Considerations for enhanced delineation of the physiological impact of high altitude stressors
Dal Cappello T
MetadataShow full item record
Acute hypobaric hypoxic (HH) exposure in healthy subjects is commonly associated with complex pathophysiological acute mountain sickness (AMS) symptomology. Specifically, failure to adequately adapt to HH during rapid ascent to high altitude can result in hypoxemia and tissue oxidative stress (OxS). However, the validity of potential surrogate measures for accurate definition of adaptive or maladaptive response to hypoxia remains under investigation. A prospective study to monitor human physiological parameters on acute HH exposure of 16 healthy individuals to 3830 m was conducted via direct helicopter ascent to Mount Ortles glacier. Neurological signs and symptoms of AMS, HACE, clinical parameters, ultrasonography of ONSD and biological samples were prospectively assessed at baseline (262m) and after ascent (9, 24 and 72h. Reactive oxygen species (ROS) production rate was determined by means of an electron paramagnetic resonance method. OxS biomarkers were assessed by immune and/or enzymatic methods. ONSD increased with exposure to altitude in all participants (p = 0.003), more so in those with AMS (p < 0.001). After 24h the imbalance between ROS production (+141%) and scavenging (- 41%) reflected an increase in OxS related damages by 50%-85% (p <0.05). Despite the concurrent increase of ONSD, regression analysis did not infer a causal relationship between OxS biomarkers and changes in ONSD. These results provide new insight regarding ROS homeostasis and potential pathophysiological mechanisms of acute exposure to HH. However, further validation is recommended, as there remain limitations to the applicable diagnostic utility of such relatively non-invasive measures, within such challenging high altitude environments.