Abstract

Omega-3 fatty acids have been implicated in the amelioration of cardiovascular disease in humans. Since these fatty acids are found in salmonid fish and are known to be essential for all salmonids, this study was undertaken to determine the effect of a high dietary intake of omega-3 fatty acids on the function of trout myocardium. Rainbow trout (Oncorhynchus mykiss) from a single stock population were divided into two groups and fed either a diet high in omega-3 fatty acids (i.e. 4.0%) or low in omega-3 fatty acids (i.e. 2.1%) for 3 months. Heart function was studied at the whole heart and isolated muscle level. In whole heart preparations, peak developed pressures in freely ejecting hearts from salmonids fed the high omega-3 fatty acid diet were significantly greater than the hearts from salmonids fed the low omega-3 fatty acid diet (21 +/- 1.5 vs. 11.5 +/- 0.9 mmHg respectively, P < 0.05). These data correlated with results from isolated muscle preparations of myocardium from fish fed high and low omega-3 fatty acid diets (4.12 +/- 0.32 vs. 3.08 +/- 0.28 mN/mm2 respectively, P < 0.05). The calcium uptake rate of heart homogenates from fish fed the high omega-3 diet was slower and sarcoplasmic reticulum Ca2+ ATPase activity was lower. The myofilament force-calcium relationship in myocardium from trout fed the low omega-3 diet was shifted leftward on the calcium axis to lower intracellular calcium concentrations (delta 0.4 pCa units) compared to mammalian myocardium. This resulted in greater activation at lower intracellular calcium concentrations. However, trouts fed diets high in omega-3 fatty acids had [Ca2+] required for half maximal activation more similar to what has been reported for mammalian myocardium (delta 0.1 pCa unit). Furthermore, the myofilaments of trout hearts appear to show less cooperativity (Hill coefficient approximately 1) than has been found in mammalian myocardium (Hill coefficient > or = 2). Our experimental results demonstrate for the first time that dietary omega-3 fatty acid content affects myocardial force of contraction by affecting calcium metabolism and myofilament calcium-activation.

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