Comprehensive Physiology Wiley Online Library

Exercise in the Prevention and Treatment of Type 2 Diabetes

Full Article on Wiley Online Library



Abstract

Type 2 diabetes is a systemic, multifactorial disease that is a leading cause of morbidity and mortality globally. Despite a rise in the number of available medications and treatments available for management, exercise remains a first‐line prevention and intervention strategy due to established safety, efficacy, and tolerability in the general population. Herein we review the predisposing risk factors for, prevention, pathophysiology, and treatment of type 2 diabetes. We emphasize key cellular and molecular adaptive processes that provide insight into our evolving understanding of how, when, and what types of exercise may improve glycemic control. © 2023 American Physiological Society. Compr Physiol 13:4559‐4585, 2023.

Keywords: exercise; type 2 diabetes; insulin resistance; metabolic syndrome; obesity; lifestyle intervention

Figure 1. Figure 1. Exercise improves glucose homeostasis. Exercise improves glucose effectiveness by increasing insulin secretion and sensitivity while lowering hepatic glucose production. Aerobic, resistance, and combination exercise training improve glucose homeostasis in varying magnitudes based on the volume, intensity, duration, and mode, with greatest benefits seen with combination training.
Figure 2. Figure 2. Mechanistic actions of exercise on the treatment of multiorgan symptoms of type 2 diabetes. Exercise induces tissue‐specific effects that contribute to improvements of whole‐body markers of type 2 diabetes. Primary systemic improvements are achieved via activated pathways in skeletal muscle, adipose tissue, and the cardiorespiratory system. Exercise‐mediated enhancements in glucose regulation, insulin sensitivity, and substrate utilization at the tissue level contribute to the reduction of inflammatory cytokine production and systemic inflammation and improvements in whole‐body outcomes. AKT, protein kinase B; GLUT4, glucose transporter type 4; IFN‐γ, interferon gamma; IL‐1β, interleukin 1 beta; IL‐6, interleukin 6; IRS‐1, insulin receptor substrate 1; PI3K, phosphatidylinositol 3‐kinase; mTOR, mammalian target of rapamycin; TNF‐α, tumor necrosis factor‐alpha.


Figure 1. Exercise improves glucose homeostasis. Exercise improves glucose effectiveness by increasing insulin secretion and sensitivity while lowering hepatic glucose production. Aerobic, resistance, and combination exercise training improve glucose homeostasis in varying magnitudes based on the volume, intensity, duration, and mode, with greatest benefits seen with combination training.


Figure 2. Mechanistic actions of exercise on the treatment of multiorgan symptoms of type 2 diabetes. Exercise induces tissue‐specific effects that contribute to improvements of whole‐body markers of type 2 diabetes. Primary systemic improvements are achieved via activated pathways in skeletal muscle, adipose tissue, and the cardiorespiratory system. Exercise‐mediated enhancements in glucose regulation, insulin sensitivity, and substrate utilization at the tissue level contribute to the reduction of inflammatory cytokine production and systemic inflammation and improvements in whole‐body outcomes. AKT, protein kinase B; GLUT4, glucose transporter type 4; IFN‐γ, interferon gamma; IL‐1β, interleukin 1 beta; IL‐6, interleukin 6; IRS‐1, insulin receptor substrate 1; PI3K, phosphatidylinositol 3‐kinase; mTOR, mammalian target of rapamycin; TNF‐α, tumor necrosis factor‐alpha.
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John P. Kirwan, Elizabeth C. Heintz, Candida J. Rebello, Christopher L. Axelrod. Exercise in the Prevention and Treatment of Type 2 Diabetes. Compr Physiol 2023, 13: 4559-4585. doi: 10.1002/cphy.c220009