High-intensity interval training attenuates impairment in regulatory protein machinery of mitochondrial quality control in skeletal muscle of diet-induced obese mice.

Autor: Tincknell JB; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., Kugler BA; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., Spicuzza H; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., Berger N; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., Yan H; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., You T; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA., Zou K; Department of Exercise and Health SciencesManning College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA.
Jazyk: angličtina
Zdroj: Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme [Appl Physiol Nutr Metab] 2024 Feb 01; Vol. 49 (2), pp. 236-249. Date of Electronic Publication: 2023 Oct 18.
DOI: 10.1139/apnm-2023-0286
Abstrakt: Mitochondrial quality control processes are essential in governing mitochondrial integrity and function. The purpose of the study was to examine the effects of 10 weeks of high-intensity interval training (HIIT) on the regulatory protein machinery of skeletal muscle mitochondrial quality control and whole-body glucose homeostasis in diet-induced obese mice. Male C57BL/6 mice were assigned to low-fat diet (LFD) or high-fat diet (HFD) group. After 10 weeks, HFD-fed mice were divided into sedentary and HIIT (HFD + HIIT) groups for another 10 weeks ( n  = 9/group). Graded exercise test, glucose and insulin tolerance tests, mitochondrial respiration, and protein markers of mitochondrial quality control processes were determined. HFD-fed mice exhibited lower ADP-stimulated mitochondrial respiration ( p  < 0.05). However, 10 weeks of HIIT prevented this impairment ( p  < 0.05). Importantly, the ratio of Drp1(Ser 616 ) over Drp1(Ser 637 ) phosphorylation, an indicator of mitochondrial fission, was significantly higher in HFD-fed mice ( p  < 0.05), but such increase was attenuated in HFD-HIIT compared to HFD (-35.7%, p  < 0.05). Regarding autophagy, skeletal muscle p62 content was lower in the HFD group than the LFD group (-35.1%, p  < 0.05); however, such reduction was disappeared in the HFD + HIIT group. In addition, LC3B II/I ratio was higher in the HFD group than the LFD group (15.5%, p  < 0.05) but was ameliorated in the HFD + HIIT group (-29.9%, p  < 0.05). Overall, our study demonstrated that 10 weeks of HIIT was effective in improving skeletal muscle mitochondrial respiration and the regulatory protein machinery of mitochondrial quality control in diet-induced obese mice through the alterations of mitochondrial fission protein Drp1 phosphorylations and p62/LC3B-mediated regulatory machinery of autophagy.
Competing Interests: The authors declare there are no competing interests.
Databáze: MEDLINE