Strength training improves insulin resistance and differently affects mitochondria in skeletal muscle and visceral adipose tissue in high-fat fed mice

Abstract

Aims: Strength training (ST) improves insulin resistance and glucose tolerance by yet unknown mechanisms. The aims of this study were to investigate the effects of ST on mitochondrial adaptation in skeletal muscle and adipose tissue, on heat shock protein 72 (Hsp72) in skeletal muscle, and on visceral adipocyte size in mice with high-fat diet (HFD)-induced insulin resistance.

Materials and methods: Male Balb/c mice were divided into sedentary control-chow (C-chow), strength trained-chow (ST-chow), sedentary control-HFD (C-HFD) and strength trained-HFD (ST-HFD). Diet was provided for 12 weeks, while ladder climbing ST was performed for the final six weeks of the study at a frequency of three days per week.

Key findings: Strength training led to increased strength, muscular endurance, and skeletal muscle hypertrophy. Compared to the C-HFD group, mice in the ST-HFD group decreased their whole-body insulin resistance, improved their glucose tolerance, and had higher activation of the insulin pathway in skeletal muscle. ST increased citrate synthase (CS) activity in skeletal muscle, but this increase was blunted in ST-HFD. Conversely, HFD reduced adipose tissue CS activity regardless of training status. Hsp72 content was reduced in C-HFD, but returned to control levels in ST-HFD. Finally, reduced epididymal adipocyte size was observed in ST-HFD.

Significance: These results suggest that the improvement in insulin resistance induced by ST is related to mitochondrial adaptation in skeletal muscle, but not in adipose tissue. Moreover, this improvement might be related to increased skeletal muscle Hsp72 and reduced epididymal adipocyte size.

Keywords: Glucose metabolism; Glucose tolerance; Heat shock protein 72; Mitochondria; Obesity; Resistance training.