Effects of nifedipine on responses to exercise in normal subjects

Abstract

The responses to sublingual nifedipine (20 mg) and placebo were compared in normal subjects during two studies on cycle ergometer [progressive exercise and constant work-load exercise at approximately 60% of maximal O2 consumption (VO2max)]. The use of nifedipine did not modify maximal power, ventilation (VE), VO2, and heart rate (HR) at the end of the multistage progressive exercise (30-W increments every 3 min). Over the 45 min of the constant-load exercise and the ensuing 30-min recovery we observed with nifedipine compared with placebo 1) no differences in VO2, VE, respiratory exchange ratio, and systolic arterial blood pressure; 2) a higher HR (P less than 0.001) and lower diastolic arterial blood pressure (P less than 0.01); 3) a greater and more prolonged rise in norepinephrine (P less than 0.01) and growth hormone (P less than 0.001); 4) no significant differences in epinephrine and insulin and a lesser increase in glucagon during recovery (P less than 0.01); and 5) a lesser fall in blood glucose (P less than 0.01) and greater increase in acetoacetate (P less than 0.001), beta-hydroxybutyrate (P less than 0.05), and blood lactate (P less than 0.001). Our data do not support the hypothesis that nifedipine reduces hormonal secretions in vivo and are best explained by an enhanced secretion of catecholamines compensating for the primary vasodilator effect of nifedipine.

Administration of slow-release nifedipine does not affect lactate threshold, hormone release during exercise, and quality of life in normal subjects

“…have not shown any effect on VO2max or maximal work load [5,25]. Likewise, the effect of single-dose nifedipine-C on ~'Qmax has not yet been proven.…”

“…Likewise, the effect of single-dose nifedipine-C on ~'Qmax has not yet been proven. Moreover, significant reductions in blood pressure and increases in heart rate during exercise were observed in normotensive subjects after the administration of single-dose nifedipine-C [5,26]. The reduction in blood pressure was most likely due to a reduction in systemic vascular resistance, and the increased heart rate was secondary to baroreceptor stimulation.…”

“…nephrine and norepinephrine levels [2,5]. The infusion of epinephrine and norepinephrine has been shown to increase maximal net lactate output during skeletal muscular contractions because the elevated catecholamines stimulate glycogenolysis not only in the liver, but also in exercising muscle [27].…”

“…To elucidate the effects of antihypertensive agents on exercise peformance, several studies have been conducted in normal subjects [1][2][3]. Administration of a single dose of nifedipine capsule (nifedipine-C), one of the calciumchannel blocking agents, increased lactate levels and decreased lactate threshold (LT) in healthy volunteers [4,5]. The question remains unanswered, however, as to the effects of slow-release nifedipine (nifedipine-SR) on these parametens.…”

The effect of 8 weeks treatment with the calcium antagonist felodipine on blood pressure, heart rate, working capacity, plasma renin activity, plasma angiotensin II, urinary catecholamines and aldosterone in patients with essential hypertension.

“…This could explain the decrease in maximal working capacity found in the present study. The unaltered maximal work load after acute nifedipine administration to normotensive subjects in the study by Raffestin et al (1985) may be due to a less pronounced vasodilatory action of calcium antagonists in normotensive as compared to hypertensive subjects (Hulthen et al, 1982;Robinson et al, 1982;Hulthen et al, 1983;Yokoyama & Kaburagi, 1983).…”