We investigated the effect of high-altitude acclimatization on peripheral fatigue
compared with sea level and acute hypoxia.
At sea level (350 m), acute hypoxia (environmental chamber), and chronic hypoxia (5050 m, 5–9 d) (partial pressure of inspired oxygen = 140, 74 and 76 mm Hg, respectively), 12 participants (11 in chronic hypoxia) had the quadriceps of their dominant leg fatigued by three bouts of 75 intermittent electrically evoked contractions (12 pulses at 15 Hz, 1.6 s between train onsets, and 15 s between bouts). The initial peak force was ~30% of maximal voluntary force. Recovery was assessed by single trains at 1, 2, and 3 min postprotocol. Tissue oxygenation of rectus femoris was recorded by near-infrared spectroscopy.
At the end of the fatigue protocol, the impairments of peak force and peak rates of force development and relaxation were greater (all P <
0.05) in acute hypoxia (~51%, 53%, and 64%, respectively) than sea level (~43%, 43%, and 52%) and chronic hypoxia (~38%, 35%, and 48%). Peak force and rate of force development recovered faster (P <
0.05) in chronic hypoxia (pooled data for 1–3 min: ~84% and 74% baseline, respectively) compared with sea level (~73% and 63% baseline) and acute hypoxia (~70% and 55% baseline). Tissue oxygenation did not differ among conditions for fatigue or recovery (P >
Muscle adaptations occurring with chronic hypoxia, independent of other adaptations, positively influence muscle contractility
during and after repeated contractions at high altitude