Abstract
Purpose Exercise training induces beneficial effects also by increasing levels of Sirtuin 1 (Sirt1) and β-hydroxybutyrate (βOHB). Up to date, no studies investigated the role of exercise training-based cardiac rehabilitation (ET-CR) programs on βOHB levels. Therefore, the present study is aimed at investigating whether a supervised 4-week ET-CR program was able to induce changes in Sirt1 activity and βOHB levels and to evaluate the possible relationship between such parameters, in Heart Failure with preserved Ejection Fraction (HFpEF) patients. Methods A prospective longitudinal observational study was conducted on patients consecutively admitted to the Cardiology and Cardiac Rehabilitation Units of “San Gennaro dei Poveri” Hospital in Naples, Italy. In fifty elderly patients affected by HFpEF, in NYHA II and III class, Sirt1 activity, Trolox Equivalent Antioxidant Capacity (TEAC), βOHB, and Oxidized Low-Density Lipoprotein (Ox-LDL) levels were measured before and at the end of the ET-CR program. A control group of 20 HFpEF patients was also recruited, and the same parameters were evaluated 4 weeks after the beginning of the study. Results ET-CR induced an increase of Sirt1 activity, βOHB levels, and antioxidant capacity. Moreover, it was associated with a rise in NAD+ and NAD+/NADH ratio levels and a reduction in Ox-LDL. No changes affected the controls. Conclusion The characterization of the ET-CR effects from a metabolic viewpoint might represent an important step to improve the HFpEF management.
Highlights
Despite recent advances in both pharmacological and nonpharmacological therapies, heart failure (HF) is still a prevalent cause of death or permanent invalidity worldwide [1]
In fifty elderly patients affected by Heart Failure with preserved Ejection Fraction (HFpEF), in NYHA II and III class, Sirtuin 1 (Sirt1) activity, Trolox Equivalent Antioxidant Capacity (TEAC), βOHB, and Oxidized Low-Density Lipoprotein (Ox-LDL) levels were measured before and at the end of the exercise training-based cardiac rehabilitation (ET-CR) program
No differences in medical therapy were found between the groups, and no therapeutic changes occurred during the study period (Table 1)
Summary
Despite recent advances in both pharmacological and nonpharmacological therapies, heart failure (HF) is still a prevalent cause of death or permanent invalidity worldwide [1]. Oxidative stress, which occurs when reactive oxygen species (ROS) are produced in excess and overcome the action of Oxidative Medicine and Cellular Longevity the endogenous antioxidants mechanisms, is implicated in the pathophysiology of HF. This is proved by a correlation between oxidative stress markers and HF in human and animal studies [3, 4] and by direct molecular evidence about an etiological role of ROS [5] in cardiovascular diseases, including HF
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