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Sahlin, Kent
Publications (10 of 53) Show all publications
Sahlin, K. (2016). Mitochondrial function during exercise. Paper presented at 95th Annual Meeting of the German Physiological Society, Lübeck, 3–5 March 2016. Acta Physiologica, 216(S707), S06-1
Open this publication in new window or tab >>Mitochondrial function during exercise
2016 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 216, no S707, p. S06-1-Article in journal, Meeting abstract (Refereed) Published
National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-4412 (URN)000372285400046 ()
Conference
95th Annual Meeting of the German Physiological Society, Lübeck, 3–5 March 2016
Available from: 2016-04-18 Created: 2016-04-18 Last updated: 2017-11-30Bibliographically approved
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
Jensen, L., Gejl, K. D., Ørtenblad, N., Nielsen, J. L., Bech, R. D., Nygaard, T., . . . Frandsen, U. (2015). Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes.. Physiological Reports, 3(2)
Open this publication in new window or tab >>Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes.
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2015 (English)In: Physiological Reports, E-ISSN 2051-817X, Vol. 3, no 2Article in journal (Refereed) Published
Abstract [en]

The aim was to determine if the metabolic adaptations, particularly PGC-1α and downstream metabolic genes were affected by restricting CHO following an endurance exercise bout in trained endurance athletes. A second aim was to compare baseline expression level of these genes to untrained. Elite endurance athletes (VO2max 66 ± 2 mL·kg(-1)·min(-1), n = 15) completed 4 h cycling at ~56% VO2max. During the first 4 h recovery subjects were provided with either CHO or only H2O and thereafter both groups received CHO. Muscle biopsies were collected before, after, and 4 and 24 h after exercise. Also, resting biopsies were collected from untrained subjects (n = 8). Exercise decreased glycogen by 67.7 ± 4.0% (from 699 ± 26.1 to 239 ± 29.5 mmol·kg(-1)·dw(-1)) with no difference between groups. Whereas 4 h of recovery with CHO partly replenished glycogen, the H2O group remained at post exercise level; nevertheless, the gene expression was not different between groups. Glycogen and most gene expression levels returned to baseline by 24 h in both CHO and H2O. Baseline mRNA expression of NRF-1, COX-IV, GLUT4 and PPAR-α gene targets were higher in trained compared to untrained. Additionally, the proportion of type I muscle fibers positively correlated with baseline mRNA for PGC-1α, TFAM, NRF-1, COX-IV, PPAR-α, and GLUT4 for both trained and untrained. CHO restriction during recovery from glycogen depleting exercise does not improve the mRNA response of markers of mitochondrial biogenesis. Further, baseline gene expression of key metabolic pathways is higher in trained than untrained.

National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3774 (URN)10.14814/phy2.12184 (DOI)25677542 (PubMedID)
Available from: 2015-03-13 Created: 2015-03-13 Last updated: 2017-12-04
Sahlin, K. (2014). Fysiologisk forskning åren 1992-2013. In: Suzanne Lundvall (Ed.), Från Kungl. Gymnastiska Centralinstitutet till Gymnastik- och idrottshögskolan: en betraktelse av de senaste 25 åren som del av en 200-årig historia (pp. 194-199). Stockholm: Gymnastik- och idrottshögskolan, GIH
Open this publication in new window or tab >>Fysiologisk forskning åren 1992-2013
2014 (Swedish)In: Från Kungl. Gymnastiska Centralinstitutet till Gymnastik- och idrottshögskolan: en betraktelse av de senaste 25 åren som del av en 200-årig historia / [ed] Suzanne Lundvall, Stockholm: Gymnastik- och idrottshögskolan, GIH , 2014, p. 194-199Chapter in book (Other (popular science, discussion, etc.))
Place, publisher, year, edition, pages
Stockholm: Gymnastik- och idrottshögskolan, GIH, 2014
National Category
History
Research subject
Social Sciences/Humanities
Identifiers
urn:nbn:se:gih:diva-3664 (URN)
Available from: 2015-01-09 Created: 2015-01-09 Last updated: 2017-06-01Bibliographically approved
Boushel, R., Lundby, C., Qvortrup, K. & Sahlin, K. (2014). Mitochondrial plasticity with exercise training and extreme environments.. Exercise and sport sciences reviews, 42(4), 169-74
Open this publication in new window or tab >>Mitochondrial plasticity with exercise training and extreme environments.
2014 (English)In: Exercise and sport sciences reviews, ISSN 0091-6331, E-ISSN 1538-3008, Vol. 42, no 4, p. 169-74Article in journal (Refereed) Published
Abstract [en]

Mitochondria form a reticulum in skeletal muscle. Exercise training stimulates mitochondrial biogenesis, yet an emerging hypothesis is that training also induces qualitative regulatory changes. Substrate oxidation, oxygen affinity, and biochemical coupling efficiency may be regulated differentially with training and exposure to extreme environments. Threshold training doses inducing mitochondrial upregulation remain to be elucidated considering fitness level.

