Parkinson’s disease (PD) is a progressive neurodegenerative disorder that causes both motor and non-motor symptoms and is becoming an increasingly important public health challenge as populations age. Researchers have also identified sarcopenia—the age-related loss of muscle mass, strength, and function—as an important contributor to frailty and disability. In people with PD, sarcopenia has been linked to poorer outcomes, including a greater risk of falls, cognitive decline, and reduced quality of life. These findings have prompted growing interest in understanding how maintaining muscle health could help improve outcomes for people living with Parkinson’s.
Exercise has long been recognised for its benefits in healthy ageing and in chronic conditions such as cancer, dementia, and Parkinson’s disease. Scientists are now exploring whether the molecular changes triggered by exercise can directly protect the brain. To better understand this connection, a research team led by Dr. Miguel Germán Borda reviewed evidence from 129 experimental, observational, and clinical studies. Their comprehensive review, published in Neuroprotection, examined the emerging concept of muscle–brain communication and its potential role in slowing the progression of Parkinson’s disease.
“Our goal was to bring together the available evidence on the relationship between muscle health, exercise, and Parkinson’s disease,” says first author Dr. Salomón Páez-García. The review found that several forms of exercise—including aerobic activities such as walking and jogging, resistance training, balance exercises such as Tai Chi, and programmes combining multiple exercise types—consistently improved physical and cognitive function. Regular exercise enhanced walking ability, balance, muscle strength, mood, thinking skills, and overall quality of life, while reducing falls and disability.
The researchers explain that muscles are far more than structures responsible for movement. During exercise, contracting muscles release hormone-like signalling molecules known as exerkines, allowing muscles to function much like an endocrine organ. These molecules—including brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), irisin, cathepsin B, myostatin, and growth/differentiation factor 15 (GDF15)—enter the bloodstream and communicate with organs throughout the body, including the brain.
According to Dr. Páez-García, exerkines appear to provide the biological link between exercising muscles and brain health. Rather than simply responding to signals from the brain, active muscles send beneficial messages back through these molecules. The review found that exerkines reduce inflammation and oxidative stress, improve mitochondrial function, and help protect dopamine-producing neurons in the substantia nigra, the region most affected in Parkinson’s disease. They also appear to promote neuroplasticity, enabling the brain to adapt and form new neural connections that may improve resilience against disease-related damage.
Current clinical guidelines already recommend beginning exercise early after a Parkinson’s diagnosis and maintaining it throughout the course of the disease. A combination of aerobic, strength, and balance training, tailored to each individual’s abilities, is considered the most effective approach. While more research is needed to determine the optimal exercise dose and identify the exerkines with the greatest long-term neuroprotective effects, the evidence suggests that exercise benefits far more than muscles. By strengthening the body’s natural muscle–brain communication system, regular physical activity may help preserve brain function, slow aspects of disease progression, and improve quality of life for people living with Parkinson’s disease.
More information: Salomón Páez-García et al, Exercise, exerkines, and muscle–brain crosstalk in Parkinson’s disease, Neuroprotection. DOI: 10.1002/nep3.70032
Journal information: Neuroprotection Provided by Chinese Medical Journals Publishing House Co., Ltd.
