Exercise protects the cardiovascular system: effects beyond traditional risk factors

Abstract

In humans, exercise training and moderate to high levels of physical activity are protective against cardiovascular disease. In fact they are 40% more protective than predicted based on the changes in traditional risk factors (blood lipids, hypertension, diabetes etc.) that they cause. In this review, we highlight the positive effects of exercise on endothelial function and the autonomic nervous system. We also ask if these effects alone, or in combination, might explain the protective effects of exercise against cardiovascular disease that appear to be independent of traditional risk factor modification. Our goal is to use selected data from our own work and that of others to stimulate debate on the nature and cause of the 'risk factor gap' associated with exercise and physical activity.

Figure 1. Differences in sudden death cardiovascular mortality in physically active London bus conductors vs. sedentary bus drivers

This was the first example showing that physical activity (exercise) was protective against cardiovascular disease. Data from Blair & Morris (2009).

Figure 2. Effects of >1500 versus <200 calories per week of exercise/physical activity on risk factors and their impact on coronary heart disease and cardiovascular disease

The filled bars show the risk reduction due to high levels of physical activity for all traditional risk factors in combination and for specific individual risk factors. The effects of exercise on traditional risk factors explained less than half the risk of coronary heart disease and ∼60% of cardiovascular disease. Data from Mora et al. (2007). HbA1c = elevated glycosylated haemoglobin.

Figure 3. Effects of reduced (lowest quartile) high-frequency (HF) or low-frequency (LF) heart rate variability on morbidity and mortality in diabetic patients form the ARIC study

A, B, C and D reflect specific outcomes as follows: A, coronary heart disease; B, myocardial infarction; C, fatal coronary heart disease; and D, total mortality. Diabetic subjects with any marker of reduced heart rate variability had increased morbidity and mortality. Data from Liao et al. (2002).

Figure 4. Effects of systemic nitric oxide synthase inhibition with l-NMMA on blood pressure in healthy male subjects with high vs. low levels of baseline muscle sympathetic nerve activity

Low- and moderate-dose nitric oxide synthase inhibition causes larger increases in blood pressure in the subset of subjects with high baseline levels of MSNA. *P < 0.05, differences between the groups. Data from Charkoudian et al. (2006). Open circles = high MSNA subjects; closed circles = low MSNA subjects.

Figure 5. A 5 kg weight gain causes a marked increase in muscle sympathetic nerve activity in young subjects

Data from Gentile et al. (2007).

Figure 6. Schematic diagram of the interactions proposed in this paper

In the endurance exercise-trained state or with high levels of physical activity, endothelial function and parasympathetic tone (augmented heart rate variability) are enhanced. Large conducting vessels remain compliant, and the effects of high sympathetic outflow, when present, are buffered. These positive interactions may account for observations showing that exercise is more protective against cardiovascular risk than predicted by its effects on traditional risk factors. With physical inactivity, there is a loss of endothelial function during middle age, a potential accumulation of risk factors, and increased vessel stiffness. These effects of physical inactivity permit the effects of high sympathetic tone to be more fully expressed while parasympathetic tone is progressively lost. These negative interactions may account for observations showing that physical inactivity is a more potent cardiovascular risk factor than widely appreciated.