Corticotroph axis sensitivity after exercise in endurance‐trained athletes

Duclos, Martine; Corcuff, J.-B.; Arsac, Laurent M.; Moreau‐Gaudry, François; Rashedi, M; Roger, Patrick; Tabarin, Antoine; Manier, G.

doi:10.1046/j.1365-2265.1998.00334.x

Cited by 74 publications

(53 citation statements)

References 40 publications

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“…Consequently, the majority of studies aimed at identifying markers of ensuing OTS are actually reporting markers of excessive exercise stress resulting in the acute condition of OR and not the chronic condition of OTS. The mechanism of the OTS could be difficult to examine in detail maybe because the stress caused by excessive training load, in REVISION : Consensus Statement "Overtraining" (17-07-2012) 26 combination with other stressors might trigger different "defence mechanisms" such as the immunological, neuroendocrine and other physiological systems that all interact and probably therefore cannot be pinpointed as the "sole" cause of the OTS. It might be that as in other syndromes (e.g., chronic fatigue syndrome, or burnout) the psychoneuroimmunology (study of brainbehaviour-immune interrelationships) might shed a light on the possible mechanisms of the OTS, but until there is no definite diagnostic tool, it is of utmost importance to standardise measures that are now thought to provide a good inventory of the training status of the athlete.…”

Section: Resultsmentioning

confidence: 99%

“…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.…”

Section: Biochemistry and Hormones Biochemistrymentioning

confidence: 99%

See 1 more Smart Citation

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)

Meeusen¹,

Duclos²,

Foster³

et al. 2012

European Journal of Sport Science

617

934

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Successful training must involve overload, but also must avoid the combination of excessive overload plus inadequate recovery. Athletes can experience short-term performance decrement, without severe psychological, or lasting other negative symptoms. This Functional Overreaching (FOR) will eventually lead to an improvement in performance after recovery. When athletes do not sufficiently respect the balance between training and recovery, Non-Functional Overreaching (NFOR) can occur. The distinction between NFOR and the Overtraining Syndrome (OTS) is very difficult and will depend on the clinical outcome and exclusion diagnosis. The athlete will often show the same clinical, hormonal and other signs and symptoms. A keyword in the recognition of OTS might be 'prolonged maladaptation' not only of the athlete, but also of several biological, neurochemical, and hormonal regulation mechanisms. It is generally thought that symptoms of OTS, such as fatigue, performance decline and mood disturbances, are more severe than those of NFOR. However, there is no scientific evidence to either confirmor refute this suggestion. One approach to understanding the aetiology of OTS involves the exclusion of organic diseases or infections and factors such as dietary caloric restriction (negative energy balance) and insufficient carbohydrate and/or protein intake, iron deficiency, magnesium deficiency, allergies, etc., together with identification of initiating events or triggers. In this paper, we provide the recent status of possible markers for the detection of OTS. Currently several markers (hormones, performance tests, psychological tests, biochemical and immune markers) are used, but none of them meets all criteria to make its use generally accepted.

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Section: Resultsmentioning

confidence: 99%

Section: Biochemistry and Hormones Biochemistrymentioning

confidence: 99%

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)

Meeusen¹,

Duclos²,

Foster³

et al. 2012

European Journal of Sport Science

617

934

View full text Add to dashboard Cite

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“…Marathon runners have normal resting GC concentrations, despite higher concentrations of ACTH, suggesting that training may decrease adrenal sensitivity to ACTH (11,37). In rodents, the effect of exercise on diurnal HPA activity and adrenal sensitivity to ACTH is also unclear.…”

Section: Discussionmentioning

confidence: 99%

Voluntary wheel running initially increases adrenal sensitivity to adrenocorticotrophic hormone, which is attenuated with long-term training

