The evidence that a sedentary lifestyle leads to CHD, and particularly myocardial infarction (MI) or sudden death, is based on observational studies in the general population and in specific groups, on experimental studies that compare a sedentary group with one doing more exercise. There is evidence that regular PA, together with other risk reduction behaviors, can help prevent first cardiac and stroke events, reduces the risk of their recurrence and helps patients recover after MI, surgical revascularization or coronary angioplasty (PCI). In relation to CHD, biological mechanisms have been identified through which PA and exercise training may contribute to primary and secondary prevention: it maintains or increases myocardial oxygen supply, decreases myocardial work and reduces cardiac work and oxygen demand, increases myocardial function and electrical stability of myocardium by a favorable modulation of autonomic balance—induces ischemic pre-conditioning of the myocardium, increasing their tolerance to more ischemic stress. The underlying cardioprotective mechanisms involve changes in the coronary arteries, myocardial heat shock proteins and cyclooxygenase-2 activity, endoplasmic reticulum stress proteins, nitric oxide, sarcolemmal and/or mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels and myocardial antioxidant capacity, antioxidant enzymes, mitochondrial phenotype that protect against apoptotic stimuli [7]. At another level, PA has a positive effect on established risk factors for CVDs, leading to improvements in blood pressure, glucose intolerance, diabetes, dyslipidemia, and obesity. Specifically, it helps to control body weight, prevents or delays the development of hypertension in normotensive subjects and reduces blood pressure in hypertensive patients, improves lipoprotein profile—increases HDL cholesterol levels, improves carbohydrate metabolism, the body’s use of insulin—lowering the risk of developing type 2 diabetes mellitus, particularly in those at high risk of diabetes, improves glycemic control and reduces type 2 diabetes medications and increases exercise capacity [1, 8]. In short, antiatherogenic effects of PA and exercise training are well documented by changes on the body fat mass, lipoprotein metabolism, carbohydrate intolerance, regression of coronary lesions, vascular reactivity and structure, and neurohormonal modulation [9].

The first studies to examine the relationship between CHD and PA were based on occupational activities. It all began with the Morris’s landmark study, the first rigorous epidemiological study in the field of PA, showing that men in physically demanding occupations (bus conductors and postmen) had a significantly lower risk of heart disease than individuals who worked in less demanding jobs (bus drivers and office workers). Since then, many investigations have focused on occupational activity and leisure-time physical activity (LTPA), although with different qualitative and quantitative assessments. The procedures to assessing PA in epidemiological research are critical both for understanding the relation between PA, or opposite physical inactivity, and measures of health as for comparability of data around the world. Nevertheless, the research to date has been consistent and compelling: regular PA reduces markedly the risk for CVDs and has other documented benefits. Indeed, there is strong evidence that PA is associated with healthier body mass and composition, increased cardio-respiratory fitness, reduced rates of high blood pressure, metabolic syndrome, type 2 diabetes, CHD, and stroke [2, 10].

Worldwide, the relative risk (95 % CI) associated with physical inactivity, activity level insufficient to meet WHO recommendations [2], adjusted for confounders, for incidence of CHD and diabetes is, respectively, 1.16 (1.04–1.30) and 1.20 (1.10–1.33) [6]. These numbers are consistent with findings from INTERHEART study, a case–control study conducted in 52 countries throughout Africa, Asia, Australia, Europe, Middle East, and North and South America, in which the adjusted OR for MI associated with physical inactivity was 1.16 (1.03–1.32) [11].

Numerous reviews or meta-analyses strengthened the evidence that PA has an independent role in primary prevention of CHD, with a 20–30 % lower risk of CHD [10]. A meta-analysis of prospective cohort studies of occupational and LTPA and CVDs (CHD and stroke), with follow-up ≥5 years, exploring the dose–response relationship, shows that high level of LTPA and moderate level of occupational PA reduces the risk of incidental events of CHD and stroke among men and women by 20–30 % and 10–20 %, respectively [12]. On the other hand, the reduction in risk of all-cause and cardiovascular mortality derived from systematic review is significant, 30–40 % [10] to 20–30 % [1], with a stronger dose–response gradient for fitness than for PA [13]. Fitness has direct dose–response relations between intensity, frequency, duration and volume for CVDs and CHD. The weaker relation of PA than cardiorespiratory fitness with health benefit may result from bias in the measurement method (objectively versus self-reports) and resultant misclassification. The procedures to assessing PA in epidemiological research are critical both for understanding the relation between PA, or opposite physical inactivity, and measures of health as for comparability of data around the world. Recent technological advances (accelerometers and heart rate monitors) will increase in the future the accuracy of the PA assessment.

The-Lancet-Series-Physical-Activity highlights global burden of physical inactivity and suggests that it’s responsible for 5.8 % of the burden of CHD worldwide, ranging from 3.2 % in Southeast Asia to 7.8 % in the Eastern Mediterranean. In addition, physical inactivity accounts for 11.9 % of the burden of CHD in the Cook Islands and Malta, 11.4 % in Swaziland and Saudi Arabia, 11.3 % in Argentina, 10.5 % in the UK, 6.7 % in the US, and 5.6 % in Canada. Similarly, the burden of diabetes attributable to physical inactivity is 7.2 % worldwide, ranging from 3.9 % in Southeast Asia to 9.6 % in the Eastern Mediterranean [6].