We employed the work-loop method to study the ability of ventricular and atrial trabeculae from Atlantic cod to sustain power production during repeated contractions at acclimation temperatures (10°C) and when acutely warmed (20°C). Oxygen tension (PO₂) was lowered from 450 to 34% air saturation to augment the thermal stress. Preparations worked under conditions simulating either a large stroke volume (35 min^-1 contraction rate, 8-12% muscle strain) or a high heart rate (70 min^-1 rate, 2-4% strain), with power initially equal under both conditions. The effect of declining PO₂ on power was similar under both conditions, but was temperature and tissue dependent. In ventricular trabeculae at 10°C (and atria at 20°C), shortening power declined across the full range of PO₂ studied whereas the power required to lengthen the muscle was unaffected. Conversely, in ventricular trabeculae at 20°C, there was no decline in shortening power but an increase in lengthening power when PO₂ fell below 100% air saturation. Finally, when ventricular trabeculae were paced at rates up to 115 min^-1 at 20°C (vs. the maximum of 70 min^-1 in vivo), they showed marked increases in both shortening and lengthening power. Our results suggest that while elevated heart rates may not impair ventricular power as they commonly do isometric force, limited atrial power and the increased work required to expand the ventricle during diastole may compromise ventricular filling, and hence stroke volume, in Atlantic cod at warm temperatures. Neither large strains nor high contraction rates convey an apparent advantage in circumventing this.