Exercise training modifies myocardial mitochondria and myofibril growth in spontaneously hypertensive rats.
We tested the hypothesis that exercise training provides a stimulus that could modify the decrement in mitochondria-to-myofibril volume ratio characteristic of myocardial cells hypertrophied in response to a pressure overload. Spontaneously hypertensive rats (SHR) were trained 5 days/wk on a treadmill at 70-90% maximal VO2 between the ages of 6 and 16 wk corresponding to the development of hypertension and cardiac hypertrophy. The training program increased maximal VO2 and effected a resting bradycardia but did not alter blood pressure, left ventricular hypertrophy, or peak cardiac output. Our stereological data from electron micrographs shows that the decrement in mitochondrial volume density and the increase in myofibril volume density characteristic of SHR compared with their normotensive controls (WKY, Wistar-Kyoto rats) were reversed. Thus the relative volumes of mitochondria and myofibrils and their ratio in trained SHR were similar to those of the WKY group. The similarity was noted in myocytes from both the subepicardium and subendocardium. These data suggest that exercise training facilitates a proportional growth of energy-producing and energy-consuming organelles in SHR and that this effect is not secondary to modification of blood pressure or left ventricular mass.
D000818:Animals; D002455:Cell Division; D006128:Growth; D006439:Hemodynamics; D006973:Hypertension / Q000503:physiopathology*; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D009210:Myofibrils / Q000502:physiology*; D009929:Organ Size; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal; D010807:Physical Endurance; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains