Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers

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...

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Published in:Cell metabolism Vol. 33; no. 5; p. 957
Main Authors: Flockhart, Mikael, Nilsson, Lina C, Tais, Senna, Ekblom, Björn, Apró, William, Larsen, Filip J
Format: Journal Article
Language:English
Published: United States 04.05.2021
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ISSN:1932-7420, 1932-7420
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Abstract 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.
AbstractList 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.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.
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.
Author Ekblom, Björn
Tais, Senna
Flockhart, Mikael
Apró, William
Larsen, Filip J
Nilsson, Lina C
Author_xml – sequence: 1
  givenname: Mikael
  surname: Flockhart
  fullname: Flockhart, Mikael
  email: mikael.flockhart@gih.se
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden. Electronic address: mikael.flockhart@gih.se
– sequence: 2
  givenname: Lina C
  surname: Nilsson
  fullname: Nilsson, Lina C
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden
– sequence: 3
  givenname: Senna
  surname: Tais
  fullname: Tais, Senna
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden
– sequence: 4
  givenname: Björn
  surname: Ekblom
  fullname: Ekblom, Björn
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden
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  givenname: William
  surname: Apró
  fullname: Apró, William
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden; Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
– sequence: 6
  givenname: Filip J
  surname: Larsen
  fullname: Larsen, Filip J
  email: filip.larsen@gih.se
  organization: The Swedish School of Sport and Health Sciences, GIH, Åstrand Laboratory, Department of Physiology, Nutrition and Biomechanics, Stockholm 114 33, Sweden. Electronic address: filip.larsen@gih.se
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Keywords high-intensity interval training
mitochondria
metabolic dysfunction
exercise adaptations
exercise
athletes
mitochondrial dysfunction
continuous glucose monitoring
glucose tolerance
insulin resistance
mitochondrial dynamics
Language English
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33948017 - Nat Rev Endocrinol. 2021 Jul;17(7):385-386
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Snippet Exercise training positively affects metabolic health through increased mitochondrial oxidative capacity and improved glucose regulation and is the first line...
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SubjectTerms Blood Glucose - analysis
Catalase - metabolism
Glucose Tolerance Test
Glucose Transporter Type 4 - metabolism
Glycogen - metabolism
Healthy Volunteers
Humans
Hydrogen Peroxide - metabolism
Mitochondria - metabolism
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
NF-E2-Related Factor 2 - metabolism
Oxidative Stress
Physical Endurance
Superoxide Dismutase - metabolism
Title Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers
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