Ascorbic acid or vitamin C is involved in a number of biochemical pathways that are important to exercise metabolism and the health of exercising individuals. This review reports the results of studies investigating the requirement for vitamin C with exercise on the basis of dietary vitamin C intakes, the response to supplementation and alterations in plasma, serum, and leukocyte ascorbic acid concentration following both acute exercise and regular training. The possible physiological significance of changes in ascorbic acid with exercise is also addressed. Exercise generally causes a transient increase in circulating ascorbic acid in the hours following exercise, but a decline below pre-exercise levels occurs in the days after prolonged exercise. These changes could be associated with increased exercise-induced oxidative stress. On the basis of alterations in the concentration of ascorbic acid within the blood, it remains unclear if regular exercise increases the metabolism of vitamin C. However, the similar dietary intakes and responses to supplementation between athletes and nonathletes suggest that regular exercise does not increase the requirement for vitamin C in athletes. Two novel hypotheses are put forward to explain recent findings of attenuated levels of cortisol postexercise following supplementation with high doses of vitamin C.
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André L. Estrela, Aline Zaparte, Jeferson D. da Silva, José Cláudio Moreira, James E. Turner, and Moisés E. Bauer
adaptation in response to regular exercise ( Struder et al., 1998 ) (even in the low-training group who undertook approximately 4 hr of exercise per week), the lack of a cortisol response is likely to be governed by other factors. For example, the magnitude of cortisol release from the adrenal gland during
Tony Adebero, Brandon John McKinlay, Alexandros Theocharidis, Zach Root, Andrea R. Josse, Panagiota Klentrou, and Bareket Falk
cortisol above the CBG binding point likely reflects the complexity of the hypothalamus-pituitary-adrenal gland axis response to stress, which may be differentially manifested in blood and saliva. In this study, the salivary free cortisol concentration values did not exceed the CBG binding point, and there
Carlo Pruneti, Simone Ferrari, and Sara Guidotti
reactions was called general adaptation syndrome (GAS). The univocal response to any adverse stimulus occurs in three phases ( Selye, 1956 , 1998 ). The activation of the sympathetic nervous system (SANS) with consequent activation of the medullary portion of the adrenal glands and secretion of adrenaline
Travis Anderson, Laurie Wideman, Flavio A. Cadegiani, and Claudio E. Kater
39 and is an active area of continued research. It is possible that a combination of reduced ACTH output and altered sympathetic input to the adrenal gland interact to cause the lowered CAR observed in the present study. Besides the direct corticoadrenal regulation by the sympathetic neural
Matthew Springham, Robert U. Newton, Anthony J. Strudwick, and Mark Waldron
pituitary gland, which increases cholesterol concentration and the cellular activity of desmolase in the inner mitochondrial membrane of the adrenal gland. Cholesterol is then converted to pregnenolone and progesterone, which converts to 17-A-hydroxyprogesterone, 11-deoxycortisol, and then cortisol, which
Teri J. Hepler and Matt Andre
before and after stress induction: salivary cortisol and heart rate variability (HRV). Cortisol is a glucocorticoid that is released by the adrenal gland following exposure to mental and physical stressors ( Putman, Antypa, Crysovergi, & van der Does, 2010 ). Salivary cortisol provides a simple, painless
Len De Nys, Esther F. Ofosu, Gemma C. Ryde, Jenni Connelly, and Anna C. Whittaker
training protocols, which may acutely increase the activation of adrenal glands and stimulate cortisol production ( Ahn & Kim, 2018 ). Yet, no important differences in effect sizes were found in the present meta-analysis when exploring subgroup differences by intervention type (aerobic vs. resistance vs
