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Altitudeomics on the consequences of high altitude acclimatization for the development of fatigue during locomotor exercise in humans

Altitudeomics on the consequences of high altitude acclimatization for the development of fatigue during locomotor exercise in humans

The development of muscle fatigue is O2-delivery sensitive (arterial O2-content [CaO2] x limb blood flow [QL]). Locomotor exercise in acute-hypoxia (AH) is, compared to sea-level (SL), associated with reduced CaO2 and exaggerated inspiratory muscle work (Winsp; which impairs QL), both of which individually exacerbate fatigue by compromising O2-delivery. Since chronic-hypoxia (CH) normalizes CaO2, but exacerbates Winsp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138±14W; 11±1min) at SL (PIO2 147.1±0.5mmHg), in AH (73.8±0.2mmHg) and in CH (75.7±0.1mmHg). Peripheral fatigue was expressed as pre- to post-exercise percent reduction in electrically-evoked quadriceps twitch-force (Qtw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (VA). Resting CaO2 at SL and CH were similar, but CaO2 in AH was lower compared to SL and CH (17.3±0.5, 19.3±0.7, 20.3±1.3mlO2/dl, respectively). Winsp during exercise increased with acclimatization (SL: 387±36, AH: 503±53, CH: 608±67 cmH2O s min-1; P<0.01). Exercise at SL did not induce central or peripheral fatigue. Qtw,pot was significant but similar in AH and CH (21±2% and 19±3%; P=0.24). VA was significant in both hypoxic conditions, but smaller in CH vs AH (4±1% vs 8±2%; p<0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH.

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