PNF Basic Principle: The Stretch Reflex and The Myth of Reciprocal “Inhibition”
It’s fair to say that when it comes to movement, the stretch reflex is somehow always involved. Whether we are trying to improve mobility or motor control in either the neurological or orthopedic outpatient setting, understanding the science and clinical application of the stretch reflex is a powerful clinical tool.
the Neurophysiology of the stretch reflex
Lets get deep into the micro science and then zoom back out to clinical practice. Our muscles have both intrafusal (spindle) and extrafusal fibers (regular muscle fiber). In the diagram below, the intrafusal fibers - 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 “mini-monitors/calibrators” of resting tension & neurological tone within our muscles that are there to ’protect’ us from injury.
The spindle has sensory receptors (Ia axon in diagram) that are activated anytime the muscle gets stretched. When the length of our connective tissues change during movement, the sensory Ia fibers automatically activate the alpha 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 sensitive to length changes in new ranges 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.
It’s widely accepted that the central nervous system (CNS), specifically subcortical regions of the brain, set the sensitivity of the spindle receptors thus we have no conscious control of this mechanism so it helps to understand it, and work with it, rather than against it in clinical practice.
As discussed in the Traction and Approximation article, with respect to the action potential threshold and joint mechanoreceptors, the CNS will pre-set the action potential threshold of the spindle stretch receptor based on previous injury, previous movement experience, and available force generating capacity at a given range of motion (length-tension curve).
We can’t change a previous injury, but as clinicians and coaches, we can influence movement experience at various joint angles as well as strength (force generating capacity) at various joint angles. This is the reason why contract-relax and post-isometric relaxation techniques can demonstrate short term gains in mobility, and long term gains if done over the course of weeks &/or months.
We’re essentially manipulating the the sensitivity of the receptor’s AP threshold as shown in the image on the right. The zig-zag line that is closer to the dotted line (AP threshold) has less room for activity before a reflex contract is sparked. As oppose to the zig zag line farther from the dotted line.
The myth behind reciprocal “inhibition”
Notice that I did not say that these techniques work because they “relax” our muscles, because the muscles actually don’t relax. Back in the ‘70s and ‘80s, Markos PD and Osternig LR performed EMG studies during PNF contract-relax techniques and they found that as the muscle increases length, post isometric contraction, EMG activity actually increased as the muscle approached end range. If true relaxation was going on, then EMG activity would decrease in the muscle. I think Ian Chrier’s literature review from ‘Evidence-Based Sports Medicine’ by MacAuley and Best (Chapter 7) does a good job at summarizing this. Here is a quote worth including in this discussion:
“When it was first proposed, PNF techniques were based upon the basic science finding that activity of the antagonist muscle creates reciprocal inhibition of the agonist muscle. When tested, PNF techniques were indeed shown to increase ROM more than static stretching. However, these initial studies did not measure muscle activity so the reason for the increased ROM was not known. In fact, when EMG was recorded in 1979, the reciprocal inhibition theory was disproved.(1) Although these results have been confirmed more recently, (2,3,4) the myth of reciprocal inhibition continues to be promoted in textbooks and the medical literature. In fact, muscles are electrically silent during normal stretches until the end ROM is neared. Surprisingly, PNF techniques actually increase the electrical activity of the muscle during the stretch, (1,3-4) even though the range of motion is increased (2,1,5).”
Thus the logical physiological conclusion is that the action potential threshold or sensitivity of the peripheral spindle receptor is being “de-sensitized” by the CNS. So rather than calling this phenomenon autogenic or reciprocal “inhibition” maybe we should call it autogenic or reciprocal “recalibration” as the CNS seems to essentially be re-calibrating the stretch reflex as depicted in the image below.
The image on the left depicts a very sensitive spindle (low dotted line) in the biceps, thus limiting mobility into elbow extension. The image to the right depicts a de-sensitized spindle (higher dotted line) after an isometric contraction of bicep near its previous end range of motion.
As discussed in the reflex model section of this article, according to Mark L. Latash, “Charles Sherrington viewed muscle reflexes not as hardwired stereotypical responses to stimuli but rather as tunable mechanisms that formed the basis of motor behavior. Control of movements, according to Sherrington, was performed by changing parameters of reflexes, in particular of the tonic stretch reflex, an idea very close in spirit to the EP-hypothesis” (See article by Latash: Evolution of Motor Control: From Reflexes and Motor Programs to the Equilibrium-Point Hypothesis)
As a side note, you’ll realize that various articles define agonist/antagonist contract relax differently. the definition of agonist/antagonist contract relax according to the roots of PNF is: 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.” It’s important to make this distinction, so make sure you clarify for yourself how each article or text define the terms before reading.
