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Frank, Per
Alternative names
Publications (6 of 6) Show all publications
Frank, P., Andersson, E., Pontén, M., Ekblom, B., Ekblom, M. & Sahlin, K. (2016). Strength training improves muscle aerobic capacity and glucose tolerance in elderly. Scandinavian Journal of Medicine and Science in Sports, 26(7), 764-773
Open this publication in new window or tab >>Strength training improves muscle aerobic capacity and glucose tolerance in elderly
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2016 (English)In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 26, no 7, p. 764-773Article 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: 2018-03-19Bibliographically approved
Psilander, N., Frank, P., Flockhart, M. & Sahlin, K. (2015). Adding strength to endurance training does not enhance aerobic capacity in cyclists. Scandinavian Journal of Medicine and Science in Sports, 25(4), e353-e359
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, p. e353-e359Article 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: 2018-01-11Bibliographically approved
Frank, P. (2014). Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis. (Doctoral dissertation). Karolinska institutet
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: 2018-03-19Bibliographically approved
Frank, P., Katz, A., Andersson, E. & Sahlin, K. (2013). Acute exercise reverses starvation-mediated insulin resistance in humans.. American Journal of Physiology. Endocrinology and Metabolism, 304(4), E436-43
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, p. E436-43Article 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: 2018-01-11Bibliographically approved
Berthelson, P., Katz, A., Andersson, E. & Sahlin, K. (2012). Acute exercise and starvation induced insulin resistance. In: Medicine & Science In Sports & Exercise, 2012, S498 Vol. 44 No. 5 Supplement. 2661.. Paper presented at ACSM's 59th Annual Meeting and 3rd World Congress on Exercise is Medicine®, San Francisco, USA, May-Jun, 2012 (pp. 2661).
Open this publication in new window or tab >>Acute exercise and starvation induced insulin resistance
2012 (English)In: Medicine & Science In Sports & Exercise, 2012, S498 Vol. 44 No. 5 Supplement. 2661., 2012, p. 2661-Conference paper, Oral presentation with published abstract (Other academic)
Abstract [en]

It is well known that starvation causes insulin resistance. The mechanism is unclear but may relate disturbances in lipid metabolism i.e. incomplete mitochondrial FA oxidation and/or accumulation of lipid intermediates. Exercise results in increased substrate oxidation and may thus remove interfering lipid metabolites and reverse starvation-induced insulin resistance. However, the effect of acute exercise and starvation on insulin sensitivity is not known.

Purpose: The aim of this study was to investigate the effect of exercise on starvation-induced insulin resistance and to elucidate potential mechanisms.

Methods: Nine healthy lean subjects underwent 84h starvation on two occasions separated by at least 2 weeks. The starvation period was followed by either exercise (EX; 5x10 min intervals with 2-4 min rest, starting at 70 %VO2 max) or an equal period of rest (NE). Before and after the starvation period (3h after exercise/rest) subjects were investigated with muscle biopsies, bloo samples and an intravenous glucose tolerance test. Muscle samples were used for measurement of mitochondrial respiration in permeabilized muscle fibers (Oroboros oxygraph), glycogen content and activation of signaling proteins.

Results: Insulin sensitivity was significantly higher in the EX group compared to the NE group (p<0.05). After starvation mitochondrial respiration was lower in both groups with complex I substrates whereas respiration with complex I+II substrates was higher in EX (p<0.05 vs. basal and NE). Muscle glycogen was decreased to 73% (NE) and 31% (EX) of the basal values. The EX group had a significant increased activation of AS160. Plasma FA increased 3-4 fold to 1.39±0.32(NE) and 1.80±0.49 (EX) (mmol/l) after starvation and plasma beta-hydroxybutyrate increased about 50-fold to 6.43±2.01(NE) and 7.12±1.59 (EX)(mmol/l).

Conclusion: Acute exercise reverses starvation-induced insulin resistance. Plasma FA and BOH were increased to similar extent after NE and EX and cannot explain the changes in insulin sensitivity. However, an increased substrate oxidation together with the observed increased capacity for mitochondrial FA oxidation after EX may be involved in the activation of AS160 and the reversal of starvation-induced insulin resistance.

National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-2599 (URN)
Conference
ACSM's 59th Annual Meeting and 3rd World Congress on Exercise is Medicine®, San Francisco, USA, May-Jun, 2012
Note

 

 

Available from: 2013-01-02 Created: 2013-01-02 Last updated: 2016-08-10Bibliographically approved
Frank, P., Katz, A., Andersson, E. & Sahlin, K. (2012). Acute exercise during starvation improves insulin sensitivity and increases mitochondrial FA oxidation. Paper presented at 15th International Biochemistry of Exercise Congress (IBEC) in Stockholm, Sweden, June 17-21, 2012.
Open this publication in new window or tab >>Acute exercise during starvation improves insulin sensitivity and increases mitochondrial FA oxidation
2012 (English)Conference paper, Published paper (Other academic)
Abstract [en]

Aim: To investigate if exercise can reverse starvation-induced insulin resistance and to elucidate the mechanism. Methods: Nine subjects underwent 87 h of starvation with (EX) or without (NE) one exercise session at the end. Before and after starvation (3 h post-exercise) subjects underwent an intravenous glucose tolerance test and muscle biopsy. Results: Insulin sensitivity decreased after starvation (NE) but increased after exercise (EX). Glycogen stores were reduced and plasma FA and β-Hydroxybutyrate increased in both conditions. Mitochondrial respiration with FA substrate increased in EX but was unchanged in NE. RCR and mitochondrial ROS production decreased in both conditions. Phosphorylation of Acetyl-CoA carboxylase (ACC) and Akt substrate of 160 kDA (AS160) proteins increased in EX. Conclusion: Exercise improves starvation induced insulin resistance, probably by increased mitochondrial FA oxidation, reduced glycogen stores and alterations in signaling proteins involved in glucose uptake and FA metabolism.

National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-2600 (URN)
Conference
15th International Biochemistry of Exercise Congress (IBEC) in Stockholm, Sweden, June 17-21, 2012
Available from: 2013-01-02 Created: 2013-01-02 Last updated: 2016-08-10Bibliographically approved
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