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

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claim that exercise-induced cardioprotection following few exercise sessions is


similar to long-term physical training [ 24 , 62 ]. Given that exercise-induced cardio-


protection is a multifactorial process, it is tempting to assume that it involves differ-


ent mediators and magnitude according to the exercise protocol duration. Clarifying


this issue would be important considering that the potential mechanisms involved in


this response are still largely debated.


4.3 Exercise Training Intensity


When it comes to exercise intensity, the first question we ask is how much exercise


is needed to protect the heart. Is there a minimum amount of exercise to achieve


cardioprotection? Many researchers have been trying to answer this question, as the


dose-response impact of aerobic exercise intensity on cardioprotection is extremely


important. And the truth is that although findings from several studies provide


insight into this matter [ 24 ], definitive answers remain unknown.


Before reviewing existing data on the effect of exercise intensity over cardiopro-

tection, it is important to revisit a concept of exercise prescription. There are two


different methodologies to deal with aerobic exercise intensity: continuous or inter-


val exercise. Continuous exercise consists of maintaining submaximal power output


and VO 2 constant throughout the entire session, whilst interval exercise alternates


periods of greater and lower intensity within an exercise session [ 84 ].


In one of the first investigations into the role of long-term exercise intensity in

providing cardioprotection [ 85 ], rats were treadmill trained for 11–16 week at low


intensity (20  m/min, 0% grade, 60  min/day), moderate (30  m/min, 5% grade,


60 min/day) or intense (10 bouts of alternating 2-min runs at 16 and 60 m/min, 5%


grade). After submitted to 25 min of global ischemia, all trained groups presented


significantly greater post-ischemic cardiac output and work compared to sedentary


rats. However, as intensity increased the greater was myocardial recovery.


Interestingly, a previous study [ 67 ] exercised rats daily for 6 week at low (20 m/

min, 0% grade, 60 min/day) or high intensity (5 bouts of alternating 1-min runs at


75 and 20 m/min, 15% grade, 10 min/day). The high-intensity protocol improved


myocardial functional recovery following 20 min of global ischemia in an isolated


Langendorff perfusion model, but the low-intensity program did not. The same


result was found by Starnes et  al. [ 81 ], who showed that exercise training for 16


week, 5  days/week 40  min/day below 55–60% VO2max did not achieve protection


against IRI. Unfortunately, the earlier studies did not provide information regarding


exercise intensity used in terms of VO2max. Regardless, it is feasible that there may


be an exercise intensity threshold above which cardioprotection is achieved and that


the amount of cardioprotection is proportional to exercise intensity [ 24 , 86 ].


Controversially, Lennon et al. [ 87 ] concluded that both moderate- (i.e., 60 min/

day at 50% VO2max) and relatively high-intensity exercise (i.e., 60 min/day at 70%


VO2max) performed during three consecutive days appear to be equally protective


against IR-induced myocardial stunning. The discrepancy in results may be due to


10 Cardiac Ischemia/Reperfusion Injury: The Bene cial Effects of Exercise

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