Food deprivation
Long periods of starvation, which occur naturally (Holdway and Beamish, 1984
), and may produce mortality, e.g. in Atlantic cod (Dutil and Lambert, 2000), roach (Griffiths and Kirkwood, 1995) and smallmouth bass (Adams et al., 1982), can significantly decrease swimming endurance (e.g. Atlantic cod; Martinez et al., 2003). Given the importance of cardiac function to aerobic swimming performance (Hughes et al., 1988; Kolok and Farrell, 1994; Keen and Farrell, 1994), one might expect that cardiac alterations after extended periods of food deprivation could seriously compromise heart function. This hypothesis was recently tested by depriving Atlantic cod Gadus morhua of food for 10 weeks at 8°C (A. K. Gamperl et al., unpublished), and measuring cardiac morphometrics, biochemistry, and in situ cardiac performance. Cod deprived of food for 10 weeks were in poor condition (25% lighter, with a 85% decrease in hepatosomatic index), and had smaller hearts that contained dramatically reduced levels of energy substrates (Table 1). However, relative ventricular mass, ventricular protein levels and mass-specific maximum cardiac output (
max expressed in ml min–1 g–1 ventricle, rather than ml min–1 kg–1 body mass) were unchanged (Table 2). These results show that although the heart was not spared during prolonged negative energy balance, the relative performance of the cod heart, and thus its capacity to support swimming capacity, was unaffected. Additional evidence of cardiac remodeling with food deprivation was provided by the 15% reduction in intrinsic fH in food-deprived cod (Table 2). Agnisola et al. (1996) earlier reported a 30% lower heart rate in sturgeon Acipenser naccarii Bonaparte fed diets enriched with either omega-3 polyunsaturated fatty acids or saturated fatty acids. Thus, it is possible that starvation altered the membrane lipid composition of the cardiac pacemaker cells, and effected the change in heart rate.
Exercise training
Aerobic training alters various components of the salmonid cardiovascular system, inducing cardiac growth (Hochachka, 1961; Farrell et al., 1990), and increasing max, certain cardiac enzymes, haematocrit, arterial O2 content, skeletal muscle capillarity and tissue O2 extraction (Hochahcka, 1961; Davie et al., 1986; Farrell et al., 1991; Gallaugher et al., 2001). These exercise-induced changes, however, are often small and variable (Davison, 1989), and even the 25% increase in 
O2max brought about by a 3 month intense training regime (Fig. 1) is small relative to the twofold variability in 
O2max that often exists among individual fish. Thus, although many individual components responsible for internal arterial O2 convection show plasticity, the sum of the changes in individual components produce, at best, about a 25% improvement in metabolic capacity.
Because tissue O2 extraction can increase with training, and the O2 supply to the heart's spongy myocardium comes from oxygen-depleted venous blood (Davie and Farrell, 1991; Farrell and Clutterham, 2003), the possibility exists that training-induced cardiac growth occurs predominantly in the compact myocardium, which receives oxygen-rich coronary arterial blood. This pattern of cardiac growth would be consistent with that seen in sexually maturing male trout (see above); however, this possibility remains to be studied.
Aquaculture
Aquaculture conditions contrast with food deprivation and exercise-training studies in that fish become less active and are often overfed, and cardiac morphology certainly changes in salmonids raised for aquaculture. The normally distinct pyramidal structure of the ventricle (Fig. 2A) becomes more rounded (Fig. 2B,D), resembling the morphology of sedentary fish species (see Santer et al., 1983). Fat deposition can increase around the heart (Fig. 2B,C) and cardiac deformities may develop (Fig. 2E vs F). Further, studies show that the enhanced growth rates associated with aquaculture increase the rate of development of coronary arteriosclerosis (Saunders et al., 1992; Farrell, 2002), and that cultured salmonids have a decreased swimming capacity compared to wild fish (Duthie, 1987; Brauner, 1994; MacDonald et al., 1998). While these observations all point to diminished cardiac performance, direct measurements of cardiac performance in fish displaying the above morphological changes have not been performed. Moreover, two recent studies indicate that maximum cardiac function may not be different between wild and hatchery-reared salmonids. Dunmall and Schreer (2003) examined whether there is a genetic component to domestication by measuring swimming performance and in vivo maximum cardiac function in genetically distinct adult farmed and wild Atlantic salmon raised in identical conditions, and found no difference between the two groups. Further, maximum in situ cardiac function for two groups of pond-reared (domesticated) rainbow trout was found to be no different from either wild or sea-ranched (fish from wild stock, raised in hatcheries until smolts and then released into the wild) steelhead trout (Table 3; A. K. Gamperl et al., unpublished data).
While a definitive answer as to whether aquaculture/domestication affects maximum cardiac function requires more refined/controlled studies, aquaculture practices such as triploidy certainly alter cardiac physiology. Cardiomyocytes are 60% larger in triploid brown trout than in diploid rainbow trout, and they have an increased sensitivity to ryanodine (a blocker of SR Ca2+ release; Mercier et al., 2002). Perhaps the enhanced role for SR calcium release in the contraction of triploid cardiac muscle reflects the decrease in cellular surface to volume ratio associated with cell enlargement and a concomitant limitation to ICavia L-type Ca2+ channels.
When growth rate is further enhanced using growth hormone (GH) transgenic fish, swimming performance and O2max can be either reduced (Farrell et al., 1997; Lee et al., 2003a) or no different (Stevens et al., 1998; McKenzie et al., 2000). With respect to the potential for cardiac changes in GH transgenic fish, we are only aware of one study. Pitkänen et al. (2001) found that the relative ventricular mass (RVM) of GH transgenic animals was enhanced by 60% vs size-matched controls, and suggested, based on non-significant differences in myocardial DNA contents (2.54 mg g–1 in transgenics vs 2.69 mg g–1 in size-matched controls), that this difference was due to hypertrophy alone.
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