Redox basis of exercise physiology

Margaritelis, N. V.; Paschalis, V.; Theodorou, A. A.; Kyparos, A.; Nikolaidis, M. G.

doi:10.1016/j.redox.2020.101499

Javascript is disabled or not supported in your browser. JavaScript must be enabled in order for you to use WIKINDX fully. Enable JavaScript through your browser options then try again, otherwise, try using a different browser.

BioAcyl Corp

WIKINDX Resources

Margaritelis, N. V., Paschalis, V., Theodorou, A. A., Kyparos, A., & Nikolaidis, M. G. (2020). Redox basis of exercise physiology. Redox Biology, 35.
Added by: Dr. Enrique Feoli (14/10/2020, 20:34) Last edited by: Dr. Enrique Feoli (15/10/2020, 18:09)

Resource type: Journal Article
DOI: 10.1016/j.redox.2020.101499
BibTeX citation key: Margaritelis2020
View all bibliographic details

Categories: BioAcyl Corp
Subcategories: Sports performance
Creators: Kyparos, Margaritelis, Nikolaidis, Paschalis, Theodorou
Collection: Redox Biology

Views: 4/267

Abstract

Redox reactions control fundamental processes of human biology. Therefore, it is safe to assume that the responses and adaptations to exercise are, at least in part, mediated by redox reactions. In this review, we are trying to show that redox reactions are the basis of exercise physiology by outlining the redox signaling pathways that regulate four characteristic acute exercise-induced responses (muscle contractile function, glucose uptake, blood flow and bioenergetics) and four chronic exercise-induced adaptations (mitochondrial biogenesis, muscle hypertrophy, angiogenesis and redox homeostasis). Based on our analysis, we argue that redox regulation should be acknowledged as central to exercise physiology.
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli

Notes

Redox homeostasis

Collectively, it is clear that the upgraded redox homeostasis after exercise training is mediated by delicate redox processes (Fig. 8). In particular, RONS activate a series of transcription factors that rapidly turn on gene coding for the expression of antioxidant enzymes. The improved repair mechanisms that facilitate more rapid and efficient turnover of oxidatively modified proteins and DNA, as well as the increased resistance to redox modifications in response to a following stimulus, corroborate also towards a more solid redox homeostasis. For an in-depth analysis of the topic, the reader is referred to reviews about the upregulation of antioxidant genes by exercise training [9,318], the oxidative stress biomarkers and the oxidation repair mechanisms [255,370,371] and the regulation of the two central redox-sensitive transcription factors, NFkB and Nrf2 [340,344,372].

Fig. 8

Proposed mechanisms on how RONS regulate redox homeostasis. Panel A based on [9,318]; Panel B based on [344,372]; Panel C based on [255,370]. ARE, antioxidant response element; DNA, deoxyribonucleic acid; IKK, IκB kinase; Keap1, Kelch-like ECH-associated protein 1; NFkB, nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf2, nuclear factor erythroid 2-related factor 2; OGG1, 8-oxoguanine glycosylase; ROS, reactive oxygen species.

Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli