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Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis
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. Karolinska institutet, Inst för fysiologi och farmakologi.
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: urn:nbn:se:gih:diva-3502ISBN: 978-91-7549-712-9 (print)OAI: oai:DiVA.org:gih-3502DiVA: diva2:756270
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
List of papers
1. Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle.
Open this publication in new window or tab >>Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle.
2013 (English)In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 113, no 4, 951-963 p.Article in journal (Refereed) Published
Abstract [en]

Recent studies suggest that carbohydrate restriction can improve the training-induced adaptation of muscle oxidative capacity. However, the importance of low muscle glycogen on the molecular signaling of mitochondrial biogenesis remains unclear. Here, we compare the effects of exercise with low (LG) and normal (NG) glycogen on different molecular factors involved in the regulation of mitochondrial biogenesis. Ten highly trained cyclists (VO(2max) 65 ± 1 ml/kg/min, W (max) 387 ± 8 W) exercised for 60 min at approximately 64 % VO(2max) with either low [166 ± 21 mmol/kg dry weight (dw)] or normal (478 ± 33 mmol/kg dw) muscle glycogen levels achieved by prior exercise/diet intervention. Muscle biopsies were taken before, and 3 h after, exercise. The mRNA of peroxisome proliferator-activated receptor-γ coactivator-1 was enhanced to a greater extent when exercise was performed with low compared with normal glycogen levels (8.1-fold vs. 2.5-fold increase). Cytochrome c oxidase subunit I and pyruvate dehydrogenase kinase isozyme 4 mRNA were increased after LG (1.3- and 114-fold increase, respectively), but not after NG. Phosphorylation of AMP-activated protein kinase, p38 mitogen-activated protein kinases and acetyl-CoA carboxylase was not changed 3 h post-exercise. Mitochondrial reactive oxygen species production and glutathione oxidative status tended to be reduced 3 h post-exercise. We conclude that exercise with low glycogen levels amplifies the expression of the major genetic marker for mitochondrial biogenesis in highly trained cyclists. The results suggest that low glycogen exercise may be beneficial for improving muscle oxidative capacity.

National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-2481 (URN)10.1007/s00421-012-2504-8 (DOI)23053125 (PubMedID)
Available from: 2012-11-19 Created: 2012-11-19 Last updated: 2016-12-05Bibliographically approved
2. Adding strength to endurance training does not enhance aerobic capacity in cyclists
Open this publication in new window or tab >>Adding strength to endurance training does not enhance aerobic capacity in cyclists
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.

National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3500 (URN)10.1111/sms.12338 (DOI)25438613 (PubMedID)
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
3. Acute exercise reverses starvation-mediated insulin resistance in humans.
Open this publication in new window or tab >>Acute exercise reverses starvation-mediated insulin resistance in humans.
2013 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 304, no 4, E436-43 p.Article in journal (Refereed) Published
Abstract [en]

Within 2-3 days of starvation, pronounced insulin resistance develops, possibly mediated by increased lipid load. Here, we show that one exercise bout increases mitochondrial fatty acid (FA) oxidation and reverses starvation-induced insulin resistance. Nine healthy subjects underwent 75-h starvation on two occasions: with no exercise (NE) or with one exercise session at the end of the starvation period (EX). Muscle biopsies were analyzed for mitochondrial function, contents of glycogen, and phosphorylation of regulatory proteins. Glucose tolerance and insulin sensitivity, measured with an intravenous glucose tolerance test (IVGTT), were impaired after starvation, but in EX the response was attenuated or abolished. Glycogen stores were reduced, and plasma FA was increased in both conditions, with a more pronounced effect in EX. After starvation, mitochondrial respiration decreased with complex I substrate (NE and EX), but in EX there was an increased respiration with complex I + II substrate. EX altered regulatory proteins associated with increases in glucose disposal (decreased phosphorylation of glycogen synthase), glucose transport (increased phosphorylation of Akt substrate of 160 kDa), and FA oxidation (increased phosphorylation of acetyl-CoA carboxylase). In conclusion, exercise reversed starvation-induced insulin resistance and was accompanied by reduced glycogen stores, increased lipid oxidation capacity, and activation of signaling proteins involved in glucose transport and FA metabolism.

National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-2852 (URN)10.1152/ajpendo.00416.2012 (DOI)23269410 (PubMedID)
Available from: 2013-08-05 Created: 2013-08-05 Last updated: 2016-08-10Bibliographically approved
4. Strength training improves muscle aerobic capacity and glucose tolerance in elderly
Open this publication in new window or tab >>Strength training improves muscle aerobic capacity and glucose tolerance in elderly
Show others...
2016 (English)In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 26, no 7, 764-773 p.Article in journal (Refereed) Published
Abstract [en]

The primary aim of this study was to investigate the effect of short-term resistance training (RET) on mitochondrial protein content and glucose tolerance in elderly. Elderly women and men (age 71 ± 1, mean ± SEM) were assigned to a group performing 8 weeks of resistance training (RET, n = 12) or no training (CON, n = 9). The RET group increased in (i) knee extensor strength (concentric +11 ± 3%, eccentric +8 ± 3% and static +12 ± 3%), (ii) initial (0-30 ms) rate of force development (+52 ± 26%) and (iii) contents of proteins related to signaling of muscle protein synthesis (Akt +69 ± 20 and mammalian target of rapamycin +69 ± 32%). Muscle fiber type composition changed to a more oxidative profile in RET with increased amount of type IIa fibers (+26.9 ± 6.8%) and a trend for decreased amount of type IIx fibers (-16.4 ± 18.2%, P = 0.068). Mitochondrial proteins (OXPHOS complex II, IV, and citrate synthase) increased in RET by +30 ± 11%, +99 ± 31% and +29 ± 8%, respectively. RET resulted in improved oral glucose tolerance measured as reduced area under curve for glucose (-21 ± 26%) and reduced plasma glucose 2 h post-glucose intake (-14 ± 5%). In CON parameters were unchanged or impaired. In conclusion, short-term resistance training in elderly not only improves muscular strength, but results in robust increases in several parameters related to muscle aerobic capacity.

National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3501 (URN)10.1111/sms.12537 (DOI)000379758500006 ()26271931 (PubMedID)
Note

At the time of Per Frank's dissertation this article was accepted.

Available from: 2014-10-16 Created: 2014-10-16 Last updated: 2017-03-31Bibliographically approved

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