End points of lactate and glucose metabolism after exhausting exercise

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 two substrates. Oxygen consumption (VO₂) declined rapidly for the first 15 min after exercise; thereafter, (VO₂) declined slowly and remained elevated above resting levels for 120 min. The slow phase of decline in (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 HCO^-₃ (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. It is suggested that classical explanations of excess postexercise O₂ consumption (i.e., 'O₂ debt') are too simplistic.