Exercise is an important part of healthy living for everyone. However, for people with PD exercise is not only healthy, but a vital component to maintaining balance, mobility and daily living activities. Doing exercise is associated with a better sense of well being, even across stages and severity of the disease. There is a growing consensus amongst researchers about the short- and long-term benefits of exercise for people with PD.

Exercise can benefit in two ways:

Symptom management. Research has shown that exercise can improve gait, balance, tremor, flexibility, grip strength and motor coordination. Exercise such as treadmill training and biking have all been shown to benefit, as has tai chi and yoga (although more studies are needed).
Possibly slowing disease progression. There is a strong consensus among physicians and physical therapists that improved mobility decreases the risk of falls and some other complications of Parkinson’s. They agree that practicing movement—physical therapy, occupational therapy, and participating in an exercise program—improves mobility. By avoiding complications, you can avoid some of the things that can make PD worse. Beyond this, we know that people who exercise intensely, for example by doing things like running or riding a bicycle, have fewer changes in their brains caused by aging. Studies in animals suggest that Parkinson’s disease is also improved by exercise.

How does exercise change the brain?

What happens in the brain to produce these visible benefits? Researchers at the University of Southern California (Fisher et al.) looked at the brains of the mice that had exercised under conditions parallel to a human treadmill study. They found that:

Exercising changed neither the amount of dopamine nor the amount of neurons in the animals’ brains.
But in the ones that had exercised, the brain cells were using dopamine more efficiently.
They also found that exercise improves that efficiency by modifying the areas of the brain where dopamine signals are received — thesubstantia nigra and basal ganglia.

Scientists at University of Pittsburgh found that in animal models, exercise induces and increases the beneficial neurotrophic factors, particularly GDNF (glial-derived neurotrophic factor), which reduces the vulnerability of dopamine neurons to damage.

At the molecular level, at least two things are happening to make dopamine use more efficient:

Dopamine travels across a space between two adjacent brain cells called a synapse. This process is called signaling and it is essential for normal functioning. To end the signal, a protein complex called thedopamine transporter normally retrieves dopamine from the synapse. The first thing Fisher et al. found is that animals that had exercised possessed less of the dopamine transporter, meaning that dopamine stayed in their synapses longer, and their dopamine signals lasted longer.
Secondly, they found that the cells receiving the dopamine signal had more places for the dopamine to bind in animals that exercised, and so could receive a stronger signal. This binding site is called theD2 receptor.
They also studied the D2 receptor in a subset of the human subjects who were within one year of diagnosis and not on any medications, using the imaging technique known as positron emission tomography(PET). They found that in humans, too, exercise increased the number of D2 receptors.

Should exercise be done well before major motor symptoms of PD occur?

YES! Everyone should exercise more, whether they have PD or not.

In PD, a special kind of neuron—brain cells—that produces the chemical transmitter dopamine gets damaged and lost.
However, there is a lag between the time when the loss of neurons begins and the time when Parkinson’s motor symptoms start to show.
In fact, by the time most people are diagnosed, as much as 40-60 percent of their dopamine neurons are already gone.
The reason that people with Parkinson’s don’t experience symptoms until they reach this point is that the brain can compensate for the loss of dopamine neurons by gradually changing to adapt to the situation.
In fact, the brain reshapes itself throughout life in response to experience. Scientists call this ability to change and compensate experience-dependent neuroplasticity.

The Current Research

At Rhodes University in Memphis, TN, Dr. Gerecke et al. report that exercise can protect mice against toxic exposure. MPTP is a neurotoxin that is used as an animal model for Parkinson’s disease, as it selectively kills dopamine neurons in the substantia nigra, the same nucleus that degenerates in Parkinson’s disease. Dr. gerecke showed that 3 months of exercise provided complete protection against MPTP-induced neurotoxicity in mice. Also, if the duration of running was limited to either 1 or 2 months, or if the amount of running daily was decreased, the protective effects of exercise was abolished. Thus, daily, sustained exercise was necessary for full protection. In addition, Gerecke performed proteomic analysis to identify possible mechanisms of this protection, and found that 3 months of exercise induces changes in proteins related to energy regulation, cellular metabolism, cytoskeleton dynamics, and intracellular signaling events.
At the University of Pittsburgh, Dr. Zigmond et al. found that exercise reduces the impairments elicited by the dopaminergic neurotoxins as well as the loss of DA neurons. This study is focused on one of several possible explanations for the beneficial effects of exercise: an exercise-induced increase in the expression of neurotrophic factors, particularly GDNF (glial-derived neurotrophic factors). Observations indicate that GDNF can reduce the vulnerability of DA neurons, in part due to the activation of key intracellular cascades. This raises the possibility that some individuals with Parkinson's disease suffer from a reduction of these neuroprotectivemechanisms, and that treatments that boost these mechanisms - including exercise - may provide therapeutic benefit.
A review of 14 studies on treadmill training found that three studies show an immediate effect of increased walking speed, longer stride length and improved balance as early as after one treadmill session. Longer-term trials, numbering 11 in all, demonstrated not only safety, but positive benefits in gait speed, strike length and related quality of life even several weeks later.
And at the Cleveland Clinic, Dr. Alberts et al. found that when people with Parkinson’s pedaled on a stationery bike 30% faster than their preferred “voluntary” rate (or forced exertion), they not only gained in aerobic fitness, but also showed improvement in motor function and coordination as well as manual dexterity. This improvement was retained some weeks after the exercise stopped.
In a recent study conducted by Beth Fisher et al., researchers at the University of Southern California found that exercise may have an effect on the brain.On a day-to-day basis, people with PD who exercised moved more normally than those who did not. Based on these findings, they believe that exercise may be helping the brain to maintain old connections, form new ones and restore lost ones. They suggest that, in certain situations, the neuroplasticity created from exercise in patients with PD may actually outweigh the effects of neurodegeneration.
The above are just some of the mounting evidence that shows that for people with Parkinson’s, exercise is an essential part of managing the disease. Many researchers are working to better understand this, what makes it happen, and how to achieve the best results and the National Parkinson Foundation is supporting their efforts.

Source parkinson.org