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

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the use of different exercise protocols in regards to: a) exercise training duration

(long or short-term) that possibly alters the underlying mechanisms for cardiopro-

tection; and b) methodology for imposing intensity (continuous or interval) that

could interfere in the amount of cardioprotection afforded. Besides investigating

these issues, it would be interesting to assess the effects of exercise intensity follow-

ing different levels of IRI other than myocardial stunning, as all previous data in this

matter were found after applying ischemia up to 25 min [ 67 , 81 , 85 , 87 ].

Recently, to overload the physiological system and stimulate greater adaptations

due to an increased shear stress, high intensity interval training (HIIT) has been

increasingly prescribed to patients with cardiovascular diseases. Indeed, well-

controlled clinical studies in patients with heart failure indicated that interval exer-

cise affords greater benefits in mitochondrial biogenesis, insulin sensitivity [ 88 ],

and body fat reduction [ 89 ] than continuous exercise training. However, the poten-

tial role of HIIT in providing protection against IRI is still little understood.

Importantly, regardless of the choice for interval or continuous exercise, studies

investigating the influence of training intensity on cardioprotection should use exer-

cise bouts with equal volume (understood as the interaction between training inten-

sity, duration and frequency) [ 90 ]. Otherwise, exercise sessions performed with a

higher intensity might have a greater volume, which introduces bias in such experi-

ments designed to determine whether a given outcome was exclusively produced by

exercise intensity or not. Unfortunately, exercise induced-cardioprotection has

never been studied in exercise sessions with different intensities but equal volume.

4.4 Time Course for Exercise Cardioprotection

Similar to the ischemic preconditioning phenomenon, an interesting study revealed

that exercise-induced cardioprotection is biphasic [ 12 ]. In this study, rats were exer-

cised for a single bout for 30 min at 30 m/min and then underwent regional cardiac

ischemia/reperfusion (20 min/48 h) at 0.5, 3, 24, 36, 48, 60, and 72 h after exercise.

The authors observed that the size of myocardial infarct after IRI in rats at 3, 24 and

72 h after exercise was similar to untrained rats. However, rats subjected to ischemia

at 0.5, 36, 48, and 60 h after the exercise session exhibited a significantly decrease

in infarcted area in comparison to control rats. Thus, the first phase of cardioprotec-

tion is believed to start rapidly following an acute exercise bout (i.e., 0.5  h after

exercise). Nonetheless, this early cardioprotection is quickly lost within 3 h post-

exercise. The second or late phase of exercise-induced cardioprotection is acquired

within 24 h after the exercise bout and persists for several days.

As important as the time required to achieve cardioprotection is for how long

after detraining the acquired phenotype is maintained. In Lennon’s study, short-term

exercised animals (3 days of 60 min/day at 30 m/min) kept a higher cardiac work

after global ischemia/reperfusion (20.5 min/30 min) at 1, 3, and 9 days post- exercise.

The exercise-induced cardioprotection vanished by 18 days after exercise cessation

[ 20 ]. As for long-term exercise, cardioprotection against IRI seems to persist for a

J.P. Borges and K. da Silva Verdoorn