The Power of Facilitation: How to supercharge your run.

While running intervalsone morning, something dawned on me. My left knee was hurting from some patellar tracking issues, but only on initial contact and toe off. I generally run with a midfoot strike. I began concentrating on my feet, lifted and spread my toes and voila! my knee pain instantly improved. Very cool, and that is why I am writing this today. 

Without getting bogged down in the mire of quad/hamstring facilitation patterns, lets look at what happened.

I contracted the long extensors of the toes: the extensor digitorum longus and the extensor hallicus longus; the short extensors of my toes: the extensor digitorum brevis, the extensor hallucis brevis: as well as the dorsal interossei.the peroneus longus, brevis and tertius were probably involved as well.

Do you note a central theme here? They are all extensors. So what, you say. Hmmm… 

Lets think about this from a neurological perspective:

In the nervous system, we have 2 principles called convergence and divergence. Convergence is when many neurons synapse on one (or a group of fewer) neuron(s). It takes information and “simplifies” it, making information processing easier or more streamlined. Divergence is the opposite, where one(or a few) neurons synapse on a larger group. It takes information and makes it more complicated, or offers it more options.

In the spinal cord, motor neurons are arranged in sections or “pools” as we like to call them in the gray matter of the cord. These pools receive afferent information  and perform segmental processing (all the info coming in at that spinal cord segment) before the information travels up to higher centers (like the cerebellum and cortex). One of these pools fires the extensor muscles and another fires the flexor muscles.. 

If someone in the movie theater keeps kicking the back of our seat, after a while, you will say (or do) something to try and get them to stop. You have reached the threshold of your patience. Neurons also have a threshold for firing.  If they don’t reach threshold, they don’t fire; to them it is black and white. Stimuli applied to the neuron either takes them closer to or farther from threshold.  When a stimulus takes them closer to firing, we say they are “facilitating” the neuron. If it affects a “pool” of neurons, then that neuronal pool is facilitated. If that pool of neurons happens to fire extensor muscles, then that “extensor pool” is facilitated.

When I consciously fired my extensor muscles, two things happened: 1. Through divergence, I sent information from my brain (fewer neurons in the cortico spinal pathway) to the motor neuron pools of my extensor muscles (larger groups of motor neurons) facilitating them and bringing them closer to threshold for firing and 2. When my extensor muscles fired, they sent that information (via muscle spindles, golgi tendon organs, joint mechnoreceptors, etc) back to my cerebellum, brain stem and cortex (convergence) to monitor and modulate the response.

When I fired my extensor muscles, I facilitated ALL the neuronal pools of ALL the extensors of the foot and lower kinetic chain. This was enough to create balance between my flexors and extensors and normalize my knee mechanics.

If you have followed us for any amount of time, you know that it is often “all about the extensors” and this post exemplifies that fact.

 Next time you are running, have a consciousness of your extensors. Think about lifting and spreading our toes, or consciously not clenching them. Attempt to dorsiflex your ankles and engage your glutes. It just may make your knees feel better!

Gaining Anterior Length, Through Posterior Strength. A Lesson in Reciprocal Inhibition

Gaining Anterior Length, Through Posterior Strength and vice versa….A Lesson in Reciprocal Inhibition

I found a really cool article, quite by accident. I was leafing through an older copy of one of, if not my favorite Journals “Lower Extremity Review” and there it was. An article entitled “Athletes with hip flexor tightness have reduced gluteus maximus activation”. Wow, I thought! Now there is a great article on reciprocal inhibition! This reminded me of a piece we wrote some time ago

What is reciprocal inhibition, also called “reciprocal innervation” you ask? The concept, was 1st observed as early as 1626 by Rene Descartes though observed in the 19th century, was not fully understood and accepted until it earned a Nobel prize for its creditor, Sir Charles Sherrington, in 1932.

Simply put, when a muscle contracts, its antagonist is neurologically inhibited (see the diagram above) When your hip flexors contract, your hip extensors are inhibited. This holds true whether you actively contract the muscle or if the muscle is irritated in some manner, causing contraction. The reflex has to do with muscle spindles and Type I and Type II afferents which I have covered in an article I wrote some time ago.

We can (and often do) take advantage of this concept with treating the bellies of hip flexors (iliopsoas, tensor fascia lata, rectus femoris, iliacus, iliocapsularis) and extensors (gluteus maximus, posterior fibers of gluteus medius). This is especially important in folks with low back pain, as they often have increased psoas activity and cross sectional area, especially in the presence of degenerative changes.

There also appears to be a correlation between decreased hip extension and low back pain, with a difference of as little as 10 degrees being significant. Take the time to do a thorough history and exam and pay attention to hip extension and ankle dorsiflexion as they should be the same, with at least 10 degrees seeming to be the “clinical” minimum. Since the psoas should only fire at the end of terminal stance/preswing and into early swing, problems begin to arise when it fires for longer periods.

Can you see now how taking advantage of reciprocal inhibition can improve your outcomes? Even something as simple as taping the gluteus can have a positive effect! Try this today or this week in the clinic, not only with your patients hip flexors, but with all muscle groups, always thinking about agonist/antagonist relationships.

