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Resistance exercise...
Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle.
- Article/chapterEnglish2011
Publisher, publication year, extent ...
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American Physiological Society,2011
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Numbers
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LIBRIS-ID:oai:DiVA.org:gih-1930
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https://urn.kb.se/resolve?urn=urn:nbn:se:gih:diva-1930URI
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https://doi.org/10.1152/japplphysiol.00086.2011DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:123682317URI
Supplementary language notes
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Language:English
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Summary in:English
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Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E: 1h cycling at ~65% of VO(2max)) or endurance exercise followed by resistance exercise (ER: 1h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3h Post cycling). The mRNA of genes related to mitochondrial biogenesis (PGC-1α, PRC) and substrate regulation (PDK4) increased after both E and ER, but the mRNA levels were about 2-fold higher after ER (P<0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis (mTOR, S6K1 and eEF2) was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMPK, ACC and Akt increased similarly at 1h Post (P<0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that resistance exercise, performed after endurance exercise, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a crosstalk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.
Subject headings and genre
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PGC
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AMPK
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endurance
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exercise
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resistance
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mTOR
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Medicin/Teknik
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Medicine/Technology
Added entries (persons, corporate bodies, meetings, titles ...)
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Psilander, Niklas,1975-Gymnastik- och idrottshögskolan,Forskningsgruppen Mitokondriell funktion och metabol kontroll(Swepub:gih)niklasp
(author)
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Blomstrand, EvaGymnastik- och idrottshögskolan,Eva Blomstrands forskningsgrupp(Swepub:gih)evab
(author)
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Mascher, HenrikKarolinska Institutet,Gymnastik- och idrottshögskolan,Forskningsgruppen Mitokondriell funktion och metabol kontroll(Swepub:gih)henrikm
(author)
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Sahlin, KentGymnastik- och idrottshögskolan,Forskningsgruppen Mitokondriell funktion och metabol kontroll(Swepub:gih)kents
(author)
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Gymnastik- och idrottshögskolanForskningsgruppen Mitokondriell funktion och metabol kontroll
(creator_code:org_t)
Related titles
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In:Journal of applied physiology: American Physiological Society111:5, s. 1335-13448750-75871522-1601
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