The potential regulatory roles of cortisol in recovery from exhaustive exercise in rainbow trout

Abstract

Exercise to exhaustion, as indicated by near depletion of muscle glycogen stores, resulted in a 2- to 3-fold increase in the levels of plasma cortisol, but there was no consistent effect of exercise on plasma insulin, glucagon, T₃ or T₄ levels. Treatment of rainbow trout (Oncorhynchus mykiss) with metyrapone (which inhibits cortisol synthesis) 1 h or dexamethasone (which inhibits cortisol release) 24 h prior to exercise successfully blocked the exercise-induced rise in plasma cortisol. Neither metyrapone nor dexamethasone treatment had any effect on exercise performance, as muscle glycogen was depleted and lactate accumulated to the same extent in control and treated fish. Control fish showed the typical blood lactate response to exhaustive exercise: [lactate] peaked at 10–15 μmol∙mL⁻¹ about 2–4 h post exercise and returned to pre-exercise levels within 8 h. The response of blood lactate in cortisol-blocked fish was significantly different: post-exercise levels were rarely greater than 5 μmol∙mL⁻¹ and had returned to resting levels by 2 h. Analysis of tissue metabolite and acid–base status indicated that cortisol-blocked fish recovered faster than did controls. In treated fish, muscle glycogen and lactate levels had returned to pre-exercise levels within 2 h. Blood pH and muscle intracellular pH were also restored to pre-exercise values within 2 h. In contrast, restoration of tissue metabolite and acid–base status in control fish required up to 8 h. The fact that both metyrapone and dexamethasone treatment had the same effects on recovery metabolism suggests that it is the absence of the rise in plasma cortisol, rather than the drug treatment itself, which is responsible for the enhancement of metabolic recovery.