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    Circulating tumor necrosis factor alpha may modulate the short-term detraining induced muscle mass loss following prolonged resistance training

    McMahon, G, Morse, CI ORCID logoORCID: https://orcid.org/0000-0002-5261-2637, Winwood, K ORCID logoORCID: https://orcid.org/0000-0002-8696-9976, Burden, A ORCID logoORCID: https://orcid.org/0000-0002-1105-312X and Onambélé, GL (2019) Circulating tumor necrosis factor alpha may modulate the short-term detraining induced muscle mass loss following prolonged resistance training. Frontiers in Physiology, 10. ISSN 1664-042X

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    Abstract

    Copyright © 2019 McMahon, Morse, Winwood, Burden and Onambélé. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Introduction: Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that has been shown to modulate muscle mass, and is responsive to exercise training. The effects of resistance training (RT) followed by a short period of detraining on muscle size, architecture and function in combination with circulating TNFα levels have not been previously investigated in a young, healthy population. Methods: Sixteen participants (8 males and 8 females) were randomly assigned to a training group (TRA; age 20 ± 3 years, mass 76 ± 7 kg), whilst fourteen participants (7 males and 7 females) age 22 ± 2 years, mass 77 ± 6 kg were assigned to a control group (CON). Measures of vastus lateralis (VL) muscle size (normalized physiological cross-sectional area allometrically scaled to body mass; npCSA), architecture (fascicle length; LF, pennation angle Pθ), strength (knee extensor maximal voluntary contraction; KE MVC), specific force, subcutaneous fat (SF) and circulating TNFα were assessed at baseline (BL), post 8 weeks RT (PT), and at two (DT1) and four (DT2) weeks of detraining. Results: Pooled BL TNFα was 0.87 ± 0.28 pg/mL with no differences between groups. BL TNFα tended to be correlated with npCSA (p = 0.055) and KEMVC (p = 0.085) but not specific force (p = 0.671) or SF (p = 0.995). There were significant (p < 0.05) increases in npCSA compared to BL and CON in TRA at PT, DT1, and DT2, despite significant (p < 0.05) decreases in npCSA compared to PT at DT1 and DT2. There were significant (p < 0.05) increases in LF, Pθ and KE MVC at PT but only LF and torque at DT1. There were no significant (p > 0.05) changes in SF, specific force or TNFα at any time points. There was a significant correlation (p = 0.022, r = 0.57) between the relative changes in TNFα and npCSA at DT2 compared to PT. Discussion: Neither RT nor a period of short term detraining altered the quality of muscle (i.e., specific force) despite changes in morphology and function. TNFα does not appear to have any impact on RT-induced gains in muscle size or function, however, TNFα may play a role in inflammatory-status mediated muscle mass loss during subsequent detraining in healthy adults.

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