TY - JOUR
T1 - Effect of β-blockade on the drift in O2 consumption during prolonged exercise
AU - Kalis, J. K.
AU - Freund, B. J.
AU - Joyner, M. J.
AU - Jilka, S. M.
AU - Nittolo, J.
AU - Wilmore, J. H.
PY - 1988
Y1 - 1988
N2 - The effect of β-adrenergic blockade on the drift in O2 consumption (V̇O2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (V̇O(2 max)). After an initial maximum cycle ergometer test to determine the subject's control V̇O(2 max), subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control V̇O(2 max) for 90 min on a cycle ergometer in a warm (31.7±0.3°C) moderately humid (44.7±4.7%) environment. β-Blockade caused significant (P<0.05) reductions in V̇O(2 max), maximal minute ventilation (V̇E(max)), maximal heart rate (HR(max)), and maximal exercise time. Significantly greater decreases in V̇O2(max), V̇E(max), and HR(max) were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, β-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (V̇O2) and minute ventilation (V̇E) were observed with propranolol compared with atenolol or placebo. Furthermore, V̇O2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial. These results suggest that the lower submaximal V̇O2 and the absence of V̇O2 drift with propranolol were due primarily to its effects on the β2-receptors, resulting in a greater reliance on carbohydrates for substrate, a lower V̇E, and by blocking the actions of circulating catecholamines.
AB - The effect of β-adrenergic blockade on the drift in O2 consumption (V̇O2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (V̇O(2 max)). After an initial maximum cycle ergometer test to determine the subject's control V̇O(2 max), subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control V̇O(2 max) for 90 min on a cycle ergometer in a warm (31.7±0.3°C) moderately humid (44.7±4.7%) environment. β-Blockade caused significant (P<0.05) reductions in V̇O(2 max), maximal minute ventilation (V̇E(max)), maximal heart rate (HR(max)), and maximal exercise time. Significantly greater decreases in V̇O2(max), V̇E(max), and HR(max) were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, β-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (V̇O2) and minute ventilation (V̇E) were observed with propranolol compared with atenolol or placebo. Furthermore, V̇O2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial. These results suggest that the lower submaximal V̇O2 and the absence of V̇O2 drift with propranolol were due primarily to its effects on the β2-receptors, resulting in a greater reliance on carbohydrates for substrate, a lower V̇E, and by blocking the actions of circulating catecholamines.
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M3 - Article
C2 - 3372432
AN - SCOPUS:0023861066
SN - 0161-7567
VL - 64
SP - 753
EP - 758
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 2
ER -