Timing and frequency of high temperature events bend the onset of behavioural thermoregulation in Atlantic salmon (Salmo salar).

The role of temperature on biological activities and the correspondent exponential relationship with temperature has been known for over a century. However, lacking to date is knowledge relating to (a) the recovery of ectotherms subjected to extreme temperatures in the wild, and (b) the effects repeated extreme temperatures have on the temperatures that induce behavioural thermoregulation (aggregations). We examined these questions by testing the hypothesis that thermal thresholds which initiate aggregations in juvenile Atlantic salmon (AS) (Salmo salar) are not static, but are temporally dynamic across a summer and follow a hysteresis loop. To test our hypothesis, we deployed custom-made underwater camera (UWC) systems in known AS thermal refuges to observe the timing of aggregation events in a natural system and used these data to develop and test models that predict the temperatures that induce thermal aggregations. Consistent with our hypothesis our UWC observations revealed a range of aggregation onset temperatures (AOT) ranging from 24.2°C to 27.1°C, thus confirming our hypothesis that AOTs are dynamic across summer. Our models suggest it take ~ 11 days of non-thermally taxing temperatures for the AOT to rebound in the study river. Conversely, we found that as the frequency of events increased, the AOT declined, from 27.1°C to 24.2°C. Integrating both model components led to more robust model performance. Further, when these models were tested against an independent data set from the same river, the results remained robust. Our findings illustrate the complexity underlying behavioural thermoregulation in AS-a complexity that most likely extends to other salmonids. The frequency of extreme heat events is predicted to increase, and this has the capacity to decrease AOT thresholds in AS, ultimately reducing their resilience to extreme temperature events.

Maternal age alters offspring lifespan, fitness, and lifespan extension under caloric restriction.

Maternal age has a negative effect on offspring lifespan in a range of taxa and is hypothesized to influence the evolution of aging. However, the mechanisms of maternal age effects are unknown, and it remains unclear if maternal age alters offspring response to therapeutic interventions to aging. Here, we evaluate maternal age effects on offspring lifespan, reproduction, and the response to caloric restriction, and investigate maternal investment as a source of maternal age effects using the rotifer, Brachionus manjavacas, an aquatic invertebrate. We found that offspring lifespan and fecundity decline with increasing maternal age. Caloric restriction increases lifespan in all offspring, but the magnitude of lifespan extension is greater in the offspring from older mothers. The trade-off between reproduction and lifespan extension under low food conditions expected by life history theory is observed in young-mother offspring, but not in old-mother offspring. Age-related changes in maternal resource allocation to reproduction do not drive changes in offspring fitness or plasticity under caloric restriction in B. manjavacas. Our results suggest that the declines in reproduction in old-mother offspring negate the evolutionary fitness benefits of lifespan extension under caloric restriction.

Congeneric variability in lifespan extension and onset of senescence suggest active regulation of aging in response to low temperature.

Lifespan extension under low temperature is well conserved across both endothermic and exothermic taxa, but the mechanism underlying this change in aging is poorly understood. Low temperature is thought to decrease metabolic rate, thus slowing the accumulation of cellular damage from reactive oxygen species, although recent evidence suggests involvement of specific cold-sensing biochemical pathways. We tested the effect of low temperature on aging in 11 strains of Brachionus rotifers, with the hypothesis that if the mechanism of lifespan extension is purely thermodynamic, all strains should have a similar increase in lifespan. We found differences in change in median lifespan ranging from a 6% decrease to a 100% increase, as well as differences in maximum and relative lifespan extension and in mortality rate. Low temperature delays reproductive senescence in most strains, suggesting an extension of healthspan, even in strains with little to no change in lifespan. The combination of low temperature and caloric restriction in one strain resulted in an additive lifespan increase, indicating these interventions may work via non- or partially-overlapping pathways. The known low temperature sensor TRPA1 is present in the rotifer genome, but chemical TRPA1 agonists did not affect lifespan, suggesting that this gene may be involved in low temperature sensation but not in chemoreception in rotifers. The congeneric variability in response to low temperature suggests that the mechanism of low temperature lifespan extension is an active genetic process rather than a passive thermodynamic one and is dependent upon genotype.

Physiological effects of environmentally relevant, multi-day thermal stress on wild juvenile Atlantic salmon (Salmo salar).

The frequency of extreme thermal events in temperate freshwater systems is expected to increase alongside global surface temperature. The Miramichi River, located in eastern Canada, is a prominent Atlantic salmon (Salmo salar) river where water temperatures can exceed the proposed upper thermal limit for the species (~27°C). Current legislation closes the river to recreational angling when water temperatures exceed 20°C for two consecutive nights. We aimed to examine how natural thermal variation, representative of extreme high thermal events, affected the thermal tolerance and physiology of wild, juvenile Atlantic salmon. We acclimated fish to four thermal cycles, characteristic of real-world thermal conditions while varying daily thermal minima (16°C, 18°C, 20°C or 22°C) and diel thermal fluctuation (e.g. Δ5°C-Δ9°C). In each cycling condition, we assessed the role that thermal minima played on the acute thermal tolerance (critical thermal maximum, (CTMax)), physiological (e.g. heat shock protein 70 (HSP70), ubiquitin) and energetic (e.g. hepatic glycogen, blood glucose and lactate) status of juvenile Atlantic salmon throughout repeated thermal cycles. Exposure to 16-21°C significantly increased CTMax (+0.9°C) compared to a stable acclimation temperature (16°C), as did exposure to diel thermal fluctuations of 18-27°C, 20-27°C and 22-27°C, yet repeated exposure provided no further increases in acute thermal tolerance. In comparison to the reference condition (16-21°C), consecutive days of high temperature cycling with different thermal minima resulted in significant increases in HSP70 and ubiquitin, a significant decrease in liver glycogen, and no significant cumulative effect on either blood glucose or lactate. However, comparison between thermally taxed treatments suggested the diel thermal minima had little influence on the physiological or energetic response of juvenile salmon, despite the variable thermal cycling condition. Our results suggest that relatively cooler night temperatures in the summer months may play a limited role in mitigating physiological stress throughout warm diel cycle events.