Exposure to hypobaric hypoxia at high altitude (HA) is associated with worsening of hypoxemia during sleep. Since the endocrine system is involved in the adaptation to hypoxia, we assessed the effects of sleeping at HA (5050 m) on serum glucose, insulin, and cortisol levels and plasma leptin. Fasting venous blood samples were obtained in seven healthy subjects (M/F: 5/2, mean age±SD 41.9±13.7 yr) at sea level in the morning (SL), and at HA before (PRE) and after one night (POST) during which oxyhemoglobin saturation (SaO2) was recorded by pulse-oximetry. Mean nocturnal and mean lowest SaO2 decreased from 95±2% and 84±6% at SL, respectively, to 74± 5% and 64±7% at HA. Serum glucose was similar under all experimental conditions, while insulin at awakening decreased at HA (PRE: 16.2±8.2; POST: 6.3±1.8 mU/L, p<0.02; SL: 14.8±21.6 mU/L). Cortisol concentration was higher during both wakefulness and sleep at HA compared to SL (PRE: 125.8±53.8; POST: 315.4±68.7 ng/ml, p<0.0001; SL: 81.9±47.3 ng/ml). Plasma leptin did not show any significant difference. Insulin sensitivity, estimated by the homeostatic model (HOMA), increased from PRE to POST at HA (p<0.03). These results suggest that constant plasma glucose during sleep at HA is associated with increased insulin sensitivity. Increased cortisol level at HA suggests possible hypoxia-induced stress.

Metabolic effects of hypoxia and sleep at hight altitude (5050)

COGO, Annaluisa;
2010

Abstract

Exposure to hypobaric hypoxia at high altitude (HA) is associated with worsening of hypoxemia during sleep. Since the endocrine system is involved in the adaptation to hypoxia, we assessed the effects of sleeping at HA (5050 m) on serum glucose, insulin, and cortisol levels and plasma leptin. Fasting venous blood samples were obtained in seven healthy subjects (M/F: 5/2, mean age±SD 41.9±13.7 yr) at sea level in the morning (SL), and at HA before (PRE) and after one night (POST) during which oxyhemoglobin saturation (SaO2) was recorded by pulse-oximetry. Mean nocturnal and mean lowest SaO2 decreased from 95±2% and 84±6% at SL, respectively, to 74± 5% and 64±7% at HA. Serum glucose was similar under all experimental conditions, while insulin at awakening decreased at HA (PRE: 16.2±8.2; POST: 6.3±1.8 mU/L, p<0.02; SL: 14.8±21.6 mU/L). Cortisol concentration was higher during both wakefulness and sleep at HA compared to SL (PRE: 125.8±53.8; POST: 315.4±68.7 ng/ml, p<0.0001; SL: 81.9±47.3 ng/ml). Plasma leptin did not show any significant difference. Insulin sensitivity, estimated by the homeostatic model (HOMA), increased from PRE to POST at HA (p<0.03). These results suggest that constant plasma glucose during sleep at HA is associated with increased insulin sensitivity. Increased cortisol level at HA suggests possible hypoxia-induced stress.
2010
physiology; hipoxia; biomarkers
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1403545
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