Alterations in the oxygen deficit‐oxygen debt relationships with beta‐adrenergic receptor blockade in man.

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Abstract
The effects of .beta.-adrenergic receptor blockade (100 mg oral metoprolol) or matched placebo on gas exchange kinetics were studied in 6 males. Ventilation and gas exchange were monitored in 4 transitions for each treatment from loadless pedaling (0 W) to a selected work rate (100 W) and back to 0 W. Breath-by-breath data were averaged for analysis. O2 uptake (.ovrhdot.VO2) kinetics were significantly slowed at the onset of exercise and recovery by .beta.-blockade. This resulted in larger O2 deficit and O2 debt (671 .+-. 115, 586 .+-. 87 ml O2, respectively) for .beta.-blockade than for placebo (497 .+-. 87, 474 .+-. 104 ml O2). O2 deficit was significantly larger than O2 debt during .beta.-blockade tests. This can be explained by greater utilization of O2 and creatine phosphate stores as well as anaerobic glycolysis at the onset of 100 W exercise with .beta.-blockade. CO2 output (.ovrhdot.VCO2) kinetics were significantly slowed by .beta.-blockade only at the onset of exercise. Expired ventilation (.ovrhdot.VE) kinetics were not affected by .beta.-blockade. At 0 W, .ovrhdot.VE was significantly reduced by .beta.-blockade. Heart rate was lower at all times with .beta.-blockade. Kinetics of heart rate were not affected. At the start and end of exercise and even in moderate-intensity exercise, lactic acid production can contribute significantly to energy supply. The use of the term alactic to describe the deficit and debt associated with this exercise is not appropriate.