Abstract

Type 2 diabetes mellitus (T2D) is characterized by insulin resistance, impaired glycogen synthesis, lipid accumulation, and impaired mitochondrial function. Exercise training has received increasing recognition as a cornerstone in the prevention and treatment of T2D. Emerging research suggests that resistance training (RT) has the power to combat metabolic dysfunction in patients with T2D and seems to be an effective measure to improve overall metabolic health and reduce metabolic risk factors in diabetic patients. However, there is limited mechanistic insight into how these adaptations occur. This review provides an overview of the intervention data on the impact of RT on glucose metabolism. In addition, the molecular mechanisms that lead to adaptation in skeletal muscle in response to RT and that are associated with possible beneficial metabolic responses are discussed. Some of the beneficial adaptations exerted by RT include increased GLUT4 translocation in skeletal muscle, increased insulin sensitivity and hence restored metabolic flexibility. Increased energy expenditure and excess postexercise oxygen consumption in response to RT may be other beneficial effects. RT is increasingly establishing itself as an effective measure to improve overall metabolic health and reduce metabolic risk factors in diabetic patients.

Highlights

  • The global epidemic of obesity has contributed to a concomitant increase in the prevalence of type 2 diabetes mellitus (T2D)

  • According to the Health Professionals Follow-up Study who observed >32,000 men over a period of 18 years, subjects engaging in resistance training (RT) over >150 min/week showed a 34% reduction in risk of T2D, after adjustment for aerobic activities and body mass index (BMI)

  • The first significant finding of this investigation was the clear demonstration of an RT-induced increase in mitochondrial content in the skeletal muscle of T2D patients after 9 months of training, and these changes were significantly associated with clinical improvements (i.e., HBA1c, VO2max)

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Summary

Introduction

The global epidemic of obesity has contributed to a concomitant increase in the prevalence of type 2 diabetes mellitus (T2D). Before the year 1990, neither the American Heart Association nor the American College of Sports Medicine (ACSM) included guidelines for recommendation of RT for exercise training and rehabilitation It was in 1990 when the ACSM recognized RT as a contributing factor to a comprehensive fitness program for healthy adults of all ages. A 40% reduction in mitochondrial function with aging, obesity, and T2D may contribute to declines in glucose uptake and the development of insulin resistance, possibly arising from increases in intracellular lipid stores [30]. Evidence indicates metabolic dysfunction in skeletal muscle in patients with T2D, characterized by insulin resistance, impaired glycogen synthesis, lipid accumulation, and impaired mitochondrial function.

Implications of Resistance Training
Cellular and Molecular Mechanisms
Findings
Conclusion
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