Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Adding strength to endurance training does not enhance aerobic capacity in cyclists
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, 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, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
2015 (English)In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 25, no 4, e353-e359 p.Article in journal (Refereed) Published
Abstract [en]

The molecular signaling of mitochondrial biogenesis is enhanced when resistance exercise is added to a bout of endurance exercise. The purpose of the present study was to examine if this mode of concurrent training translates into increased mitochondrial content and improved endurance performance. Moderately trained cyclists performed 8 weeks (two sessions per week) of endurance training only (E, n = 10; 60-min cycling) or endurance training followed by strength training (ES, n = 9; 60-min cycling + leg press). Muscle biopsies were obtained before and after the training period and analyzed for enzyme activities and protein content. Only the ES group increased in leg strength (+19%, P < 0.01), sprint peak power (+5%, P < 0.05), and short-term endurance (+9%, P < 0.01). In contrast, only the E group increased in muscle citrate synthase activity (+11%, P = 0.06), lactate threshold intensity (+3%, P < 0.05), and long-term endurance performance (+4%, P < 0.05). Content of mitochondrial proteins and cycling economy was not affected by training. Contrary to our hypothesis, the results demonstrate that concurrent training does not enhance muscle aerobic capacity and endurance performance in cyclists.

Place, publisher, year, edition, pages
2015. Vol. 25, no 4, e353-e359 p.
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-3500DOI: 10.1111/sms.12338PubMedID: 25438613OAI: oai:DiVA.org:gih-3500DiVA: diva2:756265
Note

At the time of Per Frank's and Niklas Psilander's dissertations the article was accepted for publication.

Available from: 2014-10-16 Created: 2014-10-16 Last updated: 2016-12-05Bibliographically approved
In thesis
1. Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis
Open this publication in new window or tab >>Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Regular exercise plays a key role in the maintenance of health and physical capabilities. Extensive research shows that exercise is an efficient method to prevent diabetes. Both resistance and aerobic exercise training are well known countermeasures for insulin resistance. However, depending on factors like purpose, capability and accessibility, different exercise modes need to be evaluated on both applied and molecular levels. In addition, exercise is the means to improve performance. New training strategies have emerged, like training with low glycogen stores or combining strength with endurance training, and guidelines based on empirical data are needed. Although knowledge of exercise physiology has advanced, much more needs to be learned before we can exploit the full potential of exercise with regard to health and performance. Therefore, the overall aim of this thesis is to provide knowledge of how different exercise strategies improve performance and insulin sensitivity. The mitochondria represent a central part of this thesis considering their key role in both health and performance. Study I was an acute crossover investigation of the effect of exercise with low glycogen levels on markers of mitochondrial biogenesis. Study II investigated the effect of concurrent resistance and endurance training on mitochondrial density and endurance performance. Study III investigated the acute effect of exercise on starvation-induced insulin resistance. In Study IV, the effect of resistance exercise training on health and performance in the elderly was investigated. The main findings were:

  • Training with low glycogen levels enhanced the response in markers of mitochondrial biogenesis.
  • Adding resistance training to endurance training did not improve mitochondrial density or endurance performance in trained individuals. 
  • Resistance training for only eight weeks is an efficient strategy to improve strength, heart rate (HR) during submaximal cycling and glucose tolerance in elderly. It also improves muscular quality by increasing mitochondrial and hypertrophy signaling proteins. 
  • Starvation-induced insulin resistance is attenuated by exercise. Mitochondrial respiration and reactive oxygen species (ROS) production is reduced during starvation. Exercise during starvation reduced glycogen stores and resulted in the activation of enzymes involved in glucose metabolism.
  • When exercise was performed during starvation there was an increase in markers for mitochondrial lipid oxidation.


In conclusion, training with low glycogen stores seems to be a promising strategy to increase mitochondrial density. In contrast to our previous acute findings, concurrent training had no effect on mitochondrial biogenesis or endurance performance. Exercise can reverse yet another mode of insulin resistance (starvation) which strengthens its role in the treatment for other states of insulin resistance, e.g. Type 2 diabetes (T2D). Resistance exercise training is an efficient and safe strategy for the elderly to improve health and performance.

Place, publisher, year, edition, pages
Karolinska institutet, 2014
National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3502 (URN)978-91-7549-712-9 (ISBN)
Public defence
2014-11-07, Aulan, GIH, Lidingövägen 1, Stockholm, 09:00 (English)
Opponent
Supervisors
Available from: 2014-10-16 Created: 2014-10-16 Last updated: 2014-10-16Bibliographically approved
2. 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)
Opponent
Supervisors
Available from: 2014-11-28 Created: 2014-11-28 Last updated: 2016-12-05Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Psilander, NiklasFrank, PerFlockhart, MikaelSahlin, Kent
By organisation
Research group for Mitokondriell funktion och metabolisk kontroll
In the same journal
Scandinavian Journal of Medicine and Science in Sports
Physiology

Search outside of DiVA

GoogleGoogle Scholar

Altmetric score

Total: 1396 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf