On the hemodynamic response to exercise in Parkinson’s disease: does neurogenic orthostatic hypotension matter?

Fabio Giuseppe Laginestra; Danilo Iannetta; Erin Suttman; Jeremy Alpenglow; Kanokwan Bunsawat; Ryan Broxterman; Guillaume Lamotte; Markus Amann

doi:10.1152/physiol.2026.41.S1.2346830

Abstract only Parkinson’s disease is a neurodegenerative disorder characterized by a spectrum of motor and non-motor symptoms. Cardiovascular autonomic dysfunction is a major non-motor manifestation that affects roughly half of all people with Parkinson’s and can manifest as neurogenic orthostatic hypotension (OH) upon standing. Despite growing interest in this area, data describing cardiovascular responses to physical activity in people with Parkinson’s disease are limited and lack distinction between patients with vs. without OH. Moreover, the impact of cardiovascular autonomic dysfunction (i.e., OH) on circulatory adjustments to exercise in people with Parkinson’s is unknown. Therefore, the aim of this study was to characterize and compare central and peripheral hemodynamic responses to exercise in people with Parkinson’s disease with (PD-OH) and without (PD) OH, and to contrast these responses with those observed in healthy individuals. Five PD (age: 67±10 years, 1 female), 4 PD-OH (73±6 years, 1 female), and 7 matched healthy controls (CTRL; 64±4 years, 2 females) were recruited for this study. Both patient groups remained on their optimal pharmacological treatment strategy using carbidopa/levodopa. All participants performed an incremental dynamic single-leg knee-extension test with either 5 W (males) or 3 W (females) increments every 2 minutes. Leg blood flow (LBF) was quantified using Doppler ultrasound during the second minute of each stage. Mean arterial pressure (MAP) and cardiac output (CO) were continuously measured using finger photoplethysmography and averaged over the final minute of each stage. Leg vascular conductance (LVC) and systemic vascular conductance (SVC) were calculated as LBF/MAP and CO/MAP, respectively. Linear mixed models were used to quantify the slopes that characterized how each outcome variable changed in relation to absolute work rate. Baseline cardiovascular responses before starting exercise were not different between groups (all P > 0.27). Peak work rates for CTRL, PD, and PD-OH were 41 ± 17 W, 34 ± 16 W, and 27 ± 14 W, respectively. During exercise, the slope determined by the change in MAP over work rate differed between PD-OH vs CTRL and PD (both P < 0.01), but it was not different between CTRL and PD (P = 0.13). Of note, MAP did not increase throughout exercise in the PD-OH group (slope not significantly different from zero). LBF and LVC significantly increased with work rate in all groups. While the LBF slope was not different between CTRL and PD (P = 0.99), it was higher in PD-OH (both P < 0.02). Similarly, the LVC slope was not different between CTRL and PD (P = 0.44), but it was substantially higher in PD-OH (both P < 0.001). The CO response to exercise was not different between groups (P > 0.10). SVC significantly increased with work rate in all groups. However, the SVC slope was not different between CTRL and PD (P = 0.94), but it was significantly higher in PD-OH (both P < 0.001). The current data indicate that the abnormal cardiovascular response to exercise in Parkinson’s disease is not ubiquitous, but specific to the presence of cardiovascular autonomic dysfunction. Specifically, while PD exhibited hemodynamic adjustments comparable to CTRL (i.e., normal increases in MAP, LVC, and SVC), PD-OH demonstrated a profound pressor deficit. This issue does not appear to stem from compromised CO response, but rather from exaggerated peripheral and systemic vasodilation. These findings are consistent with reduced sympathetic vasoconstrictor restraint, which hinders the normal increase in MAP during physical exertion. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

On the hemodynamic response to exercise in Parkinson’s disease: does neurogenic orthostatic hypotension matter?

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