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1 Introduction
Cardiovascular disease (CVD) remains the leading cause of death in the world. The
dramatic clinical events, such as unstable angina (UA), myocardial infarction (MI)
and stroke are all caused by atherosclerotic process. Atherosclerosis can start to form
as early as childhood, and progress to adulthood [ 1 ]. Over the last several decades,
people have become more obese and less physically active. Thus, the incidence of
disease related to metabolic dysfunction, such as diabetes, hypertension and hyper-
lipidemuia, has been increased dramatically. In addition, according to the WHO data-
base, about 80% of CVD related mortalities are caused by unhealthy behaviors, such
as high fat diets, physical inactivity, alcohol abuse and so on. It has been accepted that
changing lifestyle could reduce the incidence of these disease. One of the most cost-
effective intervention is physical exercise [ 2 , 3 ]. Recent studies have revealed that
physical exercise decreases CVD related morbidity and mortality through systemic
and cardiac-specific adaptations. Furthermore, physical exercise has been proven to
be a very promising tool in both primary and secondary prevention of CVD [ 4 – 6 ].
Atherosclerosis has been considered as a chronic inflammatory artery disease,which is responsible for approximate 50% of deaths worldwide. Risk factors to ath-
erosclerotic diseases include smoking, diabetes, hypertension, hyperlipidemia and
lack of physical activity [ 7 ]. This process is initiated by circulating plasma low-
density lipoprotein (LDL) entering the sub-endothelial space in the blood vessel. In
artery with normal endothelial function, LDL would be cleared. However, if endothe-
lial malfunction exists, the balance of entering and clearance would be broken and
LDL would keep accumulating. With time goes by, the accumulated LDL would
build up plaque inside the arterial wall, which could result in narrowing of the lumen.
Consequently, the narrowed lumen reduces blood supply to the end organs. In some
circumstances, the plaque could become vulnerable and finally ruptures. The ruptured
plaque could lead to thrombus formation, which critically obstructs the blood flow.
To date, it has been well established that atherosclerosis is the result of interac-tions of increased oxidative stress, inflammation, macrophage dysfunction, endo-
thelial injury, lipid deposition, and genetic predisposition [ 8 , 9 ]. Physical inactivity
has been widely believed to be an independent risk factor for atherosclerosis and
cardiovascular complications [ 10 ]. It contributes to the accumulation of visceral fat
and the activation of inflammatory pathways that promote the development of meta-
bolic disorders [ 11 – 13 ]. Nevertheless, evidence suggested that physical exercise
was able to reverse this pathological changes [ 14 , 15 ].
2 Physical Activity and Atherosclerosis
Atherosclerosis is a complicated process involving various reactions. It is started
from LDL entering the sub-endothelial space in the blood vessel, which is later
oxidized by reactive oxygen species (ROS). Oxidized LDL upregulates adhesion
molecules and induces the expression of chemotactic agents in endothelial cells
J. Yang et al.