Corticotroph axis sensitivity after exercise: Comparison between elite athletes and sedentary subjects

Minetto, Marco Alessandro; Lanfranco, Fabio; Baldi, Matteo; Termine, A; Kuipers, H.; Ghigo, Ezio; Rainoldi, Alberto

doi:10.1007/bf03347428

Cited by 44 publications

(55 citation statements)

References 23 publications

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“…It is well known that physical and mental stress elicit the release of cortisol from HPA axis, by which stress can modulate various immune responses 33) . Exercise in the present study could cause comparable increases in saliva cortisol levels to those observed in previous studies 34,35) . Cortisol is important hormone in the regulation of intermediate metabolism and stress.…”

Section: ⅳ．Discussionsupporting

confidence: 89%

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Usui

Yoshikawa

Ueda

et al. 2011

Jpn. J. Phys. Fitness Sports Med.

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The aim of the present study was to examine whether amount of oral cortisol, immunoglobulin A (IgA), chromogranin A (CgA) and inflammatory cytokines, might be affected by prolonged strenuous exercise. Ten young male volunteers either exercised on recumbent ergometer at 75 % V 4 O 2 max for 60 min (exercise session) or sat quietly (resting session). Saliva samples were obtained at 60 min intervals during sessions for measurements of salivary stress markers (cortisol, IgA and CgA), salivary inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) and osmolality. Saliva flow rate was decreased and saliva osmolality was increased during the 60-min exercise. Saliva cortisol and CgA concentrations and secretion rates were increased during and after the exercise, whereas saliva IgA concentration and secretion rates were decreased after the exercise. Salivary inflammatory cytokines was increased during and after the exercise. The present findings suggested a single bout of prolonged strenuous exercise caused a transient increase in the salivary cortisol, CgA and inflammatory cytokines levels, whereas salivary IgA concentration and secretion rates were decreased after the exercise. Further studies, however, are needed to delineate whether or not salivary stress markers and inflammatory cytokines may be used as biological markers to determine the host responses to acute prolonged strenuous exercise.(Jpn. J. Phys. Fitness Sports Med., 60（ 3 ）: 295-304 (2011))

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Section: ⅳ．Discussionsupporting

confidence: 89%

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Usui

Yoshikawa

Ueda

et al. 2011

Jpn. J. Phys. Fitness Sports Med.

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“…A hypothesis based on the presence of GRE in MASP2 promoter and the antiinflammatory response of glucocorticoids in general is that in control subjects exercise induces cortisol secretion that inhibits MASP2 transcription through GRE, whereas at least in a subgroup of CFS subjects, exercise-induced cortisol secretion is below a threshold (hypocortisolism) required to inhibit MASP2 expression. Although cortisol was not measured in this study, other studies have reported significant increases in cortisol and its correlation with postexercise performance in healthy subjects (50)(51)(52)(53). Accumulating evidence suggests that physical exercise, depending on the kind of exercise and subject characteristics, can act as a powerful modulator of the HPA axis and influence central nervous system functions in general (54,55).…”

Section: Discussionmentioning

confidence: 66%

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Sorensen

Jones

Vernon

et al. 2009

Mol Med

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Complement activation resulting in significant increases of C4a split product may be a marker of postexertional malaise in individuals with chronic fatigue syndrome (CFS). This study focused on identification of the transcriptional control that may contribute to the increased C4a in CFS subjects after exercise. We used quantitative reverse-transcription polymerase chain reaction to evaluate differential expression of genes in the classical and lectin pathways in peripheral blood mononuclear cells (PBMCs). Calibrated expression values were normalized to the internal reference gene peptidylpropyl isomerase B (PPIB), the external reference gene ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit (rbcL), or the geometric mean (GM) of the genes ribosomal protein, large, P0 (RPLP0) and phosphoglycerate kinase 1 (PGK1). All nine genes tested, except mannose-binding lectin 2 (MBL2), were expressed in PBMCs. At 1 hour postexercise, C4, mannan-binding lectin serine protease 2 (MASP2) and ficolin 1 (FCN1) transcripts were detected at higher levels (≥2-fold) in at least 50% (4 of 8) of CFS subjects and were detected in 88% (7 of 8) CFS subjects when subjects with overexpression of either C4 or MASP2 were combined. Only an increase in the MASP2 transcript was statistically significant (PPIB, P = 0.001; GM, P = 0.047; rbcL, P = 0.045). This result may be due to the significant but transient downregulation of MASP2 in control subjects (PPIB, P = 0.023; rbcL, P = 0.027). By 6 hours postexercise, MASP2 expression was similar in both groups. In conclusion, lectin pathway responded to exercise differentially in CFS than in control subjects. MASP2 downregulation may act as an antiinflammatory acute-phase response in healthy subjects, whereas its elevated level may account for increased C4a and inflammation-mediated postexertional malaise in CFS subjects.

