scholarly journals Locomotor muscle fatigue modifies central motor drive in healthy humans and imposes a limitation to exercise performance

2008 ◽  
Vol 586 (1) ◽  
pp. 161-173 ◽  
Author(s):  
Markus Amann ◽  
Jerome A. Dempsey
2007 ◽  
Vol 581 (1) ◽  
pp. 389-403 ◽  
Author(s):  
Markus Amann ◽  
Lee M. Romer ◽  
Andrew W. Subudhi ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

1991 ◽  
Vol 70 (5) ◽  
pp. 2059-2065 ◽  
Author(s):  
M. J. Mador ◽  
F. A. Acevedo

The purpose of this study was to determine whether induction of inspiratory muscle fatigue might impair subsequent exercise performance. Ten healthy subjects cycled to volitional exhaustion at 90% of their maximal capacity. Oxygen consumption, breathing pattern, and a visual analogue scale for respiratory effort were measured. Exercise was performed on three separate occasions, once immediately after induction of fatigue, whereas the other two episodes served as controls. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating 80% of their predetermined maximal mouth pressure until they could no longer reach the target pressure. After induction of fatigue, exercise time was reduced compared with control, 238 +/- 69 vs. 311 +/- 96 (SD) s (P less than 0.001). During the last minute of exercise, oxygen consumption and heart rate were lower after induction of fatigue than during control, 2,234 +/- 472 vs. 2,533 +/- 548 ml/min (P less than 0.002) and 167 +/- 15 vs. 177 +/- 12 beats/min (P less than 0.002). At exercise isotime, minutes ventilation and the visual analogue scale for respiratory effort were larger after induction of fatigue than during control. In addition, at exercise isotime, relative tachypnea was observed after induction of fatigue. We conclude that induction of inspiratory muscle fatigue can impair subsequent performance of high-intensity exercise and alter the pattern of breathing during such exercise.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Zafeiris Louvaris ◽  
IOANNIS VOGIATZIS ◽  
ATHANASOPOULOS DIMITRIS ◽  
ANDRIANOPOULOS VASILIS ◽  
ALEXOPOULOS PANAGIOTIS ◽  
...  

2019 ◽  
Vol 44 (2) ◽  
pp. 208-215 ◽  
Author(s):  
Paul T. Morgan ◽  
Anni Vanhatalo ◽  
Joanna L. Bowtell ◽  
Andrew M. Jones ◽  
Stephen J. Bailey

Recent research suggests that acute consumption of pharmacological analgesics can improve exercise performance, but the ergogenic potential of ibuprofen (IBP) administration is poorly understood. This study tested the hypothesis that IBP administration would enhance maximal exercise performance. In one study, 13 physically active males completed 60 × 3-s maximal voluntary contractions (MVCs) of the knee extensors interspersed with 2-s passive recovery periods, on 2 occasions, with the critical torque (CT) estimated as the mean torque over the last 12 contractions (part A). In another study, 16 active males completed two 3-min all-out tests against a fixed resistance on an electronically braked cycle ergometer, with the critical power estimated from the mean power output over the final 30 s of the test (part B). All tests were completed 60 min after ingestion of maltodextrin (placebo, PL) or 400 mg of IBP. Peripheral nerve stimulation was administered at regular intervals and electromyography was measured throughout. For part A, mean torque (IBP: 60% ± 13% of pre-exercise MVC; PL: 58% ± 14% of pre-exercise MVC) and CT (IBP: 41% ± 16% of pre-exercise MVC; PL: 40% ± 15% of pre-exercise MVC) were not different between conditions (P > 0.05). For part B, end-test power output (IBP: 292 ± 28 W; PL: 288 ± 31 W) and work done (IBP: 65.9 ± 5.9 kJ; PL: 65.4 ± 6.4 kJ) during the 3-min all-out cycling tests were not different between conditions (all P > 0.05). For both studies, neuromuscular fatigue declined at a similar rate in both conditions (P > 0.05). In conclusion, acute ingestion of 400 mg of IBP does not improve single-leg or maximal cycling performance in healthy humans.


