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Aerobic Exercise Alters Skeletal Muscle Molecular Responses to Resistance Exercise
Mittuniversitetet, Fakulteten för humanvetenskap, Institutionen för hälsovetenskap.
Institute of Biomedicine, University of León, León, Spain.
Department of Laboratory Medicine, Division of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Mittuniversitetet, Fakulteten för humanvetenskap, Institutionen för hälsovetenskap.
2012 (Engelska)Ingår i: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 44, nr 9, s. 1680-1688Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

LUNDBERG, T. R., R. FERNANDEZ-GONZALO, T. GUSTAFSSON, and P. A. TESCH. Aerobic Exercise Alters Skeletal Muscle Molecular Responses to Resistance Exercise. Med. Sci. Sports Exerc., Vol. 44, No. 9, pp. 1680-1688, 2012. Purpose: This study assessed the influence of an acute aerobic exercise bout on molecular responses to subsequent resistance exercise (RE). Methods: Nine physically active men performed a 45-min one-legged cycle ergometry exercise and 4 x 7 maximal concentric eccentric knee extensions for each leg 6 h later. Thus, one limb was subjected to aerobic and resistance exercise (AE+RE), and the contralateral limb to resistance exercise (RE) only. Knee extensor peak power was determined. Biopsies were obtained from the m vastus lateralis before (PRE) and 15 mm (POST1) and 3 h after RE. Analysis determined glycogen content, mRNA levels (vascular endothelial growth factor, peroxisome proliferator activated receptor-gamma coactivator-1, muscle RING-finger protein-1, atrogin-1, myostatin), and phosphorylated proteins (mammalian target of rapamycin, p70S6 kinase, ribosomal protein S6, eukaryotic elongation factor 2). Results: Peak power was similar in AE + RE and RE. After RE, the time course of glycogen utilization and protein signaling was similar across legs. However, phosphorylation of mammalian target of rapamycin and p70S6 kinase was elevated in AE + RE versus RE (main effect, P < 0.05). Vascular endothelial growth factor and peroxisome proliferator activated receptor-gamma coactivator-1 were higher in AE + RE than in RE at PRE and POST1 (P < 0.05). Myostatin was lower in AE + RE versus RE at PRE and POST1 (P < 0.05) and downregulated after resistance exercise only. Atrogin-1 was higher in AE + RE than in RE at PRE and POST1 (P < 0.05) and decreased after RE in AE + RE. Muscle RING-finger protein-1 was similar across legs. No difference for any marker was evident 3 h after RE. Conclusions: These results suggest that acute aerobic exercise alters molecular events regulating muscle protein turnover during the early recovery period from subsequent RE.

Ort, förlag, år, upplaga, sidor
2012. Vol. 44, nr 9, s. 1680-1688
Nyckelord [en]
ENDURANCE, HUMAN SKELETAL MUSCLE, mTOR, MUSCLE POWER, PGC-1 alpha, P70S6K
Nationell ämneskategori
Idrottsvetenskap och fitness
Identifikatorer
URN: urn:nbn:se:miun:diva-17251DOI: 10.1249/MSS.0b013e318256fbe8ISI: 000307624600008Scopus ID: 2-s2.0-84865529379OAI: oai:DiVA.org:miun-17251DiVA, id: diva2:563207
Tillgänglig från: 2012-10-29 Skapad: 2012-10-27 Senast uppdaterad: 2025-09-25Bibliografiskt granskad
Ingår i avhandling
1. The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
Öppna denna publikation i ny flik eller fönster >>The Effects of Aerobic Exercise on Human Skeletal Muscle Adaptations to Resistance Exercise
2014 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
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.

Ort, förlag, år, upplaga, sidor
Östersund: Mittuniversitetet, 2014. s. 73
Serie
Mid Sweden University doctoral thesis, ISSN 1652-893X ; 181
Nyckelord
concurrent training, endurance, gene expression, hypertrophy, muscle strength and power, protein phosphorylation
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:miun:diva-21917 (URN)978-91-87557-41-5 (ISBN)
Disputation
2014-05-15, F229, Östersund, 13:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2014-05-08 Skapad: 2014-05-08 Senast uppdaterad: 2025-09-25Bibliografiskt granskad

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Lundberg, Tommy R.Tesch, Per A.

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