Blunted Cardiovascular Responses to Exercise in Parkinson Disease Patients: Role of the Muscle Metaboreflex

Parkinson's Disease (PD) is a neurodegenerative disorder characterized by motor dysfunctions, and non‐motor symptoms, such as autonomic and cardiovascular dysfunctions. Importantly, these impairments have a significant impact on patient's quality of life. Several studies have shown that PD patients exhibit attenuated cardiovascular responses to exercise. Unfortunately, the underlying mechanisms that are potentially contributing to these impairments are not fully understood. The isolation of muscle metaboreflex by post‐exercise circulatory arrest of active limb, called post‐exercise ischemia (PEI), is a well‐known mechanism related to the increase in sympathetic nerve activity and partially maintains exercise‐induced increases in blood pressure in healthy populations. Due its predominant role in mediating sympathetic and pressor response, we reasoned that blunted cardiovascular responses during isolated muscle metaboreflex activation could be one of underling mechanisms related to the impaired cardiovascular responses to exercise in PD patients. Herein, the purpose of the present study was to test the hypothesis that patients with PD would have blunted cardiovascular responses to isolated muscle metaboreflex activation during PEI when compared with age‐matched controls. Mean arterial pressure (MAP), cardiac output (CO) and total peripheral resistance (TPR) were measured in a beat‐to‐beat basis by using finger photoplethysmography and modelflow method, respectively in 11 PD patients [66 ± 2 yrs; (H&Y: 2 ± 1 a.u. and diagnose time: 7 ± 1 yrs] and eight age‐matched controls (66 ± 3 yrs). Measurements were made at baseline (5 min), during 90‐s of isometric handgrip exercise (IHG) performed at 40% maximal voluntary contraction and during isolated muscle metaboreflex activation by PEI (3 min). In addition, a non‐exercise sympathoexcitatory stimulus (cold pressor test, CPT) was performed to determine if the hypothesized attenuated responses in PD patients were specific to exercise and/or metaboreflex activation and not representative of a blunted overall reactivity to cardiovascular stressors. Changes in MAP from baseline were attenuated in PD patients during IHG (PD patients: Δ25 ± 2 mmHg vs. controls: Δ30 ± 3 mmHg; P < 0.05), and these group differences were maintained during PEI (Δ18 ± 1 mmHg vs. Δ24 ± 1 mmHg, respectively; P < 0.01). Additionally, changes in TPR from baseline were attenuated in PD patients during PEI (PD patients: Δ3 ± 1 mmHg −1 L min −1 vs. controls: Δ6 ± 1 mmHg −1 L min −1 , respectively; P < 0.05), indicating blunted reflex vasoconstriction. CO responses to both exercise and PEI were similar between groups. In addition, cardiovascular responses to CPT were not different between groups, suggesting no group differences in generalized sympathetic responsiveness. In summary, compared with control subjects, patients with PD exhibit attenuated blood pressure and vasoconstrictory responses to PEI but preserved cardiovascular responses to CPT. Collectively, these data are consistent with the concept that the attenuated cardiovascular responses to exercise in PD patients are, in part, mediated by the skeletal muscle metaboreflex. Support or Funding Information Brazilian National Council of Scientific and Technological Development (CNPq), Foundation for Research Support of Federal District (FAPDF), Brazilian Federal Agency for Support and Evaluation of Graduate Education (CAPES). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .