Peyton Manning and the Power of Plasticity
Neuroplasticity can be influenced by prior training and current effort.
Posted Jan 22, 2014
This post is about Peyton Manning’s recovery from neck injury and surgery. It’s really about the power of plasticity of the human nervous system. So it has a lot to do with you, too, even if you’re not a future Hall of Fame NFL quarterback.
Peyton Manning experienced considerable neck discomfort and weakness in his arm arising that finally led to a surgical intervention in May of 2011. Unfortunately, further and more invasive surgery was required and in September of the same year he had a fusion of his cervical vertebrae. The recovery after this procedure forced him to miss the entire 2011 NFL season.
Given his outstanding level of play, it was a very frustrating recovery for sure. As reported on ESPN.com, Peyton’s brother Eli Manning said “It just wasn't the same. ... It was frustrating and scary for him. He would look at me and say, 'What looks wrong? Why is it coming out without any pop?” The reduced strength, sensation, and throwing ability are to be expected when nerves are compressed. Compressing a nerve leads to nerve damage. And they were both compressed and damaged by the underlying neck injury and subsequent surgical procedure Peyton Manning experienced.
The effect has to do with what’s in your nerves—bundles of axons. Axons are the output wiring—or information superhighways—of our neurons. Using the metaphor of a highway, we have information in the form of electrical “action potentials” moving down our axons. If they are sensory axons, connected to the skin for example, they can carry information about touch or heat. If they are motor axons, coming from the spinal cord and going out to the muscles, they carry commands about making muscle fibers contract. And when they get compressed, those axons can get sleepy and eventually can die. This can lead to patchy sensation and weakness.
In the peripheral nervous system—that’s the parts that are basically outside our spinal cord and brain—where sensation is coming in and motor commands are going out, those axons have an interesting property—they can regenerate. They can regrow back to the original (or similar) targets and other axons can grow and “sprout” to help reconnect the nervous system. This neuroplasticity takes a while, though.
Regenerating axons—just like the concept of a highway and laying down new asphalt—is a slow but steady process. During his recovery, the axons in the affected cervical nerves of Peyton Manning would regrow at about 1 mm each day. Considering the size of the human body, this means that months would pass before any “reconnections” could be made.
There’s another problem, too. Regeneration is a very similar process to what happened during growth and development but the mature nervous system is a different place. During development there are lots of signs and signaling molecules (called neurotrophins or neurotrophic factors) that helped guide axons to the right places. We still have neurotrophic activity in the mature adult nervous system, but the best environment for growth was, well, when we were growing. This means it’s not easy for the regenerating axons to find the right targets and they can often go to the wrong places.
This zooms us back up from the cellular level of Peyton Manning’s nervous system to Peyton Manning the NFL quarterback with a prodigious work ethic. He has always worked and trained incessantly and fully. By all reports he took this same approach to his recovery and rehabilitation regimen. His nervous system is therefore very highly trained and tuned. Does this mean he can recover more quickly and effectively than an untrained person? It turns out that the answer is “yes, probably”.
There isn’t much evidence that training experience or effort can increase the speed of 1 mm per day that our axons regenerate. But there is evidence that activity can help drive more efficient plasticity. This is a kind of “activity-dependent” neuroplasticity.
At Emory University, Arthur English, Manning Sabatier and colleagues showed that treadmill training could improve and enhance recovery from peripheral nerve injury in the mouse. Compared with mice that weren’t active, relatively modest daily treadmill training enhanced neurotrophic activity to produce longer regenerating axons that found their targets with less misdirection. Physical activity led to a more efficient and effective regenerative process and, importantly, had the functional benefit of more faithfully reconnecting the spinal cord with its originally intended targets.
I’m not suggesting that being active and having a well-trained nervous system will somehow protect you from neurological injury. Instead what I’m suggesting is viewing an active lifestyle as a kind of insurance policy we pay into every time we learn or practice an activity. If we have an injury and have to cash in that “neurological insurance policy”, we have already given ourselves the opportunity to have the best recovery possible.
© E. Paul Zehr (2014)