Lets use an example. With lower back pain, we tend to see a common pattern where the CNS increases the stretch reflex sensitivity of the hamstrings, limiting the active straight leg raise (ASLR). This increases neurological tone which makes the hamstring prematurely contract before the true end range of the ASLR. 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 the muscle will just contract back and fight you as you try to stretch it, that is neurological tone. This is why you’ll hear most people say: “I stretch all the time but I’m still tight.” Helping clients understand the basics of the stretch reflex can help them understand why stretching or the way they are stretching is not working.
So are we just not suppose to stretch?
I think we need to change our intent and mindset as to what the goal of stretching really is.
We need to stretch with the intent to convince our CNS that we are in control of any new motion that we gain during a "stretching" session. How do we convince the CNS that we are in control of new motion? Breath work and progressive isometrics while being keen on time under tension (TUT) seems to be the safest and most effective entry point.
This is when the principle of Appropriate Resistance is critical as it relates to the modulation of the stretch reflex and optimizing access new ranges of motion for the purpose of mobility &/or motor control. Interestingly this starts to feel a lot more like a strength training session rather than the typical “mobility or stretching” session.
Remember that the CNS sets the stretch reflex sensitivity based on previous injury, previous movement experience, and available force generating capacity at a given range of motion. If we want long term changes in mobility &/or motor control we have to prove to the CNS that we are resilient and can produce force in any range of motion that we want to readily access and sustain for the long term.
How could the stretch reflex show up clinically?
Understanding what happens in neurologically compromised situations can enhance our practical understanding with orthopedic cases.
In a neurologically altered situation, i.e a stroke or brain injury, the descending modulation neuro-pathways get damaged and for some reason this makes the spindle fibers extremely sensitive to almost any stimuli (including emotions or a night of minimal sleep). Clinically we see severe abnormal tonal synergies in the limbs which can make voluntary functional use of the limbs almost impossible in certain cases.
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.
In the neurological setting, we can achieve profound functional use of the limbs when we switch focus to optimizing control of proximal segments of the trunk i.e scapula & pelvis while intermittently performing isometrics peripherally.
The same applies in an orthopedic situation when the limited ROM is due to this increase in neurological tone. For example, rather than trying to stretch the hamstrings in someone with low back pain with the intent to passively lengthen the tissue, we’re seeing better results with performing progressive angular isometrics on the hamstrings with intermittent anti-extension core drills to optimize proximal stability for distal mobility.
From a neurological perspective, “tight hamstrings” may be one of the only ways for the CNS to solve “the degrees of freedom problem” in the presence of poor lumbopelvic trunk control. “The degrees of freedom problem” was born from the dynamic systems model of motor control brought fourth by Nicolai Bernstein and is extensively discussed in this article: Dynamic Systems Theory of Motor Development: The Complete Guide for Sports Rehab Professionals.
Clinically, Dr. Kabat and Maggie Knott utilized the neurophysiological principles of the spindle fibers, founded by Dr. Sherrington 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. Understanding the stretch reflex at this level can help re-set our clinical mindset about improving mobility &/or motor control with our clients.
In the clinic, neurological or orthopedic setting, when we see same session improvements with a movement pre-post test this is simply a manifestation of the CNS re-calibrating the stretch reflex. Whether we use isometric techniques, proximal stabilization strategies, or postural challenges we can directly influence the CNS modulation of the stretch reflex in order to optimize mobility and motor control.
references
1. Moore MA, Hutton RS. Electromyographic investigation of muscle stretching techniques. Med Sci Sports Exercise 1980;12:322-9.
2. Magnusson SP, Simonsen EB, Aagaard P, Dyhre-Poulsen P, McHugh MP, Kjaer M. Mechanical and physiological responses to stretching with and without pre-isometric contraction in human skeletal muscle. Arch Phys Med Rehabil 1996;77:373-8.
3. Markos PD. Ipsilateral and contralateral effects of proprioceptive neuromuscular facilitation techniques on hip motion and electromyographic activity. Phys Ther 1979;59:1366-73.
4. Osternig LR, Robertson R, Troxel R, Hansen P. Muscle activation during proprioceptive neuromuscular facilitation (PNF) stretching techniques. Am J Phys Med 1987;66:298-307.
5. Halbertsma JPK, Goeken LNH. Stretching exercises: Effect on passive extensibility and stiffness in short hamstrings of healthy subjects. Arch Phys Med Rehabil 1994;75:976-81.
