A regulatory role for cortisol in muscle glycogen metabolism in rainbow troutOncorhynchus mykissWalbaum

Abstract

SUMMARY To test the hypothesis that cortisol has a regulatory role in fish muscle glycogenesis post-exercise, rainbow trout were treated 1 h prior to exercise with either saline (control) or metyrapone (2-methyl-1,2-di-3-pyridyl-1-propanone) to block cortisol synthesis. Following exercise(time 0), half of the metyrapone-treated fish received a single injection of cortisol, to mimic the post-exercise rise usually observed. Muscle glycogen and the relative activities of glycogen phosphorylase a (Phos a) and glycogen synthase I (GSase I), regulatory enzymes for glycogen resynthesis, were monitored 4 h post-exercise. Metyrapone treatment succeeded in blocking the post-exercise rise in plasma cortisol(17±2 vs 118±13 ng ml–1 in controls at time 0), and cortisol injection resulted in a larger and more prolonged cortisol increase than in controls (159±22 vs 121±14 ng ml–1 in controls at 1 h). Muscle glycogen was completely restored in the metyrapone-treated fish within 2 h after exercise(8.3±0.6 vs 8±0.7 μmol g–1pre-exercise), only partially restored in control fish at 4 h (5.4±01.4 vs 8.8±1.3 μmol g–1 pre-exercise), and not at all in cortisol-treated fish (1.0±0.5 μmol g–1at 4 h). The rapid glycogen resynthesis in the metyrapone-treated fish was associated with a more rapid inactivation of Phos a and stimulation of GSase I compared to controls. In cortisol-treated fish, Phos a activity persisted throughout 4 h post-exercise; there was also a significant stimulation of GSase I activity. As a consequence of dual activation of Phos a and GSase I, glycogen cycling probably occurred, thus preventing net synthesis. This explains why the post-exercise elevation of cortisol inhibits net glycogen synthesis in trout muscle.

Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout

“…The observed time course of inotropic effects in the rainbow trout ventricle agrees with previous studies showing rapid effects of C on muscle glycogen metabolism (Milligan, 2003) and similar effects in rat cardiac tissue (Rubín et al, 1999). However, we cannot rule out the possibility that a genomic mechanism is responsible.…”

Effects of swimming on metabolic recovery from anoxia in the painted turtle

“…Despite a similar effect of exercise on the recovery processes of fish and mammals after exercise, the mechanisms for the enhanced recovery are very different between the two classes. In trout, swimming during recovery decreases circulating cortisol, a hormone that inhibits glycogen repletion from lactate in muscle, thereby hastening overall lactate clearance (Milligan, 2003). It is unlikely, however, that corticosteroids play a major role in lactate metabolism during recovery from anoxic submergence in turtles.…”

“…The mechanism for enhanced lactate clearance during active recovery is thought to be increased lactate oxidation, which generates ATP to help sustain the exercise. Active recovery following lactic acid accumulation by strenuous exercise has also been shown to enhance metabolic recovery in trout (Milligan et al, 2000), although the suggested mechanism is thought to be related to the inhibitory effects of cortisol on glycogen repletion in muscle (Milligan, 2003). The effect of active recovery has yet to investigated in reptiles recovering from lactic acidosis or any animal recovering from hypoxia or anoxia.…”

Physiological Mechanism and Application of Fish Exercise Training in Aquaculture

“…after exercise and lasted for several hours15. Both of these hormones are closely related to the metabolic regulation of carbohydrates, proteins, amino acids and lipids after exercise, and the mechanism of the regulation is related to the hormone receptors [15][16][17].…”