Abstract
Background: Although engaging in physical exercise has been shown to reduce the incidence of cardiovascular events, the molecular mechanisms by which exercise mediates these benefits remain unclear. Based on epidemiological evidence, reductions in traditional risk factors only accounts for 50% of the protective effects of exercise, leaving the remaining mechanisms unexplained. The objective of this study was to determine whether engaging in a regular exercise program in a real world clinical setting mediates cardiovascular protection via modulation of non-traditional risk factors, such as those involved in coagulation, inflammation and metabolic regulation.Methods and Results: We performed a prospective, cohort study in 52 sedentary patients with cardiovascular disease or cardiovascular risk factors at two tertiary medical centers between January 1, 2016 and December 31, 2019. Prior to and at the completion of an 8-week exercise program, we collected information on traditional cardiovascular risk factors, exercise capacity, and physical activity and performed plasma analysis to measure levels of fibrinolytic, inflammatory and metabolic biomarkers to assess changes in non-traditional cardiovascular risk factors. The median weight change, improvement in physical fitness, and change in physical activity for the entire cohort were: −4.6 pounds (IQR: +2 pounds, −11.8 pounds), 0.37 METs (IQR: −0.076 METs, 1.06 METs), and 252.7 kcals/week (IQR: −119, 921.2 kcals/week). In addition to improvement in blood pressure and cholesterol, patients who lost at least 5 pounds, expended at least 1,000 additional kcals/week, and/or achieved ≥0.5 MET increase in fitness had a significant reduction in plasminogen activator inhibitor-1 [9.07 ng/mL (95% CI: 2.78–15.35 ng/mL); P = 0.026], platelet derived growth factor beta [376.077 pg/mL (95% CI: 44.69–707.46 pg/mL); P = 0.026); and angiopoietin-1 [(1104.11 pg/mL (95% CI: 2.92–2205.30 pg/mL); P = 0.049)].Conclusion: Modest improvements in physical fitness, physical activity, and/or weight loss through a short-term exercise program was associated with decreased plasma levels of plasminogen activator inhibitor, platelet derived growth factor beta, and angiopoietin, which have been associated with impaired fibrinolysis and inflammation.
Highlights
It is well-known that exercise reduces morbidity and mortality associated with cardiovascular disease
We found that patients engaged in a supervised, remote-monitoring program compared to those participating in supervised in-person traditional programs or unsupervised programs were the most successful in achieving modest improvements in weight loss (≥5 pounds), physical fitness (≥0.5 metabolic equivalents (METs)), and/or physical activity (≥1,000 kcals/week)
In addition to improvement in cardiac risk factors in patients enrolled in short-term exercise programs, we demonstrate that modest gains in weight, physical fitness, and/or activity can reduce PAI, PDGF-beta-1, and ANG-1
Summary
It is well-known that exercise reduces morbidity and mortality associated with cardiovascular disease. The mechanisms by which exercise mediates cardioprotection remain poorly understood. Previous studies have demonstrated exercise reduces novel risk factors in addition to traditional risk factors, these studies have been limited to the measurement of only a handful of biomarkers [8,9,10,11,12] and a reliance on self-reported measures of physical activity, fitness or weight loss [8,9,10, 13]. Reductions in traditional risk factors only accounts for 50% of the protective effects of exercise, leaving the remaining mechanisms unexplained. The objective of this study was to determine whether engaging in a regular exercise program in a real world clinical setting mediates cardiovascular protection via modulation of non-traditional risk factors, such as those involved in coagulation, inflammation and metabolic regulation
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