Key result
Inhibiting nocturnal periodic breathing at high altitude fails to alter hypoxia-induced increases in MSNA burst frequency.
Why the study?
During prolonged high-altitude exposure, sympathetic nerve activity and ventilation increase; the study investigated whether nocturnal periodic breathing contributes to these progressive increases.
Does inhibiting nocturnal periodic breathing reduce sympathetic nerve activity and hyperventilation in healthy men exposed to high altitude?
RCT (n=12)
placebo-controlled
randomised crossover
Does inhibiting nocturnal periodic breathing reduce sympathetic nerve activity and hyperventilation in healthy men exposed to high altitude?
Absolute Event Rate: 104% vs 94%
p-value: p=0.789
Inhibiting nocturnal periodic breathing does not reduce the sympathoexcitation and hyperventilation associated with acute exposure to high altitude in healthy men.
No effect of nocturnal periodic breathing inhibition on MSNA in hypoxia; leaves open chemoreflex contributions to altitude-induced sympathetic activation.
During acute exposure to the hypoxia of high altitude, activation of the peripheral chemoreflex increases sympathetic nerve activity (SNA) and pulmonary ventilation. If exposure extends over several days, SNA and ventilation further increase and we investigated whether nocturnal periodic breathing (nPB) – a form of sleep‐disordered breathing that is common at high altitude – contributes to these further increases. In a randomised, placebo‐controlled, crossover protocol, twelve healthy men completed two 3‐day sojourns in hypobaric hypoxia equivalent to 4000 m altitude. nPB was inhibited by increasing inspiratory CO 2 fraction during the nights of one (nPB−), but not the other sojourn (nPB+). Ventilation and plasma catecholamines were measured daily, while muscle SNA (MSNA) was assessed before and at the end of sojourns, without and with peripheral chemoreflex inhibition (transient hyperoxia). The hypoxia‐induced increases in MSNA burst frequency (nPB−, +104%; nPB+, +94%; P = 0.789) and incidence (nPB−, +47%; nPB+, +50%; P = 0.791) were not different between sojourns. Catecholamine concentrations throughout the sojourns were also similar (sojourn: P ≥ 0.271, time × sojourn: P ≥ 0.495). Ventilatory variables were not different between sojourns (sojourn: all P ≥ 0.090, time×sojourn: all P ≥ 0.062) except for a slightly greater tidal volume throughout nPB+ (sojourn: P = 0.047, time × sojourn: P P = 0.482). Chemoreflex inhibition induced similar reductions in ventilation during both sojourns (all P ≥ 0.151) and larger reductions in MSNA burst frequency (nPB−: −7.3 ± 2.7 bursts min −1 , nPB+: −4.4 ± 5.1 bursts min −1 , P = 0.037) and incidence after the nPB− (−0.9 ± 5.7 bursts (100 heart beats (HB)) −1 ) than after the nPB+ sojourn (+2.4 ± 7.3 bursts (100 HB) −1 , P = 0.046). We thus conclude that nPB does not contribute to the sympathoexcitation and hyperventilation associated with 3 days of exposure to high altitude. image Key points Prolonged exposure to high altitude leads to progressive increases in sympathetic nerve activity and pulmonary ventilation. Nocturnal periodic breathing (nPB), a form of sleep‐disordered breathing that is common at high altitude, may contribute to these progressive increases in sympathetic nerve activity and ventilation. In this randomised, placebo‐controlled, crossover study, twelve healthy men completed two 3‐day sojourns in hypobaric hypoxia where nPB was either inhibited or not. The hypoxia‐induced increases in sympathetic nerve activity and ventilation were not different between the two sojourns. We conclude that nPB does not contribute to the sympathoexcitation and hyperventilation associated with 3 days of exposure to high altitude.
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Roche et al. (2025) conducted an RCT in Healthy men exposed to high altitude (n=12). Inhibition of nocturnal periodic breathing (nPB) via increased inspiratory CO2 vs. No inhibition of nPB (nPB+) was evaluated on Hypoxia-induced increases in MSNA burst frequency (p=0.789). Inhibiting nocturnal periodic breathing during 3-day exposure to high altitude did not significantly alter the hypoxia-induced increases in MSNA burst frequency (+104% vs +94%; P=0.789).
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