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Acute molecular responses in untrained and trained muscle subjected to aerobic and resistance exercise training versus resistance training alone
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
Mittuniversitetet, Fakulteten för humanvetenskap, Avdelningen för hälsovetenskap.
Mittuniversitetet, Fakulteten för humanvetenskap, Avdelningen för hälsovetenskap. Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
2013 (engelsk)Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 209, nr 4, s. 283-294Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

AimThis study assessed and compared acute muscle molecular responses before and after 5-week training, employing either aerobic (AE) and resistance exercise (RE) or RE only. MethodsTen men performed one-legged RE, while the contralateral limb performed AE followed by RE 6h later (AE+RE). Before (untrained) and after (trained) the intervention, acute bouts of RE were performed with or without preceding AE. Biopsies were obtained from m. vastus lateralis of each leg pre- and 3h post-RE to determine mRNA levels of VEGF, PGC-1, MuRF-1, atrogin-1, myostatin and phosphorylation of mTOR, p70S6K, rpS6 and eEF2. ResultsPGC-1 and VEGF expression increased (P<0.05) after acute RE in the untrained, but not the trained state. These markers showed greater response after AE+RE than RE in either condition. Myostatin was lower after AE+RE than RE, both before and after training. AE+RE showed higher MuRF-1 and atrogin-1 expression than RE in the untrained, not the trained state. Exercise increased (P<0.05) p70S6K phosphorylation both before and after training, yet this increase tended to be more prominent for AE+RE than RE before training. Phosphorylation of p70S6K was greater in trained muscle. Changes in these markers did not correlate with exercise-induced alterations in strength or muscle size. ConclusionConcurrent exercise in untrained skeletal muscle prompts global molecular responses consistent with resulting whole muscle adaptations. Yet, training blunts the more robust anabolic response shown after AE+RE compared with RE. This study challenges the concept that single molecular markers could predict training-induced changes in muscle size or strength.

sted, utgiver, år, opplag, sider
2013. Vol. 209, nr 4, s. 283-294
Emneord [en]
concurrent exercise, gene expression, human skeletal muscle, mammalian target of rapamycin, p70S6 kinase
HSV kategori
Identifikatorer
URN: urn:nbn:se:miun:diva-20644DOI: 10.1111/apha.12174ISI: 000326924300007Scopus ID: 2-s2.0-84887535632OAI: oai:DiVA.org:miun-20644DiVA, id: diva2:678273
Tilgjengelig fra: 2013-12-11 Laget: 2013-12-11 Sist oppdatert: 2017-12-06bibliografisk kontrollert
Inngår i avhandling
1. The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
Åpne denne publikasjonen i ny fane eller vindu >>The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
2014 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Aerobic exercise (AE) may interfere with muscle adaptations induced by resistance exercise (RE). Three experimental campaigns were conducted to explore the influence of AE on molecular, functional and muscular adaptations to acute and chronic RE. Twenty-nine men performed unilateral knee extensor RE preceded by AE (AE+RE). The contralateral leg did RE only. First, the influence of acute AE on muscle molecular responses to RE performed 6 h later was studied. Subsequently, this exercise regimen was implemented over 5 weeks training. The relationships between acute and chronic outcomes were examined and molecular responses to acute exercise were assessed in untrained and trained muscle. Finally, acute and chronic responses to AE+RE, interspersed by only 15 min recovery, were investigated.Phosphorylation of mTOR and p70S6K was greater after AE+RE than after RE. In parallel, myostatin was suppressed for a longer time after AE+RE. These results suggest that AE+RE enhance skeletal muscle anabolic environment more than RE alone (Paper I). After 5 weeks training, improvements in muscle strength and power were similar across legs. However, AE+RE prompted a greater increase in muscle size than RE, suggesting that AE potentiates the hypertrophic stimulus to RE training without altering muscle function progress (Paper II). Consistent with changes in whole-muscle size, AE+RE showed greater anabolic molecular responses than RE. As chronic training blunted this effect, it appears that AE offers a synergistic hypertrophic stimulus to RE only during short-term training (Paper III). Although putative regulators of hypertrophy such as p70S6K, myostatin and PGC-1a4 were examined, no molecular marker correlated with changes in muscle size, strength or power induced by training. Hence, this study challenges the concept that single molecular markers are viable predictors of training-induced muscle adaptations (Paper III–IV). When recovery time between exercise bouts was reduced to 15 min, AE+RE still produced a more substantial increase in muscle size than RE. However, progression of concentric strength was blunted. Thus, while restored muscle function between exercise bouts is a prerequisite for achieving maximal gains in strength and power, incomplete recovery appears not to compromise muscle hypertrophy (Paper V).Collectively, the results suggest that outcomes of AE+RE are impacted by chronic training and time allowed for recovery between exercise modes. Yet, the current study offers no support to the view that AE interferes with muscle hypertrophy induced by RE.

sted, utgiver, år, opplag, sider
Östersund: Mittuniversitetet, 2014. s. 73
Serie
Mid Sweden University doctoral thesis, ISSN 1652-893X ; 181
Emneord
concurrent training, endurance, gene expression, hypertrophy, muscle strength and power, protein phosphorylation
HSV kategori
Identifikatorer
urn:nbn:se:miun:diva-21917 (URN)978-91-87557-41-5 (ISBN)
Disputas
2014-05-15, F229, Östersund, 13:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2014-05-08 Laget: 2014-05-08 Sist oppdatert: 2014-05-09bibliografisk kontrollert

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