maximal force.

Whereas a variety of pre-exercise activities have been incorporated as part of a "warm-up" prior to work, combat, and athletic activities for millennia, the inclusion of static stretching (SS) within a warm-up has lost favour in the last 25 years. Research emphasised the possibility of SSinduced impairments in subsequent performance following prolonged stretching without proper dynamic warm-up activities. Proposed mechanisms underlying stretch-induced deficits include both neural (i.e. decreased voluntary activation, persistent inward current effects on motoneurone excitability) and morphological (i.e. changes in the force-length relationship, decreased Ca 2+ sensitivity, alterations in parallel elastic component) factors. Psychological influences such as a mental energy deficit and nocebo effects could also adversely affect performance. However, significant practical limitations exist within published studies, e.g. long stretching durations, stretching exercises with little task specificity, lack of warm-up before/after stretching, testing performed immediately after stretch completion, and risk of investigator and participant bias.Recent research indicates that appropriate durations of static stretching performed within a full warm-up (i.e. aerobic activities before and task-specific dynamic stretching and intense physical activities after SS) have trivial effects on subsequent performance with some evidence of improved force output at longer muscle lengths. For conditions in which muscular force production is compromised by stretching, knowledge of the underlying mechanisms would aid development of mitigation strategies. However, these mechanisms are yet to be perfectly defined. More information is needed to better understand both the warm-up components and mechanisms that contribute to performance enhancements or impairments when SS is incorporated within a pre-activity warm-up.

This study aims to evaluate the acute effects of different stretching exercises on muscular endurance in men, in terms of the number of sets, set duration, and type of stretching. Two experiments were conducted; in the first one (E1), the subjects (n = 19) were evaluated to test the effect on the number of sets, and, in the second one (E2), the subjects (n = 15) were tested for the effect of set duration and type of stretching. After a warm-up of 10-15 repetitions of a bench press (BP) with submaximal effort, a one-repetition maximum (1RM) test was applied. For E1, BP endurance was evaluated after static stretching comprising one set of 20 seconds (1 x 20), two sets of 20 seconds (2 x 20), and three sets of 20 seconds (3 x 20). For E2, BP endurance was evaluated after static stretching comprising one set of 20 seconds (1 x 20), one set of 40 seconds (1 x 40), and proprioceptive neuromuscular facilitation (PNF) stretching. All tests were performed 48-72 hours apart, at which time the muscular endurance was assessed through the maximal number of repetitions (NR) of BP at 85% of 1RM until fatigue. The NR and the overload volume (OV) were compared among tests through repeated-measures analysis of variance. No significant effect of the number of sets on muscular endurance was observed because no statistically significant difference was found when comparing all stretching exercises of E1 in terms of NS (p = 0.5377) and OV (p = 0.5723). However, significant reductions were obtained in the set duration and PNF on NR (p < 0.0001) and OV (p < 0.0001), as observed in E2. The results suggest that a stretching protocol can influence BP endurance, whereas a decrease in endurance is suggested to be attributable to set duration and PNF. On the other hand, a low volume of static stretching does not seem to have a significant effect on muscular endurance.