Irisin, a product of the post-translational processing of fibronectin type III domain-containing protein 5 (FNDC5), is a novel myokine which is upregulated during exercise. This hormone not only promotes the transformation of white adipose tissue into a brown-fat-like phenotype but also enhances energy expenditure and mitigates fat accumulation. Its role is crucial in the management of certain metabolic disorders such as diabetes and heart disease. Of note, the type of exercise performed significantly affects blood irisin levels, indicating the critical role of physical activity in regulating this hormone. This article aims to summarize the current scientific understanding of the role of irisin and the mechanisms through which it mediates cardiovascular protection through exercise. Moreover, this article aims to establish irisin as a potential target for preventing and treating cardiovascular diseases.

Background: The COVID-19 has been shown to have negative effects on the cardiovascular system, but it is unclear how long these effects last in college students. This study aimed to assess the long-term impact of COVID-19 on arterial stiffness, endothelial function, and blood pressure in college students.Methods: We enrolled 37 college students who had been infected with COVID-19 for more than 2 months. Brachial artery flow-mediated dilation (FMD) was used to assess endothelial function, while arterial stiffness was evaluated using the ABI Systems 100, including variables such as ankle-brachial index (ABI), brachial-ankle pulse wave velocity (baPWV), carotid-femoral pulse wave velocity (cfPWV), heart rate (HR), and blood pressure (BP).Results: Our results showed that FMD was significantly impaired after COVID-19 infection (p < 0.001), while cfPWV and systolic blood pressure (SBP) were significantly increased (p < 0.05). Simple linear regression models revealed a significant negative correlation between post-COVID-19 measurement time and baPWV change (p < 0.01), indicating an improvement in arterial stiffness over time. However, there was a significant positive correlation between post-COVID-19 measurement time and diastolic blood pressure (DBP) change (p < 0.05), suggesting an increase in BP over time. There were no significant differences in ABI and HR between pre- and post-COVID-19 measurements, and no significant correlations were observed with other variables (p > 0.05). Conclusion: Our study demonstrated that COVID-19 has long-term detrimental effects on vascular function in college students. However, arterial stiffness tends to improve over time, while BP may exhibit the opposite trend.

This study aimed to analyze the association of lifestyle habits (physical activity, sleep habits, and eating habits) with cardiovascular risk (arterial stiffness and autonomic nervous system function) among sedentary adults. Sixty adults of sedentariness and physical activity were evaluated by accelerometers; sleep and eating habits were assessed by questionnaires; cardiovascular risks were assessed by pulse wave velocity (PWV), ankle-brachial index, flow mediated dilation, and heart rate variability; circulating biomarkers were also determined. Prolonged sitting (represented by longer maximum length of sedentary bouts, lower length of sedentary breaks, and more total time of sitting) were ( P < .05) significantly associated with matrix metalloproteinases, neuropeptide Y, C-reactive protein, peptide Y, ghrelin, and leptin; significant associations ( P < .05) were also observed of total time in physical activity with most circulating biomarkers except interleukin-6, tumor necrosis factor-α, and adiponectin. Sleep habits, especially sleep efficiency, were ( P < .05) significantly associated with PWV, ankle-brachial index, and circulating biomarkers. Eating habits (including emotional overeating and enjoyment of food) were ( P < .05) significantly associated with PWVs and flow mediated dilation; satiety responsiveness and enjoyment of food were ( P < .05) significantly associated with low-frequency spectral component expressed in normalized units, high frequency spectral component expressed in normalized units, and ratio between low-frequency/high frequency spectral component expressed in normalized units. The findings indicated that several lifestyle habits among sedentary adults were closely associated with increased cardiovascular risk. Sedentary people were encouraged to live with sufficient physical activity, good sleep, and healthy eating habits for decreasing arterial stiffness and balancing autonomic nervous function.

Regular exercise enhances heart function and metabolism. The N6-methyladenosine (m⁶A) RNA modification is related to myocardial homeostasis, with the demethylase fat mass and obesity-associated protein (FTO) crucial for myocardial remodeling. However, its role in exercise-induced heart protection is unclear. We analyzed m⁶A levels and methylation enzymes to evaluate FTO changes in transverse aortic constriction (TAC) mice hearts after six weeks of treadmill exercise. Further in vivo experiments explored the effect of FTO. High-throughput sequencing identified the target gene enoyl-CoA delta isomerase 1 (Eci1). Cardiac-specific Eci1 knockout mice were used to assess the role of Eci1. The influence of FTO on Eci1 expression was explored by eliminating demethylase activity. The results showed that exercise increased FTO expression in TAC mice hearts. Reducing FTO in the heart diminishes exercise benefits. The differential m⁶A-modified genes in TAC mice hearts were enriched in fatty acid metabolism, with increased methylation of Eci1 m⁶A and decreased protein levels, leading to abnormal lipid accumulation. Exercise could reverse these effects. Eci1 knockout partially weakened exercise benefits. FTO regulated Eci1 expression via m⁶A modification, and inhibiting FTO demethylase activity blunted its protective effects on hypertrophic cardiomyocytes. Thus, FTO modulates Eci1 expression through m⁶A-dependent mechanisms, facilitates fatty acid metabolism and mitigates pressure overload-induced heart failure during exercise.