DE LAAT Exercise PD

 https://www.nature.com/articles/s41531-024-00641-1

Heart-rate chest-strap Participants wore chest straps with a Polar H7 heart rate (HR) monitor (Polar Electro Oy, Kempele, Finland) starting five minutes before, and continuing throughout every exercise session. The target HR for each participant was defined as 80% of his/her maximum HR. Maximum HR was determined according to the formula: Maximum HR = 220-age. Beat-to-beat interval data were collected with the EliteHRV app and filtered using a Butterworth filter to minimize high frequency art

220-70 = 150    220-60 = 160.

nature  npj parkinson's disease  articles  article

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Published: 09 February 2024

Intense exercise increases dopamine transporter and neuromelanin concentrations in the substantia nigra in Parkinson’s disease

Bart de Laat, Jocelyn Hoye, Gelsina Stanley, Michelle Hespeler, Jennifer Ligi, Varsha Mohan, Dustin W. Wooten, Xiaomeng Zhang, Thanh D. Nguyen, Jose Key, Giulia Colonna, Yiyun Huang, Nabeel Nabulsi, Amar Patel, David Matuskey, Evan D. Morris & Sule Tinaz 

npj Parkinson's Disease volume 10, Article number: 34 (2024) Cite this article

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Abstract

Parkinson’s disease (PD) is characterized by a progressive loss of dopaminergic neurons. Exercise has been reported to slow the clinical progression of PD. We evaluated the dopaminergic system of patients with mild and early PD before and after a six-month program of intense exercise. Using 18F-FE-PE2I PET imaging, we measured dopamine transporter (DAT) availability in the striatum and substantia nigra. Using NM-MRI, we evaluated the neuromelanin content in the substantia nigra. Exercise reversed the expected decrease in DAT availability into a significant increase in both the substantia nigra and putamen. Exercise also reversed the expected decrease in neuromelanin concentration in the substantia nigra into a significant increase. These findings suggest improved functionality in the remaining dopaminergic neurons after exercise. Further research is needed to validate our findings and to pinpoint the source of any true neuromodulatory and neuroprotective effects of exercise in PD in large clinical trials.

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Introduction

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN)1. A growing literature has demonstrated the benefits of exercise programs for controlling motor symptoms of PD2,3,4,5. The reported benefits vary according to the type, intensity, and duration of the exercise. Moderate-to-high-intensity exercise multiple times per week for prolonged periods (e.g., 6 months) has been shown to ameliorate the motor severity of PD in clinical trials6,7,8.

Rodent models of PD have shown that exercise-induced improvements in motor performance were accompanied by neuroprotective effects on the dopaminergic neurons in the SN9,10,11,12,13,14,15,16. These neuroprotective effects of exercise are thought to be mediated through neurotrophic, anti-inflammatory, and angiogenic factors. It has been suggested that the interplay between these factors facilitates rescuing of the dopaminergic neurons and increased signaling capacity of healthy dopaminergic neurons17,18. In humans, indirect clinical evidence suggests that exercise may be neuroprotective. Exercise studies in patients with PD support the mediator role of neurotrophic and anti-inflammatory factors in clinical improvement19,20,21. Low pro-inflammatory microglial activation has been proposed as a pathway linking physical activity to brain health based on postmortem examination of older adults without PD but with varying degrees of physical activity22. Postmortem nigral volumes and white matter integrity have been found to be positively correlated with physical activity in older adults without PD23. A positron emission tomography (PET) study using [11C]-raclopride in people with PD demonstrated that a single bout of vigorous cycling by habitual exercisers released significantly more dopamine in the caudate nucleus than the same activity performed by those who were sedentary24. These findings suggest that the benefits of exercise may be due to neuromodulatory effects, such as the preservation of the dopaminergic reserves and enhanced dopamine transmission. However, these putative effects have not been directly investigated in humans with PD in vivo.