End points of lactate and glucose metabolism after exhausting exercise

Abstract

To determine the extent of metabolite oxidation, rats were injected with [U-14C]lactate, -glucose or -bicarbonate (n = 5, each) during rest or after continuous (CE) and intermittent (IE) exercises to exhaustion. Tissue analyses of resting rats, or rats killed following CE and IE and pulse injection with [14C]lactate or -glucose (n = 72, each) were used to determine the metabolic pathways of these 2 substrates. Oxygen consumption .ovrhdot.VO2 declined rapidly for the 1st 15 min after exercise; thereafter, .ovrhdot.VO2 declined slowly and remained elevated above resting levels for 120 min. The slow phase of decline in .ovrhdot.VO2 during recovery did not coincide with lactate removal, which occurred within 15 min. Two-dimensional radiochromatograms produced from blood, kidney, liver, skeletal muscle and heart indicated a rapid incorporation of 14C into several amino acid pools, including alanine, glutamine, glutamate and aspartate. Four-hour postexercise recoveries (means of CE and IE) of injected [14C]lactate were lactate (0.75%), glucose (0.52%), protein (8.57%), glycogen (18.30%), CO2 (45.18%) and HCO3- (17.72%). Greater (P < 0.05) incorporation of 14C into protein and glycogen constituents after exercise, compared with rest, was demonstrated. Incorporation of [14C]lactate into glycogen represented a significant but only minor fraction of the metabolism of lactate after exhausting exercise. Classical explanations of excess postexercise O2 consumption (i.e., O2 debt) are too simplistic.