The effect of sleep restriction (SR) on the physiological responses to normobaric hypoxia (NH) remains unknown. This study examined whether acute SR the night prior to a 5-h exposure to 3,500 m NH impacts (i) the resting ventilatory response, (ii) circulating pro- and anti-inflammatory cytokines, and (iii) their potential association. Seventeen healthy men (31 ± 7 yr; 77.1 ± 8.5 kg) were exposed to 5 h of NH (FIO2 = 13.6%, 3,500 m) in a randomized crossover design following one night of habitual (> 6 h) or restricted (≤ 3 h) sleep, separated by at least one week. Minute ventilation (V̇E), carbon dioxide output (V̇CO2), oxygen uptake (V̇O2), tidal volume (VT), and respiratory rate (RR) were assessed after 1.5 h of NH. Plasma cytokines (TNF-α, IL-8, IL-10) were measured following 1.5 h and 5 h of NH. SR increased VT (0.67 ± 0.34 vs. 0.63 ± 0.33 L, p = 0.031) following 1.5 h of NH. TNF-α was elevated following SR at both 1.5 h (0.98 ± 0.38 vs. 0.86 ± 0.41 pg/mL, p = 0.012) and 5 h (1.00 ± 0.45 vs. 0.79 ± 0.35 pg/mL, p = 0.004) of NH exposure. IL-10 levels increased after 5 h of NH following SR (0.94 ± 0.65 vs. 0.78 ± 0.73 pg/mL, p = 0.040). Ventilatory responses (VT, V̇E, V̇O2, V̇CO2, RER, V̇E/V̇O2, V̇E/V̇CO2, PETO2, V̇A, SpO2) positively correlated with IL-10 after 1.5 h of NH (r ranged from 0.433 to 0.659, p < 0.05). PETCO2 negatively correlated with IL-10 (r = −0.411, p = 0.033). Acute SR modulates the ventilatory and inflammatory responses to NH which may influence altitude tolerance. IL-10 may influence ventilatory responses to NH. In this context, IL-10 is associated with ventilatory responses to NH.
David et al. (Wed,) studied this question.