Abstract
Irisin, a recently identified myokine, plays an important physiological role in modulating energy homeostasis. However, the role of irisin in cardiac function during exercise has not been evaluated. In this study, we investigated the effect of exercise on irisin, pro-inflammatory cytokines, and cardiac function during 12 weeks of exercise in rats. Eight-week-old Sprague-Dawley male rats were randomly divided into two groups (n = 9 per group): sedentary control (CON) and exercise (EXE) groups. The EXE group was trained on a motorized treadmill at 20 m/min, for 60 min/day, five times/week for 12 weeks. The EXE group showed a decrease in abdominal visceral fat (p < 0.05), epididymal fat (p < 0.01), and total cholesterol (TC) (p < 0.05) and an increase in irisin levels (p < 0.01). Irisin negatively correlated with abdominal visceral (p < 0.05) and epididymal fat (p < 0.05) and positively correlated with the ejection fraction (p < 0.05), fractional shortening (p < 0.05), and cardiac output (p < 0.05). In conclusion, exercise decreases the abdominal visceral and epididymal fat and TC levels, possibly caused by elevated irisin levels, thus improving the cardiac function. This suggests that exercise-induced circulating irisin levels correlate with improved cardiac function in rats.
Highlights
Exercise can prevent a number of chronic diseases [1,2,3]
Our results show improved cardiac output, stroke volume, diastolic volume, and systolic volume after exercise, which were correlated with irisin levels
Irisin upregulated Ki67 of proliferative markers and phosphorylated histone 3 and reduced histone deacetylase 4 to increase p38 in cardiac progenitor cells (CPC) [52]. These results suggest that exercise-induced irisin can improve Nkx2.5+ cells to protect against cardiovascular damage and improve cardiac function via increasing PGC-1α expression [53]
Summary
The contraction of skeletal muscles releases molecules called myokines [4]. Myokines are involved in the autocrine regulation of metabolism in the muscles, adipose tissue, liver, and brain [5]. One such myokine, irisin, is cleaved and secreted from a type I membrane protein called fibronectin type III domain-containing protein 5 (FNDC5) [6]. Irisin is predominantly released from the skeletal muscles and is regulated by increased expression of a receptor activated by peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) to stimulate intracellular mitochondrial biogenesis (e.g., mitochondrial uncoupling protein mRNA 1 (UCP1)) [7,8] and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) [9]. Irisin increases energy expenditure, which promotes weight loss and improves insulin resistance [6]. Circulating irisin has been shown to improve the clinical course of acute coronary syndrome [11] and to promote umbilical vein endothelial proliferation [12] through the ERK signaling pathway [9,13]
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