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Publications (8 of 8) Show all publications
Nilsson, L., Flockhart, M., Apro, W., Ekblom, B. & Larsen, F. J. (2019). Biphasic relationship between training load and glucose tolerance. In: : . Paper presented at Cell Symposia, Exercise Metabolism. May 5-7 2019, Sitges Spain.
Open this publication in new window or tab >>Biphasic relationship between training load and glucose tolerance
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2019 (English)Conference paper, Poster (with or without abstract) (Other academic)
Abstract [sv]

Biphasic relationship between training load and glucose tolerance

Nilsson, L, Flockhart M, Bergman K, Apro W, Ekblom B, Larsen FJ

 

There is a well-established construct regarding the positive effects of exercise on glucose tolerance and insulin sensitivity, as well as muscle glycogen storage. In insulin resistance, physical activity is an essential part of the treatment. However, the optimal dose is unknown. Reduced muscular glycogen stores, resulting from exercise, should stimulate an increased uptake of blood glucose. In this study we investigated the relation between training load, glucose tolerance and insulin sensitivity during three weeks of increasing interval training. Three times during the intervention, oral glucose tests were conducted to investigate the rate of glucose uptake. We found a biphasic dose-response relationship between training load and glucose tolerance, where an excessive training load led to a paradoxical reduction in glucose tolerance and impaired insulin release despite an unchanged amount of muscle glycogen. In light of these results, an upper limit of physical exercise exist where the negative effects overpowers the positive.

National Category
Cell Biology
Research subject
Medicine/Technology; Medicine/Technology; Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-5933 (URN)
Conference
Cell Symposia, Exercise Metabolism. May 5-7 2019, Sitges Spain
Funder
Swedish National Centre for Research in Sports
Available from: 2019-11-29 Created: 2019-11-29 Last updated: 2019-12-09Bibliographically approved
Nilsson, A., Björnson, E., Flockhart, M., Larsen, F. J. & Nielsen, J. (2019). Complex I is bypassed during high intensity exercise.. Nature Communications, 10(1), Article ID 5072.
Open this publication in new window or tab >>Complex I is bypassed during high intensity exercise.
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2019 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, no 1, article id 5072Article in journal (Refereed) Published
Abstract [en]

Human muscles are tailored towards ATP synthesis. When exercising at high work rates muscles convert glucose to lactate, which is less nutrient efficient than respiration. There is hence a trade-off between endurance and power. Metabolic models have been developed to study how limited catalytic capacity of enzymes affects ATP synthesis. Here we integrate an enzyme-constrained metabolic model with proteomics data from muscle fibers. We find that ATP synthesis is constrained by several enzymes. A metabolic bypass of mitochondrial complex I is found to increase the ATP synthesis rate per gram of protein compared to full respiration. To test if this metabolic mode occurs in vivo, we conduct a high resolved incremental exercise tests for five subjects. Their gas exchange at different work rates is accurately reproduced by a whole-body metabolic model incorporating complex I bypass. The study therefore shows how proteome allocation influences metabolism during high intensity exercise.

Place, publisher, year, edition, pages
Nature Publishing Group, 2019
National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-5909 (URN)10.1038/s41467-019-12934-8 (DOI)000494938600006 ()31699973 (PubMedID)
Available from: 2019-11-11 Created: 2019-11-11 Last updated: 2019-12-19
Flockhart, M., Nilsson, L., Apro, W., Ekblom, B. & Larsen, F. J. (2019). Dose-response relationship between exercise load and mitochondrial function. In: : . Paper presented at Cell Symposia: Exercise Metabolism, May 5-7 2019, Sitges Spain.
Open this publication in new window or tab >>Dose-response relationship between exercise load and mitochondrial function
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2019 (English)Conference paper, Poster (with or without abstract) (Other academic)
Abstract [en]

