
Mitochondrial Capacity and Muscle Endurance in Individuals with Parkinson’s Disease
Author(s) -
Nivita D. Sharma,
Megan Ware,
Kevin K. McCully
Publication year - 2021
Publication title -
medical research archives
Language(s) - English
Resource type - Journals
eISSN - 2375-1924
pISSN - 2375-1916
DOI - 10.18103/mra.v9i1.2325
Subject(s) - skeletal muscle , medicine , vo2 max , stimulation , ischemia , endurance training , oxygen , mitochondrion , mitochondrial myopathy , oxygen metabolism , endocrinology , cardiology , chemistry , mitochondrial dna , heart rate , blood pressure , biochemistry , organic chemistry , gene
Parkinson's disease (PD) is associated with loss of motor control and difficulty exercising. This study measured skeletal muscle mitochondrial capacity and endurance in individuals with and without PD using novel non-invasive methods. We hypothesized that individuals with PD will have decreased mitochondrial capacity, reduced oxygen recovery, and decreased endurance compared to controls. Methods: Eight participants with PD and nine healthy controls were tested. Mitochondrial capacity was measured as the rate of recovery of muscle metabolism after electrical stimulation using near-infrared spectroscopy (NIRS) and repeated short arterial occlusions. Oxygen recovery was measured as the half time of recovery of oxygen levels after 5 minutes of ischemia. Muscle endurance was determined from changes in twitch contraction acceleration during electrical stimulation at 2, 4, and 6 Hz. Results: Mitochondrial capacity was lower in individuals with PD compared to controls (1.5±0.1min-1 vs. 1.7±0.1min-1, p=0.02). Individuals with PD had slower oxygen recovery after ischemia compared to controls (8.9±2.3s vs. 5.4±0.8s, p=0.01). Endurance was not different between groups at 6 Hz (PD vs controls: 58±23% vs. 69±16%, p=0.34). The effect sizes for mitochondrial capacity and oxygen recovery were large (Cohen's d >0.8). The Cohen's d for endurance was 1.11. Conclusion: Individuals with PD had slight impairments in mitochondrial capacity and blood flow but did not have reduced muscle endurance. While our study suggests that muscle metabolic dysfunction may play a minor role in exercise intolerance in people with PD, it demonstrates the use of noninvasive technologies to evaluate muscle function in people with neurological disorders.