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Low responders to endurance training exhibit impaired hypertrophy and divergent biological process responses in rat skeletal muscle

West, DWD, Doering, TM, Thompson, J-LM, Budiono, BP, Lessard, SJ, Koch, LG, Britton, SL, Steck, R, Byrne, NM ORCID: 0000-0001-5310-6640, Brown, MA, Peake, JM, Ashton, KJ and Coffey, VG 2021 , 'Low responders to endurance training exhibit impaired hypertrophy and divergent biological process responses in rat skeletal muscle' , Experimental Physiology, vol. 106 , 714–725 , doi: 10.1113/EP089301.

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Divergent skeletal muscle phenotypes result from chronic resistance-type versusendurance-type contraction, reflecting the principle of training specificity. Our aimwas to determine whether there is a common set of genetic factors that influenceskeletal muscle adaptation to divergent contractile stimuli. Female rats were obtainedfrom a genetically heterogeneous rat population and were selectively bred from highresponders to endurance training (HRT) or low responders to endurance training(LRT; n = 6/group; generation 19). Both groups underwent 14 days of synergistablation to induce functional overload of the plantaris muscle before comparison tonon-overloaded controls of the same phenotype. RNA sequencing was performedto identify Gene Ontology biological processes with differential (LRT vs. HRT) geneset enrichment. We found that running distance, determined in advance of synergistablation, increased in response to aerobic training in HRT but not LRT (65 ± 26 vs.−6 ± 18%, mean ± SD, P < 0.0001). The hypertrophy response to functional overload was attenuated in LRT versus HRT (20.1 ± 5.6 vs. 41.6 ± 16.1%, P = 0.015).Between-group differences were observed in the magnitude of response of 96upregulated and 101 downregulated pathways. A further 27 pathways showed contrasting upregulation or downregulation in LRT versus HRT in response to functionaloverload. In conclusion, low responders to aerobic endurance training were alsolow responders for compensatory hypertrophy, and attenuated hypertrophy wasassociated with differential gene set regulation. Our findings suggest that geneticfactors that underpin aerobic training maladaptation might also dysregulate thetranscriptional regulation of biological processes that contribute to adaptation tomechanical overload.

Item Type: Article
Authors/Creators:West, DWD and Doering, TM and Thompson, J-LM and Budiono, BP and Lessard, SJ and Koch, LG and Britton, SL and Steck, R and Byrne, NM and Brown, MA and Peake, JM and Ashton, KJ and Coffey, VG
Keywords: heritable factors, molecular networks, skeletal muscle plasticity, specificity of adaptation
Journal or Publication Title: Experimental Physiology
Publisher: Wiley-Blackwell Publishing Ltd.
ISSN: 1469-445X
DOI / ID Number: 10.1113/EP089301
Copyright Information:

Copyright 2021 the authors

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