In Japan, spiked fish in a pre-rigor state have extremely high commercial value, similar to that of live fish. It has been claimed that the progress of rigor mortis is slower in carp acclimated to 10°C than in fish acclimated to 30°C during storage at either 0°C or I0°C. Wild specimens of plaice captured from cold waters in winter also show retarded rigor-mortis progress at 10°C compared with fish captured from warm water in other seasons.
Two factors are supposed to be associated with such temperature-dependent rigor-mortis progress in fish. One is intracellular Ca²⁺ concentration and myofibrillar adenosine triphosphate (ATP) consumption-enhanced by the increase of Ca²⁺, which is released from the sarcoplasmic reticulum (SR; the Ca²⁺-storing organelle in muscle) via nervous stimuli. Ca²⁺ uptake by SR is very low at 0°C due to a low activity of Ca²⁺-ATPase for the Ca²⁺ pump. Subsequently, fish rigor mortis is accelerated at 0°C due to the increase of intracellular Ca²⁺ concentration. The other factor is ATP synthesis in mitochondria. We have recently found that the content of mitochondrial ATP synthase (FoF1-ATPase) was higher in carp acclimated to 10°C than in fish acclimated to 30°C. Oligomycin-sensitive FoF1-ATPase activity per mitochondrial protein weight was three times higher in carp acclimated to 10°C than 30°C. Furthermore, plaice and red seabream adapted to about 10°C contained larger quantities of ATP synthase than fish acclimated to about 25°C, irrespective of species. These changes suggest that alterations in FoF1-ATPase, functioning at the final step of ATP production, are related to the progress of rigor mortis in
fish.