Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Abstract

Our aim was to isolate the independent effects of 1) inspiratory muscle work (Wb) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O2 fraction (FIO 2 ) ϭ 0.15, arterial hemoglobin saturation (SaO 2 ) ϭ 81 Ϯ 1%; 8.6 Ϯ 0.5 min, 273 Ϯ 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (SaO 2 ϭ 95 Ϯ 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO 2 , were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of SaO 2 (P ϭ 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Qtw,pot) decreased by 30 Ϯ 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 Ϯ 4%; P ϭ 0.0007). This effect of Wb on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of reduced SaO 2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 15 Ϯ 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (Ϫ22 Ϯ 3%; P ϭ 0.034). We conclude that both arterial hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, Wb has no effect on peripheral fatigue. work of breathing; arterial oxygen content; altitude; limb blood flow; expiratory flow limitation ON THE BASIS OF STUDIES that mimicked the work of breathing (W b ) obtained during heavy and maximum exercise (1, 2) and unloaded the W b in maximal exercise (34), it has been estimated that the oxygen cost of breathing or the cardiac output devoted to the respiratory muscles approximates 10 -16% of maximal O 2 consumption (V O 2max ) or maximal cardiac output in healthy trained and untrained subjects. More direct microsphere measurements of blood flow distribution during maximal exercise in equines also showed that ϳ15-16% of cardiac output was distributed to the inspiratory and expiratory muscles of the chest wall and abdomen (47). One mechanism protecting blood flow to the respiratory muscles in heavy exercise may be the respiratory muscle metaboreflex, which has been shown to cause sympathetically mediated vasoconstriction of the exercising limb vasculature during heavy exercise in the face of developing inspiratory or expiratory muscle fatigue (32,56,57,59).We (4 -6) and others (48, 53, 62) have shown previously that whole body exercise in acute hypoxia significantly increases the rate of develo...

Changes in heart rate recovery index after a programme of strength/endurance training in hypoxia

“…because of the difficulty of maintaining the same intensities as at sea level. 35 In our case, the execution of squat jumps were technically maintained and performed equally by both groups.…”

Cerebral perturbations during exercise in hypoxia

“…By changing FI O 2 and/or the work of breathing (by using pressure-assisted ventilation) during exercise, it has been demonstrated that the increased work of breathing during hypoxic exercise independently enhances locomotor muscle fatigue during cycling, probably by reducing blood flow to the legs (9). Given these results, it can be hypothesized that brain perfusion during high-intensity hypoxic exercise might be compromised by 1) competition for blood flow distribution in face of increased locomotor muscle perfusion compensating for reduced arterial oxygenation (17), and 2) the increased work of breathing potentially impairing blood flow to other regions of the body (9). In support, greater alteration in brain versus muscle oxygenation (as determined by NIRS) in hypoxia compared with normoxia was reported during rest and exercise (2,102), leading the authors to suggest that a "steal" of blood from cerebral circulation to the muscle may occur in hypoxia.…”

Exercise-induced respiratory muscle fatigue: implications for performance

“…Exercise in hypoxia would also be expected to exacerbate the effects of respiratory muscle work on limb fatigue and exercise tolerance. Recent evidence suggests that the increased work of breathing during acute moderate hypoxia (arterial O 2 saturation 81%) accounts for at least one-third of the total limb locomotor muscle fatigue induced by exercise and a significant part of the hypoxia-induced reduction in exercise tolerance (8). The effects of augmented respiratory muscle work in acute hypoxia on limb fatigue and exercise tolerance may be especially significant in chronic hypoxia during which the hyperventilatory response and work of breathing are greatly magnified (129).…”