The thyroid gland contributes immensely to the basal metabolic rate, and hence, thermogenesis in mammals. Its response to the thermal environment is, however, slow and may require several days to adjust. A rapid thyrosuppressive mechanism (“Wolff–Chaikoff” phenomenon; WC) is inducible by high dietary iodine ingestion. The current study aimed to examine the WC on thermophysiology of rats exposed to acute heat stress (HS). Biotelemetry was used to assess real-time core body temperature (T_core), locomotive activity (LA) and heart rate (HR) in rats (N = 12). Animals were randomly assigned to two treatment groups: a control (CN) group had ad libitum access to tap water throughout the trial; a second group (KI) received potassium iodide (0.5%) in drinking water, 3 h before HS. Climatic conditions during the 10-day experimental period were set to 4 days at thermoneutrality (TN; T_a = 23.60 ± 0.05 °C), then HS (T_a = 33.22 ± 0.25 °C, for 4 h) and finally back to TN until the end of trial. Serum samples were collected right after the HS, to measure free thyroxine (FT4), triiodothyronine (FT3) and total antioxidant capacity (TAO), from 12 other equivalent rats.

The KI induced the WC, as evidenced with lower FT3 (1.66 and 1.91 ± 0.08 pg/mL) than the CN treatment, respectively. This momentary goitrogenic response by KI mitigated hyperthermia, compared to CN (T_core maxima of 38.90 and 39.54 ± 0.09 °C). Furthermore, KI resulted in higher TAO than KI-free rats (238.30 and 198.80 ± 9.10 µM copper reducing equivalents). While instigating an instant suppression in LA, KI caused a delayed 25% elevation in HR along with a rebound in T_core, likely due to the “escape phenomenon.”

The employed WC protocol alleviated HS impact on rats. Research on other mammals awaits further investigation.