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Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.ORCID iD: 0000-0003-1848-5491
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.ORCID iD: 0000-0002-6537-042X
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
Show others and affiliations
2011 (English)In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 111, no 5, 1335-1344 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2011. Vol. 111, no 5, 1335-1344 p.
Keyword [en]
PGC, AMPK, endurance, exercise, resistance, mTOR
National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-1930DOI: 10.1152/japplphysiol.00086.2011PubMedID: 21836044OAI: oai:DiVA.org:gih-1930DiVA: diva2:449009
Available from: 2011-10-19 Created: 2011-10-19 Last updated: 2016-12-05Bibliographically approved
In thesis
1. The effect of different exercise regimens on mitochondrial biogenesis and performance
Open this publication in new window or tab >>The effect of different exercise regimens on mitochondrial biogenesis and performance
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Endurance training is a powerful tool to improve both health and performance. Physical activity is now recognized as an effective treatment and prevention therapy for a wide range of diseases. One of the most profound adaptations to endurance training is increased mitochondrial function and content within the exercising muscles. Mitochondrial quality and quantity are closely related to several of the positive health effects reported after training. High mitochondrial content strongly correlates with muscle oxidative capacity and endurance performance. Even though it is well known that endurance training increases mitochondrial content, it is unclear which type of training is the most efficient to promote mitochondrial biogenesis. Therefore, the basis for current exercise recommendations relative to mitochondrial biogenesis is poor or absent. Thus, the main objective of this thesis was to evaluate the effect of different training strategies on mitochondrial biogenesis.

Recent developments in molecular methods have made it possible to study the initial adaptations to training through measurement of mRNA gene expression of exercise induced genes. One such gene is transcriptional coactivator peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α). PGC-1α is a key regulator of mitochondrial biogenesis and the expression of PGC-1α can therefore be used as a marker of this process.

The first four studies presented in this thesis are acute exercise studies where two different exercise models were compared using a cross-over design. Muscle biopsies were obtained pre and post exercise and analysed for gene expression and glycogen, apart from study II. The final study was a long-term training study where muscle biopsies were obtained before and after the training period and analysed for mitochondrial enzyme activities and protein content.

Study I: The expression of PGC-1α and related genes were examined after 90 min of continuous and interval exercise in untrained subjects. The exercise protocols influenced the expression of genes involved in mitochondrial biogenesis and oxidative metabolism in a similar manner. Both interval and continuous exercise were potent training strategies for relatively sedentary individuals.

Study II: The expression of PGC-1α and related genes were examined after low-volume sprint interval (SIT) and high-volume interval (IE) exercise in highly trained cyclists. SIT induced a similar increase in PGC-1α expression as IE despite a much lower time commitment and work completed. Sprint interval exercise might, therefore, be a time efficient training strategy for highly trained individuals.

Study III: The expression of PGC-1α and related genes, as well as the activity of upstream proteins, were examined after concurrent (ER: cycling + leg press) and single-mode (E: cycling only) exercise in untrained subjects. PGC-1α expression doubled after ER compared with E. It was concluded that concurrent training might be beneficial for mitochondrial biogenesis in untrained individuals.

Study IV: The expression of PGC-1α and related genes were examined after exercise performed with low (LG) and normal (NG) muscle glycogen in well-trained cyclists. PGC-1α expression increased approximately three times more after LG compared with NG. This finding suggested that low glycogen exercise is a potent inducer of mitochondrial biogenesis in well-trained individuals.

Study V: Mitochondrial enzyme activity, protein content and endurance performance were examined after eight weeks of concurrent (ES: cycling + leg press) or single-mode (E: cycling only) training in cyclists. ES did not affect enzyme activity, protein content or endurance performance differently than E. The beneficial effect previously observed in untrained subjects did not translate to higher numbers of mitochondria in trained individuals.

In three of the studies, I, III, and IV, both glycogen and PGC-1α expression were measured after exercise. These data were then pooled and examined. The highest PGC-1α mRNA expression levels were identified when glycogen levels were low, and vice versa. This suggests that low glycogen might play an important role in the regulation of mitochondrial biogenesis also during interval and concurrent strength and endurance exercise.

In conclusion, key markers of mitochondrial biogenesis can be effectively up-regulated by interval, concurrent and low glycogen exercise. A possible explanation for this might be that though the exercise protocols are quite divergent in nature, they all have a pronounced effect on muscle glycogen and/or perturbation in energetic stress.

Place, publisher, year, edition, pages
Karolinska insitutet, 2014
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3579 (URN)978-91-7549-774-7 (ISBN)
Public defence
2014-12-19, Aulan, GIH, Lidingövägen 1, Stockholm, 09:00 (English)
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Supervisors
Available from: 2014-11-28 Created: 2014-11-28 Last updated: 2016-12-05Bibliographically approved

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