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Aerobic exercise does not compromise muscle hypertrophy response to short-term resistance training
Mittuniversitetet, Fakulteten för humanvetenskap, Avdelningen för hälsovetenskap.
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Department of Laboratory Medicine, Section for Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Mittuniversitetet, Fakulteten för humanvetenskap, Avdelningen för hälsovetenskap.
2013 (engelsk)Inngår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 114, nr 1, s. 81-89Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

This study tested the hypothesis that chronic aerobic and resistance exercise (AE+RE) would elicit greater muscle hypertrophy than resistance exercise only (RE). Ten men (25±4 yrs) performed 5 wks unilateral knee extensor AE+RE. The opposing limb was subjected to RE. AE completed 6 hrs prior to RE, consisted of ~45 min one-legged cycle ergometry. RE comprised 4 x 7 maximal concentric-eccentric knee extensions. Various indices of in vivo knee extensor function were measured before and after training. Magnetic resonance imaging (MRI) assessed m. quadricep femoris (QF) cross-sectional area (CSA), volume, and signal intensity (SI). Biopsies obtained from m. vastus lateralis determined fiber CSA, enzyme levels and gene expression of myostatin, atrogin-1, MuRF-1, PGC-1α and VEGF. Increases (P < 0.05) in isometric strength and peak power, respectively were comparable in AE+RE (9 and 29%) and RE (11 and 24%). AE+RE showed greater increase (14%; P < 0.05) in QF volume than RE (8%). Muscle fiber CSA increased 17% after AE+RE (P < 0.05) and 9% after RE (P > 0.05). QF SI increased (12%; P < 0.05) after AE+RE, but not RE. Neither AE+RE nor RE showed altered mRNA-levels. Citrate Synthase activity increased (P < 0.05) after AE+RE. The results suggest that the increased aerobic capacity shown with AE+RE, was accompanied by a more robust increase in muscle size compared with RE. While this response was not carried over to greater improvement in muscle function, it remains that intense AE can be executed prior to RE without compromising performance outcome.

sted, utgiver, år, opplag, sider
2013. Vol. 114, nr 1, s. 81-89
Emneord [en]
Endurance; Gene expression; Muscle cross-sectional area; Muscle power and strength
HSV kategori
Identifikatorer
URN: urn:nbn:se:miun:diva-17710DOI: 10.1152/japplphysiol.01013.2012ISI: 000313051000011Scopus ID: 2-s2.0-84871782994OAI: oai:DiVA.org:miun-17710DiVA, id: diva2:576781
Tilgjengelig fra: 2012-12-13 Laget: 2012-12-13 Sist oppdatert: 2025-09-25bibliografisk 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: 2025-09-25bibliografisk kontrollert

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