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“…In contrast, the need for both nuclear FOXO1 and activated GR to fully activate MuRF1 may be protective and prevent unnecessary muscle breakdown. For example, following intense exhaustive exercise, circulating cortisol levels increase (6,31), yet elevated cortisol is generally not associated with an increase in the breakdown of contractile proteins, nor is loss of muscle mass a consequence of endurance training (33). Thus, the need for additional factors to fully activate MuRF1 gene expression could protect the muscle from breakdown under certain physiological conditions.…”

Section: Discussionmentioning

confidence: 99%

The glucocorticoid receptor and FOXO1 synergistically activate the skeletal muscle atrophy-associated MuRF1 gene

Waddell¹,

Baehr²,

Brandt³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

291

268

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The muscle specific ubiquitin E3 ligase MuRF1 has been implicated as a key regulator of muscle atrophy under a variety of conditions, such as during synthetic glucocorticoid treatment. FOXO class transcription factors have been proposed as important regulators of MuRF1 expression, but its regulation by glucocorticoids is not well understood. The MuRF1 promoter contains a near-perfect palindromic glucocorticoid response element (GRE) 200 base pairs upstream of the transcription start site. The GRE is highly conserved in the mouse, rat, and human genes along with a directly adjacent FOXO binding element (FBE). Transient transfection assays in HepG2 cells and C 2C12 myotubes demonstrate that the MuRF1 promoter is responsive to both the dexamethasone (DEX)-activated glucocorticoid receptor (GR) and FOXO1, whereas coexpression of GR and FOXO1 leads to a dramatic synergistic increase in reporter gene activity. Mutation of either the GRE or the FBE significantly impairs activation of the MuRF1 promoter. Consistent with these findings, DEXinduced upregulation of MuRF1 is significantly attenuated in mice expressing a homodimerization-deficient GR despite no effect on the degree of muscle loss in these mice vs. their wild-type counterparts. Finally, chromatin immunoprecipitation analysis reveals that both GR and FOXO1 bind to the endogenous MuRF1 promoter in C 2C12 myotubes, and IGF-I inhibition of DEX-induced MuRF1 expression correlates with the loss of FOXO1 binding. These findings present new insights into the role of the GR and FOXO family of transcription factors in the transcriptional regulation of the MuRF1 gene, a direct target of the GR in skeletal muscle.forkhead transcription factor class O; muscle RING finger 1; glucocorticoid receptor SKELETAL MUSCLE IS A DYNAMIC TISSUE that has the capacity to continuously regulate its size in response to a variety of external cues, including mechanical load, neural activity, hormones/growth factors, stress, and nutritional status. In addition, skeletal muscle serves as the most significant repository for protein in the body, a source that is tapped to provide a pool of amino acids for tissue repair and gluconeogenesis under conditions of starvation and other metabolic stresses. Muscle loss or "atrophy" occurs as the result of a number of disparate conditions, including aging, immobilization, metabolic diseases, cancer, and neurodegenerative diseases, and as a serious side effect of therapeutic corticosteroid hormone treatment (15,27,32). The recently identified E3 ubiquitin ligase, muscle RING finger 1 (MuRF1

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Corticotroph axis sensitivity after exercise: Comparison between elite athletes and sedentary subjects

Cited by 44 publications

References 23 publications

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

The glucocorticoid receptor and FOXO1 synergistically activate the skeletal muscle atrophy-associated MuRF1 gene

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