Microvascular and biochemical compensation during ventricular hypertrophy in male rainbow trout

We investigated whether there are compensatory changes in the coronary microvasculature, cardiac lipid metabolism, and myocyte ultrastructure associated with ventricular enlargement in male rainbow trout. Epicardial tissue was sampled at different stages of sexual maturation, and we estimated arterial capillary density, intercapillary diffusion distance, and applied a diffusion model to predict PO₂ at different workloads. We also measured biochemical indices of lipid metabolism and estimated fractional volumes of mitochondria and myofibrils in myocytes. Immature fish with nonenlarged ventricles had the highest capillary length densities (1620±158 mm mm⁻³). Maturing trout with moderate ventricular hypertrophy had lower capillary length densities (1103±58 mm mm⁻³) and similar diffusion distances (13.9±0.7 μm) compared with immature fish (11.7±0.9 μm). The largest ventricles had intermediate capillary length densities (1457±288 mm mm⁻³) and diffusion distances (12.8±0.8 μm). Modelling predicted that enlarged ventricles would not become anoxic even at maximal workloads. Biochemical markers of fatty acid metabolism and aerobic capacity were unchanged with hypertrophy. Volume densities of mitochondria and myofibrils were also not influenced by cardiac growth. In summary, ventricle hypertrophy results in expansion of the coronary capillary bed and the maintenance of the epicardial capacities for fat and oxidative metabolism.