Aim: Parkinson’s disease is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction and reduced expression of PGC-1α, TFAM, and COX play a fundamental role in its pathophysiology. Exercise is recognized as a stimulator of mitochondrial biogenesis; however, its effect on neuronal mitochondrial markers in Parkinson’s disease is less clear. This study aimed to investigate the effects of eight weeks of aerobic, resistance, and combined exercise on the expression of these genes in a 6-OHDA-induced Parkinsonian rat model.
Methods: Fifty Wistar rats were assigned to five groups (control, Parkinsonian, and three exercise groups: aerobic, resistance, and combined). Parkinsonism was induced by 6-OHDA injection, and exercise protocols were performed for 8 weeks (5 days per week), including treadmill running, weighted ladder climbing, or their combination. Then, brain tissues were extracted and the expression of PGC-1α, TFAM, and COX genes was measured by qPCR.
Results: All three types of exercise significantly improved the disease-induced reduction in gene expression (p≤0.05). Combined exercise showed the greatest effect and significantly surpassed aerobic or resistance training alone (p≤0.01). Aerobic training also produced notable positive effects, while resistance training resulted in smaller improvements.
Conclusion: Exercise training, particularly the combination of aerobic and resistance modalities, is an effective strategy to enhance mitochondrial biogenesis markers in the Parkinsonian brain. This molecular adaptation acts as a neuroprotective mechanism and provides strong scientific justification for the clinical application of structured exercise as a non-pharmacological intervention in the management of Parkinson’s disease.
