Impact of acute sleep restriction on resting ventilation and cytokine levels in normobaric hypoxia, and their association

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.