Does exercise alter anaerobic threshold in coronary artery disease during beta blockade?

Abstract

The effect of propranolol on cardiac patients undergoing exercise training is reported to increase exercise tolerance and maximum oxygen uptake (VO2 max) but its effect on anaerobic threshold (AT) is unknown. It was the purpose of this study to determine the role of exercise training with propranolol on AT in patients with coronary artery disease (CAD). Eight men and one woman with significant (CAD) were selected for this study. Each patient completed a maximum treadmill stress test (MTST) following the Bruce protocol on propranolol 40-160 mg/day as a control study. Cardiorespiratory variables were measured at rest and at each stage of the treadmill test. These patients underwent an exercise training programme for 12-16 weeks on the same dose of propranolol. Training sessions were for a minimum of 30-40 minutes, 3 times a week, with training heart rate of 75%-85% of the pretraining peak heart rate. Training heart rate ranged from 98 to 128 beats/min. They were retested with a MTST after the training programme, on the same dose of propranolol. AT was calculated noninvasively by measuring respiratory variables every 30 seconds in relation to work increment. AT was identified by measuring the time course of VE, VCO2, VE/VO2, etc. in relation to incremental work. The mean values of VO2, O2P and % VO2 max at AT before and after training on propanolol were as follows: VO2 = 1.43 L/min +/- .25 and 1.86 L/min +/- .44, O2P = 14.35 +/- 2.40 and 18.73 +/- 4.00 ml/beat, % of VO2 max = 68.20 +/- 6.31 and 73.59 +/- 5.84. The mean changes of VO2 O2P, and % of VO2 max were + 0.43 L/min +/- 0.20 (P < .003), + 4.38 +/- 2.55 (P < .003) and +/- 5.07% +/- 4.84 (P < .001). After exercise training on propanolol, the mean peak exercise tolerance time and absolute VO2 max increased by 2.8 min (from 9.0 to 11.8 min) (P < .001) and 22.7% (P < .007), respectively. We conclude that the increase in anaerobic threshold in patients with coronary artery disease may be due to improvement in VO2 max, increased stroke volume, and peripheral O2 extraction.