TOWARDS A MOLECULAR EXPLANATION OF THE HIGH-PERFORMANCE OF THE TUNA HEART

The tuna heart is capable of sustaining cardiac outputs that are high relative to other active teleost species. The question as to whether t here are known molecular mechanisms to explain this phenomenon is exam ined. Unfortunately, the evidence at present is scant but the paper at tempts to put existing knowledge into a contextual framework. It is kn own that the high cardiac outputs in tuna are due to the maximum heart races that are high relative to other active teleost species. While t he normalized stroke volume (ml/kg body weight) in tuna is in the same range as that of trout several important points are worth noting. The stroke volume in the tuna heart is generated in the face of an afterl oad that is two-fold higher (due to high ventral aortic pressure) than that observed in the trout or other teleosts. Since the stroke volume is predicated on the strength of ventricular contraction, the questio n then arises as to whether this is a consequence of factors intrinsic or extrinsic to the design of the cardiomyocytes that make up the myo cardium. Two important extrinsic factors must be noted: the substantia lly higher normal operating temperatures and the apparent cardiac hype rplasia in the tuna. While the merit of these factors is discussed, th e paper focuses on intrinsic factors. There is very little that has be en determined to date that would indicate substantive changes in the d esign of the myocyte in the tuna heart compared to that of trout. Are these extrinsic factors alone then sufficient to account for the impre ssive cardiac output capabilities in the tuna?