Atherosclerosis and its complications are leading causes of death and disability in western countries (Anderson et al., 2006). Cardiovascular diseases are the world's most prevalent causes of mortality claiming 17.1 million lives a year (WHO, 2010). The total cost, directly and indirectly of cardiovascular disease in 2001 was estimated at $299 billion dollars (Reed, 2002).
The following paper will discuss the mechanisms which cause atherosclerosis and examine through the review of empirical evidence the link between regular aerobic exercise and a reduction in the risk of developing atherosclerosis.
Atherosclerosis (not to be confused with arteriosclerosis) is a cardiovascular disease which affects various regions of the circulatory system and manifests itself depending on the circulatory bed affected (Fauci et al., 2008). Atherosclerosis is the main pathological process leading to CHD (coronary heart disease), (Mendis et al., 2005). It is a chronic inflammatory disease occurring usually over a period of years; it can present itself in a variety of fashions. (Blasi, 2008). It can remain "silent" and present as chronic (e.g. angina pectoris), acute (e.g. stroke, sudden cardiac death) or may not be discovered until post-mortem (Fauci et al., 2008). Fig. 1 shows the development of atherosclerosis over time. It is evidenced from this that it primarily begins occurring as early as the second/third decade of life (REF FIG 1.). Predisposition to atherosclerosis includes genetic (age, gender, hypercholesterolemia, diabetes), and behavioural risk factors (smoking, physical inactivity, hypertension and obesity (Mendis et al., 2005). Individuals with blood cholesterol level above 200mg are at serious risk (Reed, 2002). According to Davison, 2009 increased levels of LDL (low density lipoprotein) cholesterol and reduced levels of HDL-C (high density lipoprotein) cholesterol within artery walls are also a contributor to the development and progression of atherosclerosis.
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Fig.1: Timeline of Atherosclerosis (adapted from Pecsvarady, 2010)
Atherosclerosis is a disease which initiates with lesions known as "fatty streaks" (characterised as lipid laden macrophages) within the lining of the artery which is followed by atheroma (caused by thrombosis and TGF-Î² growing smooth muscle and transforming a simple foam cell accumulation into a fibro-fatty lesion), usually followed by a more advanced atherosclerotic plaque (Fauci et al., 2008). The right and coronary arteries have been documented as being particularly vulnerable (Mendis et al., 2005). As they advance, these plagues also accumulate calcium and become more fibrous (Fauci et al., 2008) and further increase artery lumen size. This is visible in fig. 2 below.
Fig. 2: Timeline of Atherosclerosis (adapted from Pecsvarady, 2010)
Protection against atherosclerosis:
HDL-C has been documented to protect against the development of atherosclerosis via its antiatherogenic properties (Brewer, 2004). Although literature also recognises Anti-inflammatory and antioxident properties may also contribute to HDL atheroprotective effects (Fauci et al., 2008). Evidence shows aerobic physical activity and weight loss can raise HDL-C and lower triglycerides (McArdle, et al., 1996) and also improve glucose and lipid metabolism (Harding et al., 2001).
Early stages of atherosclerosis
Although the exact sequence is not yet fully understood, monocytes, macrophages, smooth muscle cells and lymphocytes play large roles (Mendis et al., 2005). The primary aspects associated with its development are elevated cholesterol, triglycerides and LDL levels and also reduced HDL levels (Reed, 2002). Atherogenesis begins with the uptake of oxidised LDL by endothelial macrophages, foam cell formation in the intima of the artery and fatty streak formation (Reed, 2002). Some controversy surrounds the foam cells within early lesions but it may be that smooth muscle cell Î±-actin accumulates fewer lipids than macrophages (Mendis et al., 2005). Increased T-lymphocyte numbers present in fatty streaks than initial lesions may suggest their possible role in fatty streak lesion formation (Fauci et al., 2008).
