Temperature has a dramatic effect on the physiology of ectothermic animals, impacting most of their biology. When temperatures increase above optimal for an animal, their growth gradually decreases. The main mechanism behind this growth rate reduction is unknown. Here, we suggest the 'aerobic scope protection' hypothesis as a mechanistic explanation for the reduction in growth. After a meal, metabolic rate, and hence oxygen consumption rate, transiently increases in a process called specific dynamic action (SDA). At warmer temperatures, the SDA response usually becomes temporally compressed, leading to a higher peak oxygen consumption rate. This peak in oxygen consumption rate takes up much of the animal's aerobic scope (the difference between resting and maximum rates of oxygen consumption), leaving little residual aerobic scope for other functions (e.g. foraging, predator avoidance, immune function). We propose that water-breathing ectothermic animals will protect their postprandial residual aerobic scope by reducing meal sizes in order to regulate the peak SDA response during times of warming, leading to reductions in growth. This hypothesis is consistent with the published literature on fishes, and we suggest predictions to test it.
Temperature has a dramatic effect on the physiology of ectothermic animals, impacting most of their biology. When temperatures increase above optimal for an animal, their growth rate tends to decrease. The mechanism behind this growth rate reduction is unknown. Here, we suggest the aerobic scope protection hypothesis as a mechanistic explanation for the reduction in growth. After a meal, metabolic rate, and hence oxygen consumption rate, transiently increases in a process called specific dynamic action (SDA). At warmer temperatures, the SDA response becomes temporally compressed, leading to a higher peak oxygen consumption rate. This peak in oxygen consumption rate takes up much of the animal’s aerobic scope (the difference between maximum and resting rates of oxygen consumption), leaving little residual aerobic scope for other functions. We propose that animals will actively protect their postprandial residual aerobic scope by reducing meal sizes in order to regulate the peak SDA response. This hypothesis is consistent with the published literature and we suggest further predictions to test it.
The 2010 Deepwater Horizon (DWH) oil spill in the Gulf of Mexico was the largest spill in recent history and led to the exposure of many commercially and ecologically important fish species. Crude-oil exposure is known to result in compromised cardiorespiratory function and swim performance of fishes, presumably altering ecological performance by impairing the ability to capture prey or evade predators. However, this has yet to be empirically tested. This study assessed the impacts of oil exposure on thigmotaxis (avoidance of exposed areas), routine activity, and prey-capture ability in larval red drum (Sciaenops ocellatus) by using environmentally relevant concentrations of weathered-oil water-accommodated fractions (0–55.9µgL–1 of total polycyclic aromatic hydrocarbons, ΣPAH). Oil exposure caused a dose-dependent increase in time spent in the exposed area of the arena, with an average three-fold increase at the highest dose, suggesting increased risk-taking. Although increased risk-taking resulted in 14% more area explored, oil-exposed individuals were significantly slower to catch prey and caught 67% less prey overall. Prey-capture ability did not appear to be related to cardiorespiratory or swimming impairments, because oil-exposed fish exhibited routine swim speeds and the distance travelled similar to those of the control, suggesting an alternate route of toxicity, such as cognitive impairments.
Winter dormancy is a seasonal survival strategy common among temperate ectotherms, characterized by inactivity, fasting, and low metabolic rates. Previous reports of metabolic rate depression (MRD) in winter-dormant ectotherms, including many fishes, may result from confounding influences of temperature-dependent variation in activity on metabolic rate measurements. We hypothesize that, as demonstrated recently in the winter-dormant cunner (Tautogolabrus adspersus), inactivity and the passive physicochemical (Arrhenius) effect of cold on standard metabolic rate (SMR) are the common primary mechanisms underlying the low metabolic rates among winter-dormant fishes. Using automated video tracking, we investigated threshold temperatures for winter dormancy onset (major reductions in activity, increased sheltering, and fasting) in four phylogenetically-diverse teleost species reported to be winter dormant: cunner, pumpkinseed sunfish (Lepomis gibbosus), American eel (Anguilla rostrata), and mummichog (Fundulus heteroclitus). All species showed large activity and feeding reductions, but the magnitude of change and dormancy threshold temperature was species-specific. We propose that a continuum of overwintering responses exists among fishes from dormant to lethargic to active. The relationship between activity and metabolic rate was then measured using video-recorded automated respirometry during acute cooling and following cold acclimation in pumpkinseed, mummichog, and eel. In all species, activity and metabolic rate were strongly correlated at all temperatures, and cooling caused reduced activity and metabolic rate. When variation in activity was controlled for across temperatures spanning the dormancy thresholds, the thermal sensitivity of metabolic rate including SMR indicated the predominance of passive physicochemical influences (mean Q10<3.5), rather than active MRD. Activity reductions and physicochemical slowing of metabolism due to cold appear to be the primary energy saving mechanisms in overwintering fishes.
Fishes exposed to crude oil have shown reduced sociability and poor habitat selection, which corresponded with increased predation risk. However, the contribution of oil-induced cardiorespiratory impairments to these findings is uncertain. This study explores the effect of oil exposure on predation risk in a model fish species, Sciaenops ocellatus, across a suite of physiological and behavioral end points to elucidate the mechanisms through which any observed effects are manifested. Using mesocosms to assess group predator avoidance, oil exposure to 36.3 μg l–1 ΣPAH reduced the time to 50% mortality from a mean time of 80.0 (74.1–86.0 95% confidence interval [CI]) min to 39.2 (35.6–42.8 95% CI) min. The influence of oil impaired cardiorespiratory and behavioral pathways on predation risk was assessed based on respiratory performance, swim performance, sociability, and routine activity. Swim trials demonstrated that cardiorespiratory and swim performance were unaffected by exposures to 26.6 or 100.8 μg l–1 ΣPAH. Interestingly, behavioral tests revealed that exposure to 26.6 μg l–1 ΣPAH increased distance moved, speed, acceleration, and burst activity. These data indicate that behavioral impairment is more sensitive than cardiorespiratory injury and may be a more important driver of downstream ecological risk following oil exposure in marine species.
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