Jan Estoppey1, Bertrand Léger2, Philippe Vuistiner2, Claudio Sartori3, Bengt Kayser1. 1. Institute of Sport Sciences, Synathlon, Uni-Centre, Lausanne, Switzerland. 2. Department of Medical Research, Romandie Clinic for Rehabilitation, Sion, Switzerland. 3. Department of Internal Medicine, University Hospital, Lausanne, Switzerland.
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.
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.