Fig. 3-6 show artery wall early plague formation stages:
C:\Users\Sony\Pictures\Artery wall structure & function.PNG Fig. 3: Structure & function
C:\Users\Sony\Pictures\1. Fatty streak.PNG Fig. 4: Fatty Streak
C:\Users\Sony\Pictures\2. Fibrous cap.PNG Fig. 5: Fibrous cap
Progression of atherosclerosis
C:\Users\Sony\Pictures\3. Lipid core.PNG Fig. 6: Fibrous cap
As fig. 4 shows, with continued build up of fatty deposits narrowing the artery wall, less and less blood is pumped through. This increases the strain on the heart, thus increasing risk of heart failure, stroke (blockage in brain) or myocardial infarction (blockage in artery), (Fauci et al., 2008). Atherosclerosis of coronary arteries impedes blood flow and leads to ischemic heart disease (Reed, 2002). Impaired blood flow to smaller vasculature can lead to blindness and other negative consequences (Fauci et al., 2008).
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Aerobic Exercise & Atherosclerosis
Exercise is a subset of physical activity as set out by Caspersen et al., 1985, designed to improve fitness and health through energy expenditure.
In a study conducted by (Raurama et al., 2004), where atherosclerotic and healthy subjects participated in a progressive and longitudinal (six years) regular aerobic exercise regimen, it was concluded that aerobic exercise produces many beneficial and favourable changes relating to the associated variables of atherosclerosis such as blood pressure, body adiposity, plasma lipid levels as well as plasma glucose and insulin levels (Raurama et al., 2004).
Further longitudinal intervention studies have been carried out in this area however lack of compliance and adherence to an exercise regimen generally restricts the long term clinical benefits of such interventions (Praet et al., 2008).
However, evidence supports that the implementation of aerobic exercise results in a decrease in plasma triglyceride level, increased HDL cholesterol and improvement in mild hypertension (Sato et al., 2007), "thus physical exercise exerts an inhibitory effect on the development and progression of atherosclerosis through a number of mechanisms" (Sato et al., 2007).
In 2007, McClean et al. conducted a study with the aim of measuring markers of postprandial oxidative stress and also pulse wave velocity (PWV) before and after an acute bout of moderate exercise. The study consisted of a randomised cross-over design of ten trained male participants (age 21.5 Â± 2.5years, VO2 max 58.5Â±7.1 ml.kg.-1min-1) as follows:
Group 1 - High fat meal alone
Group 2 - High fat meal followed 2 hours later by acute bout of exercise of 60% max HR.
PVW was measured before and postprandial levels were taken each hour after the meal for four hours. It was found that in group 2, at hour 3 (immediately post exercise) and hour 4 (1 hour post exercise), circulating triglycerides decreased. There was no change in HDL-C levels in group 2 while group 1 had increased HDL-C levels. These findings demonstrate the benefits of exercise to offset the negative and atherogenic affects which a high fat meal produces (triglyceride and HDL-C responses). The researchers found that the aerobic exercise session blunted the postprandial increases in PWV demonstrated in the control trial (and supported by other: Gaenzer et al., 2001; Ceriello et al., 2002). The findings of this study are visible in fig. 4 below.
Fig 7: Biochemical markers following ingestion of high fat meal & exercise (adapted from McClean et al., 2007).
Interestingly, a study conducted by Metsios (Metsios et al, 2010) found that aerobic exercise has significant positive effects on the endothelial system, both acutely and long term, which has implications for atherosclerosis. As previously stated above and as is visible in fig 1, endothelial dysfunction plays a large role in the very early development of this disease. According to Metsios (Metsios et al, 2010) exercise acutely increases expression of endothelial progenitor (repair) cells and also increases circulating angiogenic cells which promote endothelial cell growth. This supports the view that exercise has enormous benefits for the prevention of atherosclerosis as fig 4 shows below.
Fig. 8: The effects of exercise on endothelial function, atherosclerosis and inflammation (adapted from 12 pg. 91).
Reflection & Conclusion
Upon review of the evidence it is abundantly clear that the implementation of aerobic exercise results in a decrease in plasma triglyceride level, increased HDL cholesterol and improvement in mild hypertension (Sato et al., 2007), "thus physical exercise exerts an inhibitory effect on the development and progression of atherosclerosis through a number of mechanisms" (Sato et al., 2007).
Current estimates predict that by 2020 cardiovascular diseases, notably atherosclerosis, will become the leading global cause of disease (Fauci et al., 2008). If this estimate is to be reduced then aerobic exercise must be incorporated into preventative and management strategies. From reviewing the empirical evidence, aerobic exercise must be thought of as an essential aspect of maintaining good health and preventing, delaying or managing atherosclerosis effectively.