Thermal relations in sled dogs before and after exercise.

Regulation of internal body temperature (Tb), or thermoregulation, is an evolutionarily conserved trait that places demand on basal metabolic rate of endothermic animals. Across species, athletes generate increased quantities of heat in comparison to their nonathletic counterparts and, therefore, must mediate physiological unbalance by upregulating the effectiveness of their heat dissipation abilities. Canine athletes are no exception to this phenomenon, however, with literature denoting body temperatures lower than nonathletic canines, it is clear they must possess adaptations to mitigate this demand. With VO2 max measurements of more than 200 mL/kg/min in sled dogs with mild training to 300 mL/kg/min in highly trained animals, sled dogs are a prime example of athleticism in canines. Seeking to determine correlations between Tear and body mass, morphology, and age of canine athletes, core body temperature (Tb) was measured with an instant ear thermometer, using Tear as a correlate before and after a 2-mile run. In addition, we employed thermal imaging analysis to capture body-wide heat dissipation patterns in sled dogs, and focused on thermal variation of mouth (Tmouth), nose (Tnose), and eyes (Teye). Furthermore, we looked at correlations between thermal variability across these four tissues and head morphology of each dog. Tear was consistently the highest temperature across all tissues measured, with a 1.5°C increase between pre- to postexercise (p < 0.001). Thermal imaging revealed significant positive correlations between Tmouth and body mass 15 min postexercise (p = 0.0023) as well as significantly negative correlations between Tnose and body mass at before exercise (p = 0.0468), Teye and nose length after run (p = 0.0076), and Tmouth and nose length after run (p = 0.0110). As body temperature rises during exercise, it becomes increasingly important to regulate blood flow throughout the body to supply working tissues with oxygen. This demand is offset by the role of the snout in evaporative cooling through panting, functioning as a prime location for heat dissipation and therefore maintaining significant relationships with many other vascularized tissues.

Cellular metabolic pathways of aging in dogs: could p53 and SIRT1 be at play?

Aging and cancer seem to be closely associated, such that cancer is generally considered a disease of the elderly in both humans and dogs. Additionally, cancer is a metabolic shift in itself towards aerobic glycolysis. Larger dog breeds with shorter lifespans, and increased glycolytic cellular metabolic rates, die of cancer more often than smaller breeds. The tumor suppressor p53 factor is a key suppressor oncogene, and the p53 pathway arrests cellular proliferation and prevents DNA mutations from accumulating during cellular stress. The p53 pathway is also associated with the control of cellular metabolism to prevent cellular metabolic shifts common to cancerous phenotypes. SIRT1 deacetylates the p53 tumor suppressor protein, downregulating p53 via effects on stability and activity during stress. Here, we used primary fibroblast cells from small and large puppies and old dogs. Using UV radiation to upregulate the p53 system (100 J/m2), control cells and UV-treated cells were used to measure aerobic and glycolytic metabolic rates using a Seahorse XFe96 oxygen flux analyzer. We also quantified p53 expression and SIRT1 concentration in canine primary fibroblasts before and after UV treatment. We demonstrate that, due to a higher p53 nuclear to cytoplasmic ratio in large breed dogs after UV treatment, p53 could have a more regulatory effect on large breed dogs' metabolism compared with smaller breeds. Thus, there may be a link between p53 upregulation and inhibition of glycolysis in large breed dogs during times of cellular stress compared with small breed dogs. However, SIRT1 concentrations decrease with age in domestic dogs of both size classes, suggesting a possible release of inhibition of p53 through the SIRT1 pathway with age. This may lead to increased incidences of cancer, especially due to the more pronounced upregulation of p53 with cellular stress.