Flockhart 2021 Cell Metab
Flockhart M, Nilsson LC, Tais S, Ekblom B, Apro W, Larsen FJ (2021) Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers. Cell Metab 33:957-70. |
Flockhart Mikael, Nilsson Lina C, Tais Senna, Ekblom Bjoern, Apro William, Larsen Filip J (2021) Cell Metab
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. β’ Keywords: Athletes, Continuous glucose monitoring, Exercise, Exercise adaptations, Glucose tolerance, High-intensity interval training, Insulin resistance, Metabolic dysfunction, Mitochondria, Mitochondrial dynamics, Mitochondrial dysfunction β’ Bioblast editor: Reiswig R β’ O2k-Network Lab: SE Stockholm Larsen FJ
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, Patients
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS, ET
Pathway: F, N, S, NS
2021-08, AmR