Effects of Exercise to Improve Cardiovascular Health

Abstract

Obesity is a complex disease that affects whole body metabolism and is associated with an increased risk of cardiovascular disease (CVD) and Type 2 diabetes (T2D). Physical exercise results in numerous health benefits and is an important tool to combat obesity and its co-morbidities, including cardiovascular disease. Exercise prevents both the onset and development of cardiovascular disease and is an important therapeutic tool to improve outcomes for patients with cardiovascular disease. Some benefits of exercise include enhanced mitochondrial function, restoration and improvement of vasculature, and the release of myokines from skeletal muscle that preserve or augment cardiovascular function. In this review we will discuss the mechanisms through which exercise promotes cardiovascular health.

Keywords: cardiovascular; exercise; myokines; obesity—complications; type 2 diabetes.

Figure 1

Exercise improves cardiovascular health by inducing changes in oxygen delivery, vasculature, peripheral tissues, and inflammation. (A) Exercise improves oxygen delivery throughout the body through promotion of vasodilation and angiogenesis (–110). (B) Exercise increases mitochondrial biogenesis in adipocytes (104, 111, 112), skeletal muscle myotubes (113), and cardiomyocytes (14, 114, 115). (C) Exercise causes a long-term anti-inflammatory effect (which is inversely related to the increased inflammation typically seen in CVD and obesity) (116). Myokines released from skeletal muscle during physical exercise partially mediate these anti-inflammatory effects, and promote inter-tissue cross talk to mediate further cardiovascular benefits (–120).

Figure 2

Exercise-induced myokines mediate organ cross-talk and improve cardiometabolic health. (A) The myokine IL-6 inhibits TNF-α (186), reducing inflammation and protecting against the formation of atherosclerosis (187); stimulates GLP-1 secretion causing improved insulin secretion (188); increases lipolysis and fatty acid oxidation in adipose tissue (189) and increases glucose uptake through the AMPK signaling pathway (190, 191). (B) Fstl1 decreases ischemic injury size through activation of the Akt/AMPK pathway (activating eNOS and enhancing revascularization) (118, 119) and early fibroblast stimulation (which aids in repair after ischemia-reperfusion) (192). (C) Myonectin (MyoN) increases fatty acid uptake in adipocytes and hepatocytes (117), and promotes protects against ischemic injury in the heart, possibly through Akt activation (193). (D) NDNF improves survival after myocardial infarction (MI) by reducing apoptosis (120) through stimulation of the Akt/AMPK/eNOS pathway (enhancing revascularization) (194).