Influence of oxygen supply on activation of group IV muscle afferents after low‐frequency muscle stimulation

Anaerobic muscle metabolism and local release of inflammatory mediators play key roles in the mechanism of postfatigue-induced activation of group IV muscle afferents. The present study focused on activation of these muscle afferents after a 3-min period of low-frequency muscle stimulation (LFMS) in different conditions of muscle oxygenation, such as occur in patients with respiratory insufficiency and subjects living at high altitude. In anesthetized rabbits, spontaneous activity of group IV afferents (conduction velocity = 1.52 ± 0.13 m.s -1 ) from the tibialis anterior muscle was recorded at rest (baseline) and then after LFMS under normoxic (PaO 2 = 113 mmHg), hyperoxic (PaO 2 = 186 mmHg), or hypoxic (PaO 2 = 35 mmHg) conditions. The maximal force decay at the end of LFMS did not differ significantly with respect to conditions of muscle oxygenation. Compared with normoxia, hypoxia significantly increased the baseline activity of group IV muscle afferents, whereas no effect was noted when hypoxia followed a period of hyperoxia. LFMS-induced activation of group IV afferents occurred in all circumstances, except when hypoxia was first tested. The activation of group IV muscle afferents after LFMS was markedly reduced when hypoxia followed normoxia (+14% versus +27%) or hyperoxia (+55% versus +144%), whereas it was accentuated when hyperoxia followed hypoxia (+25% versus +8%). We concluded that the sensorimotor control of skeletal muscles may be altered during acute hypoxia but facilitated after reoxygenation.