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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Melinda M. Manore
This paper presents an overview of vitamin
Javier T. Gonzalez and Andy J. King
endogenous glucose being labeled with 13 C is extremely unlikely. In contrast, [6,6 2 H 2 ]-glucose is often used as an infused tracer since there is almost no chance that both of the 2 H atoms will be recycled back into the same C-6 position that they started in after glycolysis and gluconeogenesis
Alexander-Stephan Henze, Jochen Huth, and Frieder Mauch
-intensity exercise can also lead to an increase in urea due to the breakdown of structural and functional proteins for gluconeogenesis after depleting glycogen stores. 23 – 25 Relevant protein catabolism for energy production occurs in sport after 60 to 70 minutes of exercise. Therefore, urea is suitable as an
Christopher C. Webster, Jeroen Swart, Timothy D. Noakes, and James A. Smith
. Webster CC , Noakes TD , Chacko SK , Swart J , Kohn TA , Smith JA . Gluconeogenesis during endurance exercise in cyclists habituated to a long-term low carbohydrate high-fat diet . J Physiol . 2016 ; 594 ( 15 ): 4389 – 4405 . PubMed ID: 26918583 doi:10.1113/JP271934 10.1113/JP271934
John Stoszkowski and Hans Amato
adrenaline are increased to mobilize fat from fat stores as a backup fuel and convert our muscle and organ tissue into glucose via gluconeogenesis, an inefficient and energetically wasteful process ( Veldhorst et al., 2009 ). Glucose is considered the obligatory energy substrate in the adult brain, with the
Mark Glaister and Conor Gissane
balance between lactate production and clearance; with approximately 70% to 80% of the latter achieved through oxidation and the remainder by gluconeogenesis. 50 As such, the caffeine-induced increase in [BLa] determined in this meta-analysis could be due to either an increase in lactate production
Ralph Beneke, Tobias G.J. Weber, and Renate M. Leithäuser
mitochondrion for subsequent aerobic utilization. 25 , 26 Consequently, aerobic lactate oxidation reflects the ultimate reliance on carbohydrate (CHO) during exercise and prevents the option to use lactate/pyruvate as a substrate of gluconeogenesis. Aerobic lactate/pyruvate oxidation is defined by V ˙ O 2
Bruno P. Melo, Débora A. Guariglia, Rafael E. Pedro, Dennis A. Bertolini, Solange de Paula Ramos, Sidney B. Peres, and Solange M. Franzói de Moraes
potentiating gluconeogenesis, contributes to the energy metabolism. 13 On the other hand, chronically high cortisol concentrations at rest have been associated with physiological stress, immunosuppression, and homeostatic disturbance in several populations, including older adults with hypertension, diabetes
Emma L. Sweeney, Daniel J. Peart, Irene Kyza, Thomas Harkes, Jason G. Ellis, and Ian H. Walshe
improvements in the late rather than total postprandial response after a bout of exercise. High-intensity exercise is known to temporarily increase glucose due to gluconeogenesis and possible carbohydrate sparing for glycogen repletion ( Marliss et al., 1992 ). It may be possible that as glucose regulation was