Modulating exercise-induced hormesis: does less equal more?

Peake, Jonathan M., Markworth, James F., Nosaka, Kazunori, Raastad, Truls, Wadley, Glenn D. and Coffey, Vernon G. 2015, Modulating exercise-induced hormesis: does less equal more?, Journal of applied physiology, vol. 119, no. 3, pp. 172-189, doi: 10.1152/japplphysiol.01055.2014.

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Title Modulating exercise-induced hormesis: does less equal more?
Author(s) Peake, Jonathan M.
Markworth, James F.
Nosaka, Kazunori
Raastad, Truls
Wadley, Glenn D.ORCID iD for Wadley, Glenn D. orcid.org/0000-0002-6617-4359
Coffey, Vernon G.
Journal name Journal of applied physiology
Volume number 119
Issue number 3
Start page 172
End page 189
Total pages 18
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2015-08-01
ISSN 1522-1601
Keyword(s) adaptation
preconditioning
stress
Science & Technology
Life Sciences & Biomedicine
Physiology
Sport Sciences
HUMAN SKELETAL-MUSCLE
BLOOD-FLOW RESTRICTION
INTENSITY RESISTANCE EXERCISE
LOCAL NSAID INFUSION
REDUCED CARBOHYDRATE AVAILABILITY
INDUCED MITOCHONDRIAL BIOGENESIS
COACTIVATOR 1-ALPHA PGC-1-ALPHA
INTRAMUSCULAR METABOLIC STRESS
MAXIMAL ISOMETRIC CONTRACTIONS
XANTHINE-OXIDASE INHIBITION
Summary Hormesis encompasses the notion that low levels of stress stimulate or upregulate existing cellular and molecular pathways that improve the capacity of cells and organisms to withstand greater stress. This notion underlies much of what we know about how exercise conditions the body and induces long-term adaptations. During exercise, the body is exposed to various forms of stress, including thermal, metabolic, hypoxic, oxidative, and mechanical stress. These stressors activate biochemical messengers, which in turn activate various signaling pathways that regulate gene expression and adaptive responses. Historically, antioxidant supplements, nonsteroidal anti-inflammatory drugs, and cryotherapy have been favored to attenuate or counteract exercise-induced oxidative stress and inflammation. However, reactive oxygen species and inflammatory mediators are key signaling molecules in muscle, and such strategies may mitigate adaptations to exercise. Conversely, withholding dietary carbohydrate and restricting muscle blood flow during exercise may augment adaptations to exercise. In this review article, we combine, integrate, and apply knowledge about the fundamental mechanisms of exercise adaptation. We also critically evaluate the rationale for using interventions that target these mechanisms under the overarching concept of hormesis. There is currently insufficient evidence to establish whether these treatments exert dose-dependent effects on muscle adaptation. However, there appears to be some dissociation between the biochemical/molecular effects and functional/performance outcomes of some of these treatments. Although several of these treatments influence common kinases, transcription factors, and proteins, it remains to be determined if these interventions complement or negate each other, and whether such effects are strong enough to influence adaptations to exercise.
Language eng
DOI 10.1152/japplphysiol.01055.2014
Field of Research 110699 Human Movement and Sports Science not elsewhere classified
Socio Economic Objective 929999 Health not elsewhere classified
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2015, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30077488

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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