Dose-response relationship between exercise load and mitochondrial function

Flockhart M, Nilsson L, Bergman K, Apro W, Ekblom B, Larsen FJ

A dose-dependent relationship exists between exercise load and muscular adaptation. Mitochondria adapt to the increased ATP-demand by alterations in mass and/or quality. How mitochondrial mass and quality changes as a function of exercise load is not well investigated and we have previously found mitochondrial dysfunction after short-term intensive exercise. We therefore aimed to study mitochondrial function by altering exercise load during a three week interval training regimen to understand the dose-response relationship between exercise load and mitochondrial function. We took four muscle biopsies throughout the study, and as expected, mitochondrial function was positively affected during the first two weeks. After the third week, a dramatic mitochondrial dysfunction was evident as mitochondrial intrinsic respiration was reduced by 26% despite a 32% increase in mitochondrial yield. We hereby present evidence of a striking exercise-induced reduction in mitochondrial function after a period of very intense interval training.

National Category
Cell Biology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-5932 (URN)
Conference
Cell Symposia: Exercise Metabolism, May 5-7 2019, Sitges Spain
Funder
Swedish National Centre for Research in Sports
Available from: 2019-11-29 Created: 2019-11-29 Last updated: 2019-12-09Bibliographically approved
Flockhart, M. & Larsen, F. J. (2019). Physiological adaptation of aerobic efficiency: when less is more. [Letter to the editor]. Journal of applied physiology, 127(6), Article ID 1821.
Open this publication in new window or tab >>Physiological adaptation of aerobic efficiency: when less is more.
2019 (English)In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 127, no 6, article id 1821Article in journal, Letter (Other academic) Published
Place, publisher, year, edition, pages
American Physiological Society, 2019
National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-5961 (URN)10.1152/japplphysiol.00649.2019 (DOI)000504408200042 ()31829830 (PubMedID)
Available from: 2019-12-18 Created: 2019-12-18 Last updated: 2020-01-09Bibliographically 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
Flockhart, M., Mattsson, M. & Ekblom, B. (2014). Fysiologisk analys av utbildningsmomentet "Markstrid grundkurs (GK) 1, Fjällmarsch". Gymnastik- och idrottshögskolan, GIH
Open this publication in new window or tab >>Fysiologisk analys av utbildningsmomentet "Markstrid grundkurs (GK) 1, Fjällmarsch"
2014 (Swedish)Report (Other academic)
Abstract [sv]

Denna observationsstudie av militär grundutbildning för kadetter visar mycket tydligt att förflyttning i fjällmiljö leder till stort energiunderskott, till viss del beroende på ökade energiutgifter i och med bärande av utrustning, men framför beroende på otillräckligt energiintag.

Den genomsnittliga energiförbrukningen över övningens 100 timmarna och ca 78 km förflyttning var ca 260 kcal/h, medan energiintaget endast 135 kcal/h. Även om en typ av rations (mjukkonserv) gav i genomsnitt högre energiintag än två rations av frystorkat blev det genomsnittliga energiunderskottet för samtliga rations nästan 50 %.

Mätningarna visade stora variationer mellan olika deltagare vilket dock endast delvis kan förklaras med tekniken av att bära tungt.

Skjutprov (precision) visade att stridsvärdet påverkats negativt, genom en klart försämrad träffbild efter övningen. De fysiologiska testerna visar ökad hjärtfrekvens och upplevd ansträngning på submaximala belastningar, medan de maximala nivåerna av de fysiologiska kapaciteterna kondition, muskelstyrka i hand och ben i stort sett var oförändrade.

Kommande undersökningar på motsvarande övningar bör inriktas på interventionsstudier på fördelning av utrustningsvikter, samt hur kostintaget bör förbättras för att nå ökat energiintag.

På längre sikt bör träningsmodeller för att förbättra förmågan att bära tung utrustning utvärderas.

