Discussion
Our work shows that low-intensity PA applied to sedentary overweight and obese postmenopausal women improves several parameters associated with cardiovascular health and that there is high adherence to such a PA program. International recommendations by different scientific societies establish at least 2.5 to 5 hours/week of moderate-intensity walking to reduce cardiovascular risk. However, even this small amount of activity cannot be met by many older, handicapped, or metabolically limited people, such as those with obesity. Therefore, an evaluation of the impact of exercise levels below these recommendations is warranted. A low-intensity PA intervention results in an augmented antioxidant system, measured by the activity of the enzymes superoxide dismutase and glutathione peroxidase. The increases in these enzymes suggest better antioxidant status, although we did not observe any effect on plasma lipid oxidation, as measured with oxidized low-density lipoprotein levels. saRHI, a surrogate of endothelial function, showed a nonstatistically significant improvement trend. Albeit nonsignificant, the saRHI increase was positively associated with the increase in PA and the improvement in oxidative parameters, and inversely associated with ADMA levels and RHR, in concordance with an overall benefit on cardiovascular health parameters.
Current evidence suggests that PA improves several classical cardiovascular risk factors and measures of the new biomarkers of cardiovascular risk, including oxidative stress, endothelial wall dysfunction, and high RHR. Weight loss, especially visceral fat loss (but also subcutaneous fat loss), is one of the main determinants of these changes. By assessing body fat patterns with standardized echography methods, we observed that our results were independent of changes in body weight loss or body fat distribution. Moreover, our group has recently published that a moderate increase in PA decreases a marker of adipose tissue distribution, such as FABP4 levels; specifically, an increase of 30 METs/hour/week decreases FABP4 by 10.3 U. In the present study, the low increase in PA has not been associated with FABP4 changes.
We found that ADMA levels decrease significantly with low-intensity PA. Exercise training has been documented to decrease ADMA levels, but no data on low-intensity PA are available. ADMA acts as a strong endogenous endothelial NO synthase inhibitor by blocking NO synthesis from the amino acid L-arginine, which contributes to the initiation and progression of atherosclerosis. Therefore, the reduction of ADMA and the increase in saRHI might also contribute to endothelial function improvement in postmenopausal women undergoing low-intensity PA. Even though we cannot obtain mechanistic data from this study, our results support improvements in oxidative status and small artery endothelial function markers. These results were confirmed in multivariate analyses showing that both PA and antioxidant enzymes play a role in the observed improvement in endothelial function.
Another relevant finding is the significant decrease in RHR observed after the intervention. High RHR has been identified as a potential accelerator of atherosclerosis via its negative effects on the endothelium attributed to shear and mechanical stress. In fact, modifications of the hemodynamic environment by an accelerated heart rate probably contribute to enhanced atherosclerosis in certain parts of the vascular tree. It is known that physical exercise improves heart function by reducing RHR; however, small amounts of PA already have a positive impact. Interestingly, changes in RHR were among the determinants of saRHI changes, supporting the idea that heart functionality is linked to overall endothelial function. In accordance with this observation, clinical trials with ivabradine, a selective inhibitor of I(f) channels, showed a relationship between decreased RHR and improved endothelial function. This association is not fully understood, but evidence derived from ivabradine studies produced two possible explanations for this effect. First, with slowing heart rate, shear stress becomes more constant, and thus flow is more constant, leading to a reduced burden on arterial wall function. Second, with high RHR (which is associated with mechanical stress from each heartbeat), the wall becomes stiffer; this is associated with accelerated endothelial cell turnover, premature senescence of the endothelium, and high shear stress. Our results support these observations and extend them to clinical practice, suggesting a benefit of low-intensity PA on overweight and obese postmenopausal women.
Study Limitations
Our study has some limitations. Because the study was conducted in a specific group of overweight and obese postmenopausal women, the results cannot be generalized to other specific populations. Because the study has not introduced a control group, we cannot exclude from the results the effects of time and regression-to-the-mean phenomenon. Although not described, the pharmacological agents being taken by the participants or the interactions between the pharmacological agents and PA changes could have influenced changes in oxidative stress or endothelial function. PA is measured objectively by self-reports that may lead to misclassification and bias toward weaker PA or health benefit associations. Nevertheless, the PA sessions were directed by healthcare and physical education professionals, and participants signed an attendance list before every session. Considering that the intervention lasted for only 4 months, long-term follow-up may provide a better perspective of the observed changes.