Gymnastik- och idrottshögskolan, GIH

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Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers.
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. (Åstrandlaboratoriet)ORCID iD: 0000-0002-7743-9295
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. (Åstrandlaboratoriet)ORCID iD: 0000-0001-8314-7814
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. (Åstrandlaboratoriet)
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. (Åstrandlaboratoriet)ORCID iD: 0000-0002-4030-5437
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2021 (English)In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 33, no 5, p. 957-970, article id S1550-4131(21)00102-9Article in journal (Refereed) Published
Abstract [en]

Exercise training positively affects metabolic health through increased mitochondrial oxidative capacity and improved glucose regulation and is the first line of treatment in several metabolic diseases. However, the upper limit of the amount of exercise associated with beneficial therapeutic effects has not been clearly identified. Here, we used a training model with a progressively increasing exercise load during an intervention over 4 weeks. We closely followed changes in glucose tolerance, mitochondrial function and dynamics, physical exercise capacity, and whole-body metabolism. Following the week with the highest exercise load, we found a striking reduction in intrinsic mitochondrial function that coincided with a disturbance in glucose tolerance and insulin secretion. We also assessed continuous blood glucose profiles in world-class endurance athletes and found that they had impaired glucose control compared with a matched control group.

Place, publisher, year, edition, pages
Cell Press , 2021. Vol. 33, no 5, p. 957-970, article id S1550-4131(21)00102-9
Keywords [en]
athletes, continuous glucose monitoring, exercise, exercise adaptations, glucose tolerance, high-intensity interval training, insulin resistance, metabolic dysfunction, mitochondria, mitochondrial dynamics, mitochondrial dysfunction
National Category
Endocrinology and Diabetes
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-6622DOI: 10.1016/j.cmet.2021.02.017ISI: 000647175300002PubMedID: 33740420OAI: oai:DiVA.org:gih-6622DiVA, id: diva2:1541145
Available from: 2021-03-31 Created: 2021-03-31 Last updated: 2025-09-16Bibliographically approved
In thesis
1. Exercising on the edge: mitochondrial and metabolic responses to intense training
Open this publication in new window or tab >>Exercising on the edge: mitochondrial and metabolic responses to intense training
2022 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Exercise and exercise training induces several physiological adaptations that increase the oxidative capacity of the muscles and improve glucose regulation. While the positive metabolic adaptations and effects on glucose regulation after exercise and exercise training have been extensively studied, negative outcomes have not. This thesis aims to address these questions and investigate possible negative effects of intensified training on mitochondrial parameters and glucose regulation.

In two separate interventions, we studied these outcomes after progressive exercise training, and after different intensities of exercise. Mitochondrial respiration was assessed in muscle biopsies taken from m. vastus lateralis 14 hours after exercise and oral glucose tolerance tests were performed at the same time point.

In paper I, we demonstrate that there is an upper limit of training load that can be tolerated without the manifestation of negative outcomes. After administrating almost daily sessions of high-intensity interval training, mitochondrial function and glucose control were impaired. In paper II, we used mitochondrial function as a novel biomarker of maladaptive training loads and constructed a diagnostic model that can be used for the early detection of maladaptations to exercise training. In paper III, we further demonstrated that endurance-trained athletes can have decreased glucose tolerance and increased insulin resistance the day after three hours of continuous cycling whereas these responses were not accentuated in healthy controls. Our results indicate that a metabolic switch in favor of lipid metabolism is the probable cause of this phenomenon. In paper IV, we briefly commented on a publication that described changes in whole-body VO2 responses to work rates in the athlete with the highest recorded VO2max. We provided arguments that the observed changes in VO2 and gross efficiency can in part have their origin in the mitochondria.

We here combine measurements in muscle tissue with physiological measurements in an applied context. Using this integrated approach, we investigated the effects of intensified training on health-related and performance outcomes, thereby presenting insights into what maladaptations to exercise can constitute. We hope that our results and conclusions can help to further understand the complex relationship between exercise and health and to guide athletes and coaches to optimize training outcomes.

Place, publisher, year, edition, pages
Stockholm: Gymnastik och idrottshögskolan, GIH, 2022. p. 67
Series
Avhandlingsserie för Gymnastik- och idrottshögskolan ; 25
Keywords
Exercise, training, mitochondria, performance, glucose tolerance, proteins, oxygen uptake, metabolism, cycling
National Category
Sport and Fitness Sciences Endocrinology and Diabetes Physiology and Anatomy
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-7114 (URN)978-91-986490-7-9 (ISBN)
Public defence
2022-09-22, Aulan, Lidingövägen 1, Stockholm, 09:00 (English)
Opponent
Supervisors
Funder
Swedish National Centre for Research in Sports
Available from: 2022-08-24 Created: 2022-08-23 Last updated: 2025-09-16Bibliographically approved

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Flockhart, MikaelNilsson, Lina C.Tais, SennaEkblom, BjörnApro, WilliamLarsen, Filip J

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