Date of Graduation

5-2015

Document Type

Thesis

Degree Name

Bachelor of Science Education

Degree Level

Undergraduate

Department

Health, Human Performance and Recreation

Advisor

Ganio, Matthew S

Reader

Washington, Tyrone A

Second Reader

Hammig, Bart J

Abstract

Arterial compliance (i.e., arterial elasticity) is a major contributor to the pathophysiology of cardiovascular disease (CVD) and has been recognized as an independent risk factor for CVD. Smokers have poor arterial compliance compared to non-smokers. In non-smokers, passive heat stress has been shown to acutely improve arterial compliance. It is unknown how passive heat stress affects arterial compliance in smokers. The purpose of this pilot study was to test the hypothesis that passive heat stress improves arterial compliance in smokers to a greater extent than non-smokers. This pilot study involved 2 male smokers and 2 male non-smokers, ages 18-21. Smokers and non-smokers underwent a control (no heat) and passive heat stress trial in a randomized, counter-balanced fashion. Passive heating was achieved by circulating hot water through a water-perfused, tube-lined suit that covered the entire body except the head, face, hands, feet, and right forearm. Measures were obtained prior to heating and after a 0.5, 1.0, and 1.5°C elevation in core body temperature or equivalent time points in the non-heated control trial. At each time point, mean skin temperature was measured via thermocouples and heart rate and blood pressure were measured using an automated sphygmometer with ECG. Arterial compliance was assessed with pulse wave velocity (PWV) measured from a Doppler ultrasound. During heat stress in the smokers, central PWV tended to decrease from 681.36 ± 31.21 cm/s at baseline to 634.91 ± 96.87 cm/s at the 0.5°C time point. From 1.0° to 1.5°C there was an increase in central PWV (699.33 ± 135.46 to 747.11 ± 0.00 cm/s). The non-smokers central PWV tended to decrease during the heat stress from 660.03 ± 86.49 cm/s at baseline to 562.89 ± 23.41 cm/s at 1.5°C. Peripheral PWV in the smokers decreased from 724.00 ± 23.46 cm/s at baseline to 701.73 ± 5.43 cm/s at 0.5°C and 703.77 ± 23.22 cm/s at 1.0°C, but there was a later increase in peripheral PWV at 1.5°C (725.95 ± 43.45 cm/s). For the non-smoker heat stress trial, peripheral PWV saw a steady decrease from 701.73 ± 1.52 cm/s at baseline to 603.30 ± 30.64 cm/s at 1.5°C. In conclusion we observed decreases in PWV (i.e., increases in arterial compliance) in non-smokers, but relatively no change in smokers when heat stressed. Future research should investigate the mechanisms by which arterial compliance may or may not change during passive heat stress in smokers and non-smokers.

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