Autonomic Function in Patients With Parkinson's Disease: From Rest to Exercise

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder classically characterized by symptoms of motor impairment (e.g., tremor and rigidity), but also presenting with important non-motor impairments. There is evidence for the reduced activity of both the parasympathetic and sympathetic limbs of the autonomic nervous system at rest in PD. Moreover, inappropriate autonomic adjustments accompany exercise, which can lead to inadequate hemodynamic responses, the failure to match the metabolic demands of working skeletal muscle and exercise intolerance. The underlying mechanisms remain unclear, but relevant alterations in several discrete central regions (e.g., dorsal motor nucleus of the vagus nerve, intermediolateral cell column) have been identified. Herein, we critically evaluate the clinically significant and complex associations between the autonomic dysfunction, fatigue and exercise capacity in PD.

Keywords: blood pressure; dorsal motor nucleus of the vagus nerve; exercise; parasympathetic activity; sympathetic activity.

FIGURE 1

Heart rate and LF/HF ratio in response to active standing in controls and in patients with PDwith (PD + OH) and without (PD – OH) orthostatic hypotension (A and B, respectively). Non-variable (0V – a proxy of sympathetic activity, C) and very variable (2V – a proxy of parasympathetic activity, D) category of symbolic dynamics analyses of heart rate variability. *P < 0.05 compared with control group. ^†P < 0.05 compared with PD – OH group. Mean data from Vianna et al. (2016).

FIGURE 2

Hypothetical model from Sabino-Carvalho and Vianna (2020) of the potential deleterious consequences of altered group III and IV skeletal muscle afferent activity in PD. Diminished skeletal muscle afferent signaling, together with central degeneration in PD, can result in a blunted sympathetic vasoconstriction leading to a blunted pressor response and, consequently, to lower increase blood flow to the active muscle, which may lead to metabolic distress, tissue/brain hypoperfusion, fatigue, cardiac autonomic imbalance, and an impaired exercise capacity.

FIGURE 3

Mean and individual data from Sabino-Carvalho et al. (2018) demonstrated that mean BP (MBP) responses to exercise and post-exercise ischemia (PEI) are attenuated in patients with PD compared to healthy control (CT) subjects. These blunted cardiovascular responses to isometric handgrip exercise in patients with PD are partially attributable to an altered metaboreflex. CO, Cardiac output; TPR, total peripheral resistance.