Next Monday I will be running in the Boston Marathon. Six days after that I take on the London Marathon. Later, in the fall, I expect to toe the starting lines in Berlin, Chicago, and New York City.
My recent marathon efforts have been lackluster and this year’s challenge may further expose my inadequacies. Hence, I have spent some time researching how I might become a better runner.
I’m also curious as to why I am able to take on such exploits given my Parkinson’s disease (PD). Indeed, I have reported many times previously that vigorous exercise has been proven to slow the progression of PD. But why is that exactly? How does this work?
I recently pinged the internet for answers and in reply I got a plethora of technical publications. Reading through them is not for the technologically faint of heart; thankfully I am a man of science.
However I am neither a physician nor an expert in exercise physiology. In fact, I may have learned only just enough to be dangerous. To be sure, PD is like fingerprints, no two people have the exact same manifestation. Thus, you will want to run the following ideas by your medical care teams before embracing them. Please do and let me know what they say.
Notwithstanding, here’s the gist: In performing this research, I am struck by some similarities between what it takes to be a better runner and the strategies for slowing the progression of Parkinson’s disease.
It’s like living in the metaverse of Everything Everywhere All at Once and the verse-jumping point between these two realms is a tiny organelle that powers all cellular activity: the mitochondria.
Here’s to mitochondria!
Mitochondria are life-giving. They make ATP (adenosine triphosphate) from aerobic respiration and ATP is the energy source for many of the critical functions that go on in a cell.
Running requires a lot of energy. Thus, well-functioning mitochondria in sufficient number are necessary for peak performance during a run.
Moreover, when a cell’s mitochondria cease to provide the necessary energy to perform its functions, the cell dies.
Parkinson’s disease, the hallmark of which is a loss of control over motor functions, is caused by the death of certain neurons in the brain that produce the neurotransmitter dopamine. Dopamine is essential for proper motor control. The death of these neurons has been linked to dysfunction of their mitochondria from a variety of factors including mitochondrial clumping of the protein alpha-synuclein.
Protect them.
I’ve read some articles about practices for improving one’s mitochondria. The topic is somewhat controversial. However, a common recommendation is to reduce caloric intake and lessen the amount of highly processed carbohydrates (sugar) in one’s diet. The idea is to lower the stress on the mitochondria — it gets complicated and this post is already on the long side so I won’t go into the details.
But I will report this: There is a class of drugs used for treating PD called MAO-B inhibitors (Selegiline, Rasagiline, among others) that come into play here. MAO-B degrades dopamine such that it can’t be used effectively as a neurotransmitter. These drugs inhibit MAO-B thus increasing the availability of dopamine.
But that’s not all that MAO-B inhibitors can do for people living with Parkinson’s.
Interestingly, the degraded dopamine that MAO-B creates has been linked to processes that damage mitochondria. Hence, the use of MAO-B inhibitors has a protective effect on mitochondria and can therefore boost ATP production.
I have been using Sinemet, a combination of Carbidopa and Levodopa, since my diagnosis in 2018. Beginning in 2020, I have also been taking 10 mg of Selegiline daily. Last year, in an attempt to optimize my dosages, I experimented by stopping all medications for one week and then gradually re-introducing them. I anticipated that my training sessions would go better with the meds. True this, but I was totally surprised by how effective Selegiline was. I ran far better with the combination of the two drugs than with Sinemet alone. In hindsight, it seems likely that the improvement that I got from Selegiline was an enhancement of ATP production and utilization.
May they be fruitful and multiply.
It’s the strangest thing. The theory is that more than a billion years ago when they were both mucking about in the primordial soup, a primitive cell engulfed a bacterium. Their symbiosis became the ancestor of present day animal cells with the bacterium evolving into today’s mitochondria with the responsibility for supplying energy for the organism.
Consequently, mitochondria have their own genome separate from the cell’s nuclear DNA. Also, they are capable of replication, by fission, separately from that of a cell. Mitochondria will replicate due to the energy demands on them. Although there is still some debate about the ideal intensity for stimulating mitochondria counts, most runners and other endurance athletes understand that their workouts can increase the number of mitochondria in their muscles.
Improvement to an athlete’s VO2max — her ability to utilize the oxygen she breaths in — is driven by workouts that create more mitochondria.
Yet, brain cells also have a high demand for energy and it turns out that exercise promotes mitochondria replication in them as well.
Therein lies the best explanation I have at present for running’s ability to slow the progression of Parkinson’s disease. The aerobic exercise that has been shown to increase the quality and quantity of mitochondria in skeletal muscle also does the same for neurons in the brain. With more and better functioning mitochondria, death of the neurons is mitigated and the progression of PD is slowed. Additionally, credit Selegiline with a neuroprotective assist for its ability to pacify MAO-B.
I have only scratched the surface here. There’s more to say regarding the beneficial commonality of specific strength training exercises both to running and Parkinson’s disease. Perhaps I will go into that in later posts.
It’s too late for me to do much more with my mitochondria before my next races. But I’ve got plenty of time to work on this before my fall marathons.
I’ll let you know how it goes in Boston and London.
(Some references used for this post are cited below.)
In 2023, I will be running for Team Fox again. You can donate to my New York City Marathon campaign (click this link). I could use your support. If you share the passion that The Michael J. Fox Foundation (MJFF) and I have for finding a Parkinson’s cure please consider contributing. All donations are meaningful and greatly appreciated.
Alternatively, if you would like something tangible in exchange for a contribution, consider purchasing my book Run With It: A True Story of Parkinson’s, Marathons, the Pandemic, and Love. I’ve heard it’s a good read. Most of the reviews are coming in at four to five stars and it recently was named a Finalist in the 2022 Wishing Shelf Book Awards contest.
All profits from its sale are donated to MJFF. It can be found on my author’s website and Amazon. It’s cheaper on my author site (for domestic shipping), a larger percentage goes to MJFF than for Amazon sales, and you get the option of having it signed by the author.
Selected references:
- Hutchison, A. (2016 June 17). How to Maximize Your Mitochondria. Retrieved from https://www.runnersworld.com/training/a20800596/how-to-maximize-your-mitochondria/
- Nilsson, M. I., & Tarnopolsky, M. A. (2019 May 11). Mitochondria and Aging — The Role of Exercise as a Countermeasure. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627948/
- Ostadkarampour, M. & Putnins, E. E. (2021 April 30). Monoamine Oxidase Inhibitors: A Review of Their Anti-Inflammatory Therapeutic Potential and Mechanisms of Action. Retrieved from https://www.frontiersin.org/articles/10.3389/fphar.2021.676239/full
- Risiglione, P., et al. (2021 May 11). Alpha-Synuclein and Mitochondrial Dysfunction in Parkinson’s Disease: The Emerging Role of VDAC. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8170894/
- Reynolds, G. (2011 Sept 28). How Exercise Can Strengthen the Brain. Retrieved from https://archive.nytimes.com/well.blogs.nytimes.com/2011/09/28/how-exercise-can-strengthen-the-brain/
- Toomey, C. E., et al. (2022 Sept 8). Mitochondrial dysfunction is a key pathological driver of early stage Parkinson’s. Retrieved from https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-022-01424-6
