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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. [ABSTRACT FROM AUTHOR]

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.

This study tested the hypothesis that neuromuscular characteristics of plantar flexor (PF) and knee extensor (KE) muscles explain differences of both performance in vertical jump and maximal voluntary isometric contraction (MVC) between endurance-trained (END, n = 9), power-trained (POW, n = 8), and sedentary subjects (SED, n = 8). Evoked twitch characteristics of PF and KE were measured. MVC, maximal voluntary activation (%VA) of KE, and performance in vertical jump were also measured. POW have higher maximal rate of twitch force development (MRFD) than SED and END for both PF (p < 0.05) and KE (p < 0.01); %VA and MVC were higher for POW and END than SED (p < 0.01). Higher performances were measured in vertical jump for POW compared with END and SED. Significant relationships were found between the squat jump performance and MRFD for both KE and PF (R = 0.71, p < 0.0001 and R = 0.55, p < 0.01, respectively). These findings show that low MRFD on lower limbs extensors does not limit expression of MVC on subjects with high levels of activation, whereas intrinsic muscular qualities have a direct influence on performance during the vertical jump.

The aim of this study was to examine the effects of fatigue induced by a 65-km ultramarathon on the oxygen cost of running (Cr) and cycling (Ccycl). The day before and immediately after the race, a group of nine well-trained male subjects performed two submaximal 4-min exercise bouts: one cycling at a power corresponding to 1.5 W x kg(-1) body mass on an electromagnetically braked ergometer, and one running at 11 km x h(-1) on a flat asphalt roadway. Before oxygen cost determinations, the subjects performed 12 "ankle" jumps at a given frequency that was fixed by an electronic metronome (2.5 Hz). From the non-fatigued to the fatigued condition, there was a significant increase in minute ventilation for both running (P < 0.01) and cycling (P < 0.0001). Significant changes were also found in respiratory exchange ratio both for running (P = 0.01) and cycling (P < 0.0001). However, running and cycling differed in that Cycyc increased significantly by [mean (SD)] 24.2 (11.5)% (P < 0.001), suggesting an alteration of muscle efficiency, while Cr did not change with fatigue [186.8 (14.1) mlO2 x kg(-1) x km(-1) vs 186.8 (18.7) mlO2 x kg(-1) x km(-1)]. In addition, contact times during hopping increased significantly from 0.173 (0.019) ms to 0.194 (0.027) ms (P < 0.01). Analysis of the factors that determine Cr indicate that the subjects modified their movement pattern in order to decrease the mechanical cost of running in such long-term fatigue conditions.

Rats treated with ethinylestradiol (5 mg kg-1 day-1 for 5 days) secrete de novo synthesized bile acids at a markedly reduced rate (-57%). Administration of the nonionic detergent Triton WR-1339 to estradiol-treated rats rapidly restored the rate of secretion of de novo synthesized bile acids to control levels. In contrast, when Triton was administered to control rats, the secretion rate of bile acids was unaffected. The reduction in bile acid synthesis displayed by estradiol-treated rats was similar to the 50% decrease in the activity of hepatic microsomal 7 alpha-hydroxylase. The activity of 7 alpha-hydroxylase was also restored to control levels by the administration of Triton to estradiol-treated rats. We examined the possibility that estradiol acts directly on the hepatic microsomes. Adding increasing amounts of estradiol to microsomes obtained from control rats resulted in decreasing activities of 7 alpha-hydroxylase. The inhibition by estradiol of 7 alpha-hydroxylase obtained in vitro occurred with amounts of estradiol that were found to accumulate in the liver via in vivo treatment. Double-reciprocal analysis showed that at and below 50 micrograms of estradiol/0.5 mg of protein uncompetitive inhibition was displayed. Additional experiments showed that adding Triton to microsomes obtained from estradiol-treated rats increased the activity of 7 alpha-hydroxylase to control levels. In contrast, Triton did not increase the activity of 7 alpha-hydroxylase when it was added to control microsomes. These data show for the first time that the estrogenic steroid estradiol acts directly on the microsomes and inhibits both the activity of 7 alpha-hydroxylase and the rate of bile acid synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)