Exercise for Cardiovascular Disease Prevention and Treatment From Molecular to Clinical, Part 1

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The reported major mechanisms of exercise-induced cardioprotection include

(Fig. 10.4): (1) increased antioxidant capacity, (2) increased levels of HSPs, (3)

altered NO signaling pathway, (4) enhanced function of KAT P channels, and (5)

increased activation of the opioids system [ 54 ]. Other possible underlying mecha-

nisms such as: adaptations in coronary arteries (increased arteriolar diameter and

density), elevated endoplasmic reticulum stress proteins, and amplified myocardial

COX-2 activity are not manifested after an acute bout of exercise [ 23 , 24 , 62 ] and,

although can contribute to chronic exercise cardioprotection, are not considered of

critical importance.

When the body is under stress, such as hypoxia, hyperthermia, acidosis and isch-

emia, the synthesis of several important proteins that maintain homeostasis is com-

promised [ 23 ]. Our organism responds  to these stresses  by synthetizing proteins

termed HSPs that help maintaining homeostasis [ 71 ].

HSPs are classified into groups according to its molecular weight. Although

many of them are related to cardioprotection, the HSP70 family deserves attention

[ 23 ], especially HSP73 and 72. HSP73 is constitutively synthetized in all cells, and

its level increase slightly after a stressful condition. Conversely, HSP72 is found

only after stressful events, particularly IRI [ 96 ].

Not surprisingly, HSP70 is significantly increased in hearts of animals submitted

to a single bout of aerobic exercise of at least 40 min [ 97 ] due to increased body

temperature. In theory, elevated cellular levels of HSP72 can protect the myocar-

dium against IRI by repairing unfolded proteins and/or by stabilizing the function

of endoplasmic reticulum via HSP70-related autophagy [ 98 ].

Indeed, Locke et al. [ 82 ] have demonstrated that three consecutive days of exer-

cise or heat stress increased HSP72 content and promoted greater myocardial recov-

ery after IRI than controls and rats exercised only once. Others support the hypothesis

that cardioprotection induced by long-term [ 19 , 21 , 86 ] and short-term exercise [ 7 ]

can be mediated by exercise-induced increase in HSP72 levels. Controversially,

many studies compared animals submitted to exercise in a cold environment and

Enhanced

activation

of opioids

system

Increased

antioxidant

capacity

Altered

nitric oxide

signaling

pathway

Increased

levels of

heat shock

proteins

Enhanced

function of

K ATP

channels

Fig. 10.4 Candidate
mechanisms for exercise-
induced cardioprotection

J.P. Borges and K. da Silva Verdoorn