As an example of applying the evidential approach to statistical inference, we address one of the longest standing controversies in ecology, the evidence for, or against, a universal metabolic scaling relationship between metabolic rate and body mass. Using fish as our study taxa, we curated 25 studies with measurements of standard metabolic rate, temperature, and mass, with 55 independent trials and across 16 fish species and confronted this data with flexible random effects models. To quantify the body mass – metabolic rate relationship, we perform model selection using the Schwarz Information Criteria (ΔSIC), an established evidence function. Further, we formulate and justify the use of ΔSIC intervals to delineate the values of the metabolic scaling relationship that should be retained for further consideration. We found strong evidence for a metabolic scaling coefficient of 0.89 with a ΔSIC interval spanning 0.82 to 0.99, implying that mechanistically derived coefficients of 0.67, 0.75, and 1, are not supported by the data. Model selection supports the use of a random intercepts and random slopes by species, consistent with the idea that other factors, such as taxonomy or ecological or lifestyle characteristics, may be critical for discerning the underlying process giving rise to the data. The evidentialist framework applied here, allows for further refinement given additional data and more complex models.
Thermal acclimation is a key process enabling ectotherms to cope with temperature change. To undergo a successful acclimation response, ectotherms require energy and nutritional building blocks obtained from their diet. However, diet is often overlooked as a factor that can alter acclimation responses. Using a temperate omnivorous fish, opaleye (Girella nigricans), as a model system, we tested the hypotheses that 1) diet can impact the magnitude of thermal acclimation responses and 2) traits vary in their sensitivity to both temperature acclimation and diet. We fed opaleye a simple omnivorous diet (ad libitum Artemia sp. and Ulva sp.) or a carnivorous diet (ad libitum Artemia sp.) at two ecologically relevant temperatures (12 and 20°C) and measured a suite of whole animal (growth, sprint speed, metabolism), organ (cardiac thermal tolerance), and cellular-level traits (oxidative stress, glycolytic capacity). When opaleye were offered two diet options compared to one, they had reduced cardiovascular thermal performance and higher standard metabolic rate under conditions representative of the maximal seasonal temperature the population experiences (20°C). Further, sprint speed and absolute aerobic scope were insensitive to diet and temperature, while growth was highly sensitive to temperature but not diet, and standard metabolic rate and maximum heart rate were sensitive to both diet and temperature. Our results reveal that diet influences thermal performance in trait-specific ways, which could create diet trade-offs for generalist ectotherms living in thermally variable environments. Ectotherms that alter their diet may be able to regulate their performance at different environmental temperatures.
Fish physiological performance is directly regulated by their thermal environment. Intraspecific comparisons are essential to ascertain the vulnerability of fish populations to climate change and to identify which populations may be more susceptible to extirpation and which may be more resilient to continued warming. In this study, we sought to evaluate how thermal performance varies in coastal cutthroat trout (Oncorhynchus clarki clarki) across four distinct watersheds in OR, USA. Specifically, we measured oxygen consumption rates in trout from the four watersheds with variable hydrologic and thermal regimes, comparing three ecologically relevant temperature treatments (ambient, annual maximum and novel warm). Coastal cutthroat trout displayed considerable intraspecific variability in physiological performance and thermal tolerance across the four watersheds. Thermal tolerance matched the historical experience: the coastal watersheds experiencing warmer ambient temperatures had higher critical thermal tolerance compared with the interior, cooler Willamette watersheds. Physiological performance varied across all four watersheds and there was evidence of a trade-off between high aerobic performance and broad thermal tolerance. Given the evidence of climate regime shifts across the globe, the uncertainty in both the rate and extent of warming and species responses in the near and long term, a more nuanced approach to the management and conservation of native fish species must be considered.
Annual hypoxia in the Chesapeake Bay has expanded to the point where Darwinian fitness of juvenile striped bass (Morone saxatilis) may depend on their ability to perform in low-oxygen environments. The locomotion they use in predator/prey dynamics relies primarily on white (type II) muscle that is powered by anaerobic metabolic pathways and has generally been thought to be immune to aquatic hypoxia. We tested the sprint performance of 15 juvenile striped bass twice under acute hypoxia (20% air saturation [AS]) 5 wk apart and once under normoxia (>85% AS) in between. Average sprint performance was lower under the first hypoxia exposure than in normoxia and increased in the second hypoxia test relative to the first. The rank order of individual sprint performance was significantly repeatable when comparing the two hypoxia tests but not when compared with sprint performance measured under normoxic conditions. The maximum sprint performance of each individual was also significantly repeatable within a given day. Thus, sprint performance of striped bass is reduced under hypoxia, is phenotypically plastic, and improves with repetitive hypoxia exposures but is unrelated to relative sprint performance under normoxia. Since energy to fuel a sprint comes from existing ATP and creatine phosphate stores, the decline in sprint performance probably reflects reduced function of a part of the reflex chain leading from detection of aversive stimuli to activation of the muscle used to power the escape response.
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