Although the mitochondrial metabolism responses to warm acclimation have been widely studied in fish, the time course of this process is less understood. Here, we characterise changes of rainbow trout (Oncorhyncus mykiss) cardiac mitochondrial metabolism during acute warming from 10 to 16°C, and during the subsequent warm acclimation for 39 days (D). We repeatedly measured mitochondrial O2 consumption in cardiac permeabilized fibers and functional integrity of mitochondria (i.e. mitochondrial coupling and cytochrome c effect) at two assay temperatures (10 and 16°C), as well as citrate synthase (CS) and lactate dehydrogenase (LDH) activities at room temperature. LDH and CS activities significantly increased between D0 (10°C acclimated fish) and D1 (acute warming to 16°C), while mitochondrial O2 consumption measured at respective in vivo temperatures did not change. Enzymatic activities and mitochondrial O2 consumption rates significantly decreased by D2, and remained stable during warm acclimation (D2-39). The decrease in rates of O2 between D0 and D1 coincided with an increased cytochrome c effect and a decreased mitochondrial coupling, suggesting a structural/functional impairment of mitochondria during acute warming. We suggest that after two days of warm acclimation, a new homeostasis is reached, which may involve removal of dysfunctional mitochondria. Interestingly, from D2 onward, there was a lack of differences in mitochondrial O2 consumption rates between the assay temperatures, suggesting that warm acclimation reduces the acute thermal sensitivity of mitochondria. This study provides significant knowledge on the thermal sensitivity of cardiac mitochondria that is essential to delineate the contribution of cellular processes to warm acclimation.
- Received October 29, 2016.
- Accepted February 13, 2017.
- © 2017. Published by The Company of Biologists Ltd