bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2020.04.06.027623

A temperate endotherm trades thermoregulation for self-preservation: stress-induced changes in surface temperature as thermoregulatory trade-offs

Robertson, J. K.·Mastromonaco, G. F.·Burness, G.
View original source ↗Export metadata ↓

Abstract

O_LICoping with stressors can require substantial energetic investment, and when resources are limited, such investment can preclude simultaneous expenditure on other biological processes. Among endotherms, energetic demands of thermoregulation can be immense, yet whether a stress response is sufficient to induce changes in thermoregulatory investment appears unexplored. C_LIO_LIWe tested the hypothesis that stress-induced changes in surface temperature, a well-documented phenomenon across vertebrates, stem from a trade-off between thermoregulation and stress responsiveness, whereby individuals seek to reduce energetic expenditure on thermoregulation in challenging environments (the "Thermoprotective Hypothesis"). We predicted that surface temperature and dry heat loss of individuals that are resource-limited would fall under stress exposure at low ambient temperatures and rise under stress exposure at high ambient temperatures when compared with non-resource limited individuals. C_LIO_LITo test our predictions, we exposed Black-capped Chickadees to rotating stressors and control treatments (ndays/treatment = 30; paired treatments) across an ambient temperature gradient whilst remotely monitoring both feeding behaviour and surface temperature. C_LIO_LISupporting the Thermoprotective Hypothesis, our results showed that: 1) social subordinates (n = 12), who fed less than social dominants and alone suffered stress-induced declines in mass, displayed significantly larger changes in surface temperature following stress exposure than social dominants (n = 8), and 2) stress-induced changes in surface temperature significantly increased heat conservation at low ambient temperature, and heat dissipation at high ambient temperature among social subordinates alone. C_LIO_LIThese results suggest that Black-capped Chickadees adjust their thermoregulatory strategies under stress when resources are limited and support the hypothesis that stress-induced changes in temperature are functionally significant. C_LI Data Availability Statement: All data and R code used for the construction of this study are available at: https://datadryad.org/stash/share/QzmRV875_S5IYpMT0jxOYIsoO-ua0T3LX6AA9u-XpdQ.

Explore related subjects

physiologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Robertson, J. K., Mastromonaco, G. F., Burness, G.. 2020-04-07. A temperate endotherm trades thermoregulation for self-preservation: stress-induced changes in surface temperature as thermoregulatory trade-offs. https://doi.org/10.1101/2020.04.06.027623

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

KEEP EXPLORING

Related preprints

bioRxiv2026

Epigenetic Rescue of Disuse Muscle Atrophy by Histone Deacetylase Inhibitor Trichostatin A

Mechanical unloading rapidly induces skeletal muscle atrophy and functional deterioration, yet how the loss of mechanical input influences nuclear architecture, chromatin organization, and associated transcriptional programs remains poorly understood. Here, we investigated whether pharmacological inhibition of histone deacetylases (HDACs) using Trichostatin A (TSA) could attenuate the consequences of continued mechanical unloading in a murine hindlimb suspension model. Following 14 days of unloading, mice exhibited impaired locomotor activity, altered muscle architecture, and widespread transcriptional reprogramming characterized by increased expression of atrophy associated genes, inflammatory mediators, and extracellular matrix remodeling pathways, alongside suppression of mitochondrial metabolic programs. Super resolution imaging further revealed irregular Lamin A/C organization and disruption of discrete H3K9me3 associated heterochromatin foci. Systemic TSA treatment significantly attenuated the decline in locomotor activity, accompanied by trends toward reduced body weight loss, and preservation of muscle morphology. Transcriptomic analysis demonstrated a substantial shift toward the baseline expression profile, with high-dose TSA attenuating FOXO associated catabolic programs, inflammatory, and extracellular matrix-related signatures, while enhancing mitochondrial oxidative phosphorylation pathways. Quantitative gene level and pathway analyses further revealed dose dependent and selective reversal of unloading associated transcriptional changes. Notably, TSA treatment also partially preserved nuclear lamina organization and the focal distribution of H3K9me3 associated heterochromatin. Despite these muscle specific benefits, TSA did not prevent trabecular bone loss over the 14-day unloading period, although several muscle-expressed genes potentially involved in muscle to bone communication were altered by treatment. Together, these findings demonstrate that HDAC inhibition counteracts multiple functional and molecular consequences of skeletal muscle unloading and is associated with partial preservation of nuclear and heterochromatin organization. This study supports a link between mechanical unloading, nuclear architectural remodeling, and HDAC sensitive transcriptional regulation, providing a foundation for epigenetic strategies to counter disuse induced muscle deterioration.

