Cardiac enlargement that occurs in salmonids and some other species is associated with reproductive maturation in male, but not female, fish. This sexual dichotomy results in hearts from mature males being 20–90% larger than those of mature females (Luk'yanenko and Raspopov, 1972
, Franklin and Davie, 1992; Graham and Farrell, 1992; West and Driedzic, 1999). Functionally, this increases maximum cardiac stroke volume (VSmax) and power output (POmax) (Franklin and Davie, 1992), and is hypothesized to support the increased functional demands placed on the hearts of male fish during spawning. Elevated levels of androgens (testosterone, 11-ketotestosterone) stimulate this cardiac growth (Thorarensen et al., 1996; Davie and Thorarensen, 1997), and increase the proportion of compact myocardium without compromising coronary capillary density (Clark and Rodnick, 1998; R. V. Clark and K. J. Rodnick, unpublished data). However, whether androgen-induced myocardial growth is hypertrophic or hyperplastic has not been resolved. Bailey et al. (1997) concluded that cardiac enlargement in maturing rainbow trout is mainly due to hyperplasia, whereas Clark and Rodnick (1998) indicate that cardiac growth in male trout results from hypertrophy and not hyperplasia. The use of different methodologies (DNA/protein ratios vs cardiocyte morphometics) may have contributed to these opposing views, and so further study is required to resolve the relative contributions of cardiomyocyte hyperplasia and hypertrophy to heart growth in maturing male trout.
The trout heart has a significant population of androgen receptors (Pottinger, 1988; Fitzpatrick et al., 1994), which probably mediate the increased protein synthesis needed for maturation-induced cardiac enlargement in response to elevated levels of circulating androgens. However, Clark and Rodnick (1999) provide evidence for two scenarios where changes in haemodynamics with maturation may also promote ventricular hypertrophy. For example, an androgen-dependent expansion of blood volume could increase both venous pressure and VS (through the Starling response), and cause stretch-induced remodeling. Similarly, work-induced remodeling could occur if androgens increase blood pressure through alterations in vascular tone and resistance.
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