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little longer. Esposito et al. have demonstrated that, although some cardioprotection
was kept, 10-week trained rats had higher infarct size after 4 weeks of detraining [ 86 ].
4.5 Resistance Exercise Preconditioning
It is well established that resistance training induces cardiac hypertrophy due to
pressure overload during training [ 91 ]. Although there is a notion that concentric
and eccentric cardiac hypertrophy occurs in response to resistance and endurance
training, respectively; more recent evidence cast some doubts over this proposal
[ 92 , 93 ]. In addition, previous data reported benefits of resistance exercise on car-
diac performance in patients with heart failure [ 94 ]. Even though it is not clear
whether significant adaptation in cardiac structure is possible in individuals under-
going resistance exercise training, investigating the impact of this type of training
on IRI is crucial.
Although convincing evidence exists that short and long-term aerobic exerciseinduce cardioprotection against IRI, the role of resistance training in protecting the
heart in this sense is little understood. In this matter, only two studies from the same
group have been developed so far [ 91 , 95 ]. In the first one [ 95 ], rats were exercised
in a squat-training apparatus (12 repetitions/set, 4 sets/day and 5 days/wk. for
12 weeks) and after the training cessation underwent transient regional ischemia of
left anterior descending coronary artery (40 min) followed by 80 min of reperfu-
sion. The authors observed that diastolic pressure and infarct size were smaller in
trained rats whereas coronary flow and developed pressure were higher in trained
than untrained rats during and after the cardiac insult.
Interestingly, the second study included identical protocol, except for the shorterresistance training duration, but found different results. Four weeks of resistance
training did not significantly change the infarct size, apoptosis rate and myocardial
tolerance against IRI. Therefore, the duration of resistance training seems to play a
key role in inducing cardioprotection. This may be due to a required longer period
to adaptations after resistance training to occur. Nevertheless, a precise conclusion
about this issue needs more investigations.
5 Mechanisms Involved in Cardioprotection
Against Ischemia/Reperfusion Injury
As described earlier, many changes that include calcium overload, free radical pro-
duction, altered membrane lipids, protease activation, and leukocyte activation,
contribute to IRI-induced myocyte damage. In theory, any physiological effect elic-
ited by exercise that influences one or more of these events and attenuates myocyte
damage, acts as a mechanism of cardioprotection. In this sense, exercise induces
cardioprotection by multifactorial processes.
10 Cardiac Ischemia/Reperfusion Injury: The Bene cial Effects of Exercise