289 Why We Need to Fix the Mechanoreceptors (Part 2)
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Dynamic Chiropractic – September 1, 2016, Vol. 34, Issue 15

Why We Need to Fix the Mechanoreceptors (Part 2)

By Warren Hammer, MS, DC, DABCO

Editor's Note: Part 1 of this article (August 2016) introduced the importance of fixing mechanoreceptors to avoid training uncoordinated muscles and elevating the risk of re-injury.


The muscle spindle, a particular type of mechanoreceptor, is located deep within the muscle belly, encapsulated in fascia made up of intrafusal fibers, all within the extrafusal muscle fibers. According to Kendel,2 "a primary function of proprioceptive reflexes in regulating voluntary movements is to adjust the motor output according to the changing biomechanical state of the body and limbs. This adjustment ensures a coordinated pattern of motor activity during an evolving movement and compensates for the intrinsic variability of motor output."

Motor Nerves and Muscle Contraction

Two motor nerves are involved in the contraction of a muscle, both emanating from the ventral horn of the spinal cord: the alpha motor neuron and the gamma motor neuron.

Gamma motor neurons: Although both motor neurons work simultaneously, for an explanation of spindle cell function we can start with the gamma motor neuron, which causes a contraction of the intrafusal fibers. This stretches the primary and secondary sensory endings in the intrafusal muscle fibers of the spindle cell.

The spindle cell must stretch or be taut during a muscle contraction in order to stimulate afferent information back to the spinal cord. This is the prime function of the gamma neuron that represents 31 percent of the muscle motor supply, emphasizing the importance of the spindle cell.

Thus, during muscle (alpha motor) contraction, gamma motor neurons are firing in order to keep the spindle taut, which allows the spindle to function at all muscle lengths during movement. The gamma keeps the spindle cell sensitive to stretch during a muscle contraction.

When the nervous system sends information to the alpha motor neurons, it also sends information to the gamma motor neurons (alpha-gamma co-activation). The gamma causes stretching of sensory endings in the spindle, and activates type Ia and type II sensory fibers.

Two types of gamma motor neurons affect the firing of the Ia fibers differently: dynamic and static. The dynamic fibers increase the dynamic lengthening response in the Ia spindle receptors of the intrafusal fibers. The static fibers increase the static response of both Ia and II spindle afferents. They monitor the static stretch and length of the muscle. These fibers are slow adaptors and fire both while the muscle is stretching and after the muscle has stopped moving.

Alpha motor neurons: The alpha motor nerve causes a contraction of the extrafusal muscle fibers. The muscle spindle, by way of afferents to the cord, leads to excitation of the alpha motor neurons and contraction of the muscle. It has been found that fascia may become restricted, thereby limiting spindle cell stretching, and abnormally affect its communication with the CNS.

The afferent impulses to the CNS may become diminished as they enter the spinal cord, lessening the effect of the alpha motor neurons in contracting muscles.

Type Ia & II Sensory Fibers

The spindle sensory fibers report back to the CNS the rate (velocity) of change in muscle length and stretch, especially the fast-conducting primary Ia fibers, which make direct connections with the alpha motor neurons that innervate not only the same muscle, but also other muscles with a similar action.  Both sensory fibers detect muscle stretch and their firing rates are proportional to muscle length.

Ia afferent neurons also connect to interneurons, which inhibit the motor neurons that innervate the antagonist muscles (reciprocal inhibition). Ia fibers form inhibitory connections with the alpha motor neurons (Ia inhibitory interneurons).

More than just being involved in the stretch reflex they coordinate muscle contraction during voluntary movements. The interneurons also receive inputs from descending neurons that connect with the spinal motor neurons.

Secondary II spindle endings are also sensitive to muscle length, but less sensitive to rate. They monitor the static stretch and length of the muscle. These fibers are slower adapting, firing while the muscle is stretching and continuing to fire after the muscle has stopped moving.

Spindles also receive neural input from the CNS, which has the ability to modify the sensitivity of the spindles. The spindle sends its messages to the spinal cord, cerebellum, reticular activating system in the brain stem and the motor cortex.

The Benefits of Stimulating Proprioceptive Spindle Cells

There are many studies on the beneficial effects of stimulating proprioceptive spindle cell activity. For example, Riva, et al., treated professional basketball players and found improvements in proprioceptive control in single stance may be a key factor for an effective reduction in ankle sprains, knee sprains, and low back pain. This was a six-year study involving training groups two years at a time.

That said, it appears that receptors stuck in restricted fascia may temporarily respond to stimulation, but will require continuous stimulation over time. There is a strong possibility that local treatment of mechanoreceptors may literally fix them and not require repeated stimulation. Local restoration of spindles can prevent recidivism and allow long-lasting, normal function for mechanoreceptors along a fascial kinetic chain.

Altered spindle feedback results in altered stimulation to the muscles, resulting in altered function. A fascial manipulation hypothesis states that fascial alteration could alter afferent information to the CNS, causing incorrect motor unit functioning and, over time, pain in the corresponding portion of the joint maintaining dysfunction – even in absence of pain.

That old ankle sprain loses its ability to report due to persistent densified fascia; and the muscle supply to the ankle area can become deficient, resulting in repeated strain to the area and eventual compensatory hyper- / hypo-function to the knee, pelvis, hip or back. The knee or back pain patient may need the fascia of the ankle to be treated.

Patients who complain of a painful area with no apparent reason, i.e., the area was never injured, are usually complaining of a compensatory reaction that has been overworking due to possible previous involvement proximal or distal to the painful complaint area.

As often happens, treating the site of complaint may temporarily reduce the pain, but never solve the problem. Is it possible that the "overuse" injury is really an overused area compensating for previous fascial disruptions due to trauma or surgery in a nearby or distant part of the fascial system?

References

6. Leonard CT. The Neuroscience of Human Movement. St. Louis, MO: Mosby, 1998:15-69.

7. Riva D, et al. Proprioceptive training and injury prevention in a professional men's basketball team: a six-year prospective study. J Strength Cond Res, 2016 Feb;30(2):461-75.


Click here for previous articles by Warren Hammer, MS, DC, DABCO.


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