Abstract

Patients with peripheral arterial disease (PAD) have an exaggerated pressor response to dynamic exercise of the affected limb. We tested the hypothesis that this response is mediated by an increase in total peripheral resistance (TPR). We measured heart rate, blood pressure, stroke volume, cardiac output (CO), and total peripheral resistance (TPR) during exercise in 9 subjects with PAD and 9 age matched controls using continuous finger arterial pressure monitoring (Finometer). Finometer derived values were adjusted to values obtained by echocardiography, and brachial pressure at baseline. The average age and ABI was 65 ± 7 and 1.06 ± 0.07 in controls, and 66 ± 7 and 0.64 ± 0.08 in PAD. Participants performed dynamic plantar flexion at progressive workloads of 2 to 12kg (increased by 1kg/min until onset of fatigue/pain) using their symptomatic leg or leg with lower ABI. Those who reached 12kg continued exercise at a constant load until onset of fatigue/pain or a maximum of 4 minutes. Participants were then asked to perform an isometric handgrip exercise at 30% of maximum voluntary contraction (MVC) until fatigue. Results are shown in Table 1. There were no differences in hemodynamic parameters at baseline. The average weight at end of plantar flexion was 12.0 ± 0.2 and 9.2 ± 2.5 kg (p<0.0001) for control and PAD. Perceived exertion (Borg scale) and pain (NPRS scale) at end of exercise was 15 ± 2 and 0, and 15 ± 2 and 6 ± 3 in control and PAD. Plantar flexion elicited a significantly higher rise in blood pressure in PAD compared to control. TPR decreased in controls, but slightly increased in PAD. In contrast, isometric handgrip elicited a similar pressor response, as well as changes in CO and TPR in both groups. We conclude that the exaggerated pressor response in PAD is mediated by an abnormal response in TPR, which counteracts the normal vasodilatory response to dynamic leg exercise seen in controls. This response appears to be specific to dynamic plantar flexion exercise in PAD.

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