June 1, 2018Journal of the Renin-Angiotensin-Aldosterone SystemOpen Access

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

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Why the study?

Does acute normobaric hypoxia and high altitude exposure alter serum ACE, aldosterone, and cortisol levels during exercise?

Structured PICO

Does acute normobaric hypoxia and high altitude exposure alter serum ACE, aldosterone, and cortisol levels during exercise?

Population

23 participants (9 exposed to acute normobaric hypoxia, 6 controls at sea level, and 8 separate participants trekking to high altitude)

Intervention

Acute normobaric hypoxia (5 hours with 90 minutes submaximal treadmill walking) and prolonged high altitude exposure (5140 m)

Comparator

Sea level exposure with the same exercise

Outcome

Serum aldosterone, angiotensin-converting enzyme (ACE), and cortisol levelssurrogate

Acute hypoxia blunts the exercise-induced rise in aldosterone and stimulates cortisol without altering ACE activity, suggesting ACE is not the mechanism for altitude-induced aldosterone reduction.

Implication

Acute hypoxia may blunt exercise aldosterone rise independently of ACE; hypothesis-generating for mechanisms and high-altitude applicability.

Abstract

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: ) 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.