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Purpose: To examine the acute effect of a single static-stretching session of hamstring muscles on torque production in relation with individual flexibility., Methods: Maximal voluntary concentric torque of hamstring muscles was measured before and after a static-stretching session (6 × 30 s). Torque changes were correlated with the flexibility level determined at the onset of the experimental procedure., Results: The hamstring-stretching intervention significantly reduced maximal concentric torque in participants with low and high hamstring flexibility. Hamstring flexibility and torque decrease, determined immediately after the stretching procedure, were negatively correlated., Conclusions: Torque decrease measured after the static-stretching session is dependent on participant flexibility. Participants with low flexibility are much more likely to demonstrate large torque decreases poststretching.

The time course of alteration in neuromuscular function of the knee extensor muscles was characterized during a prolonged intermittent exercise. Maximal voluntary contraction (MVC) and surface EMG activity of both vastii were measured during brief interruptions before (T(0)), during (30, 60, 90, 120, 150 and 180min: T(30), T(60), T(90), T(120), T(150), T(180)) and 30min after (T(+30)) a 3h tennis match in 12 trained players. M-wave and twitch contractile properties were analyzed following single stimuli. Short tetani at 20Hz and 80Hz were also applied to six subjects at T(0) and T(180). Significant reductions in MVC (P<0.05; -9%) and electromyographic activity normalized to the M wave for both vastii (P<0.01) occurred with fatigue at T(180). No significant changes in M-wave duration and amplitude nor in twitch contractile properties were observed. The ratio between the torques evoked by 20Hz and 80Hz stimulation declined significantly (P<0.001; -12%) after exercise. Central activation failure and alterations in excitation-contraction coupling are probable mechanisms contributing to the moderate impairment of the neuromuscular function during prolonged tennis playing.

Purpose: To investigate muscle deoxygenation and neural drive-related changes during repeated cycling sprints in a fatiguing context., Methods: Nine healthy male subjects performed a repeated-sprint test (consisting of 10 x 6-s maximal sprints interspaced by 30 s of recovery). Oxygen uptake was measured breath-by-breath; muscle deoxygenation of the vastus lateralis was assessed continuously using the near-infrared spectroscopy technique. Surface electromyograms (RMS) of both vastus lateralis and biceps femoris were also recorded. Furthermore, before and after the repeated-sprint test, the percentage of muscle activation by voluntary drive (twitch-interpolated method) was measured during a maximal voluntary contraction., Results and Discussion: Consistent with previous research, our data showed a significant power decrement during repeated-sprint exercise. There was also a progressive muscle deoxygenation, but our data showed that the ability of the subjects to use available O2 throughout the entire repeated-sprint test was well preserved. Our data displayed a significant decrement in the RMS activity during the acceleration phase of each sprint across the repeated-sprint exercise. Moreover, decrement in motor drive was confirmed after exercise by a significant decrease in both percentage of voluntary activation and RMS/M-wave ratio during a maximal voluntary contraction., Conclusion: In this experimental design, our findings suggest that the ability to repeat short-duration (6 s) sprints was associated with the occurrence of both peripheral and central fatigue.

Aim: The purpose of this study was to re-examine central and peripheral origins of neuromuscular fatigue after a highly strenuous eccentric exercise of the knee extensor muscles (KE) using both voluntary/evoked contractions and electromyographic recordings (EMG)., Methods: Before, and 30 min after 15 min of intermittent one-logged downhill running, maximal percutaneous electrical stimulations (single twitch, 0.5 s tetanus at 20 Hz and 80 Hz) were applied to the femoral nerve of 10 male subjects. Electrically evoked superimposed twitches were delivered during isometric maximal voluntary contraction (MVC) to determine maximal voluntary activation (%VA). Vastus lateralis (VL), vastus medialis (VM) and biceps femoris (BF) EMG were recorded during MVC and quantified using the root mean square (RMS) value. M-wave characteristics were also determined., Results: KE MVC and %VA decreased significantly with fatigue (-19.6+/-6.1%; P<0.001 and -7.8+/-6.6%; P<0.01, respectively). Peak tetanus tension at 20 and 80 Hz (P20 and P80, respectively) declined (P<0.001), concurrently with a decrement of the P20 x P80(-1) ratio (-37.3+/-16.6%; P<0.001). Antagonist muscle coactivation, RMS to M-wave peak-to-peak amplitude and MVC x P80(-1) ratios were unchanged after the fatiguing exercise., Conclusions: The results reveal that part of the large loss in MVC may have a central origin but most of the MVC decrement is due to the presence of low-frequency fatigue while possible contractile failure cannot be excluded.

Purpose: This study aimed to evaluate the benefit of using low-intensity running or electromyostimulation (EMS) to hasten the recovery process from eccentric-contraction-induced injury., Methods: Before and 30 min, 24 h, 48 h, and 96 h after a one-legged downhill run, electrical stimulations were applied to the femoral nerve of healthy volunteers. Superimposed twitches were delivered during isometric maximal voluntary contraction (MVC) to determine the voluntary activation level (%VA). For 4 d after the exercise, each subject performed either (i) 30 min of running at 50% VO2max, (ii) 30 min of low-frequency EMS on the lower limb extensor muscles, or (iii) passive recovery., Results: Recovery time courses of the different variables did not differ significantly among the three experimental conditions. MVC decreased 30 min after the exercise and did not recover thereafter (P < 0.001). Percent VA was depressed after the exercise (P < 0.05) but did not contribute to MVC decrement thereafter. Mechanical responses to 80- and 20-Hz stimulation (P80 and P20, respectively) were significantly reduced over time (P < 0.01 and P < 0.001, respectively). Interestingly, MVC, P20, and P80 decrements were not statistically different (-9.6 +/- 14.5%, -13.2 +/- 14.2%, and -12.3 +/- 11.3%, respectively) at 48 h, and the P20.P80(-1) ratio showed complete recovery at this time., Conclusions: The different recovery modes had no significant effect on the recovery time course of contractile properties. The prolonged torque loss is mainly due to peripheral alterations. Our results suggest that an alteration of the excitation-contraction coupling might be involved during the first 2 d after the eccentric exercise. From 2 to 4 d, damage to force-generating structures could account for the remaining torque deficit.

The contribution of central and peripheral factors to muscle fatigue were quantified following a high-intensity uphill running exercise. Eight male volunteers performed an intermittent exercise at 120 % of maximal aerobic speed on a treadmill with an 18 % grade. Electrically evoked and voluntary contractions of the knee extensors and EMG of the two vastii were analyzed before and immediately after the high-intensity exercise. Isometric maximal voluntary contraction decreased slightly (-7+/-8 %; p < 0.05) after exercise but no changes were found in the level of maximal activation or in the torque produced by a 80 Hz maximal stimulation applied to the femoral nerve. Following exercise, the single twitch was characterized by lower peak torque, maximal rate of force development, and relaxation (-28+/-11%, -25+/-12%, -31+/-15% respectively, p < 0.001), and higher surface of the M-wave for both vastii. The ratio between the torques evoked by 20 Hz and 80 Hz stimulation declined significantly (-22+/-10%, p < 0.01) after exercise. These findings indicate that muscle fatigue after high-intensity running exercise is due to significant alteration in excitation-contraction coupling and that this type of exercise does not induce significant central fatigue or changes at the crossbridge level.

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 +/- 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 +/- 25.2 to 142.7 +/- 29.7 N x m; P < 0.001) as did %VA (from 98.8 +/- 1.8 to 91.3 +/- 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated (R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant (P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 +/- 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit.