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reduces the risk of CVD [ 11 , 12 ]. Further, exercise training and physical activity
have been shown to increase the longevity [ 13 – 16 ]. Understandably the effect of
exercise varies significantly among different individuals and also in comparison to
certain drug based treatments, exercise as an intervention has been shown to exert
comparably fewer benefits [ 17 , 18 ]. This depends on several factors including but
not limited to age, type of exercise, environmental conditions in which exercise is
being performed, individuals metabolic capacity and several others [ 19 – 25 ].
Importantly, an elaborative prospective study with ~27,000 human subjects indi-
cated that, although significant, only ~40 ∼ 60% of the risk reduction of CHD and
CVD is contributed by exercise and physical activity-related modification of tradi-
tional risk factors such as inflammatory, homeostatic factors, blood pressure, tradi-
tional lipids, BMI, HbA1c, homocysteine etc. [ 26 , 27 ]. Notably, physical inactivity
has been identified as the fourth leading risk factor for global mortality by the World
Health Organization [ 28 ]. Although much remains to be learned as to how and why
the exercise exerts differential effects, given the relatively less harmful effects
(unless and until appropriate type and the right amount of exercise are performed),
the positive benefits of exercise to the cardiovascular system cannot be denied.
Though several investigations have attempted towards understanding the cardio-vascular aging and aging-cardiovascular pathway, an apparent translational divide
still prevails between the basic mechanistic elucidations and clinical investigations
and/or approaches. Growing evidence from basic and clinical studies suggest that
an optimal level of endogenous reactive oxygen species and redox signaling path-
ways govern cardiovascular physiology (Fig. 13.1). Specifically, disrupted redox
Fig. 13.1 Types of stress and their impact on cardiac health. Aging or any stress initially triggers
physiological alterations (representing stress – red). In response to oxidative stress, system evokes
Nrf2-antioxidant signaling to maintain homeostatic redox and restores the normal function (repre-
senting eustress – green). Uncontrolled and/or chronic stress conditions impair the defense mecha-
nisms leading to pathological remodeling and cardiac dysfunction (representing distress – black)
M. Narasimhan and N.-S. Rajasekaran