Exaggerated Hemodynamic Responses Upon the Initiation of Thermoregulatory Behavior in ‘At Risk’ Older Adults

Abstract

Cold or heat exposure presents a challenge to blood pressure that can strain cardiovascular function. The risk of thermal induced cardiovascular morbidity and mortality is heightened in older adults who often present with co‐morbidities such as hypertension, diabetes, and hypercholesterolemia. In young healthy adults the initiation of thermoregulatory behavior is preceded by modest changes in blood pressure, which could strain cardiovascular function. We tested the hypothesis that older adults with existing cardiovascular co‐morbidities demonstrate exaggerated hyper‐ or hypo‐ tension upon the initiation of thermoregulatory behavior.We studied twelve healthy younger adults (Y, 25 ± 4 y, 6 females) and six older adults (O, 67 ± 4 y, 3 females) who each reported taking prescription medications for at least two of the following conditions: hypertension (n=2), type II diabetes (n=2), hypercholesterolemia (n=5). Participants wore shorts and a t‐shirt and underwent a 90 min test in which they voluntarily moved between cool (18.1 ± 1.8°C. RH: 29 ± 5%) and warm (40.2 ± 0.3°C, RH: 20 ± 0%) rooms when they felt ‘too cool’ or ‘too warm’. Blood pressure (Finometer), stroke volume (Model flow), cardiac output, heart rate (ECG), and mean skin and intestinal temperatures were measured continually. Data are reported as a 30 s average immediately prior to moving from cool to warm (C‐W) and warm to cool (W‐C). Data were averaged across behaviors for a given subject and are reported as a change from the pretest baseline.Time before initiating behavior did not differ between groups at C‐W (Y: 9.8 ± 4.3 min, O: 8.4 ± 2.8 min, P=0.47) or W‐C (Y: 14.5 ± 4.3 min, O: 18.9 ± 18.4 min, P=0.22). Changes in mean skin temperature were not different between groups at C‐W (Y: +0.2 ± 0.8°C, O: +0.7 ± 1.8, P=0.22) or W‐C (Y: +2.7 ± 0.6°C, O: +2.9 ± 1.9, P=0.37). Changes in intestinal temperature were also not different at C‐W (Y: 0.0 ± 0.1°C, O: +0.1 ± 0.2, P=0.06), but were higher at W‐C in O (Y: −0.1 ± 0.2°C, O: +0.1 ± 0.3°C, P=0.03). Systolic pressure at C‐W increased (Y: +10 ± 9 mmHg, O: +24 ± 17 mmHg, P=0.02) and at W‐C decreased (Y: −4 ± 13 mmHg, O: −23 ± 19 mmHg, P=0.01) to a greater extent in O. Differences were also apparent for diastolic pressure at C‐W (Y: −2 ± 4 mmHg, O: +17 ± 23 mmHg, P<0.01) and W‐C (Y: +4 ± 13 mmHg, O: −1 ± 6 mmHg, P=0.03). Changes in heart rate were not different between groups at C‐W (Y: −2 ± 3 bpm, O: −2 ± 3 bpm, P=0.45) or W‐C (Y: +6 ± 5 bpm, O: +7 ± 6 bpm, P=0.28). Stroke volume differed between groups at C‐W (Y: −6 ± 7 mL, O: +6 ± 10 mL, P<0.01), but not at W‐C (Y: −4 ± 11 mL, O: −3 ± 10 mL, P=0.43). Cardiac output differed between groups at C‐W (Y: −0.5 ± 0.5 L/min, O: +0.1 ± 0.6 L/min, P<0.01), but not at W‐C (Y: +0.1 ± 0.9 L/min, O: +0.4 ± 1.2 L/min, P=0.28). Rate pressure product, an index of myocardial O2 demand, changed to a greater extent in O at C‐W (Y: +0.5 ± 7 mmHg*bpm, O: +1.2 ± 1.0 mmHg*bpm, P=0.05) and W‐C (Y: +0.3 ± 1.0 mmHg*bpm, O: −0.5 ± 0.8 mmHg*bpm, P=0.05).Despite modest changes in body temperature, the initiation of thermoregulatory behavior in ‘at risk’ older adults is preceded by exaggerated hyper‐ and hypo‐ tensive responses that may strain cardiovascular function.