Altitude illness is related to low hypoxic chemoresponse and low oxygenation during sleep

Abstract

Altitude illness remains a major cause of mortality. Reduced chemosensitivity, irregular breathing leading to central apnoeas/hypopnoeas, and exaggerated pulmonary vasoconstriction may compromise oxygenation. All factors could enhance susceptibility to acute mountain sickness (AMS).We compared 12 AMS-susceptible individuals with recurrent and severe symptoms (AMS+) with 12 ''AMS-nonsusceptible'' subjects (AMS-), assessing sleep-breathing disorders in simulated altitude as well as chemoresponsive and pulmonary vasoconstrictive responses to hypoxia.During exposure to simulated altitude, mean blood oxygen saturation during sleep was lower in AMS+ subjects (81.6¡2. ?%; p,0.001). This represented the only significant and independent predictive factor for altitude intolerance, despite a higher increase in pulmonary artery systolic pressure in response to hypoxia, a lower lung diffusing capacity and a higher endothelin-1 level at baseline in AMS+ subjects (p,0.05). AMS+ subjects were more hypoxaemic whilst exhibiting fewer respiratory events during sleep owing to lower hypoxic (isocapnic) chemoresponsiveness.In conclusion, the reduction in peripheral hypoxic chemosensitivity appears to be a major causative factor for altitude intolerance.

Impact of Sleeping Altitude on Symptoms of Acute Mountain Sickness on Mt. Fuji

“…Fuji about 2.5-fold (Table 2), which is consistent with the findings of previous studies (Bartsch et al, 2004;Luks, 2012). It is plausible that sleeping at higher altitudes causes hypoxemia, and several studies have found that hypoxemia is associated with AMS (Erba et al, 2004;Koehle et al, 2010;Nespoulet et al, 2012;Nussbaumer-Ochsner et al, 2012). Recently, we reported that arterial oxygen saturation gradually decreased when sleeping overnight at a high altitude, ca.…”

Acclimatization to chronic intermittent hypoxia in mine workers: a challenge to mountain medicine in Chile

“…Recently, in a group of people exposed to experimental hypoxia (FIO 2 = 80% SaO 2 ), the acute hypoxic ventilatory response at 5 min (HVR5min) was greater in individuals not susceptible to AMS compared to susceptible individuals (Nespoulet et al, 2012). These results support the hypothesis of low chemoreceptor sensitivity as a marker of AMS predisposition (Moore et al, 1986), suggesting high chemo sensitivity as a protective factor for AMS.…”

Bed rest and hypoxic exposure affect sleep architecture and breathing stability

“…Sleep architecture is affected in all trials, with the most noticeable shifts occurring in the combined HBR condition. There appears to be a direct relationship between breathing stability and mean night SpO 2 when otherwise healthy adults are confined to bed, echoing published data that have reported ventilatory drive changes in patients (Schiffman et al, 1983;Chen and Tang, 1989), and lower hypoxic chemoresponsiveness in susceptible individuals at high altitude (Nespoulet et al, 2012). The initial increase in ventilation during exposure to hypoxia (i.e., hypoxic ventilatory response; HVR) is highly variable (Hirshman et al, 1975).…”

“…The initial increase in ventilation during exposure to hypoxia (i.e., hypoxic ventilatory response; HVR) is highly variable (Hirshman et al, 1975). Some studies have stratified test populations into "susceptible" and "resistant" phenotypes when characterizing one's predisposition to suffering AMS and highaltitude pulmonary edema (HAPE) (Hohenhaus et al, 1995;Nespoulet et al, 2012). In one investigation, AMS susceptible patients' night SpO 2 concentrations were ∼5% lower than their non-susceptible counterparts, yet these patients experienced significantly fewer AHI events per hour (18 vs. 33 events per hour; p = 0.038) (Nespoulet et al, 2012).…”

“…Some studies have stratified test populations into "susceptible" and "resistant" phenotypes when characterizing one's predisposition to suffering AMS and highaltitude pulmonary edema (HAPE) (Hohenhaus et al, 1995;Nespoulet et al, 2012). In one investigation, AMS susceptible patients' night SpO 2 concentrations were ∼5% lower than their non-susceptible counterparts, yet these patients experienced significantly fewer AHI events per hour (18 vs. 33 events per hour; p = 0.038) (Nespoulet et al, 2012). The present study observed a highly individualized response in breathing stability, especially after 21-days in bed rest, such that those who experienced the greatest change in breathing stability from Night 1 to Night 21 also maintained or increased night SpO 2 saturations.…”