PNF Basic Principle: The Stretch Reflex

First, let me attempt to simplify and review some neuromuscular physiology of the sensory spindle fibers (intrafusal fibers) that exist in our muscle tissue and the stretch reflex before we get into real world application. For more nerdy details check out Laurie Lundy-Ekman’s book Neuroscience: Fundamentals for Rehabilitation.


Our muscles have both intrafusal (spindle) and extrafusal fibers (regular muscle fiber). In the diagram below the spindle fiber is the skinny yellow strand.  Extrafusal fibers are what we all think of when we think of muscles: the proteins that actually contract and move.

The spindle fibers never get as much attention, even though they are a lot more interesting. Think of the spindle fibers as the “monitors/calibrators” of tension/tone within our muscles that are there to ’protect’ us from injury. 

The spindle has sensory receptors (Ia axon) that are activated anytime the muscle gets stretched. When a muscle gets stretched, the sensory Ia fibers automatically activate the alpha (shown in the diagram) and gamma motor neurons in the spinal cord. The alpha motor neurons make the actual muscles contract back a little bit in response to that stretch. 

The gamma motor neurons make the ends of the spindle fibers contract in order to keep the spindle “receptive” to length changes in the new range of motion (ROM). This is how the muscle spindle is able to stay sensitive in a moment to moment basis to length changes no matter what the joint angle / muscle length is.

So if something happens fast and delivers an unexpected quick stretch to the tissue that is potentially harmful, the spindle will send an automatic impulse to the muscle to contract back as a protective mechanism to “prevent” an overstretch injury. This is a reflex, meaning all this happens at the spinal cord level before our brains even realize what just happened. In other words we have no conscious control of this mechanism so it helps to understand it and respect it.

If the gamma motor neuron was not constantly contracting the ends of the spindle fibers and keeping it “in tune” as the muscle changes length, then the spindle fibers would only be able to protect us from an unexpected stretch at selective ranges of motion and we wouldn’t have this automatic protective mechanism.

Another interesting piece of this is that there are signals that come from the brain (originating in the subcortical areas of the brain) that can turn up the sensitivity of the spinal fibers, which would only allow us to lengthen the muscle in small ranges of motion before the muscle would contract back and not allow us to go any farther.  

An example of this is many times after a back injury the nervous system will increase the sensitivity of the spindle fibers in the hamstrings. This will increase the neurological tone (The hamstring will literally "fight/contract" against increased range of motion) in the hamstrings in order to give the low back additional stability. This is what people will sometimes think of as “tightness” like a short rope that needs to be stretched and lengthened. 

In the scenario of a“neurologically tight” muscle it would not be wise to just forcefully stretch it, because as discussed above it’s a mechanism which serves as an “internal brace” to guard/protect us against instability, so the muscle will just contract back and fight you as you try to stretch it. This is why you’ll hear most people say:

“I stretch all the time but I’m still tight.”

So are we just not suppose to stretch? 

No. That wouldn't be wise either. 

We need to change our intent/mindset as to what the goal of stretching is. 

We need to stretch with the intent to convince our nervous system that we are in control of any new motion that we gain during a "stretching" session. 

You can think of it as active stretching.

In a neurologically altered situation, when neurons in the brain get damaged (due to a stroke or brain injury) those “spindle” modulation pathways get damaged and for some reason this also makes the spindle fibers go hay wire and extremely sensitive to almost any stimuli (including emotions or a night of minimal sleep). The spindle fibers’ threshold for activation is significantly lowered and we see severe abnormal tonal synergies in the limbs which can make voluntary functional use of the limbs almost impossible in certain cases.

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Clinically, Dr. Kabat and Maggie Knott utilized the neurophysiological principles of the spindle fibers founded by Dr. Sherington in the 1930s  to either: induce voluntary muscle contractions or to reduce abnormal tone by using techniques that help to “recalibrate” the spindle sensitivity levels in those who had a neurological impairment.

When dealing with abnormal tone (in an orthopedic or neurological setting), the good old “contract relax” that PNF is known for is a great tool to help re-calibrate the spindle sensitivity level. Unfortunately the foundational intent of re-calibrating the stretch reflex is often insulted when those who use it, forget to follow up the technique with neuro re-education or in other words teach the neuromuscular system how to actively gain control of the newly acquired range of motion that the technique allowed you to “magically” gain in the first place.

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 For example, teaching the hip flexor how to contract in the new range achieved after utilizing a contract relax (post contraction relaxation) on the hamstrings allows the system to perceive a sense of control in the new range of motion. This makes that new range of motion more likely to last if hip flexion and knee extension are consistently trained in the new range of motion (ROM). In this way we can help to re-set the sensitivity of the spindles in the hamstrings, which will allow for the hamstring to enter a new range of motion without the nervous system increasing the tone or "the fight" of the hamstrings. 

There are two topics that are often very confusing that I would like to attempt to clarify. First, is the definition of agonist/antagonist contract relax. In PNF, the tissues that are limiting the ROM are defined as the “antagonists” (the bad guys) and the tissues that help contract into the desired ROM are defined as the “agonists”.

 If you look into the literature that discusses Agonist/Antagonist contract relax you’ll realize that various articles define Agonist/Antagonist contract relax differently, so make sure you clarify for yourself how each article or text define the terms before reading.

Second, is the thought that reciprocal inhibition (better thought of as reciprocal innervation) is the reason why there are long lasting changes in ROM after we “contract” the agonist. Dr. Sherington founded that reciprocal innervation is a spinal cord reflex that is short lived and that it is only manifested in the act of the agonist contracting. Reciprocal innervation actually dies out almost immediately after the agonist relaxes. Interestingly enough there were a couple studies that showed that EMG levels actually increased in the antagonist muscle when the agonist was contracting. This suggests that an eccentric contraction is going on in the antagonist (not true relaxation) as the agonist contracts concentrically. 

It may be better to think of contracting the muscles that work against the “limiting tissue” as a means of teaching the neuromuscular system how to actively utilize the new ROM by convincing the CNS that it doesn’t have to make the spindle fibers that sensitive, thus reducing the protective tone of the muscle and the perceived threat to length changes. You’re basically telling the system “I 'm in control of this motion, take off the breaks, and let go.”

Understanding this stretch stimulus principle will help guide your intent when trying to gain ROM/”stretch” tissue. It will make you want to differentiate between neurological tone tightness and actual mechanical stiffness before deciding what mobility treatment technique to use.

Dr. Andreo Spina discusses this application to soft tissue management in regards to orthopedic and sports medicine in his system Functional Range Release. I would highly recommend taking Dr. Spina’s courses as he has helped me find the connection between this stretch reflex principle and sports medicine/orthopedics application.

 If you have worked with patients that have true neurological tone secondary to a brain injury you know that you won’t get anywhere if you try to “stretch” and fight that tone with the mindset that you are going to mechanically “lengthen it”, sometimes that makes the tone actually get worse.

The same applies in an orthopedic situation when the limited ROM is due to this increase in neural tone after an injury. This can explain why people will say things like “I feel really loose and good after a massage or yoga, but after a little while the tightness comes right back”. The tightness might be coming back because the spindles have only been trained to be sensitive and reactive in that little ROM that you demonstrate/actively use. Allowing you ROM beyond where the spindles can pick up on length changes would do you a dis-service and in theory increase your risk for injury. 

So if you do a mobility routine and gain range of motion in that session, be able to demonstrate muscle contractions in that new range of motion instead of just passively pulling on stuff to make it "longer". 

Ramez Antoun