The effect of nifedipine on cardiopulmonary responses during exercise in normal subjects

• Published in: Chest Vol. 89; no. 5; p. 641
• Main Authors: Chick, T W, Halperin, A K, Jackson, J E, Van As, A
• Format: Journal Article
• Language: English
• Published: United States 01.05.1986
• Subjects: Adult; Blood Pressure - drug effects; Double-Blind Method; Female; Heart - drug effects; Heart Rate - drug effects; Humans; Lactates - blood; Lung - drug effects; Male; Nifedipine - blood; Nifedipine - pharmacology; Oxygen Consumption - drug effects; Physical Exertion - drug effects; Placebos; Pulmonary Gas Exchange - drug effects; Reference Values
• ISSN: 0012-3692
• DOI: 10.1378/chest.89.5.641

We investigated the effects of a single dose of nifedipine (10 mg orally) on exercise performance during progressive incremental cycle ergometry in nine sedentary normal subjects in a double-blind, placebo-controlled crossover study. Maximum work load after nifedipine (213 +/- 42 watts; mean +/- SD) was less than after placebo (222 +/- 41 watts; p less than 0.05). Maximum oxygen consumption was unchanged. In addition, the drug decreased lactate threshold from 19.7 +/- 4.9 ml O2/min/kg to 15.5 +/- 5.5 ml O2/min/kg (p less than 0.02); gas exchange anaerobic threshold was unaffected. There were higher plasma lactate concentrations at low and intermediate exercise intensities after nifedipine compared with placebo (p less than 0.05). Systolic blood pressure was lower at high work loads (p less than 0.05) and heart rate was higher at low work loads (p less than 0.05) after nifedipine. We conclude that the short-term administration of nifedipine limits peak performance and increases plasma concentration of lactic acid in normal subjects. One or more of the following mechanisms may account for these observations: nifedipine decreases blood flow to skeletal muscle by diverting blood to nonexercising tissues; nifedipine increases catecholamine levels, thereby augmenting lactic acid production; and nifedipine decreases skeletal muscular contractility by selectively impairing fatigue-resistant fibers.