Abstract
Inadequate cerebral O2 availability has been proposed to be an important contributing factor to the development of central fatigue during strenuous exercise. Here we tested the hypothesis that supraspinal processes of fatigue would be increased after locomotor exercise in acute hypoxia compared to normoxia, and that such change would be related to reductions in cerebral O2 delivery and tissue oxygenation. Nine endurance-trained cyclists completed three constant-load cycling exercise trials at ∼80% of maximal work rate: (1) to the limit of tolerance in acute hypoxia; (2) for the same duration but in normoxia (control); and (3) to the limit of tolerance in normoxia. Throughout each trial, prefrontal cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assessed using near-infrared spectroscopy and transcranial Doppler sonography, respectively. Cerebral O2 delivery was calculated as the product of arterial O2 content and MCAV. Before and immediately after each trial, twitch responses to supramaximal femoral nerve stimulation and transcranial magnetic stimulation were obtained to assess neuromuscular and cortical function, respectively. Exercise time was reduced by 54% in hypoxia compared to normoxia (3.6 ± 1.3 vs. 8.1 ± 2.9 min; P < 0.001). Cerebral O2 delivery, cerebral oxygenation and maximum O2 uptake were reduced whereas muscle electromyographic activity was increased in hypoxia compared to control (P < 0.05). Maximum voluntary force and potentiated quadriceps twitch force were decreased below baseline after exercise in each trial; the decreases were greater in hypoxia compared to control (P < 0.001), but were not different in the exhaustive trials (P > 0.05). Cortical voluntary activation was also decreased after exercise in all trials, but the decline in hypoxia (Δ18%) was greater than in the normoxic trials (Δ5–9%) (P < 0.05). The reductions in cortical voluntary activation were paralleled by reductions in cerebral O2 delivery. The results suggest that curtailment of exercise performance in acute severe hypoxia is due, in part, to failure of drive from the motor cortex, possibly as a consequence of diminished O2 availability in the brain.
Highlights
Muscle fatigue is characterised as an exercise-induced decrease in maximal force production or an inability to sustain further exercise at a required force (Gandevia, 2001)
We recently found that declines in cortical voluntary activation in response to single-limb knee-extensor contractions were greater in acute severe hypoxia compared to normoxia, and that the increased contribution of supraspinal fatigue to the loss of voluntary force occurred in line with the greatest cerebral deoxygenation (Goodall et al 2010)
Cortical voluntary activation declined after exercise in both conditions, but the decline was more than twofold greater for exercise performed to the limit of tolerance in hypoxia compared to the same duration of exercise in normoxia, and onefold greater compared to exercise performed to the limit of tolerance in normoxia
Summary
Muscle fatigue is characterised as an exercise-induced decrease in maximal force production or an inability to sustain further exercise at a required force (Gandevia, 2001). Central fatigue is a progressive exercise-induced reduction in voluntary activation or neural drive to the muscle due to failure of the central nervous system to excite or drive motoneurones adequately. There is not yet unequivocal evidence that central neural drive declines during exercise in normoxia or that the contribution of central processes to fatigue is increased in hypoxia (Amann & Calbet, 2008; Amann & Kayser, 2009)
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