Exercise as a Therapeutic Intervention in Gestational Diabetes Mellitus

Abstract

Gestational Diabetes Mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. Regular exercise is important for a healthy pregnancy and can lower the risk of developing GDM. For women with GDM, exercise is safe and can affect the pregnancy outcomes beneficially. A single exercise bout increases skeletal muscle glucose uptake, minimizing hyperglycemia. Regular exercise training promotes mitochondrial biogenesis, improves oxidative capacity, enhances insulin sensitivity and vascular function, and reduces systemic inflammation. Exercise may also aid in lowering the insulin dose in insulin-treated pregnant women. Despite these benefits, women with GDM are usually inactive or have poor participation in exercise training. Attractive individualized exercise programs that will increase adherence and result in optimal maternal and offspring benefits are needed. However, as women with GDM have a unique physiology, more attention is required during exercise prescription. This review (i) summarizes the cardiovascular and metabolic adaptations due to pregnancy and outlines the mechanisms through which exercise can improve glycemic control and overall health in insulin resistance states, (ii) presents the pathophysiological alterations induced by GDM that affect exercise responses, and (iii) highlights cardinal points of an exercise program for women with GDM.

Keywords: diabetes; exercise; exercise endocrinology; exercise physiology; hormones; pregnancy; pregnancy endocrinology; women’s health.

Figure 1.

During exercise, the increase in skeletal muscle blood flow and capillary recruitment increase glucose delivery. Glucose uptake by the skeletal muscle cell is facilitated by two separate pathways: (i) an insulin-dependent pathway (which begins with insulin binding to its receptor (IRS), followed by its phosphorylation (1–2). In turn, the phosphoinositide 3-kinase (PI3K) pathway (3) is activated, and through a series of reactions, the translocation of GLUT4 to the cell membrane is stimulated (4)) and (ii) a contraction dependent pathway (which is mediated by several cellular events related to muscle contraction per se (1), such as the release of Ca²⁺ by the sarcoplasmic reticulum to be used for muscle contraction and the activation the Ca²⁺/calmodulin-dependent protein kinase (CaMK), the reduction in the ATP/ADP ratio and the activation of AMP-protein kinase (AMPK), the transient increase in oxidative stress), which triggers the translocation of GLUT4 to the cell membrane. Although in insulin resistance states the insulin dependent pathway is dysfunctional, the contraction dependent pathway seems to remain intact. Therefore, exercise can promote greater glucose uptake and reduce hyperglycemia. A greater glucose uptake (vs. pre-exercise) remains in the post-exercise recovery period (depending on the characteristics of the exercise session). ROS: Reactive oxygen species; GLUT4: Glucose transporters 4.

Figure 2.

An example of an exercise program based on recommendations for pregnant women, with adjustments for women with gestational diabetes mellitus (GDM). FITT: frequency, intensity, time, and type of the exercise program.