Low-dose ASA Therapy Does Not Alter Core or Skin Temperature During Hot-dry or Warm-humid Heat Stress (PSU HEAT Project)

Nearly 40% of US adults over the age of 50 use an aspirin (ASA) therapy regimen for the primary or secondary prevention of cardiovascular disease. Chronic systemic platelet cyclooxygenase inhibition with low-dose ASA has been found to attenuate reflex cutaneous vasodilation and accelerate the rate of rise in core temperature during passive heating in a water perfused suit in middle-aged adults. Further, during passive heat stress in warm-humid ambient conditions, chronic low-dose aspirin therapy resulted in elevated core temperature and delayed onset of thermoeffector mechanisms. While low-dose ASA therapy may have detrimental effects on the ability to thermoregulate in the heat, the effect of low-dose ASA therapy on thermoregulatory and cardiovascular responses to extreme heat stress in older (>65 yrs) men and women has not been determined. Therefore, in the present study, seven older adults (3F; 65-80 yrs) were exposed to progressive heat stress in a controlled environmental chamber at metabolic rates comparable to activities of daily living (~80 W·m -2 ) in a warm-humid (WH; 36°C, 52% rh) and hot-dry (HD; 40°C, 21% rh) environment after 7 days of low-dose ASA (81 mg/day) or placebo. A subset of participants (n=4) repeated experiments following a single high-dose (650 mg) of ASA 1 hr prior to the experiment. Core temperature (T c ), skin temperature (T sk ), heart rate (HR), mean arterial pressure (MAP), and forearm blood flow (FBF) were continuously monitored and recorded. Forearm vascular conductance (FVC) and rate pressure product (RPP) were subsequently calculated. Temperature and cardiovascular responses to heat stress in each environment were compared between ASA and placebo conditions. In the HD environment, low-dose ASA had no effect on T c or T sk compared to placebo (both p>0.05) . Additionally, low-dose aspirin reduced FBF (p=0.04), FVC (p=0.04), HR (p=0.04), and RPP (p=0.005) but had no effect on MAP (p=0.60). In the WH environment, low-dose ASA had no effect on T c , T sk , FBF, FVC, HR, MAP, or RPP (all p>0.05). In the subset of participants that completed experimental trials following a single 650 mg dose no differences were observed in either environment in any of the previously listed outcome variables. These data suggest that low-dose ASA therapy does not alter core or skin temperature responses to dry or humid heat stress and may alleviate cardiovascular strain in hot-dry environments. Consistent with previous work examining the effect of platelet inhibition with low-dose ASA on thermoregulation, FBF was similarly reduced during hot-dry heat stress in the present study. These findings indicate that the use of ASA therapy for prevention of cardiovascular disease likely does not increase risk for adverse heat-related events. T32 AG049676 and R01 AG067471 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.