Cardiovascular diseases (CVD) stand at the forefront of global mortality, presenting an immense and urgent public health challenge on a global scale. Effectively addressing the associated risk factors is pivotal in not only preventing but also stabilizing and potentially reversing the progression of these conditions. Emerging research illuminates a compelling correlation between sleep disorders and CVD. Clinically, individuals afflicted with existing CVD or those possessing risk factors frequently grapple with sleep disturbances, exacerbating their conditions, particularly in severe cases where disease progression is accelerated. Even among ostensibly healthy individuals, chronic sleep deprivation exacts a toll on cardiovascular function. The strategic implementation of exercise interventions emerges as a potent tool in enhancing sleep quality, surpassing the efficacy of pharmaceutical treatments. Furthermore, the maintenance of optimal sleep patterns significantly contributes to lowering the risk of cardiovascular diseases. This comprehensive review delves deeply into the intricate relationship between exercise and the amelioration of cardiovascular disease risk associated with sleep. Moreover, it meticulously elucidates the complex mechanisms through which exercise operates, effectively reducing cardiovascular disease risk from the unique perspective of sleep science.

Background Type 2 diabetes mellitus (T2DM) is a common chronic disease that is strongly associated with cardiovascular risk. Long-term high blood glucose levels may induce cardiomyocyte apoptosis, cardiac dysfunction and suppress fetal cardiomyocyte proliferation. Recent epidemiological studies have shown a link between antioxidant carotenoids and T2DM, but a comprehensive longitudinal study of this association has not yet been conducted. Methods We included participants with biological measurements for both serum cis-β-carotene and fasting glucose from NHANES (2001–2006). We divided the participants into quartiles according to serum cis-β-carotene levels and determined the association between these levels and glucose metabolism by using multivariable regression models adjusted for confounding factors. The mechanism through which β-carotene levels regulate plasma glucose levels was further investigated in vivo and in vitro. In addition, we performed a preliminary exploration of the effects of β-carotene on diabetic rats and primary cardiomyocytes. Results Higher cis-β-carotene (quartile 4) was associated with higher LDL-cholesterol levels but lower fasting blood glucose levels. However, T2DM rats subjected to β-carotene treatment showed diminished total triglycerides and LDL-cholesterol, and their β-carotene levels were associated with better cardiac function than that in the T2DM group (P<0.05). Moreover, β-carotene was found to be an important protective factor improving cardiac and mitochondrial function in diabetes. At non-cytotoxic doses, β-carotene clearly improved glucose uptake in insulin-resistant cells. Treatment with β-carotene increased GLUT4 and p-Akt expression, and attenuated the phosphorylation of IRS-1. Our data demonstrated that β-carotene improved cardiac mitochondria biogenesis in diabetes due to activation of PGC-1β. Conclusion Our results indicate that β-carotene can be used to treat metabolic disorders through inhibition of the insulin-resistance pathway in diabetes.