physiology↗
bioRxiv2026

Residual Hearing Loss After Chronic Cochlear Implantation in Guinea Pigs is Primarily Conductive

It is desirous to preserve residual low-frequency hearing in cochlear implant recipients, as dual stimulation using electrical and acoustic signals results in superior speech-in-noise processing and musicality. However, cochlear implant recipients commonly lose their residual acoustic hearing gradually following surgical placement of the array. The governing mechanism is not understood and is likely due to multiple factors including surgical trauma, inflammation, and the foreign body induced immune response to the array, including formation of intracochlear fibrosis. Normal mechanical function of the cochlea is expected to underpin residual hearing but has not been directly studied. This function includes efficient transmission of sound to the cochlea via the middle ear, sound propagation via the basilar membrane travelling wave, mechanical tuning characteristics, and the non-linear cochlear amplification of responses to low-frequency stimulation. Here, we examined these features in cochleae and middle ears of unimplanted, acutely and chronically implanted guinea pigs using our minimally invasive preparation and optical coherence tomography vibrometry. We observed that mechanical tuning and amplification is not significantly altered by either acute or chronic implant. However, the response threshold was raised and proportional to middle ear responses. Additionally, the organ of Corti phase, and its sound intensity dependent changes, are unaltered by CI. Finally, a cluster analysis revealed sensitivity loss in chronically implanted animals is caused by middle ear dysfunction. Hence, in the guinea pig model, the dominant etiology of residual hearing loss is conductive. More research is required to establish whether residual hearing loss in humans similarly shares conductive elements.

physiology↗
bioRxiv2026

Satellite cell glucocorticoid receptor restrains myogenic commitment without mediating the effects of therapeutic glucocorticoids on muscle repair

Glucocorticoids (GCs) exert profound effects on skeletal muscle, but the contribution of satellite cell (SatC) glucocorticoid receptor (GR) signaling to muscle regeneration remains poorly understood. Here, we investigated the role of GR in SatC homeostasis and assessed whether SatC GR mediates the effects of therapeutic GCs on muscle repair. Conditional deletion of GR in SatC reduced the number of PAX7-positive cells during regeneration in young mice, but did not substantially impair muscle repair in either young or aged animals. Transcriptomic and chromatin profiling revealed that GR occupies genes involved in stem cell fate and developmental signaling, with extensive GR binding already established in quiescent SatC. GR-deficient quiescent SatC showed reduced expression of Yap1, Runx1 and Foxo1, together with increased Myog expression. Similarly, GR silencing in human myoblasts induced early myogenic differentiation markers without affecting proliferation, supporting a conserved role for GR in restraining myogenic commitment. We next examined the effects of two therapeutic GCs on muscle regeneration. Chronic prednisone treatment altered the transcriptional landscape of regenerating muscle in an age-dependent manner, without substantially affecting histological repair. In contrast, dexamethasone administration during the early inflammatory phase delayed regeneration, with persistent necrosis and increased collagen deposition. These effects were comparable in control and SatC-specific GR-deficient mice, indicating that they do not require GR in SatC. Together, these findings identify GR as a regulator of the quiescent, undifferentiated state of SatC, while showing that the effects of therapeutic GCs on muscle repair are largely independent of SatC GR. They further highlight the importance of treatment regimen and physiological context in determining the effects of GCs on skeletal muscle regeneration.

physiology↗