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

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induced by exercise, and can serve as protection against pathological cardiac remodeling

in mice. miR-222 expression were resistant to adverse wheel running-induced cardiac

remodeling and dysfunction after ischemic injury [ 55 ]. Another study found that high

intensity aerobic interval training (at 95% of peak heart rate) for about 10 weeks resulted

in an increase mitochondrial density, suggesting higher intensity in exercise training is

required to stimulate mitochondrial biogenesis and cardiac efficiency in the mice heart

[ 42 ]. This study proved the importance of training intensity for provoking metabolic

improvements in the myocardium, thus leading to therapeutic potential of high intensity

aerobic interval training for heart failure patients [ 42 ]. In addition, gender differences in

cardiac hypertrophy could be a factor, exhibiting significant changes in body weight in

response to exercise [ 17 ]. Thus, there is still a need of assessing the possible influence of

sex, age, or species [ 40 ].

Though regular exercise training plays a beneficial function in reducing cardio-

vascular risk, recent studies have documented elevated biomarker levels consistent

with cardiac damage after bouts of prolonged exercise in apparently healthy indi-

viduals without cardiovascular disease [ 64 – 66 ]. In rat exercise study, elevated myo-

cardial injury-related markers after prolonged, exhaustive exercises exceeded those

of in clinical myocardial infarction [ 66 ]. This elevation was accompanied with reac-

tive oxygen species generation-induced oxidative damage in rat myocardium [ 65 ].

Since potential limitations of a specific type of exercise and conditions of the exper-

iment can compromise the exercising rats and mice, appropriate exercise testing and

prescription must be put in place to aid in the assessment and management of car-

diovascular disease [ 23 , 43 ].

There are many inherent differences between rodent and human hearts, particu-

larly cardiac excitation and contractility, that need to be considered when using

small rodents as animal exercise models [ 6 ]. These differences can serve as a hin-

drance in the clinical translation of rodent studies to humans [ 3 , 6 ].

3.3.2 Rabbits

Rabbits are advantageous for research purposes both in cardiovascular health and dis-

ease [ 2 ]. Previous finding used rabbits documented that exercise training can increase

rabbit heart rates from 71 to 112% during peak exercise [ 67 ]. Long term exercise

modalities was applied for the rabbits in low-speed flat treadmill at a speed of 18–20

meters per minute for 40–60 minutes per day to study hypertension and cardiac heart

failure [ 68 , 69 ]. The research described that in rabbit heart failure model, exercise

training evokes an antioxidative effect [ 69 ], suggesting its possibility as a model to be

used in studying myocardial effects of endurance training [ 70 ]. Moreover, endurance

training is known to increase cardiac performance and decrease resting heart rate dur-

ing exercise. The less steep slope of end systolic pressure length relations acquired by

occlusion of the descending aorta in the trained rabbits might indicate a structural

myocardial remodeling and increased contractile reserve [ 1 , 70 ].

A greater functional similarity of rabbit myocardium to humans compared to

small rodents make them a closer representative of the human heart. In addition,

V.T. Thu et al.