Poster 213: Relationships of Risk factors For Peripheral Arterial Disease to Calf Muscle Oxygenation Responses During Calf Exercise

Abstract

Objective: To determine the relationships of risk factors for peripheral artery disease (PAD) to calf muscle oxygenation responses during calf exercise. Design: Cross-sectional repeated measures. Setting: Urban tertiary care medical center. Participants: 53 men, ages 40 through 80, without diagnosed PAD. Interventions: Participants performed 5-minute bouts of plantar flexion calf exercise at 0-watts (W), 4-W, and 8-W power output, each separated by 5 minute pre-exercise baseline rest periods. A pedal ergometer was used for resistive calf muscle exercise. Tissue oxygenation (relative HbO2 saturation, StO2, %) was acquired at the medial calf throughout the testing protocol, by near-infrared spectroscopy. Main Outcome Measures: Tissue oxygenation (StO2%) was recorded throughout the testing protocol. Risk factors were documented by review of medical records and participant report. Assessed PAD risk factors included smoking, hypertension, diabetes, dyslipidemia, obesity, advanced age (>65y), and total number of PAD risk factors (0–7). Results: Repeated measures analysis of variance with Tukey-Kramer post hoc multiple comparison tests revealed that compared with preceding baseline, 0-W, 4-W, and 8-W exercise significantly decreased mean StO2 by 7%, 11%, and 16%, respectively. Stepwise multiple linear regression indicated that total decrement in StO2 was best predicted by the presence or absence of dyslipidemia and active smoking (1=present, 0=absent): Total StO2 decrement=(34.33 dyslipidemia) + (32.37 smoking)−53.44; R2=0.373, P=0.000, CV=−2.63. Hypertension, diabetes, obesity, advanced age (>65y), and total number of PAD risk factors did not explain significant amounts of additional variance in total StO2 decrement. Conclusions: Light-to-moderate intensity calf exercise causes mild HbO2 desaturation of the medial gastrocnemius in well middle-aged to elderly men without PAD. 37% of the StO2 decrement can be explained by the risk factors of dyslipidemia and smoking.