In the moment: Sports medicine  Jordana Bieze Foster: Athletes with hip flexor tightness have reduced gluteus maximus activation  Lower Extremity review Vol 6, Number 7 2014

https://tmblr.co/ZrRYjx1VG3KYy

Mills M, Frank B, Blackburn T, et al. Effect of limited hip flexor length on gluteal activation during an overhead squat in female soccer players. J Athl Train 2014;49(3 Suppl):S-83.

Ciuffreda KJ, Stark L.  Descartes’ law of reciprocal innervation. Am J Optom Physiol Opt. 1975 Oct;52(10):663-73.
Jacobson M Foundations of Neuroscience Springer Science and Business Media, Plenum Press, NY 1993 p 277

http://www.nobelprize.org/nobel_prizes/medicine/laureates/1932/sherrington-bio.html

https://thegaitguys.tumblr.com/post/9708399904/ah-yes-the-ia-and-type-ii-afferents-one-of-our

Arbanas J, Pavlovic I, Marijancic V, et al MRI features of the psoas major muscle in patients with low back pain. Eur Spine J. 2013 Sep;22(9):1965-71. doi: 10.1007/s00586-013-2749-x. Epub 2013 Mar 31.

Roach SM, San Juan JG, Suprak DN, Lyda M, Bies AJ, Boydston CR. Passive hip range of motion is reduced in active subjects with chronic low back pain compared to controls. Int J Sports Phys Ther. 2015 Feb;10(1):13-20. Erratum in: Int J Sports Phys Ther. 2015 Aug;10(4):572.

Paatelma M Karvonen E Heiskanen J Clinical perspective: how do clinical test results differentiate chronic and subacute low back pain patients from “non‐patients”? J Man Manip Ther. 2009;17(1):11‐19.[PMC free article] [PubMed]

Evans K Refshauge KM Adams R Aliprandi L Predictors of low back pain in young adult golfers: a preliminary study. Phys Ther Sports. 2005;6:122‐130.

Mellin G Correlations of hip mobility with degree of back pain and lumbar spinal mobility in chronic low‐back pain patients. Spine. June 1988;13(6):668‐670. [PubMed]

Lewis CL, Ferris DP. Walking with Increased Ankle Pushoff Decreases Hip Muscle Moments. Journal of biomechanics. 2008;41(10):2082-2089. doi:10.1016/j.jbiomech.2008.05.013.

Nodehi-Moghadam A, Taghipour M, Goghatin Alibazi R, Baharlouei H. The comparison of spinal curves and hip and ankle range of motions between old and young persons. Medical Journal of the Islamic Republic of Iran. 2014;28:74.

Daniel Moon , MD, MS; Alberto Esquenazi , MD Instrumented Gait Analysis: A Tool in the Treatment of Spastic Gait Dysfunction JBJS Reviews, 2016 Jun; 4 (6): e1. http://dx.doi.org/10.2106/JBJS.RVW.15.00076

Kilbreath SL, Perkins S, Crosbie J, McConnell J. Gluteal taping improves hip extension during stance phase of walking following stroke. Aust J Physiother. 2006;52(1):53-6.

Taking advantage of the stretch reflex and reciprocal inhibition; or the “reverse stretch”

Reciprocal inhibition is a topic we have spoken about before on the blog (see here). The diagram above sums it up nicely. Note the direct connection from the spindle to the alpha motor neuron, which is via a Ia afferent fiber.  When the spindle is stretched, and the pathway is intact, the uscle will contract. What kind of stimulus affects the spindle? A simple “stretch” is all it takes. Remember spindles respond to changes in length. So what happens when you do a nice, slow stretch? You activate the spindle, which activates the alpha motor neuron. If you stretch long enough, you may fatigue the reflex. So why do we give folks long, slow stretches to perform? Certainly not to “relax” the muscle!

How can we “use” this reflex? How about to activate a weak or lengthened muscle? Good call.

Did you notice the other neuron in the picture? There is an axon collateral coming off the Ia afferent that goes to an inhibitory interneuron, which, in turn, inhibits the antagonist of what you just stretched or activated. So if you acitvate one muscle, you inhibit its antagonist, provided there are not too many other things acting on that inhibitory interneuron that may be inhibiting its activity. Yes, you can inhibit something that inhibits, which means you would essentially be exciting it. This is probably one of the many mechanisms that explain spasticity/hypertonicity

How can we use this? How about to inhibit a hypertonic muscle?

Lets take a common example: You have hypertonic hip flexors. You are reciprocally inhibiting your glute max. You stretch the hypertonic hip flexors, they become more hypertonic (but it feels so good, doesn’t it?) and subsequently inhibit the glute max more. Hmm. Not the clinical result you were hoping for?

How about this: you apply slow stretch to the glutes (ie “reverse stretch”) and apply pressure to the perimeter, both of which activate the spindle and make the glutes contract more. This causes the reciprocal inhibition of the hip flexors. Cool, eh? Now lightly contract the glutes while you are applying a slow stretch to them; even MORE slow stretch; even MORE activation. Double cool, eh?

Try this on yourself. Now go try it on your clients and patients. Teach others. Spread the word.

Reciprocal Inhibition anyone? Thanks to The Manual Therapist (Erson Religioso) for this great post.

What they are doing here is taking advantage of what Sherrington know many years ago. Activating a muscle (agonist for a movement) will inhibit the muscle with the opposite action (antagonist for a movement), through a disynaptic, post synaptic pathway. It is a great way to gain additional movement and remove or reduce muscular inhibition. Try it!