# Skeletal Muscle 31P Magnetic Resonance Spectroscopy Study of Patients with Parkinson’s Disease: Energy Metabolism and Exercise Performance

**Authors:** Jimin Ren, Neha Patel, Talon Johnson, Ross Querry, Staci Shearin

PMC · DOI: 10.3390/diagnostics15202573 · 2025-10-13

## TL;DR

This study finds that Parkinson’s disease patients have reduced muscle energy metabolism, and regular exercise may help improve metabolic function and mobility.

## Contribution

The study is the first to use 31P MRS to show peripheral mitochondrial dysfunction in PD and link exercise to metabolic adaptations.

## Key findings

- PD patients had significantly lower ATP synthesis rates at rest compared to controls.
- Exercise recovery of PCr and Pi correlated with weekly exercise time in PD patients.
- Calf-raise training led to modest improvements in range of motion for both PD and control groups.

## Abstract

Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor symptoms such as tremor, bradykinesia, rigidity, and postural instability. In the absence of disease-modifying therapies, exercise remains one of the few interventions shown to effectively reduce fall risk and improve mobility. However, it remains unclear whether skeletal muscle ATP metabolism is impaired in PD, and whether the benefits of exercise arise primarily from improvements in central motor control or peripheral metabolic adaptations. Methods: Fourteen individuals with PD and five healthy controls underwent kinetic 31P Magnetic Resonance Spectroscopy (MRS) to assess resting muscle ATP synthesis and dynamic 31P MRS during in-magnet exercise to evaluate oxidative phosphorylation in active muscle. Results: At rest, ATP synthesis rates mediated by ATPase and creatine kinase (CK) were on average 46 ± 23% and 24 ± 9% lower, respectively, in the PD group compared to controls (p < 0.005), suggesting peripheral mitochondrial dysfunction. During plantar flexion exercise at 15% of lean body mass, range of motion (ROM) was reduced by 22 ± 5% in PD participants (p = 0.01). Despite this, post-exercise recovery of phosphocreatine (PCr) and inorganic phosphate (Pi) was similar between groups. Recovery time constants for PCr and Pi correlated with participants’ total weekly exercise time, indicating a metabolic adaptation to regular physical activity. Modest ROM improvements were observed in both groups following calf-raise exercise training. Conclusions: Reduced skeletal muscle ATP metabolism may contribute to peripheral weakness in PD. Regular exercise appears to promote adaptive metabolic responses, highlighting the need for therapeutic strategies targeting both central and peripheral components of PD.

## Linked entities

- **Proteins:** DNAH8 (dynein axonemal heavy chain 8), CHKA (choline kinase alpha)
- **Chemicals:** phosphocreatine (PubChem CID 9548602)
- **Diseases:** Parkinson’s disease (MONDO:0005180), PD (MONDO:0005180)

## Full-text entities

- **Genes:** CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, DNAH8 (dynein axonemal heavy chain 8) [NCBI Gene 1769] {aka ATPase, SPGF46, hdhc9}
- **Diseases:** PD (MESH:D010300), peripheral weakness (MESH:D018908), tremor (MESH:D014202), rigidity (MESH:D009127), postural instability (MESH:D054972), mitochondrial dysfunction (MESH:D028361), neurodegenerative disorder (MESH:D019636), bradykinesia (MESH:D018476)
- **Chemicals:** PCr (MESH:D010725), ATP (MESH:D000255), inorganic phosphate (MESH:D010710), Pi (MESH:D010716)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12562816/full.md

---
Source: https://tomesphere.com/paper/PMC12562816