Description of the condition

Cardiovascular disease (CVD) is the major cause of morbidity and premature death worldwide; in the past it was a major problem only in wealthy, industrialized countries, but presently it is a global problem (Teo 2009). It is expected that in the year 2020 more than 80% of CVD will occur in countries with low and medium income levels (Teo 2009). There are nine modifiable factors that can explain 90% of acute myocardial infarcts (AMI): dyslipemia, smoking, diabetes, hypertension, abdominal obesity, and psychosocial factors; protective factors are a diet rich in fruits and vegetables, physical activity, and moderate consumption of alcohol (Yusuf 2004).

Those risk factors, when operating together, interact in a multiplicative manner to promote disease (Jackson 2005; Yusuf 2004). Thus, for example, a combination of smoking, elevated blood pressure, and high cholesterol cause 80% of the cases of premature arterial coronary disease (Emberson 2003). One way of predicting the impact of this combination of risk factors has been the development of formulas or risk tables that provide an estimate of the probability of developing CVD or of dying from it within a certain time span. One such formulas is the SCORE system (systematic coronary risk evaluation), which estimates the 10‐year risk of a first fatal atherosclerotic event, whether heart attack, stroke, aneurysm of the aorta or other major cardiac events. According to the SCORE criteria, everyone with a 10‐year CV mortality risk of 5% or more is at increased risk (Graham 2007).

As with the global estimate and diagnosis of risk, management of CVD should also have a multifactorial focus in order to produce greater benefits, because the effect of modifying several risk factors is also multiplicative (Graham 2007; NICE 2008). A moderate reduction of various factors can be more effective than a major reduction in only one of them (Jackson 2005). In this manner, the main objective of prevention is the control of risk factors through changes such as a healthier diet and increased physical activity.  Therapeutic efforts are directed  towards lowering blood pressure, triglycerides, and LDL cholesterol, as well as smoking cessation, increasing HDL cholesterol, and controlling glycemia, thereby reducing the probability of cardiovascular events or death (D'Agostino 2008).

Description of the intervention

Physical exercise is a planned, structured, and repetitive activity performed with the objective of maintaining or improving one or more components of the physical structure (Boraita 2008).

There are two types of physical exercise: aerobic and resistance training. Aerobic exercise has been proclaimed for a long time as the more beneficial of the two, but recent studies on resistance training show that skeletal muscle is the primary metabolic sink for glucose and triglyceride disposal and is an important determinant of the resting metabolic rate. Accordingly, it has been hypothesized that resistance training and subsequent increases in muscle mass may reduce multiple cardiovascular disease risk factors (Braith 2006).

It has been demonstrated that regular physical activity protects risk of myocardial infarction: odds ratio (OR) 0.86 (95% CI: 0.76‐0.97) and that it reduces the population attributable risk by 12% (Yusuf 2004). This effect has been observed in males and females, all ages, and different parts of the world (Yusuf 2004). Physical inactivity also has an influence on other risk factors: it has potential effects on body weight, blood pressure, obesity and blood lipids, vascular structure and function, myocardial function, and development of CVD (Metkus 2010), and accounted for 3,3% of deaths and 19 million disability‐adjusted life years (DALYs) worldwide (Bull 2004). Physical activity during adult life can increase total life expectancy and life expectancy free of CVD by 1.3 to 3.5 years (Franco 2005). Physical training – with its beneficial effects on atherosclerosis ‐ reduces total mortality by 20‐25% (Taylor 2004).

The effects of exercise on individual risk factors have been extensively studied.  In appropriate doses, regular exercise produces a decrease in blood pressure that remains during 8‐12 hours after each exercise session, as well as during the days when exercise is done compared with days of inactivity (Pescatello 1991). It has also been estimated that nearly 30% of patients who exercise regularly achieve a reduction in systolic blood pressure 10 mmHg or higher in the short term and for up to one year (NICE 2006). Furthermore, the effects of exercise can be associated with an increase of lipoprotein lipase (Grandjean 2000), as well as with a decrease in total cholesterol levels, LDL, and triglycerides in obese individuals, and with increased aerobic resistance and weight loss (Kelley 2005). Aerobic exercise does not have to take place at a very intense level in order to produce an effect on lipid levels (approximately between 1,000 and 1,200 kilo calories/week). HDL cholesterol appears to increase at different levels of exercise intensity (King 1995).

Why it is important to do this review

Among the strategies for prevention of CVD, there are different interventions in asymptomatic individuals at total risk of death ≥ 5% within ten years (Graham 2007),  from changes in lifestyle to pharmacologic treatment, all of them being supported by different levels of evidence.

There are previous systematic reviews that have evaluated the effects of exercise on each CVD risk factor. A review of studies on people with type 2 diabetes showed that exercise significantly improves glycaemic control and reduces visceral adipose tissue and plasma triglycerides, but not plasma cholesterol, even without weight loss (Thomas 2006). Two reviews that assessed the effects of exercise on blood pressure concluded that progressive resistance exercise training reduces resting systolic and diastolic blood pressure in adults (Kelley 2000) and that aerobic exercise reduces blood pressure in both hypertensive and normotensive persons (Whelton 2002). A review that included trials with overweight or obese subjects concluded that increases in maximum oxygen consumption is associated with higher levels of HDL, as well as that exercise reduces triglycerides, and that lower body weight is associated with lower levels of LDL (Kelley 2005). Another review focused on this population supports the use of exercise as a weight loss intervention, particularly when combined with dietary changes (Shaw 2006). Lastly, another review indicates that aerobic exercise training produced small but favorable modifications to blood lipids in previously sedentary adults (Halbert 1999).

There is no conclusive evidence on the relationship of exercise and smoking cessation: a review of thirteen clinical trials found that only one trial offered evidence that exercise was correlated with smoking cessation at a 12‐month follow up (Ussher 2008).

While the effect of exercise on individual risk factors seems to be outlined and understood, evidence of its effect on total cardiovascular risk is conflicting. Current available data has methodological limitations, basically a small sample size (Mendivil 2006) or restricted populations (only women and elderly) (Kemmler 2010), which is insufficient to make a definitive statement on the role of exercise on total cardiovascular risk. For doing that, it is necessary to gather evidence that assesses the effects of exercise not only on the control of risk factors but also on complete risk profiles and on the incidence of cardiovascular events.

In conclusion, this review will clarify the existing evidence on the relationship of exercise and cardiovascular disease by taking a comprehensive approach to subjects, considering that they are affected by a constellation of risk factors, thus trying to make the results more applicable to clinical practice.