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Propranolol does not impair exercise oxygen uptake in normal men at high altitude
Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 1, 1986
Summary
Beta-adrenergic blockade, using propranolol, did not impair maximal oxygen uptake (VO2max) at high altitude. Contrary to hypothesis, oxygen uptake was maintained, suggesting compensatory mechanisms preserved cardiac output.
Area of Science:
- Exercise Physiology
- Altitude Physiology
- Cardiovascular Physiology
Background:
- High altitude exposure is known to decrease maximal oxygen uptake (VO2max) and stimulate the sympathetic nervous system.
- Tachycardia, driven by beta-adrenergic stimulation, was hypothesized to defend VO2max at high altitude.
Purpose of the Study:
- To investigate the role of beta-adrenergic stimulation in defending VO2max at high altitude.
- To determine if propranolol (a beta-blocker) impairs maximal or submaximal oxygen uptake at 4,300 m.
Main Methods:
- Six healthy men received propranolol (80 mg TID) before ascent to 4,300 m; five received placebo.
- Heart rate, VO2max, and submaximal oxygen uptake during exercise were measured at sea level and high altitude.
Main Results:
- Propranolol reduced heart rate during exercise at high altitude.
- VO2max decreased similarly in both groups at high altitude, and returned to baseline after discontinuation.
- Propranolol-treated subjects maintained submaximal oxygen uptake levels comparable to placebo subjects.
Conclusions:
- Beta-adrenergic blockade did not impair maximal or submaximal oxygen uptake at high altitude.
- Compensatory mechanisms, potentially maintaining stroke volume and cardiac output, likely preserved oxygen uptake despite beta-blockade.