Running and the Envelope of Function

We’ve been talking a lot about the “envelope of function” at our clinic lately.  This is a term coined by the physician Scott Dye (who famously had his knee operated on without anesthesia to see which structures were most painful) to describe a tissue homeostasis model, specifically in the knee joint. Basically what all of this means is that you have a range of load that a joint can take before being unable to maintain homeostasis (constant conditions in the internal environment). The upper end of that range is the envelope, the zone immediately above that is the overload zone (increased loading, but not enough to cause structural damage), and past that we have the zone of structural failure. On the other end, we can have the underload zone, where we may fall out of homeostasis as well. Check out the graphs below to digest some of this definition-dense jargon:

Looking at that envelope of function, we see we can push the envelope with either a ton of load infrequently, or a little load very frequently. So what happens when we get hurt? According to this model, we push the envelope too far to the point of failure and our zone of homeostasis shrinks. At this point, maybe that 6 mile run that formerly fell within the envelope is now well outside the new envelope and causes pain. This is all a pretty simplified explanation of the model, but generalizing it leads to my next point;

This model, as well as others like Mueller’s Physical Stress Theory (the first paper we were given to read in PT school), seems to explain tissue adaptation as a whole. Knee pain? Shoulder pain? Big toe pain? What if we apply this to running injuries as a whole?

The tissue homeostasis model can pretty much explain everything, albeit very non-specifically. It doesn’t diagnose the structural damage (if any) that occurs with injury, but it sure lays out an explanation as to why it happened and how we can get back to where we were. Progressive loading/graded exposure to increase the envelope of function is the basis for all adaptation, whether it’s in the context of rehab or improving performance. What’s more is that the “load” we talk about doesn’t necessarily have to mean biomechanical load. Load is affected by a variety of psychosocial factors (stress, pressure to perform well, sleep quality, to mention a few). This explanation expands the tissue homeostasis model, as in many cases of chronic pain we don’t necessarily see tissue damage; there are other factors that lead to sensitization and pain. That’s a rabbit hole to go down in a different post, though.

Here’s an example to make sense of it all:

All winter long, my weekly mileage is low. I get to the indoor track for some workouts, but I hate running outside when it’s less than 40 degrees (so basically 9 months out of the year in Upstate NY). Let’s say that first week when it’s actually okay to get outside comes and I double my weekly mileage. All of a sudden, I’ve got some lateral knee pain at the end of the week. There wasn’t a mechanism of injury and I’m not disfigured, but it hurts to run more than one mile. What happened? Well, I exceeded my envelope of function, and in this case it wasn’t one particular incident, but a week-long increase in frequency and load that reached an overload point. Now, my envelope is lower and I need to start building back up from the bottom. How does one do that? That’s for future posts!

I should say most of my posts will be a little less jargon and a little more running application, but just like that first day of PT school it lays the groundwork for everything to make sense later.

Questions? Comments? I will answer any that don’t push my envelope.

Dr. Jason Tuori, PT, DPT, CSCS

References/cool running readings:

1. Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res. 2005; (436): 100-10.
2. Mueller MJ, Maluf KS. Tissue adaptation to physical stress: a proposed “Physical Stress Theory” to guide physical therapist practice, education, and research. Phys Ther. 2002; 82(4): 383-403.