A pilot investigation into the effects of acute normobaric hypoxia, high altitude exposure and exercise on serum angiotensin-converting enzyme, aldosterone and cortisol.

INTRODUCTION: Aldosterone decreases at high altitude (HA) but the effect of hypoxia on angiotensin-converting enzyme (ACE), a key step in the renin-angiotensin-aldosterone system, is unclear. METHODS: We investigated the effects of exercise and acute normobaric hypoxia (NH, ~11.0% FiO2) on nine participants and six controls undertaking the same exercise at sea level (SL). NH exposure lasted 5 hours with 90 minutes of submaximal treadmill walking. Blood samples for aldosterone, ACE and cortisol were taken throughout exposure and at rest during a trek to HA (5140 m) in eight separate participants. RESULTS: There was no difference in cortisol or aldosterone between groups pre-exercise. Aldosterone rose with exercise to a greater extent at SL than in NH (post-exercise: 700 ± 325 versus 335 ± 238 pmol/L, mean ± SD, p = 0.044). Conversely, cortisol rose to a greater extent in NH (post-exercise: 734 ± 165 versus 344 ± 159 nmol/L, mean ± SD, p = 0.001). There were no differences in ACE activity. During the trek to HA, resting aldosterone and cortisol reduced with no change in ACE. CONCLUSIONS: Acute NH subdues the exercise-associated rise in aldosteroe but stimulates cortisol, whereas prolonged exposure at HA reduces both resting aldosterone and cortisol. As ACE activity was unchanged in both environments, this is not the mechanism underlying the fall in aldosterone.

The Effect of Sex on Heart Rate Variability at High Altitude.

There is evidence suggesting that high altitude (HA) exposure leads to a fall in heart rate variability (HRV) that is linked to the development of acute mountain sickness (AMS). The effects of sex on changes in HRV at HA and its relationship to AMS are unknown. METHODS: HRV (5-min single-lead ECG) was measured in 63 healthy adults (41 men and 22 women) 18-56 yr of age at sea level (SL) and during a HA trek at 3619, 4600, and 5140 m, respectively. The main effects of altitude (SL, 3619 m, 4600 m, and 5140 m) and sex (men vs women) and their potential interaction were assessed using a factorial repeated-measures ANOVA. Logistic regression analyses were performed to assess the ability of HRV to predict AMS. RESULTS: Men and women were of similar age (31.2 ± 9.3 vs 31.7 ± 7.5 yr), ethnicity, and body and mass index. There was main effect for altitude on heart rate, SD of normal-to-normal (NN) intervals (SDNN), root mean square of successive differences (RMSSD), number of pairs of successive NN differing by >50 ms (NN50), NN50/total number of NN, very low-frequency power, low-frequency (LF) power, high-frequency (HF) power, and total power (TP). The most consistent effect on post hoc analysis was reduction in these HRV measures between 3619 and 5140 m at HA. Heart rate was significantly lower and SDNN, RMSSD, LF power, HF power, and TP were higher in men compared with women at HA. There was no interaction between sex and altitude for any of the HRV indices measured. HRV was not predictive of AMS development. CONCLUSIONS: Increasing HA leads to a reduction in HRV. Significant differences between men and women emerge at HA. HRV was not predictive of AMS.