Exercise and the cardiovascular system: clinical science and cardiovascular outcomes

Abstract

Substantial evidence has established the value of high levels of physical activity, exercise training (ET), and overall cardiorespiratory fitness in the prevention and treatment of cardiovascular diseases. This article reviews some basics of exercise physiology and the acute and chronic responses of ET, as well as the effect of physical activity and cardiorespiratory fitness on cardiovascular diseases. This review also surveys data from epidemiological and ET studies in the primary and secondary prevention of cardiovascular diseases, particularly coronary heart disease and heart failure. These data strongly support the routine prescription of ET to all patients and referrals for patients with cardiovascular diseases, especially coronary heart disease and heart failure, to specific cardiac rehabilitation and ET programs.

Keywords: body mass index; cardiovascular diseases; exercise; heart failure; metabolic equivalent.

Figure 1

Median changes in high-sensitivity C-reactive protein (CRP) in control patients with CHD and cardiac rehabilitation patients (data adapted from Milani RV et al, J Am Coll Cardiol 2004.

Figure 2

Impact of formal cardiac rehabilitation and exercise training programs on prevalence of adverse psychological stress parameters (depression, anxiety, and hostility) in younger and older patients with CHD (data adapted from Lavie CJ et al, Arch Intern Med 2006.

Figure 3

Daily physical activity duration and all-cause mortality reduction (reproduced from Wen CP et al, Lancet 2011).

Figure 4

Central illustration: Hazard ratios (HRs) of all-cause and cardiovascular mortality by running characteristic (weekly running time, distance, frequency, total amount, and speed). Participants were classified into 6 groups: nonrunners (reference group) and 5 quintiles of each running characteristic. All HRs were adjusted for baseline age (years), sex, examination year, smoking status (never, former, or current), alcohol consumption (heavy drinker or not), other physical activities except running (0, 1 to 499, or ≥500 metabolic equivalent-minutes/week), and parental history of cardiovascular disease (yes or no). All p values for HRs across running characteristics were <0.05 for all-cause and cardiovascular mortality except for running frequency of ≥6 times/week (p = 0.11) and speed of <6.0 miles/h (p = 0.10) for cardiovascular mortality (reproduced with permission from Lee DC et al, J Am Coll Cardiol).

Figure 5

Proposed pathogenesis of cardiomyopathy in endurance athletes. BNP = B-type natriuretic peptide; CK-MB = creatine kinase MB; LV = left ventricle; RA = right atrium; RV = right ventricle; SCD = sudden cardiac death (reproduced with permission from O’Keefe et al, Mayo Clin Proc).

Figure 6

Categorical model. Cox proportional survival analyses of the risk of CVD-related mortality vs MET-h/d run or walked. Relative risk is calculated for 1.07 to 1.8, 1.8 to 3.6, 3.6 to 5.4, 5.4 to 7.2, and 7.2 MET-h/d or more relative to the inadequate exercisers (<1.07 MET-h/d). “All CVD-related” mortality includes both “CVD as an underlying cause” and “CVD as a contributing cause for some other underlying cause.” Significance levels are coded as follows: ^aP≤.05; ^bP≤.01; ^cP≤.001. The significance levels for 7.2 MET-h/d or more vs less than 1.07 MET-h/d were all nonsignificant, that is, P=.99 for all-cause mortality, P=.68 for all CVD-related mortality, and P=.46 for CVD as the underlying cause of death. CVD = cardiovascular disease; MET-h/d = metabolic equivalent of task-h/d (reproduced with permission from Williams P et al, Mayo Clin Proc).

Figure 7

Continuous model. Cox proportional survival analyses of the risk of CVD-related mortality vs MET-h/d run or walked. In the model “αMET-h/d _Trimmed(MET-h/d if MET-h/d≤7.2, 7.2 otherwise) + βIndicator function (1=MET-h/d≥7.2, 0 otherwise) + covariates,” the hypothesis β=0 tests whether the hazard ratio is increased significantly above 7.2 MET-h/d relative to the hazard ratio at 7.2. Shown is the 15.4% average decrease in the risk for CVD-related mortality per MET-h/d between 0 and 7.2 MET-h/d (95% CI, 8.9%–21.5%; P<.001) and a 2.62-fold risk increase above 7.2 MET-h/d relative to the risk at 7.2 MET-h/d (95% CI, 1.29- to 5.06-fold; P=.009). CVD = cardiovascular disease; HR = hazard ratio; MET-h/d = metabolic equivalent of task-h/d. Reproduced with permission from Williams P et al, Mayo Clin Proc).