Key result
Acute alcohol ingestion (1.5 g/kg) in healthy men did not significantly impair exercise capacity, with a peak VO2 of 2900 ml/min compared to 3008 ml/min with water (ns).
Why the study?
Does acute alcohol ingestion reduce exercise performance or alter the stress hormone axis in healthy men?
Does acute alcohol ingestion reduce exercise performance or alter the stress hormone axis in healthy men?
Absolute Event Rate: 2900% vs 3008%
p-value: p=ns
Acute alcohol ingestion does not significantly impair maximal exercise capacity or significantly alter stress hormone levels in healthy nonhabitual drinking men.
Acute alcohol appears tolerable for exercise in healthy men; pilot data leave effects open in patients and require confirmation.
The usage of alcohol is widespread, but the effects of acute alcohol ingestion on exercise performance and the stress hormone axis are not fully elucidated.We studied 10 healthy white men, nonhabitual drinkers, by Doppler echocardiography at rest, spirometry, and maximal cardiopulmonary exercise test (CPET) in two visits (2-4 days in between), one after administration of 1.5 g/kg ethanol (whisky) diluted at 15% in water, and the other after administration of an equivalent volume of water. Plasma levels of NT-pro-BNP, cortisol, and adrenocorticotropic hormone (ACTH) were also measured 10 min before the test, at maximal effort and at the third minute of recovery. Ethanol concentration was measured from resting blood samples by gas chromatography and it increased from 0.00 ± 0.00 to 1.25 ± 0.54‰ (P < 0.001). Basal echocardiographic and spirometric parameters were normal and remained so after acute alcohol intake, whereas ACTH, cortisol, and NT-pro-BNP nonsignificantly increased in all phases of the test. CPET data suggested a trend toward a slight reduction of exercise performance (peak VO2 = 3008 ± 638 vs. 2900 ± 543 ml/min, ns; peak workload = 269 ± 53 vs. 249 ± 40 W, ns; test duration 13.7 ± 2.2 vs. 13.3 ± 1.7 min, ns; VE/VCO2 22.1 ± 1.4 vs. 23.3 ± 2.9, ns). Ventilatory equivalent for carbon dioxide at rest was higher after alcohol intake (28 ± 2.5 vs. 30.4 ± 3.2, P = 0.039) and maximal respiratory exchange ratio was lower after alcohol intake (1.17 ± 0.02 vs. 1.14 ± 0.04, P = 0.04). In conclusion, we showed that acute alcohol intake in healthy white men is associated with a nonsignificant exercise performance reduction and stress hormone stimulation, with an unchanged exercise metabolism.
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Popović et al. (2014) studied Healthy (n=10). Ethanol (whisky) vs. Equivalent volume of water was evaluated on Peak VO2 (ml/min) (p=ns). Acute alcohol ingestion (1.5 g/kg) in healthy men did not significantly impair exercise capacity, with a peak VO2 of 2900 ml/min compared to 3008 ml/min with water (ns).
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