Mechanism of Oxygen Deficit.

Abstract

In muscular exercise, a considerable O2 deficit is incurred which cannot be explained by the accumulation of lactic acid. The hypothesis that this deficit is due to the depletion of high energy phosphate in muscle and that the O2 consumption is increased by an increase in phosphate acceptor was tested in the perfused dog gastrocnemius. An estimated O2 deficit was calculated from change in lactic acid and high energy phosphate after 2 minutes of contraction. The O2 deficit was calculated from the O2 consumption determined at 5-second intervals by measurement of blood flow and arteriovenous difference. For exercise, the muscle was stimulated at 300 cps- for 1 second intervals with 1 second rest. In 14 experiments, the average values of lactic acid were 14.2 mg % at rest, and 29.2 mg % during exercise. High energy phosphate at rest was 70.3 mg % and fell to 56 mg % during stimulation. The calculated deficit was 2.3 cc O2/100 g muscle, and the measured deficit was 2.2 cc O2/100 g muscle.