Place, publisher, year, edition, pages
Gymnastik- och idrottshögskolan, GIH, 2014. p. 20
Series
Rapport från Militärmedicinska forskningsgruppen ; 3
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3232 (URN)
Available from: 2014-02-07 Created: 2014-02-07 Last updated: 2018-01-11Bibliographically approved
Hendo, G., Jakobsson, M., Mattsson, C. M., Ekblom Bak, E., Flockhart, M., Pontén, M. & Ekblom, B. (2014). Slutövning GMU: "Aldrig ge upp", Amf1, Berga örlogsbas: Muskelfysiologiska resultat. Stockholm: Gymnastik- och idrottshögskolan, GIH
Open this publication in new window or tab >>Slutövning GMU: "Aldrig ge upp", Amf1, Berga örlogsbas: Muskelfysiologiska resultat
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2014 (Swedish)Report (Other academic)
Abstract [sv]

Energistatus, muskelfysiologiska data och fysiskt stridsvärde studerades före och efter en 8 dygn långa grundmilitär slutövning (GMU) vid AMF-1 Berga Örlogsskolor i månadsskiftet oktober november 2013.

Totalt deltog 105 soldater i övningen, fördelat på 3 plutoner om vardera 35 soldater. En subgrupp på 24 soldater (8 kvinnor) bestående av 8 soldater från vardera pluton studerades mer ingående.

Medelhjärtfrekvensen för de 6 soldater (2 kvinnor) som hade i stort sett kompletta mätningar från den 187 timmar långa övningen, inklusive viloperioder, var 88 ± 7 slag/minut. Utifrån hjärtfrekvensdata beräknades den totala energiomsättningen till i genomsnitt 44 000 ± 6 600 kcal, vilket motsvarar 5 600 ± 840 kcal per dygn och 235 ± 35 kcal/tim. Total energiförbrukning var i genomsnitt 39 000 kcal för kvinnorna och 46 500 kcal för männen. I övrigt noterades inte några betydande skillnader mellan kvinnor och män. Däremot var det stora individuella variationer i energiutgift, vilka till ca hälften berodde på skillnader i kroppsvikt. Med hänsyn till kroppsvikt och buren vikt var energiförbrukningen ca 3,1 ± 0,23 kcal per timme per kg totalvikt. Den individuella variationen beror på skillnad i buren vikt, på olika uppgifter och på individuella fysiologiska skillnader.

Utifrån beräknat energiintag blev det totala energiunderskottet under övningen 12 000-15 000 kcal, vilket är ca 1 500-2 000 kcal per dygn. Viktminskningen under övningen var 2,9 kg för kvinnor och 3,7 kg för män. Denna viktminskning på >4 % leder troligen till försämrad uthållighetsförmåga.

Den maximala muskelstyrkan i armar och ben var i stort sett oförändrade efter övningen, liksom den beräknade maximala syreupptagningsförmågan. Däremot upplevdes ett lågintensivt cykelarbete som betydligt tyngre efter övningen. Muskeluthållighet mättes inte i denna studie.

Ett skjutprov om 5 skott i liggande på 100 m mot en tredjedelsfigur visade 64 deltagande soldater på en försämrad träffprocent från 90,5% före till 79,4 % efter övningen. Alla soldater hade minst en träff före medan 6 soldater hade alla bom efter övningen.

Slutsatsen från studien är att GMU-övningen resulterade i ett stort energiunderskott. Stridsvärdet, bedömt från skjutprovet var klart försämrat. Maximala fysiologiska parametrar var i stort sett oförändrade, medan skattad ansträngning och därmed uthållighetsförmåga, försämrades.

Place, publisher, year, edition, pages
Stockholm: Gymnastik- och idrottshögskolan, GIH, 2014. p. 21
Series
Rapport från Militärmedicinska forskningsgruppen ; 5
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3568 (URN)
Available from: 2014-11-21 Created: 2014-11-21 Last updated: 2018-01-11
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
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-7743-9295

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