PubMed · 15413751
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1950. ACTH and cortisone (compound E).. https://pubmed.ncbi.nlm.nih.gov/15413751/
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An increased systemic concentration of stress hormones (of the hypothalamic-pituitary adrenal axis) and some cytokines may contribute to the depression of immune cell function typically observed after prolonged exercise. The aim of the present study was to determine the effect of 2 weeks of supplementation with vitamin C (VC) on cortisol, adrenocorticotrophic hormone, interleukin-6, oxidative stress and neutrophil responses to a single bout of endurance exercise. Nine healthy endurance-trained males exercised for 2.5 h at 60% VO2max after 2 weeks of placebo (PLA) or VC (1,000 mg day(-1)) supplementation. All participants completed both trials utilising a randomised crossover design with a minimum 14 day washout period between trials. There was a significant trial x time interaction effect for plasma cortisol concentration (P = 0.039) which tended to be lower in the VC trial but post hoc analysis found no specific between trial differences. There was a significantly lower post-exercise neutrophilia (P < 0.014) in the VC trial, compared with the PLA trial. There was no trial x time interaction for measures of neutrophil function (bacteria-stimulated elastase release, fMLP or PMA-stimulated oxidative burst). However, there was a trend for higher fMLP-stimulated neutrophil oxidative burst in the VC compared with PLA trial (trial x time interaction, P = 0.075). These results suggest that supplementation with VC for a period of up to 2 weeks provides little to no protection against the depression of neutrophil function which typically occurs after endurance exercise.
The purpose of this study was to examine pituitary-adrenal (PA) hormone responses [beta-endorphin (beta-END), adrenocorticotropic hormone (ACTH) and cortisol] to arm exercise (AE) and leg exercise (LE) at 60 and 80% of the muscle-group specific VO2 peak. Eight healthy untrained men (AE VO2 peak=32.4+/-3.0 ml kg(-1) min(-1), LE VO2 peak=46.9+/-5.3 ml kg(-1) min(-1)) performed two sub-maximal AE and LE tests in random order. Plasma beta-END, ACTH and cortisol were not different (P>0.05) between AE and LE at either exercise intensity; the 60% testing elicited no changes from pre-exercise (PRE) values. For 80% testing, plasma beta-END, ACTH and cortisol were consistently, but not significantly, greater during LE than AE. In general, plasma beta-END and ACTH were higher (P<0.05) during 80% exercise, than PRE, for both AE and LE. Plasma cortisol was elevated (P<0.05) above PRE during 80% LE, and following 80% for both AE and LE. Plasma ACTH was higher (P<0.05) during 80% LE and AE versus 60% LE and AE, respectively. Plasma beta-END and cortisol were significantly higher during and immediately after 80% LE than 60% LE. Thus, plasma beta-END, ACTH and cortisol responses were similar for AE and LE at the two relative exercise intensities, with the intensity threshold occurring somewhere between 60 and 80% of VO2 peak. It appears that the smaller muscle mass associated with AE was sufficient to stimulate these PA axis hormones in a manner similar to LE, despite the higher metabolic stress (i.e., plasma La-) associated with LE.
BACKGROUND/AIMS: We have previously demonstrated that prostaglandin generation within the fetal brain augments or partially mediates fetal reflex responsiveness to hypotension. The present study was performed to test the relative roles of prostaglandin endoperoxide synthases-1 and -2 (PGHS-1 and 2, or COX-1 and 2) as potential mediators of this interaction. METHODS: Chronically catheterized and instrumented fetal sheep were subjected to transient brachiocephalic occlusion (BCO) after intracerebroventricular injection of resveratrol (PGHS-1 or COX-1 inhibitor), nimesulide (PGHS-2 or COX-2 inhibitor), or vehicle. RESULTS: BCO decreased arterial pressure perfusing the fetal brain and stimulated increases in systemic blood pressure and heart rate as well as in circulating concentrations of ACTH. Inhibition of PGHS-1 and PGHS-2 had differential effects on fetal ACTH secretion. Pre-BCO concentrations of plasma ACTH increased in response to nimesulide, while the fetal ACTH response to BCO was delayed by resveratrol. Prior to the BCO, nimesulide also increased fetal blood pressure and decreased fetal heart rate. The injections of resveratrol and nimesulide did not alter placental biosynthesis of prostaglandins and therefore acted within the fetal brain. CONCLUSION: We conclude that prostaglandin generated in the fetal brain by the action of PGHS-1 augments fetal ACTH reflex responses to BCO but that, in contrast, the action of PGHS-2 is inhibitory to ACTH secretion.