Integrating metabolic pathways in post-exercise recovery of white muscle.

Abstract

Purine nucleotides (ATP, ADP, AMP, IMP), creatine, phosphocreatine, lactate, pyruvate and glycogen were measured in rainbow trout (Oncorhynchus mykiss) white muscle following exercise to exhaustion. Estimates of intracellular pH permitted calculation of free concentrations of nucleotides ([nucleotide]f) required for most models of control of energy metabolism. Creatine charge, [PCr]/([PCr]+[Cr]), fell from 0.49 +/- 0.05 (mean +/- S.E.M.) to 0.08 +/- 0.02 with exercise but recovered completely by the first sample (2 h). Although [ATP] declined to 24% of resting levels and recovered very slowly, RATP, [ATP]/([ATP]+[ADP]f+[AMP]f), and energy charge, EC, ([ATP]+0.5[ADP]f)/([ATP]+[ADP]f+[AMP]f), recovered as quickly as creatine charge. Changes in [IMP] mirrored those in [ATP], suggesting that AMP deaminase is responsible for maintaining RATP and EC. Recovery of carbon status was much slower than recovery of energy status. Lactate increased from 4 mumol g-1 at rest to 40 mumol g-1 at exhaustion and did not recover for more than 8 h. Glycogen depletion and resynthesis followed a similar time course. During the early stages of recovery, calculated [ADP]f declined by more than 10-fold relative to the resting values. The resulting high [ATP]/[ADP]f ratios may limit the rate at which white muscle mitochondria can produce ATP to fuel glycogenesis in situ. It is postulated that the high [ATP]/[ADP]f ratios are required to drive pyruvate kinase in the reverse direction for glyconeogenesis in recovery.