In a study published in Scientific Reports, researchers from Italy evaluated the effect of regular physical activity (PA) on the microcirculatory functions and plasma antioxidant capacity in older athletes compared to sedentary controls. They studied the associated molecular and epigenetic mechanisms.
The study found that regular PA improved microcirculatory efficiency and increased plasma antioxidant capacity in elderly athletes.
Study: Regular exercise delays microvascular endothelial dysfunction by regulating antioxidant capacity and cellular metabolism. Image Credit: Ground Picture/Shutterstock.com
Background
Aging is a biological process that lays the foundation of several physical and mental ailments, including cardiovascular diseases (CVD). In particular, arteriosclerosis and endothelial dysfunction are the most significant manifestations of vascular aging.
Several cellular and molecular mechanisms are associated with aging and aging-related endothelial dysfunction, including the senescence of endothelial cells induced by a decreased bioavailability of nitric oxide (NO), redox imbalance, and oxidative stress.
An increasing amount of evidence shows that most of these mechanisms may be delayed by exercise. However, the molecular mechanisms underlying the beneficial effects of regular PA on cardiovascular health in master athletes and the elderly population are still unclear.
Therefore, this study aimed to evaluate and compare the long-term effects of regular PA on microcirculatory functions and plasma antioxidant capacity in a group of elderly athletes and sedentary individuals while shedding light on the associated molecular and epigenetic mechanisms underlying the differences.
About the study
The study included 36 long-distance runners in the test group (ATL, age range 47–74 years) and an equal number of healthy sedentary controls (SED, age range 46–77 years). No significant difference was found in the ATL and SED groups' age and body mass index.
The selected participants showed an absence of CVDs or risk factors. At the same time, individuals with coronary artery disease, cardiomyopathy, or a history of myocardial infarction, stroke, hypertension, diabetes, dyslipidemia, smoking, or alcohol consumption were excluded.
The participants' microcirculatory efficiency and endothelial function were evaluated based on a laser Doppler study of the skin blood flow (SBF). The hand blood flow (HBF) and foot blood flow (FBF) were measured at rest, post-heating to 44°C, and after a 3-min brachial artery occlusion to assess the microcirculation under hypoxia and hyperemia.
Further, venous blood samples were collected from the participants and subjected to plasma separation. The levels of sirtuin-1 (SIRT1), nitrate, and nitrite were determined in the plasma.
Real-time quantitative polymerase chain reaction (PCR) was used to analyze the levels of mRNA peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α and microRNA (miR29) in the mononuclear cells.
To study the plasma antioxidant capacity, a total oxyradical scavenging capacity (TOSC) assay was used. The statistical analysis involved the determination of the mean and standard deviation and the use of analysis of variance (ANOVA) and covariance (ANCOVA), linear regression, and Student’s t-test.
Results and discussion
The results show that while skin microcirculation was similar in ATL and SED groups at rest, HBF and FBF significantly increased (p<0.001) in response to heating and ischemia in the ATL group.
On the other hand, HBF increased to a lesser extent, and FBF increased only in response to ischemia in the SED group. The plasma concentrations of NO were significantly higher in the ATL group, indicating a preserved bioavailability of NO and an improved endothelial function and microcirculatory efficiency in the athletes.
The plasma antioxidant capacity and plasma levels of SIRT1, miR29 and mRNA PGC-1α were found to be significantly higher in the ATL group (p<0.001) compared to the SED group. These findings are significant as SIRT1 and miR29 are epigenetic regulators of cellular metabolism and redox pathways, while PGC-1α is a metabolism marker related to oxidative stress.
Additionally, a correlation was observed between clinical parameters such as NO concentration, FBF, and HBF. In the biochemical analysis, SIRT1 levels correlate with TOSC, miR29, and PGC-1α mRNA levels. The biochemical and clinical parameters were also found to be correlated with each other.
Overall, the data suggest that regular PA could prevent the endothelial dysfunction associated with aging by improving plasma antioxidant capacity and regulating redox signaling in older athletes. However, the study is limited by its small sample size and the mean age of its participants (under 50 years).
Conclusion
Together, these findings confirm that regular exercise may help prevent endothelial cell senescence by activating intracellular and epigenetic pathways, which affect redox homeostasis and the bioavailability of nitric oxide.
In conclusion, the study highlights the protective effects of regular exercise on the cardiovascular system and the positive adaptations of the underlying pathways.
Further research is required to confirm these findings and improve our understanding of the effect of regular exercise and aging on cardiovascular parameters in older populations.
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