Hemodynamic Response to Activation of the Exercise Pressor Reflex during Dynamic Plantar Flexion in Peripheral Arterial Disease Patients

Abstract

Patients with peripheral arterial disease (PAD) have an accentuated exercise pressor reflex (EPR). The underlying hemodynamic changes responsible for the exaggerated EPR, and the effect of this on blood flow to the exercising limb is unclear. We tested the hypothesis that the exaggerated EPR in PAD is mediated by an increase in total peripheral resistance (TPR), which augments redistribution of blood flow to the ischemic exercising muscle.METHODSEleven PAD patients and 11 age, and sex‐matched subjects without PAD (control) performed dynamic plantar flexion (PF) using their symptomatic leg at progressive workloads of 2 to 12 kg (increased by 1 kg/min until the onset of fatigue). We measured heart rate (HR), beat‐by‐beat blood pressure (BP), femoral blood flow velocity (FBV), and near‐infrared spectroscopy derived tissue oxygen saturation (SmO2) continuously during the exercise. Femoral blood flow (FBF) was calculated from FBV and baseline femoral artery diameter. Stroke volume (SV), cardiac output (CO), and TPR were derived from the BP tracings.RESULTSMean arterial blood pressure (MAP) was significantly augmented in PAD compared to controls during PF (P < 0.001). This was accompanied by an equal rise in CO in the two groups. Of note, TPR decreased in controls, whereas it increased in PAD. The increase in femoral blood flow velocity was greater during exercise in PAD as compared to controls (P = 0.0021), however, the increased FBF in the two groups was the same. Despite the fact the flow was not different between PAD and control group, SmO2 of the exercising limb remained significantly lower in PAD compared to control (P < 0.001).CONCLUSIONWe conclude that the exaggerated pressor response in PAD is mediated by an abnormal response in TPR, which augments redistribution of blood flow to the exercising muscle, leading to an equal rise in FBF compared to controls. However, this increase in FBF is not sufficient to normalize the SmO2 response during exercise in patients with PAD.Support or Funding InformationSupported by National Institutes of Health Grants P01 HL134609 (Sinoway) and UL1 TR002014 (Sinoway).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.