bioRxiv Science⌕ Search

bioRxiv · 10.1101/282640

Avian thermoregulation in the heat: is evaporative cooling more economical in nocturnal birds?

Abstract

Evaporative cooling is a prerequisite for avian occupancy of hot, arid environments, and is the only avenue of heat dissipation when air temperatures (Ta) exceed body temperature (Tb). Whereas diurnal birds can potentially rehydrate throughout the day, nocturnal species typically forgo drinking between sunrise and sunset. We hypothesized that nocturnal birds have evolved reduced rates of evaporative water loss (EWL) and more economical evaporative cooling mechanisms than those of diurnal species that permit them to tolerate extended periods of intense heat without becoming lethally dehydrated. We used phylogenetically-informed regressions to compare EWL and evaporative cooling efficiency (ratio of evaporative heat loss [EHL] and metabolic heat production [MHP]; EHL/MHP) among nocturnal and diurnal birds at high Ta. We analyzed variation in three response variables: 1) slope of EWL at Ta between 40 and 46{degrees}C, 2) EWL at Ta = 46{degrees}C, and 3) EHL/MHP at Ta = 46{degrees}C. Nocturnality emerged as a weak, negative predictor, with nocturnal species having slightly shallower slopes and reduced EWL compared to diurnal species of similar mass. In contrast, nocturnal activity was positively correlated with EHL/MHP, indicating a greater capacity for evaporative cooling in nocturnal birds. However, our analysis also revealed conspicuous differences among nocturnal taxa. Caprimulgids and Australian-owlet nightjars had shallower slopes and reduced EWL compared to similarly-sized diurnal species, whereas owls had EWL rates comparable to diurnal species. Consequently, our results did not unequivocally demonstrate more economical cooling among nocturnal birds. Owls predominately select refugia with cooler microclimates, but the more frequent and intense heat waves forecast for the 21st century may increase microclimate temperatures and the necessity for active heat dissipation, potentially increasing owls vulnerability to dehydration and hyperthermia.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

O'Connor, R. S., Smit, B., Talbot, W. A., Gerson, A. R., Brigham, M., Wolf, B. O., McKechnie, A. E.. 2018-03-14. Avian thermoregulation in the heat: is evaporative cooling more economical in nocturnal birds?. https://doi.org/10.1101/282640

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Age-related biological dysregulation quantified using metabolomics is composed of distinct subsystems with synergistic associations to health outcomes: An analysis of the Canadian Longitudinal Study on Aging

Resilience is a fundamental component of healthy aging, whereby an organism can efficiently respond to external stressors and return to a resting biological and physiological state, known as homeostasis. This capacity declines with age in a heterogenous manner and is aggravated by biological dysregulation, a detrimental state broadly associated with health risk factors and poor outcomes. However, the underlying structure of dysregulation remains unclear, particularly in the context of older adult health trajectories. Here, we take a novel systems-based approach to the quantification of dysregulation using metabolomic data from n=9,992 older adults enrolled in the Canadian Longitudinal Study on Aging. We show that dysregulation across different biological systems is heritable, and exhibit distinct associations with health risk factors, indicators and outcomes, and DNA methylation patterns. Importantly, the effect of systems-specific dysregulation is cumulative, resulting in a significantly higher risk of disease incidence and death in older adults. Our findings broaden our understanding of biological dysregulation as a health state and demonstrate the value of system-specific dysregulation for effective strategies in personalized medicine and risk stratification.

physiology↗

An LRH-1 agonist reverses hepatic metabolic dysfunction in obesity

Liver receptor homolog-1 (LRH-1; NR5A2) is a nuclear receptor that controls metabolic gene programs important for liver health. Here, we address two challenges with dissecting ligand-driven LRH-1 metabolism in vivo. First, we generate ME610, a potent LRH-1 agonist with favorable pharmacokinetic properties. Second, we engineer Nr5a2humLBD mice, edited to recapitulate the ligand response of the human receptor. ME610 dose-dependently induces LRH-1 target genes and reduces triglycerides in livers of Nr5a2humLBD mice. In a mouse model of diet-induced obesity (DIO), ME610 dramatically improves insulin sensitivity and reduces liver fat. Multi-omics integration of transcriptomics, lipidomics, and metabolomics data demonstrates a coordinated reversal of DIO-induced hepatic metabolic stress via changes in lipid, amino acid, and energy metabolism, with peroxisomal lipid metabolism emerging as a central process correlated to efficacy. These studies uncover new pathways through which LRH-1 regulates metabolism and demonstrate the therapeutic potential of synthetic LRH-1 agonists in obesity-associated metabolic diseases.

physiology↗

SCN- induces prestin contraction through reduced intermonomer angles and a modified transporter like movement of each monomer.

Prestin is the membrane based molecular motor responsible for outer hair cell electromotility that expands and contracts in response to transmembrane voltage. How voltage brings these about is unknown but cryoEM structures in the presence of ligands has led to the extrapolation of structures with the transporter cycle and its expansion contraction coupling. We find prestin to adopt novel increasingly contracted states that are brought about by a reduced intermonomer angles in the obligate dimers and a transmembrane contraction of each monomer at its cytoplasmic half in the presence of SCN-. These changes are associated with a loss in the intermonomer beta sheet at its N terminus. There is a hyperpolarizing shift in Vh along with increased affinity for SCN-. SCN- binding at the internal binding site likely cause the structural changes since they are reversed by SCN- displacement by salicylate.

physiology↗