Int J Sports Med 1986; 07(5): 254-258
DOI: 10.1055/s-2008-1025770
© Georg Thieme Verlag Stuttgart · New York

Effect of Acute Calcium Slow-Channel Antagonism on the Cardiorespiratory Response to Graded Exercise Testing*

N. F. Gordon, J. P. van Rensburg, D. L. Kawalsky, H. M. S. Russell, C. P. Celliers, D. P. Myburgh
  • Institute For Aviation Medicine, Pretoria; Industrial Hygiene Branch, Chamber Of Mines Of South Africa, Johannesburg; and Department Of Physiology, University Of Witwatersrand, Johannesburg, South Africa
* This study was supported by grants from Parke-Davis Research Laboratories, Knoll Pharmaceuticals, and Execucare Preventive Fitness Maintenance.
Further Information

Publication History

Publication Date:
14 March 2008 (online)

Abstract

The effect of acute calcium slow-channel antagonism on the cardiorespiratory responses of 12 healthy males was studied during multistage maximal exercise testing. Oral diltiazem (60 mg), nifedipine (10 mg), verapamil (80 mg), and placebo were administered in a randomized double-blind crossover fashion 1.5 h before an intermittent multistage cycle ergometer exercise test. At peak effort, heart rate, pulmonary ventilation, CO2 production, and respiratory exchange ratio were not significantly modified by drug ingestion. In contrast, maximal O2 consumption (2.6% reduction, P < 0.02) and performance time (6.4% reduction, P < 0.02) were reduced by nifedipine. During submaximal exercise, the chronotropic response was accentuated by nifedipine but not by diltiazem or verapamil. Furthermore, nifedipine altered the relationship of percentage of maximal O2 consumption to percentage of maximal heart rate, and both the relative and absolute O2 consumption corresponding to 70% and 85% of the maximal heart rate were significantly reduced after nifedipine ingestion. The results indicated that in persons without symptomatic coronary artery disease exercise performed at a given percentage of the maximal heart rate will yield a lower than expected relative and absolute intensity in the presence of acute nifedipine-induced calcium slow-channel antagonism.

    >