National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3474 (URN)10.1249/JES.0000000000000025 (DOI)25062000 (PubMedID)
Available from: 2014-10-03 Created: 2014-10-03 Last updated: 2017-12-05Bibliographically approved
Sahlin, K. (2014). Muscle energetics during explosive activities and potential effects of nutrition and training.. Sports Medicine, 44(Suppl 2), 167-73
Open this publication in new window or tab >>Muscle energetics during explosive activities and potential effects of nutrition and training.
2014 (English)In: Sports Medicine, ISSN 0112-1642, E-ISSN 1179-2035, Vol. 44, no Suppl 2, p. 167-73Article in journal (Refereed) Published
Abstract [en]

The high-energy demand during high-intensity exercise (HIE) necessitates that anaerobic processes cover an extensive part of the adenosine triphosphate (ATP) requirement. Anaerobic energy release results in depletion of phosphocreatine (PCr) and accumulation of lactic acid, which set an upper limit of anaerobic ATP production and thus HIE performance. This report focuses on the effects of training and ergogenic supplements on muscle energetics and HIE performance. Anaerobic capacity (i.e. the amount of ATP that can be produced) is determined by the muscle content of PCr, the buffer capacity and the volume of the contracting muscle mass. HIE training can increase buffer capacity and the contracting muscle mass but has no effect on the concentration of PCr. Dietary supplementation with creatine (Cr), bicarbonate, or beta-alanine has a documented ergogenic effect. Dietary supplementation with Cr increases muscle Cr and PCr and enhances performance, especially during repeated short periods of HIE. The ergogenic effect of Cr is related to an increase in temporal and spatial buffering of ATP and to increased muscle buffer capacity. Bicarbonate loading increases extracellular buffering and can improve performance during HIE by facilitating lactic acid removal from the contracting muscle. Supplementation with beta-alanine increases the content of muscle carnosine, which is an endogenous intracellular buffer. It is clear that performance during HIE can be improved by interventions that increase the capacity of anaerobic ATP production, suggesting that energetic constraints set a limit for performance during HIE.

National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3542 (URN)10.1007/s40279-014-0256-9 (DOI)25355190 (PubMedID)
Available from: 2014-11-03 Created: 2014-11-03 Last updated: 2017-12-05Bibliographically approved
Gejl, K., Hvid, L. G., Frandsen, U., Jensen, K., Sahlin, K. & Ortenblad, N. (2014). Muscle Glycogen Content Modifies SR Ca2 + Release Rate in Elite Endurance Athletes.. Medicine & Science in Sports & Exercise, 46(3), 496-505
Open this publication in new window or tab >>Muscle Glycogen Content Modifies SR Ca2 + Release Rate in Elite Endurance Athletes.
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2014 (English)In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 46, no 3, p. 496-505Article in journal (Refereed) Published
Abstract [en]

PURPOSE: The aim of the present study was to investigate the influence of muscle glycogen content on sarcoplasmic reticulum (SR) function and peak power output (Wpeak) in elite endurance athletes.

METHODS: Fourteen highly trained male triathletes (VO2max 66.5 ± 1.3 ml O2 kg min), performed 4h of glycogen depleting cycling exercise (HRmean 73 ± 1% of maximum). During the first 4h recovery, athletes received either water (H2O) or carbohydrate (CHO), separating alterations in muscle glycogen content from acute changes affecting SR function and performance. Thereafter, all subjects received CHO enriched food for the remaining 20h recovery.

RESULTS: Immediately following exercise, muscle glycogen content and SR Ca release rate was reduced to 32 ± 4% (225 ± 28 mmol kg dw) and 86 ± 2% of initial levels, respectively (P < 0.01). Glycogen markedly recovered after 4h recovery with CHO (61 ± 2% of pre) and SR Ca release rate returned to pre-exercise level. However, in the absence of CHO during the first 4h recovery, glycogen and SR Ca release rate remained depressed, with normalization of both parameters at the end of the 24h recovery after receiving a CHO enriched diet. Linear regression demonstrated a significant correlation between SR Ca release rate and muscle glycogen content (P < 0.01, r = 0.30). The 4h cycling exercise reduced Wpeak by 5.5-8.9% at different cadences (P < 0.05) and Wpeak was normalized after 4h recovery with CHO whereas Wpeak remained depressed (P < 0.05) following water provision. Wpeak was fully recovered after 24h in both the H2O and the CHO group.

CONCLUSION: In conclusion, the present results suggest that low muscle glycogen depresses muscle SR Ca release rate, which may contribute to fatigue and delayed recovery of Wpeak 4 hours post exercise.

National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3107 (URN)10.1249/MSS.0000000000000132 (DOI)24091991 (PubMedID)
Available from: 2013-12-09 Created: 2013-12-09 Last updated: 2017-12-06Bibliographically 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
Psilander, N., Frank, P., Flockhart, M. & Sahlin, K. (2013). Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle.. European Journal of Applied Physiology, 113(4), 951-963
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, p. 951-963Article 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: 2017-11-21Bibliographically approved
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