Abstract
Background:
Mechanisms underlying acute mountain sickness (AMS) remain unclear. Corticosteroids are effective for prevention and treatment suggesting a role for deficient endogenous cortisol. The cortisol awakening response (CAR), the increase in cortisol secretion over the first 30–45 minutes after morning awakening, better reflects the hypothalamic–pituitary–adrenal (HPA) axis than single cortisol measurements. We hypothesized that CAR may be altered in AMS-prone persons.
Methods:
Upon arrival at 4554 m (high altitude [HA]), 81 mountaineers agreed to participate. The following morning, they gave three saliva samples after awakening (S1: 0 minute, S2: 30 minutes, S3: 45 minutes). AMS was scored with the 1993 Lake Louise Score (LLS, cut-off ≥5). Minimally 4 weeks after descent, saliva was recollected by 58 of 81 participants at low altitude (LA); 382 ± 309 m, mean ± standard deviation). Cortisol was quantified by immunoassay. Three cortisol indices were analyzed: first sample on awakening (S1), CAR (area under curve with respect to S1) and total post awaking cortisol (area under the curve from ground [AUC-G]).
Results:
AMS prevalence was 30%. At HA compared to LA, S1 (450 ± 190 vs. 288 ± 159 ng/dL, p < 0.001) and AUC-G (387 ± 137 vs. 276 ± 114 ng/dL·min, p < 0.001) were greater, but CAR was not (50 ± 100 vs. 60 ± 81 ng/dL·min, p = 0.550). AMS+ compared to AMS− participants had higher S1 both at HA (495 ± 209 vs. 384 ± 176 ng/dL, p = 0.016) and LA (354 ± 160 vs. 253 ± 142 ng/dL, p = 0.015) and lower CAR at LA (24 ± 87 vs. 79 ± 72 ng/dL·min, p = 0.013). AUC-G was similar in both groups at HA and LA.
Conclusions:
Some indices of salivary cortisol response upon awakening differ between AMS+ and AMS−, both at HA and LA, suggesting a link between HPA-axis homeostasis and AMS.
Get full access to this article
View all access options for this article.
