Heat intolerance: does gene transcription contribute?

Area of Science:

• Physiology
• Thermoregulation
• Molecular Biology

Background:

• Heat intolerance (HI) during exertion in heat is linked to impaired metabolic heat dissipation.
• HI can be permanent or temporary, stemming from predisposing factors or thermoregulatory dysfunction.
• Understanding molecular mechanisms underlying HI is crucial for identifying at-risk individuals.

Purpose of the Study:

• To investigate protein and transcript levels of heat shock proteins (HSP) and transcription factors in heat-intolerant (HI) versus heat-tolerant (T) male volunteers.
• To correlate physiological strain index and vascular responsiveness with molecular markers during a heat tolerance test.

Main Methods:

• Western blot and quantitative RT-PCR were used to analyze protein and transcript levels in lymphocytes.
• Measurements included heat shock protein (HSP) 70, HSP72, HSP90, bcl-2xL, glutathione S-transferase-p, heat shock factor-1, TATA-binding protein-associated factor, and NF-kappaB.
• Physiological parameters (rectal/skin temperature, heart rate) and physiological strain index were monitored during a controlled heat tolerance test.

Main Results:

• HI subjects exhibited a significantly higher physiological strain index compared to T subjects.
• Vascular responsiveness to thermal stimuli was decreased in HI individuals.
• HSP72 levels decreased during recovery in HI subjects, contrasting with a rise in T subjects; transcription factor expression was significantly decreased in HI subjects.

Conclusions:

• Impaired transcriptional processes, indicated by reduced expression of heat shock factor-1, NF-kappaB, and TATA-binding protein-associated factor, are characteristic of heat intolerance.
• Sluggish vascular response to thermal stimuli is a predisposing factor in heat-intolerant individuals.
• These molecular and physiological deficits contribute to the heat-intolerant phenotype.