The assessment of hypoxic tolerance using physiological markers

Tolerance to hypoxia is known to be variable between individuals, although no test protocol currently exists that is able to predict hypoxic tolerance. This study aimed to validate a hypoxic exercise tolerance test using physiological markers. The test compared subjects’ responses to acute normobaric hypoxia, monitoring a range of physiological markers for comparison with acute mountain sickness (AMS) symptom appearance. Twelve, physically active males, completed a 125 min intermittent test, involving rest and walking [50% maximal oxygen uptake ( )] phases, in a normobaric hypoxic tent under three conditions [20.93%O2 (NORM), 14%O2 (HYP1) and 12%O2 (HYP2)]. The order of the tests was determined by a Latin Squares design. Physiological markers were taken that included; peripheral arterial oxygen saturation (SaO2), rectal temperature (TEMP), heart rate (HR), body mass (BM), blood measures (lactate, haemoglobin, haematocrit, glucose), minute ventilation ( ), lung function, urinary hydration measures (osmolality, specific gravity, colour and volume), thermal sensation (TSS), perceived thirst (THIRST), rating of perceived exertion (RPE) and feeling state (FS). Lake Louise Questionnaire (LLQ) scores and the difference in pre and post Environmental Symptoms Questionnaire (ESQ) scores were used as AMS symptom measures. Multiple regression and correlation analysis were used to identify whether physiological markers related to AMS scores. One way repeated measures ANOVA was used to compare between conditions. We found that SaO2, , TSS, HR, THIRST, TEMP, RPE, FS and ∆BM all correlated significantly with LLQMEAN scores and ∆ESQ (p<0.05). All of these physiological markers were also significantly different between the three conditions during the exercise phases. Neither, age, height, absolute body mass, percent body fat, , lactate threshold, lung function nor any of the blood measures from during the test, were related to AMS susceptibility. Urine measures did not correlate with AMS markers, although urine volume was different between conditions (p<0.05); being notably higher with additional hypoxic stress. The change in relative BM (∆BMREL) was the closest correlate of LLQMEAN (r=0.66, p<0.01) and ∆ESQ (r=0.840, p<0.001), suggesting increased sweat rate may be linked to the onset of AMS. In conclusion, measures of physiological strain (via HR and TEMP), SaO2 and perception scales (TSS, RPE and THIRST) may be combined to give effective prediction of an individual’s tolerance to acute normobaric hypoxia.