Mitochondrial function can provide key insights into how fish will respond to climate change, due to its important role in heart performance, energy metabolism and oxidative stress. However, whether warm acclimation can maintain or improve the energetic status of the fish heart when exposed to short-term heat stress is not well understood. We acclimated Atlantic salmon, a highly aerobic eurythermal species, to 12 and 20 °C, then measured cardiac mitochondrial functionality and integrity at 20 °C and at 24, 26 and 28 °C (this species’ critical thermal maximum ± 2 °C). Acclimation to 20 °C vs. 12 °C enhanced many aspects of mitochondrial respiratory capacity and efficiency up to 24 °C, and preserved outer mitochondrial membrane integrity up to 26 °C. Further, reactive oxygen species (ROS) production was dramatically decreased at all temperatures. These data suggest that salmon acclimated to ‘normal’ maximum summer temperatures are capable of surviving all but the most extreme ocean heat waves, and that there is no ‘tradeoff’ in heart mitochondrial function when Atlantic salmon are acclimated to high temperatures (i.e., increased oxidative phosphorylation does not result in heightened ROS production). This study suggests that fish species may show quite different acclimatory responses when exposed to prolonged high temperatures, and thus, susceptibility to climate warming.

In fishes, the capacity of thermal acclimation to preserve cardiac mitochondrial function under future warming scenarios is important to understand given the central role that cardiac energy metabolism and performance play in this taxa9s thermal tolerance. We acclimated Atlantic salmon to 12 and 20°C (for>2 months), and investigated the effects of acute and chronic warming on cardiac mitochondrial respiration and ROS production (release rate) using high-resolution fluorespirometry. Further, we compared the sensitivity of mitochondrial respiration to nitric oxide (i.e., the NO IC₅₀), and assessed the mitochondrial response to anoxia-reoxygenation (AR). Acute exposure to 20°C increased maximal mitochondrial respiration by ∼55%, however, the mitochondria9s complex I-respiratory control ratio was 17% lower and ROS production was increased by≥60%. Acclimation to 20°C: i) preserved mitochondrial coupling and aerobic capacity; ii) decreased the mitochondria9s ROS production by ∼30%; iii) increased the mitochondria9s NO IC₅₀ by ∼23%; iv) and improved mitochondrial membrane integrity at 20°C. AR did not affect mitochondrial function at 12°C, but acute exposure to 20°C and AR depressed maximal mitochondrial respiration (by ∼9%) and coupling (by ∼16%) without impacting ROS production. Finally, warm acclimation did not improve the capacity of mitochondria to recover from AR, indicating that there was no ‘cross tolerance’ between these challenges. Our findings provide compelling evidence that thermal plasticity of cardiac mitochondrial function contributes to the Atlantic salmon9s capability to survive at≥20°C for prolonged periods, but question whether this plasticity may allow them to withstand high temperatures when combined with other stressors.

In fishes, the effect of O2 limitation on cardiac mitochondrial function remains largely unexplored. The sablefish (Anoplopoma fimbria) encounters considerable variations in environmental oxygen availability, and is an interesting model for studying the effects of hypoxia on fish cardiorespiratory function. We investigated how in vivo hypoxic acclimation (6 months at 40%+3 weeks at 20% air saturation) and in vitro anoxia-reoxygenation affected sablefish cardiac mitochondrial respiration and reactive oxygen species (ROS) release rates using high-resolution fluorespirometry. Further, we investigated how hypoxic acclimation affected the sensitivity of mitochondrial respiration to nitric oxide (NO), and compared mitochondrial lipid and fatty acid (FA) composition between groups. Hypoxic acclimation did not alter mitochondrial coupled or uncoupled respiration, or respiratory control ratio, ROS release rates, P50 or superoxide dismutase activity. However, it increased citrate synthase activity (by∼20%), increased the sensitivity of mitochondrial respiration to NO inhibition [i.e., the NO IC50 was 25% lower], and enhanced the recovery of respiration (by 21%) and reduced ROS release rates (by 25-30%) post-anoxia. Further, hypoxic acclimation altered the mitochondria's FA composition [increasing arachidonic acid (20:4ω6) and eicosapentaenoic acid (20:5ω3) proportions by 11 and 14%, respectively], and SIMPER analysis revealed that the phospholipid: sterol ratio was the largest contributor (24%) to the dissimilarity between treatments. Overall, these results suggest that hypoxic acclimation may protect sablefish cardiac bioenergetic function during or after periods of O2 limitation, and that this may be related to alterations in the mitochondria's sensitivity to NO and to adaptive changes in membrane composition (fluidity).

There is growing evidence that maintenance of ion and water balance determine cold tolerance in many insects. The hindgut of terrestrial insects is critical for maintaining organismal homeostasis as it regulates solute- and water-balance of the hemolymph. Here we used ex vivo everted gut sacs of L. migratoria to examine the effects of temperature (0 - 30°C), thermal-acclimation, hypoxia, and ionic and osmotic forces on bulk water and ion (Na+, K+ and Cl−) movement across the rectal epithelium. These findings were related to simultaneous in vivo measurements of water and ion balance in locusts exposed to similar temperatures. As predicted, we observed a critical inhibition of net water and ion reabsorption at low temperature that is proportional to the in vivo loss of water and ion homeostasis. Further, cold-acclimated locust, known to defend ion and water balance at low temperature, were characterised by improved reabsorptive capacity at low temperature. These findings strongly support the hypothesis that transport mechanisms in the hindgut at low temperature are essential for cold tolerance. The loss of osmoregulatory capacity at low temperature was primarily caused by reduced active transport while rectal paracellular permeability to fluorescein isothiocyanate dextran was unchanged at 0 and 30°C. During cold exposure, water reabsorption was independent of major cation gradients across the epithelia while reduction in mucosal Cl− availability and increase in mucosal osmolality markedly depressed water reabsorption. These findings are discussed in perspective of existing knowledge and with suggestions for future physiological studies on cold acclimation and adaptation in insects.

Nitrite secures essential nitric oxide (NO) bioavailability in hypoxia at low endogenous concentrations, whereas it becomes toxic at high concentrations. We exposed brown trout to normoxic and hypoxic water in the absence and presence of added ambient nitrite to decipher the cellular metabolism and effects of nitrite at basal and elevated concentrations under different oxygen regimes. We also tested hypotheses concerning influences of nitrite on branchial nitric oxide synthase (NOS), Na⁺/K⁺-ATPase (nka) and heat shock protein (hsp70) mRNA expression. Basal plasma and erythrocyte nitrite levels were higher in hypoxia than normoxia, suggesting increased NOS activity. Nitrite exposure strongly elevated nitrite concentrations in plasma, erythrocytes, heart tissue and white muscle, which was associated with an extensive metabolism of nitrite to nitrate and to iron-nitrosylated and S-nitrosated compounds. Nitrite uptake was slightly higher in hypoxia than normoxia, and high internal nitrite levels extensively converted blood hemoglobin to methemoglobin and nitrosylhemoglobin. Hypoxia increased inducible NOS (iNOS) mRNA levels in gills, which was overruled by a strong inhibition of iNOS expression by nitrite in both normoxia and hypoxia, suggesting negative feedback regulation of iNOS gene expression by nitrite. A similar inhibition was absent for neuronal NOS. Branchial NKA activity stayed unchanged, but mRNA levels of the NKA α1a subunit increased with hypoxia and nitrite, which may have countered an initial NKA inhibition. Nitrite also increased hsp70 gene expression, probably contributing to cytoprotective effects of nitrite at low concentrations. Nitrite displays a concentration-dependent switch between positive and negative effects resembling other signaling molecules.