2012 ◽  
Vol 302 (8) ◽  
pp. R903-R916 ◽  
Author(s):  
Samuel Verges ◽  
Thomas Rupp ◽  
Marc Jubeau ◽  
Bernard Wuyam ◽  
François Esteve ◽  
...  

Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O2 delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO2. With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O2 content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O2 saturation <70–75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O2 (and CO2) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered.


2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 163
Author(s):  
Gregers Munch ◽  
Magnus Christensen ◽  
Niels Secher ◽  
Jesper H. Svendsen ◽  
José González-Alonso ◽  
...  

1991 ◽  
Vol 69 (2) ◽  
pp. 254-261 ◽  
Author(s):  
R. S. McKelvie ◽  
N. L. Jones ◽  
G. I. F. Heigenhauser

β-Adrenoceptor blockers are widely used clinically and can be classified as nonselective (β1 and β2) or selective (β1). Impairment of exercise performance is a well-known side effect of this group of drugs. This paper reviews mechanisms that could potentially be responsible for this impairment. In addition to cardiovascular and metabolic effects, β -blockade inhibits Na+–K+ ATPase pumps controlling ion movement between muscle and plasma and thus may contribute to muscle fatigue through this mechanism. To investigate the relationship between the change in plasma [K+] and exercise performance, we studied healthy male subjects taking propranolol. Eight subjects performed maximal incremental cycle ergometer exercise tests during control (no drug), low dose (LD) (40 mg daily), and high dose (HD) (265 ± 4.3 (SE) mg daily) of propranolol. The control plasma [K+] (5.8 ± 0.12 mequiv./L) during exercise was significantly lower than either the LD (6.4 ± 0.05 mequiv./L) or HD (6.1 ± 0.16 mequiv./L) values. There was no significant difference between plasma [K+] for the LD and HD of propranolol. However, maximum oxygen uptake was reduced only while taking the HD of propranolol. Six of the subjects also performed three 30-s bouts of high intensity exercise on an isokinetic cycle ergometer while taking the LD and HD of propranolol. There was no significant difference between doses for the increase in plasma [K+] (LD, 7.8 ± 0.35 mequiv./L vs. HD, 7.6 ± 0.36 mequiv./L) during exercise. However, exercise performance was significantly reduced during HD compared with LD. These results suggest that the increases in plasma [K+] with propranolol did not play a direct significant role in the reduced performance observed during the HD.Key words: exercise, potassium, performance, lactate.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2836 ◽  
Author(s):  
Wen-Ching Huang ◽  
Mon-Chien Lee ◽  
Chia-Chia Lee ◽  
Ker-Sin Ng ◽  
Yi-Ju Hsu ◽  
...  

Probiotics have been rapidly developed for health promotion, but clinical validation of the effects on exercise physiology has been limited. In a previous study, Lactobacillus plantarum TWK10 (TWK10), isolated from Taiwanese pickled cabbage as a probiotic, was demonstrated to improve exercise performance in an animal model. Thus, in the current study, we attempted to further validate the physiological function and benefits through clinical trials for the purpose of translational research. The study was designed as a double-blind placebo-controlled experiment. A total of 54 healthy participants (27 men and 27 women) aged 20–30 years without professional athletic training were enrolled and randomly allocated to the placebo, low (3 × 1010 colony forming units (CFU)), and high dose (9 × 1010 CFU) TWK10 administration groups (n = 18 per group, with equal sexes). The functional and physiological assessments were conducted by exhaustive treadmill exercise measurements (85% VO2max), and related biochemical indices were measured before and after six weeks of administration. Fatigue-associated indices, including lactic acid, blood ammonia, blood glucose, and creatinine kinase, were continuously monitored during 30 min of exercise and a 90 min rest period using fixed intensity exercise challenges (60% VO2max) to understand the physiological adaptation. The systemic inflammation and body compositions were also acquired and analyzed during the experimental process. The results showed that TWK10 significantly elevated the exercise performance in a dose-dependent manner and improved the fatigue-associated features correlated with better physiological adaptation. The change in body composition shifted in the healthy direction for TWK10 administration groups, especially for the high TWK10 dose group, which showed that body fat significantly decreased and muscle mass significantly increased. Taken together, our results suggest that TWK10 has the potential to be an ergogenic aid to improve aerobic endurance performance via physiological adaptation effects.


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