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We examined the effects of hypoxia severity on peripheral versus central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various fractions of inspired O2 fraction (FIO2 0.21/0.15/0.10). At task failure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O2 supplementation (FIO2= 0.30) and subjects were encouraged to continue exercising. Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (ΔQtw,pot) as measured pre- versus post-exercise in response to supramaximal femoral nerve stimulation. At task failure in normoxia (haemoglobin saturation (SpO2) ∼94%, 656 ± 82 s) and moderate hypoxia (SpO2∼82%, 278 ± 16 s), hyperoxygenation had no significant effect on prolonging endurance time. However, following task failure in severe hypoxia (SpO2∼67%; 125 ± 6 s), hyperoxygenation elicited a significant prolongation of time to exhaustion (171 ± 61%). The magnitude of ΔQtw,pot at exhaustion was not different among the three trials (−35% to −36%, P= 0.8). Furthermore, quadriceps integrated EMG, blood lactate, heart rate, and effort perceptions all rose significantly throughout exercise, and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe hypoxia, we repeated this trial and assessed peripheral fatigue following task failure prior to hyperoxygenation (125 ± 6 s). Although Qtw,pot was reduced from pre-exercise baseline (−23%; P < 0.01), peripheral fatigue was substantially less (P < 0.01) than that observed at task failure in normoxia and moderate hypoxia. We conclude that across the range of normoxia to severe hypoxia, the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxia-sensitive central component of fatigue, probably involving brain hypoxic effects on effort perception.
Whole-body exercise performance in aerobic activities is impaired in hypoxia. The physiological mechanisms underpinning this impairment are not fully understood (Knight et al. 1993; Fulco et al. 1998; Calbet et al. 2003a,b; Lundby et al. 2006). We have recently shown that decreases in endurance performance from hyperoxia to moderate hypoxia are associated with peripheral muscle fatigue and its subsequent effects on CNS motor output, probably acting via afferent feedback mechanisms (Amann et al. 2006a; Romer et al. 2007). Despite our proposed link between ‘peripheral’ and ‘central fatigue’ from hyperoxia to moderate hypoxia, we acknowledge that peripheral fatigue and its associated sensory feedback is not the only potential source of inhibitory influence on central neural output and thus exercise performance. On the contrary, multiple ‘peripheral’ and ‘central’ mechanisms have been proposed (Bigland-Ritchie & Vollestad, 1988; Fitts, 1994; Kjaer et al. 1999; Jones & Killian, 2000; Gandevia, 2001; Kayser, 2003; Amann et al. 2006a) and some of the causes of central fatigue have been shown to be independent of peripheral somatosensory feedback (Blomstrand et al. 1988; Meeusen & De Meirleir, 1995; Gandevia, 2001; Dalsgaard et al. 2002).
Studies in which the severity of hypoxia was increased beyond moderate levels have provided indirect evidence that severe CNS hypoxia may result in centrally mediated inhibitory effects on autonomic control and/or motor drive originating within the CNS itself (Kjaer et al. 1999; Boushel et al. 2001; Calbet et al. 2003a). For example, blunting of neural feedback from contracting limb muscles in acute severe hypoxia (arterial oxygen saturation (SaO2)53%; fraction of inspired oxygen (FIO2) 0.078 using epidural anaesthesia did not affect exercise time to exhaustion (Kjaer et al. 1999), suggesting that limitations in exercise performance in acute severe hypoxia are of central origin and independent of peripheral feedback mechanisms. Further support for this postulate stems from studies that have shown that increasing FIO2 at the point of task failure prolongs constant-load exercise in chronic severe hypoxia (SaO2 73–77%; altitude 5050 m) (Kayser et al. 1994) and increases maximal incremental exercise performance in acute severe hypoxia (SaO2 66–68%; FIO2 0.105) (Calbet et al. 2003a,b). The fact that exercise at the point of ‘exhaustion’ could be continued with hyperoxygenation argues against a peripheral mechanism as the main cause of fatigue in severe hypoxia and, by extension, suggests an independent effect of CNS hypoxia on regulating performance under such extreme conditions.
Collectively, these findings indicate that hypoxia-sensitive sources of inhibition of central motor drive exist outside any influences related to peripheral muscle fatigue and its associated afferent feedback. Thus, the purpose of the proposed study was to determine the relative effects of central and peripheral mechanisms of fatigue on whole-body exercise performance in normoxia, moderate hypoxia and severe hypoxia (induced via FIO2 0.15 and 0.10, respectively). We hypothesized that peripheral locomotor muscle fatigue would be important in limiting exercise performance in conditions of hyperoxia to moderate hypoxia, whereas central mechanisms of fatigue (i.e. as affected by CNS hypoxia) would become more dominant as the severity of hypoxia increases.