Thermal cycles impair skin-vessel responses

This hypothesis asks whether repeated heating and cooling could cause cumulative biochemical damage in skin blood vessels, impairing their sustained response. The proposed mechanism is altered coupling of nitric oxide synthase, an enzyme system that makes nitric oxide, a vessel-widening signal. Early widening and sweating could remain intact while the sustained vascular response deteriorates. Greater vapor permeability would leave the deficit in place. The test must distinguish this prediction from rivals: synchronized recovery would favor phase control; an illumination-dependent deficit relieved by shielding would favor photothermal conversion. Testing calls for repeated challenges, skin microdialysis, redox assays, synchronized measurements, and direct calorimetry.