Morphometry of exercise-induced right ventricular hypertrophy in the rat.

Abstract

In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for 7 weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria:myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.

Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats

“…At the structural level, the increase in cardiomyocyte length results from the addition of sarcomeres in series and is characteristic of volume overload cardiac hypertrophy [39], whereas the insertion of new sarcomeric units in parallel produces the transverse enlargement of cardiomyocytes present in pressure overload hypertrophy [40]. Moreover, normal myocardial levels of skeletal α-actin have been reported in volume overload states, whereas pressure overload seems to be associated with enhanced levels of this fetal protein [41,42].…”

Quantification of Extracellular and Intracellular Adenosine Production

“…The tissue inosine content (nmol/g) was converted into a concentration (mol/L), assuming that tissue inosine was restricted to intracellular regions, which constitute 0.60 mL/g tissue. 13 The respective tissue/venous perfusate concentration ratio increased from 24.5 (control) to 488 after 20 minutes of NBTI (Figure 3). …”

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

“…Until recently, findings appeared somewhat contradictory. Treadmill running with fixed exercise intensity induced only minor increments in ventricular mass and cardiomyocyte dimensions (2,3,28,29) or did not induce any effects (16,18). However, 10-20% improvements in V O 2 max and work economy had been demonstrated (16,30).…”

“…In healthy individuals, increased exercise capacity is dependent on functional and structural adaptations in skeletal muscle, blood vessels, and heart. Cardiac adaptation includes increased ventricular chamber volumes and weights, cardiomyocyte hypertrophy, increased cardiac output, and improved contractile function measured in isolated cardiomyocytes and in the intact heart (2,3).…”