Acute and chronic effects of exercise on tissue sensitivity to glucocorticoids

Abstract

The aim of this study was to address the effect of endurance training on tissue sensitivity to glucocorticoids (GC) in both resting and exercising conditions. In vitro dexamethasone inhibition of LPS-induced interleukin-6 secretion in cultures of peripheral monocytes was compared in untrained subjects (UT) and in endurance-trained men (ET) at the end of a 2-h run and during exercise recovery. We demonstrated an in vitro plasticity of sensitivity of monocytes to GC in ET men, superimposed to changes in systemic cortisol concentrations (plasma and saliva). Compared with sedentary men, similar resting cortisol levels in ET men are associated with decreased sensitivity of monocytes to GC 8 and 24 h after the end of the last training session (P < 0.05, ET vs. UT). Moreover, in these ET subjects, an acute bout of exercise increased the sensitivity of monocytes to GC (at 1000 and 1200; ET vs. UT, P > 0.05). This acute exercise-induced increase in tissue sensitivity to GC, which is synchronous with activation of the hypothalamo-pituitary adrenal axis, may act to shut off muscle inflammatory reaction and cytokine synthesis and then decrease exercise-induced muscle damage or inflammatory response. By contrast, the decreased sensitivity of monocytes to GC reported in ET men 24 h after the last bout of exercise may be related to the process of desensitization that may act to protect the body from prolonged, exercise-induced cortisol secretion. These acute and chronic effects of exercise on tissue sensitivity to GC demonstrate an adaptation of the hypothalamo-pituitary adrenal axis to repeated and prolonged exercise-induced increases in GC secretion.

Prevention, diagnosis and treatment of the overtraining syndrome: Joint consensus statement of the European College of Sport Science (ECSS) and the American College of Sports Medicine (ACSM)

“…For example, the HPA adaptation to normal training is characterised by increased ACTH/cortisol ratio only during exercise recovery (due to decreased pituitary sensitivity to cortisol) (Lehmann et al 1993b;Duclos et al 1997Duclos et al , 1998, and by modulation REVISION : Consensus Statement "Overtraining" (17-07-2012) 10 of tissue sensitivity to glucocorticoids (Duclos et al 1999(Duclos et al , 2003). However, it should be emphasized that during a resting day, in endurance-trained athletes 24 h cortisol secretion under non-exercising conditions is normal Duclos et al 1999Duclos et al , 2003. Accordingly, morning plasma cortisol concentration and 24 h urinary free cortisol (UFC) excretion in resting endurance-trained men are similar to those of age-matched sedentary subjects (Kern et al 1995;Duclos et al 1997;Gouarne et al 2005).…”

Psychosocial Stress and Cardiovascular Disease Risk

“…Following mental stress, the sensitivity of the immune system to dexamethasone inhibition (a synthetic version of the hormone cortisol that has potent anti-14 inflammatory properties) is reduced, as manifest by a reduction in this hormone's capacity to suppress the production of inflammatory cytokines (58). In endurance trained individuals, however, an acute bout of exercise has been shown to increase tissue sensitivity to glucocorticoids (59). HPA axis dysregulation and cortisol hypersecretion has been implicated in adverse mental health and cardiovascular outcomes.…”

The response of serum leptin, cortisol and zinc concentrations to concurrent training

“…[16][17][18] Cortisol is a glucocorticoid secreted by the adrenal cortex and among other functions, increases glyconeogenesis and promotes fat mobilization and utilization. 19,20 Zinc also plays an important role in appetite regulation and may thus be expected to act as a mediator of leptin effects. 21 Studies 17,22,23 have shown low leptin levels in states of zinc deficiency.…”