Abstract
Aging is the most important risk factor for cardiovascular diseases. Although exercise is known to be beneficial for the health of aging heart, the optimal exercise training intensity to prevent natural aging-induced cardiac damage has not been defined. In this study, we used 32-week-old male mice and randomly divided them into three groups, namely, untrained (UNT) mice, moderate-intensity exercise training (MET) mice, and high-intensity interval training (HIIT) mice. Mice in the two exercise training groups were subjected to exercise 5 days per week for 24 consecutive weeks. Metabolic characteristics, cardiac function and morphology, myocardial remodeling, myocardial fibrosis (collagen III, α-SMA, and TGF-β), oxidative stress (NRF2, HO-1, SOD, and NOX4), and apoptosis (BAX, Bak, Bcl-2, and Bcl-XL) were analyzed 24 weeks after the different treatments. MET improved cardiac function and reduced myocardial remodeling, myocardial fibrosis, and oxidative stress in the aging heart. MET treatment exerted an anti-apoptotic effect in the heart of the aging mice. Importantly, HIIT did not protect against cardiac damage during the natural aging process. These findings suggest that MET may be one of the main methods to prevent cardiac damage induced by natural aging.
Highlights
Aging is an important risk factor in the development of cardiovascular diseases [1], probably due to continuous changes in the structure and function of the heart with aging [2]
To determine whether exercise training protects against cardiac damage, we examined parameters related to cardiac function in mice (Figure 1A)
The untrained (UNT) mice exhibited impaired cardiac function, as evidenced by a decrease in the left ventricular rejection fraction and fraction shortening (LVEF and LVFS). These decreases were observed in the high-intensity interval training (HIIT) group, but they were significantly abrogated in the moderate-intensity exercise training (MET) group (Figure 1B)
Summary
Aging is an important risk factor in the development of cardiovascular diseases [1], probably due to continuous changes in the structure and function of the heart with aging [2]. The key molecular phenotypes of cardiac aging include changes in stress response pathways, cardiac energy metabolism, mitochondrial function, cardiomyocyte death, and extracellular matrix remodeling [3,4,5,6,7] These changes may be beneficial because they maintain cardiac function, but later, they are usually detrimental to the heart, leading to age-related cardiac remodeling and impaired cardiac reserve, which increases the risk of heart failure and other cardiovascular diseases [8]. Various parameters including cardiac function, myocardial remodeling, myocardial fibrosis, oxidative stress, apoptosis, and aging were analyzed to clarify the exercise training intensity that can prevent cardiac damage in the natural aging process
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