Relative ventricular mass, percent compact myocardium, total protein, DNA content, and myocyte size were determined for rainbow trout, Salmo gairdneri, ranging in size from 10 to 2000 g. Ventricular mass, ventricular total protein, and DNA content increased linearly with body size. The DNA to protein ratio was reduced slightly over a 100-fold range of body size. Myocyte size increased with heart size. However, the estimated 1.7-fold increase in myocyte volume for a 10-fold increase in heart weight was incompatible with a corresponding 10-fold increase in total protein. Since DNA content increased 10-fold it is suggested that long-term cardiac growth in rainbow trout involves both hyperplasia and hypertrophy.

Rainbow trout, Oncorhynchus mykiss, were exercise trained for 28–52 days. Trained fish were 13% larger and swam 12% faster in an aerobic swimming test. Training induced cardiac growth that was isometric with body growth, since ventricle mass relative to body mass was constant. The proportions of compact and spongy myocardia in the ventricle were also unchanged by training. Trained fish had significantly higher levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase in both compact and spongy myocardium. Ligation of a 0.5- to 1.0-cm section of the coronary artery produced only a temporary interruption of coronary flow to the compact myocardium because new vessels grew around the ligation site in the majority of fish during the 28- to 52-day experiment. Nonetheless, coronary ligation resulted in a significantly smaller (17%) proportion of compact myocardium with lower levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase. Exercise-induced increases in the levels of these enzymes in the compact myocardium were prevented by coronary ligation. The decrease of enzymes in the compact myocardium as a result of coronary ligation was compensated for by a 30% increase in the levels of the aerobic enzymes citrate synthase and β-hydroxyacyl CoA dehydrogenase and a 32% increase in the mass of spongy myocardium. As a result of these compensations and coronary regrowth, chronic coronary ligation did not affect maximum prolonged swimming speed. These experiments clearly reveal that cardiac plasticity allows compensatory changes that are necessary for the heart to maintain adequate oxygen delivery to exercising skeletal muscle. The compensatory changes were isometric increases in heart mass or proportionately larger increases in heart mass and compact tissue if the coronary artery was ligated and an increase in metabolic enzymes associated with ATP generation, namely, citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase.

The HemoCue haemoglobin analyser consistently overestimated haemoglobin concentration ([Hb]) in the blood of all fish species (sockeye salmon Oncorhynchus nerka, Chinook salmon Oncorhynchus tshawytscha, Pacific bluefin tuna Thunnus orientalis and chub mackerel Scomber japonicus) by 22-50% (9Á9-36Á0 g l

This review examines selected areas of cardiovascular physiology where there have been impressive gains of knowledge and indicates fertile areas for future research. Because arterial blood is usually fully saturated with oxygen, increasing cardiac output is the only means for transferring substantially more oxygen to tissues. Consequently, any behavioural or environmental change that alters oxygen uptake typically involves a change in cardiac output, which in fishes can amount to a threefold change. During exercise, not all fishes necessarily have the same ability as salmonids to increase cardiac output by increasing stroke volume; they rely more on increases in heart rate instead. The benefits associated with increasing cardiac output via stroke volume or heart rate are unclear. Regardless, all fishes examined so far show an exquisite cardiac sensitivity to filling pressure and the cellular basis for this heightened cardiac stretch sensitivity in fish is being unraveled. Even so, a fully integrated picture of cardiovascular functioning in fishes is hampered by a dearth of studies on venous circulatory control. Potent positive cardiac inotropy involves stimulation of sarcolemmal β-adrenoceptors, which increases the peak trans-sarcolemmal current for calcium and the intracellular calcium transient available for binding to troponin C. However, adrenergic sensitivity is temperature-dependent in part through effects on membrane currents and receptor density. The membrane currents contributing to the pacemaker action potential are also being studied but remain a prime area for further study. Why maximum heart rate is limited to a low rate in most fishes compared with similar-sized mammals, even when Q10 effects are considered, remains a mystery. Fish hearts have up to three oxygen supply routes. The degree of coronary capillarization circulation is of primary importance to the compact myocardium, unlike the spongy myocardium, where venous oxygen partial pressure appears to be the critical factor in terms of oxygen delivery. Air-breathing fishes can boost the venous oxygen content and oxygen partial pressure by taking an air breath, thereby providing a third myocardial oxygen supply route that perhaps compensates for the potentially precarious supply to the spongy myocardium during hypoxia and exercise. In addition to venous hypoxemia, acidemia and hyperkalemia can accompany exhaustive exercise and acute warming, perhaps impairing the heart were it not for a cardiac protection mechanism afforded by β-adrenergic stimulation. With warming, however, a mismatch between an animal’s demand for oxygen (a Q10 effect) and the capacity of the circulatory and ventilatory systems to delivery this oxygen develops beyond an optimum temperature. At temperature extremes in salmon, it is proposed that detrimental changes in venous blood composition, coupled with a breakdown of the cardiac protective mechanism, is a potential mechanism to explain the decline in maximum and cardiac arrhythmias that are observed. Furthermore, the fall off in scope for heart rate and cardiac output is used to explain the decrease in aerobic scope above the optimum temperature, which may then explain the field observation that adult sockeye salmon ( Oncorhynchus nerka (Walbaum in Artedi, 1792)) have difficulty migrating to their spawning area at temperatures above their optimum. Such mechanistic linkages to lifetime fitness, whether they are cardiovascular or not, should assist with predictions in this era of global climate change.