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Exercise-induced AMPK activation does not interfere with muscle hypertrophy in response to resistance training in men
Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
Karolinska Institutet.
Karolinska Institutet.
2014 (English)In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 116, no 6, 611-620 p.Article in journal (Refereed) Published
Abstract [en]

As aerobic exercise (AE) may interfere with adaptations to resistance exercise (RE), this study explored acute and chronic responses to consecutive AE (similar to 45 min cycling) and RE (4 X 7 maximal knee extensions) vs. RE only. Ten men performed acute unilateral AE + RE interspersed by 15 min recovery. The contralateral leg was subjected to RE. This exercise paradigm was then implemented in a 5-wk training program. Protein phosphorylation, gene expression, and glycogen content were assessed in biopsies obtained from the vastus lateralis muscle of both legs immediately before and 3 h after acute RE. Quadriceps muscle size and in vivo torque were measured, and muscle samples were analyzed for citrate synthase activity and glycogen concentration, before and after training. Acute AE reduced glycogen content (32%; P < 0.05) and increased (P < 0.05) phosphorylation of AMPK (1.5-fold) and rpS6 (1.3-fold). Phosphorylation of p70S6K and 4E-BP1 remained unchanged. Myostatin gene expression was downregulated after acute AE + RE but not RE. Muscle size showed greater (P < 0.05) increase after AE + RE (6%) than RE (3%) training. Citrate synthase activity (18%) and endurance performance (22%) increased (P < 0.05) after AE + RE but not RE. While training increased (P < 0.05) in vivo muscle strength in both legs, normalized and concentric torque increased after RE only. Thus AE activates AMPK, reduces glycogen stores, and impairs the progression of concentric force, yet muscle hypertrophic responses to chronic RE training appear not to be compromised.

Place, publisher, year, edition, pages
2014. Vol. 116, no 6, 611-620 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:miun:diva-21915DOI: 10.1152/japplphysiol.01082.2013ISI: 000333183500004Scopus ID: 2-s2.0-84901058223OAI: oai:DiVA.org:miun-21915DiVA: diva2:716113
Available from: 2014-05-08 Created: 2014-05-08 Last updated: 2017-08-29Bibliographically approved
In thesis
1. The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
Open this publication in new window or tab >>The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
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.

Place, publisher, year, edition, pages
Östersund: Mittuniversitetet, 2014. 73 p.
Series
Mid Sweden University doctoral thesis, ISSN 1652-893X ; 181
Keyword
concurrent training, endurance, gene expression, hypertrophy, muscle strength and power, protein phosphorylation
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:miun:diva-21917 (URN)978-91-87557-41-5 (ISBN)
Public defence
2014-05-15, F229, Östersund, 13:00 (English)
Opponent
Supervisors
Available from: 2014-05-08 Created: 2014-05-08 Last updated: 2014-05-09Bibliographically approved

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Citation style
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