Vascular function, oxidative stress and inflammation in South Africans with an active-and inactive lifestyle: the SABPA study
Abstract
Motivation - Cardiovascular disease was responsible for 17.5 million deaths in 2014, which made it the main cause of mortality among non-communicable diseases. Statistics from low- and middleincome countries demonstrated that South Africa had the highest prevalence of hypertension (78%), obesity (45%), and physical inactivity (59%) among individuals who are older than 50 years, compared to countries such as China, Ghana, India, Mexico, and Russia. These figures are a cause for concern, considering that there is a dose-dependent relationship between physical inactivity and cardiovascular disease. A sedentary lifestyle may for instance cause endothelial dysfunction by means of increased oxidative stress and inflammation, as well as a subsequent decrease in nitric oxide bioavailability. Physical inactivity also contributes to increases in arterial stiffness (arteriosclerosis) and the development of atherosclerosis. Pharmacological treatments for cardiovascular disease have potential side effects and can be a financial burden, which limits the use of this treatment in low- and middle-income countries such as South Africa. Physical activity has been shown to be a cost-effective preventative, alternative, and conjoining therapy, which is associated with lower cardiovascular disease mortality, independent of other cardiovascular disease risk factors. In fact, the therapeutic effects of physical activity were shown to be as effective as drug treatment for cardiovascular disease, highlighting the necessity for research in this regard. Previous research demonstrated that high intensity physical activity is required to obtain optimal cardiovascular risk-lowering benefits. However, this physical activity prescription may be difficult to adhere to, especially in older populations. Limited research is available that explores the relationship between physical inactivity and vascular dysfunction, along with these associative factors in a South African population. Further, research on physical inactivity and cardiovascular disease is generally obtained with subjective measures such as self-reported questionnaires, therefore emphasising the need for more objective research obtained by physical activity measuring devices. Aim - The aim of this study was to investigate the interplay of vascular function measures, including twenty-four hour blood pressure, total peripheral resistance, and Windkessel
compliance, with oxidative stress, inflammation, and nitric oxide synthesis capacity markers in physically active and inactive South Africans. Methodology - This cross-sectional study formed part of the second phase of the Sympathetic activity and Ambulatory Blood Pressure in Africans study. This phase of the study was conducted between February 2011 and May 2012, and included 359 black and white school teachers, between the ages of 25 and 65 years, from the Dr Kenneth Kaunda Educational District, North West Province, South Africa. After the exclusion criteria were met, a total of 216 black and white men and women were included. Exclusion criteria included an ear temperature >37.5°C, α- and β- blocker/psychotropic substance users, pregnant/lactating women, and individuals vaccinated/donated blood within three months prior to participation. Additional exclusion criteria for our study are participants with physical activity recordings that did not last the entire seven days, or recordings with more than 40 minutes daily lost time. Standardised methods were used to capture data, which included physical activity measurements with a validated Actiheart® (CamNtech Ltd., Cambridge, UK), anthropometric measurements, and questionnaires. Cardiovascular measurements comprised Windkessel compliance and total peripheral resistance measured with a validated Finometer device (Finapres Medical Systems®, Amsterdam, Netherlands). Twenty-four hour blood pressure, including systolic blood pressure, diastolic blood pressure, mean arterial pressure, and pulse pressure were also measured with a validated Meditech Cardiotens CE120® apparatus (Budapest, Hungary). Biochemical analyses included markers of oxidative stress such as glutathione reductase, glutathione peroxidase, total glutathione, gamma-glutamyltransferase, and thiobarbituric acid reactive substances. Inflammatory markers such as interleukin-6, Creactive protein, monocytes, and eutrophil/lymphocyte ratio, as well as nitric oxide synthesis capacity markers such as L-homoarginine, asymmetric dimethylarginine, and
symmetric dimethylarginine were also measured. Participants were divided into physically active (n=84) and physically inactive (n=132) groups according to the 2008 United States Physical Activity Guidelines. Means between groups were compared with the use of analyses of covariance whereas proportions were compared with Chi-square tests. Relationships of cardiovascular variables with markers of oxidative stress, inflammation and nitric oxide synthesis capacity were investigated by means of partial and multiple regression analyses.
Results and conclusions The physically active group consisted of 84 (38.9%) participants, of whom only 3 (3.57%) participants achieved high intensity physical activity levels. The physically active group included 18.3% fewer black participants (p=0.009) than the inactive group, but sex distribution was similar. Despite higher total energy expenditure and activity-related energy expenditure levels (both p≤0.001) in the physically active group, body mass index was higher (p=0.046) than in the physically inactive group. Physically active participants had higher Windkessel compliance (p=0.041) and Lhomoarginine (p=0.006) while gamma-glutamyltransferase was lower (p=0.034) when compared to the inactive group. Unexpectedly, thiobarbituric acid reactive substances (p=0.043) were higher in the physically active group. Both partial and multiple regression analyses revealed associations between twenty-four hour diastolic blood pressure and total glutathione (β=0.18; p=0.037), as well as L-homoarginine (β=0.21; p=0.028) in the physically active group. Additionally, in multiple regression analyses, twenty-four hour systolic blood pressure (β=0.18; p=0.04) and twenty-four hour mean arterial pressure (β=0.20; p=0.025) correlated with L-homoarginine. In both analyses, the physically inactive group showed relationships of twenty-four hour systolic blood pressure (β=0.25; p=0.001), twenty-four hour diastolic blood pressure (β=0.20; p=0.013), twenty-four hour mean arterial pressure (β=0.23; p=0.003), and twenty-four hour pulse pressure (β=0.21; p=0.012) with symmetric dimethylarginine. In further analyses, since cardiovascular variables did not associate with markers of inflammation in multiple regression analyses, we repeated the above analyses, with additional inclusion of C-reactive protein to the models. Associations remained unchanged, indicating that the results are independent of inflammation. In conclusion, even moderate physical activity alters vascular risk, possibly by means of
modifications in nitric oxide synthesis capacity. These results suggest that increased nitric oxide synthesis capacity due to physical activity may mitigate the development of cardiovascular disease in a South African population.
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