Introduction: Congestive heart failure (CHF) patients suffer from functional aerobic impairment. Their reduced cardiac output and impaired O2 delivery to the peripheral muscles shifts them to anaerobic metabolism. Lactate, the major product of anaerobic metabolism crosses the membrane through monocarboxylate proteins (MCT). MCT-1 uptakes lactate whereas MCT-4 expels it. We hypothesized that exercise training might change MCT expression and may affect lactate clearance.
This may explain, in part, the beneficiary effect of exercise training in CHF.
Methods: Rats underwent coronary artery occlusion. Following induction of CHF, the animals were divided into 3 groups: sedentary, moderate intensity exercise training (MAT) and high intensity training (HIT) (n=3 for each). At baseline, a month after surgery, and after exercise period completion, the rats underwent comprehensive physiological and echocardiographic evaluation.
Analyses of the expression of MCT-1 and 4 will take place later.
Results: A month after surgery, rats' exercise capacity (VO2Max) was reduced by 26% (from 94±13 ml/min/kg to 69±10 ml/min/kg), ejection fraction (EF) was reduced by 42% (from 84±7.2% to 49±11%),
GSc (Global circumferential strain) changed from -19.56±5.48% to -11.25±6.22% and end diastolic area (EDA) increased by 27% from 32±5 mm2 to 41±9 mm2. Thus, Cardiac geometry and function were attenuated. In order to evaluate the degree of CHF developed, we calculated the change from baseline (Δ) of the following parameters:,GSc, EF, (-EDA), %FAC (fractional area change). The sum of all was used as a "damage score", a score <-150 was considered significantly CHF damaged rat. The mean pre-exercise score was -235±48, while the post-exercise score was -148±66.9 in both HIT and MAT.
Conclusions: Both exercise training program improved the rats' "damage score" indicating improvement of exercise capacity, cardiac geometry and function after training. A human study will commence shortly.