Campbell

Rakhshani²,

Fediuc³

et al. 2009

Journal of Applied Physiology

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Campbell JE, Rakhshani N, Fediuc S, Bruni S, Riddell MC. Voluntary wheel running initially increases adrenal sensitivity to adrenocorticotrophic hormone, which is attenuated with long-term training. J Appl Physiol 106: 66 -72, 2009. First published November 13, 2008 doi:10.1152/japplphysiol.91128.2008.-Although exercise is a common and potent activator of the hypothalamic-pituitary adrenal (HPA) axis, the effects of exercise on the acute stress response are not well understood. Here, we investigated the effects of short-(2 wk) and long-term (8 wk) voluntary wheel running on adrenal sensitivity to ACTH stimulation and the acute stress response to restraint in male rats. Diurnal glucocorticoid patterns were measured on days 7 (all groups) and 35 (8-wk groups). Rats were subjected to 20 min of restraint stress on either week 1 or on week 7 of treatment to assess HPA activation. One week later, exogenous ACTH (75 ng/kg) was administered to assess adrenal sensitivity to ACTH. Following this, adrenals were collected and analyzed for key proteins involved in corticosterone (CORT) synthesis. By the end of week 1, exercising (E) animals had twofold higher peak diurnal CORT levels compared with sedentary (S) animals (P Ͻ 0.01). CORT values were not different between groups at week 8. In response to restraint stress at week 2, CORT values in E were approximately threefold greater than in S (P Ͻ 0.05). No difference was found between E and S rats in the response to, or recovery from, restraint at week 8. During the ACTH challenge at week 2, E demonstrated a ϳ2.5-fold increase in adrenal sensitivity compared with S, while no difference was found between E and S at week 8. The expression of steroidogenic acute regulatory protein was found to be ϳ50% higher in the adrenals in E compared with S at week 2 (P Ͻ 0.05), but no difference existed between groups at week 8. These results show that volitional wheel running initially causes hyperactivation of the HPA axis, due to enhanced adrenal sensitivity to ACTH, but that these alterations in HPA activity are completely restored by 8 wk of training. glucocorticoids; corticosterone; adrenocorticotropic hormone; voluntary exercise; circadian rhythm; restraint stress; adrenocorticotropic hormone challenge; glucocorticoid receptor THE HYPOTHALAMIC-pituitary-adrenal (HPA) axis is a vital component of the body's stress response system. This pathway is activated by a variety of stressors that increase the pituitary release of adrenocorticotropic hormone (ACTH) into the circulation. ACTH stimulates the adrenal release of glucocorticoids (GCs), which, in turn, mobilize energy sources for the increased metabolic demands placed on the body. Acutely, this recruitment of energy sources is essential for events, such as physical exercise; however, restoration of the axis is imperative to prevent overexposure to GCs. It has been well established that chronically elevated levels of plasma GCs can lead to the development of a number of harmful pathologies, including impaired insulin signaling, centr...

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“…For example, after an exercise-induced cortisol increase, the subsequent stimulation exerted by a meal does not elicit a rise of cortisol levels in sedentary men, whereas in ET men a marked cortisol increase occurs (3). These findings suggesting a decreased sensitivity to glucocorticoid negative feedback in healthy ET men may reflect allostatic modifications of the HPA axis due to repeated exercise-induced HPA axis activation (5).…”

Section: Introductionmentioning

confidence: 88%

Decreased pituitary sensitivity to glucocorticoids in endurance-trained men

Duclos

Corcuff

Péhourcq

et al. 2001

European Journal of Endocrinology

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Objective: Muscular exercise induces hypothalamo-pituitary-adrenal (HPA) axis activation and when regularly repeated, as in endurance training, leads to HPA axis adaptation. To assess whether nonprofessional endurance-trained (ET) men with a substantial training load and no clinical or biological features of HPA axis overactivity can present subtle alterations of HPA axis sensitivity to glucocorticoid negative feedback, nine ET men were subjected to HPA axis testing using the dexamethasone±corticotrophin-releasing hormone (CRH) test. Design: Nine endurance-trained men and eight healthy age-matched sedentary men were studied. Morning plasma cortisol and 24 h urinary free cortisol (UFC) were determined and a low dose dexamethasone suppression test (LDDST) was performed followed by CRH stimulation (dexamethasone±CRH test). Results: After a day without physical exercise, at 0800 h, plasma ACTH and cortisol concentrations, and the 24 h UFC and UFC/urinary creatinine (UC) ratio were similar in ET and sedentary men. By contrast, clear differences between the groups were seen in cortisol and ACTH responses to the dexamethasone±CRH test. In eight ET subjects, after LDDST, basal ACTH and cortisol levels were similar to those of sedentary men, whereas one ET subject displayed a poor suppression of cortisol level (131 nmol/l). After injection of CRH, however, three of nine ET men's cortisol levels were not suppressed by dexamethasone but instead displayed significant CRH-induced increase (peak cortisol: 88, 125 and 362 nmol/l). No sedentary subject exhibited any increase in cortisol levels. Conclusion: Three of nine ET men with a mean maximum rate of O 2 uptake (V O2, max ) of 61 ml/kg per min, running 50±70 km per week, were resistant to glucocorticoid suppression during the combined dexamethasone±CRH test.

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Corticotroph axis sensitivity after exercise in endurance‐trained athletes

Cited by 74 publications

References 40 publications

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)

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)

Voluntary wheel running initially increases adrenal sensitivity to adrenocorticotrophic hormone, which is attenuated with long-term training

Decreased pituitary sensitivity to glucocorticoids in endurance-trained men

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