Effects of Amlodipine on Exercise Performance and Cardiovascular and Skeletal Muscle Function in Physically Active Hypertensive Patients

Abstract

The effect of the long-acting dihydropyridine calcium channel antagonist, amlodipine, on the exercise performance of hypertensive patients is not known. The aim of this study was to determine the effects of amlodipine on maximal (MAX) and prolonged submaximal (PSX) exercise and on skeletal muscle function (SMF) in patients with mild hypertension. In a double-blind, randomised, crossover trial, 10 physically active hypertensive patients performed: (a) graded exercise to exhaustion for determination of maximal oxygen consumption (VO2max), peak heart rate (HR) and systolic blood pressure (SBP); (b) PSX at 75% VO2max to determine cardiorespiratory responses, cardiac output (Q), blood lactate (La), free fatty acid (FFA), glucose (G) concentrations and ratings of perceived exertion (RPE); and (c) tests of isometric SMF including maximal voluntary contraction (MVC) and time to fatigue during repetitive isometric MVCs. Tests were performed following 2-week ingestion of amlodipine (5mg daily) or placebo separated by a 2-week washout period. Resting SBP was decreased following ingestion of amlodipine [ 142 ± 13 vs 133 ± 12mm Hg, amlodipine vs placebo (mean ± SD); p < 0.05]. However, VO2max (31 ±5 vs 33 ±5ml O2/kg/min, amlodipine vs placebo), peak HR (168 ± 13 vs 165 ± 16 beats/min, amlodipine vs placebo) and peak SBP (181 ± 21 vs 170 ± 16mm Hg, amlodipine vs placebo) were not reduced following ingestion of amlodipine. Submaximal cycling time, VO2, Q, BP, HR, ventilation, RPE, FFA, La and G during PSX were unaltered following ingestion of amlodipine. Similarly, ingestion of amlodipine did not alter tests of isometric SMF. These data suggest that: (a) ingestion of amlodipine lowers resting SBP but does not alter the normal haemodynamic response during exercise; (b) MAX and PSX exercise performance and SMF are unaltered following ingestion of amlodipine in athletic hypertensive patients. These findings suggest that the regulatory mechanisms that maintain haemodynamic homeostasis during maximal and submaximal exercise are not influenced by ingestion of amlodipine in athletic hypertensive patients.