ArticlePhysiological reports2025
Adrenal steroid hormone responses to exercise under thermal stress: Potential role for nonclassic congenital adrenal hyperplasia in heat illness susceptibility.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Thermoregulatory and plasma neurobiomarker responses to heat tolerance assessment in exertional heat illness and matched controls.Experimental physiology · 2026Article
- Edaravone provides neuroprotection against chronic heat stress-induced behavioral dysfunction through adaptive proteomic remodeling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Adrenal steroid hormone responses to exercise under thermal stress: Potential role for nonclassic congenital adrenal hyperplasia in heat illness susceptibility.Physiological reports · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
We queried whether adrenal insufficiency attributable to non-classic congenital adrenal hyperplasia (21 hydroxylase deficiency, 21OHD) might contribute to heat illness susceptibility. Patients referred to a specialist heat illness clinic (n = 2 with prior hyponatremia; n = 16 lacking documentary evidence) and controls (n = 16) underwent laboratory Heat Tolerance Assessment (HTA: 60-90 min walking, 60% relative intensity, 34°C heat), synthetic adrenocorticotrophic hormone stimulation (heat illness only) and CYP21A2 genotyping (hyponatremic heat illness only). Copeptin, cortisol, 17-hydroxyprogesterone, and 21 deoxycortisol were assayed from blood at baseline and post-HTA, with precursor product [17-hydroxyprogesterone +21 deoxycortisol] expressed relative to cortisol. Saliva and urine were assayed for free cortisol (one hyponatremic case, controls). Versus controls, normonatremic heat illness exhibited greater (p < 0.05) serum cortisol across HTA, while hyponatremic heat illness showed blunted responses in aldosterone and free cortisol (salivary cortisol 1.6 and 1.6 vs. 6.0 [4.2, 19.4] and 4.2 [3.8, 19.2] nmol.L-1; urine cortisol 19 vs. 117 +/- 71 nmol.L-1). Hyponatremic heat illness demonstrated elevated precursor product consistent with 21OHD and multiple CYP21A2 mutations. One normonatremic case of heat illness also showed elevated precursor product. These data support the potential for 21OHD to precipitate heat illness under sustained physical stress and advance a case for targeted genetic screening.
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