A single rapid heat stress episode does not result in prolonged elevations in salivary cortisol and C-reactive protein production in firefighters.

In the present experiment, we evaluated the impact of rapid heat stress (RHS) on salivary cortisol and C-reactive protein production pre-RHS, post-RHS, and 24 and 48 h post-RHS exposure among firefighters. Previous research has demonstrated that RHS increases salivary cortisol during RHS and immediately post-RHS exposure. However, no research has evaluated the duration necessary to return to baseline cortisol levels following RHS. Additionally, no studies have analyzed the impact of RHS on inflammatory biomarkers, such as C-reactive protein. This study hypothesized that salivary cortisol and C-reactive protein levels would increase following RHS and then return to pre-RHS levels within 24 h post-exposure. Twenty-four participants performed a steady-state treadmill protocol in an environmental chamber (35 °C; 45% humidity) in full firefighter personal protective equipment until reaching either a core temperature (Tc) of 39 °C or a volitional maximum. The subjects had their saliva collected via the passive drool protocol pre-RHS, post-RHS, and 24 and 48 h post-RHS. Pre-RHS of 0.23 ± 0.03 µg/dL increased post-RHS to 0.51 ± 0.06 µg/dL (p < 0.001). This finding supports previous literature demonstrating the immediate impact of RHS. There were no changes in C-reactive protein. The novel finding of this study is that salivary cortisol levels return to baseline in the 24 h post-RHS exposure. This indicates that 24 h is recommended to recover from RHS and should be applied to prevent the chronic stress response.

Adipocyte Glucocorticoid Receptor Inhibits Immune Regulatory Genes to Maintain Immune Cell Homeostasis in Adipose Tissue.

Glucocorticoids acting via the glucocorticoid receptors (GR) are key regulators of metabolism and the stress response. However, uncontrolled or excessive GR signaling adversely affects adipose tissue, including endocrine, immune, and metabolic functions. Inflammation of the adipose tissue promotes systemic metabolic dysfunction; however, the molecular mechanisms underlying the role of adipocyte GR in regulating genes associated with adipose tissue inflammation are poorly understood. We performed in vivo studies using adipocyte-specific GR knockout mice in conjunction with in vitro studies to understand the contribution of adipocyte GR in regulating adipose tissue immune homeostasis. Our findings show that adipocyte-specific GR signaling regulates adipokines at both mRNA and plasma levels and immune regulatory (Coch, Pdcd1, Cemip, and Cxcr2) mRNA gene expression, which affects myeloid immune cell presence in white adipose tissue. We found that, in adipocytes, GR directly influences Cxcr2. This chemokine receptor promotes immune cell migration, indirectly affecting Pdcd1 and Cemip gene expression in nonadipocyte or stromal cells. Our findings suggest that GR adipocyte signaling suppresses inflammatory signals, maintaining immune homeostasis. We also found that GR signaling in adipose tissue in response to stress is sexually dimorphic. Understanding the molecular relationship between GR signaling and adipose tissue inflammation could help develop potential targets to improve local and systemic inflammation, insulin sensitivity, and metabolic health.