Cardiac pathology related to stress and life-style is a major cause of death in humans. It is also an emerging problem for the salmon aquaculture industry. This industry produces semi-domesticated fish in very intensive rearing regimes, and the underlying causes for heart pathology are largely unknown. A recent study showed that the “stress hormone” cortisol induces heart growth in rainbow trout (Oncorhynchus mykiss). Furthermore, increased heart size in fish is associated with up-regulation of several heart disease markers well-known from human cardiology. In the current study, we first aimed at determining the time-course for cortisol-induced heart growth. To this end, we measured relative ventricle size in rainbow trout after 2, 7 and 21 days of non-invasive cortisol administration. This experiment revealed a steep growth phase of the hearts around 21 days of cortisol treatment, with indications of marked growth even earlier. Cortisol mediates its effects on the heart through cardiac mineralocorticoid (MR) and glucocorticoid receptors (GRs). In order to investigate receptor-specific effects of cortisol on heart phenotype and cardiac markers, rainbow trout were administered feed enriched with cortisol alone or in combination with specific cortisol receptor antagonists for 21 days. In the latter experiment, relative ventricle weight was increased by 20% in cortisol-treated fish compared to controls, an increase which was not blocked by any of the antagonists. Heart growth was accompanied by increased mRNA levels of the hypertrophy markers VMHC and SMLC2. Combined with decreased levels of the proliferation marker, PCNA, this indicates that the hearts were growing mainly through hypertrophy. There was a strong tendency towards higher PCNA mRNA levels in fish treated with cortisol in combination with the GR antagonist mifepristone. Similarly, markers of collagen synthesis COL1α1 and COL1α2 mRNAs were significantly decreased by the cortisol treatment, a decrease which was partially blocked by the GR antagonist. This indicates that the suppressing effect of cortisol on COL1α1 and COL1α2, and likely PCNA as well, is mediated through the cardiac GR. No consequence of blocking the cardiac MR by use of spironolactone was seen. However, quite unexpectedly, cortisol suppressed feed intake by an apparent inhibition of the swallowing reflex, and this effect was abolished by the GR antagonist. This observation can explain frequent observations of low feed intake in stressed fish and may have important implications for the aquaculture industry. In conclusion, cortisol administration significantly induces heart growth after 21 days of cortisol treatment. The involvement of the two cortisol receptor types in inducing cardiac remodeling in salmonids remains to be clarified.