INTEGRATED RESPONSES TO EXHAUSTIVE EXERCISE AND RECOVERY IN RAINBOW-TROUT WHITE MUSCLE - ACID-BASE, PHOSPHOGEN, CARBOHYDRATE, LIPID, AMMONIA, FLUID VOLUME AND ELECTROLYTE METABOLISM

White muscle and arterial blood plasma were sampled at rest and during 4h of recovery from exhaustive exercise in rainbow trout. A compound respiratory and metabolic acidosis in the blood was accompanied by inc reases in plasma lactate (in excess of the metabolic acid load), pyruv ate, glucose, ammonia and inorganic phosphate levels, large elevations in haemoglobin concentration and haematocrit, red cell swelling, incr eases in the levels of most plasma electrolytes, but no shift of fluid out of the extracellular fluid (ECF) into the intracellular fluid (IC F) of white muscle. The decrease in white muscle pHi was comparable to that in pHe; both recovered by 4h. Creatine phosphate and ATP levels were both reduced by 40% after exercise, the former recovering within 0.25h, whereas the latter remained depressed until 4h. Changes in crea tine concentration mirrored those in creatine phosphate, whereas chang es in LMP and ammonia concentration mirrored those in ATP. White muscl e glycogen concentration was reduced 90% primarily by conversion to la ctate; recovery was slow, to only 40% of resting glycogen levels by 4h . During this period, most of the lactate and metabolic acid were reta ined in white muscle and there was excellent conservation of carbohydr ate, suggesting that in situ glycogenesis rather than oxidation was th e major fate of lactate. The redox state ([NAD(+)]/[NADH]) of the musc le cytoplasm, estimated from ICF lactate and pyruvate levels and pHi, remained unchanged from resting levels, challenging the traditional vi ew of the 'anaerobic' production of lactate. Furthermore, the membrane potential, estimated from levels of ICF and ECF electrolytes using th e Goldman equation, remained unchanged throughout, challenging the vie w that white muscle becomes depolarized after exhaustive exercise. Ind eed, ICF K+ concentration was elevated. Lactate was distributed well o ut of electrochemical equilibrium with either the membrane potential ( Em) or the pHe-pHi difference, supporting the view that lactate is act ively retained in white muscle. In contrast, H+ was actively extruded. Ammonia was distributed passively according to E(m) rather than pHe-p Hi throughout recovery, providing a mechanism for retaining high ICF a mmonia levels for adenylate resynthesis in situ. Although lipid is not traditionally considered to be a fuel for burst exercise, substantial decreases in free carnitine and elevations in acyl-carnitines and ace tyl-CoA concentrations indicated an important contribution of fatty ac id oxidation by white muscle during both exercise and recovery.