What do you know about the Ia Afferents?

This is a nice study looking at lateral gastroc activity and changing firing patterns with speed of movement. Great if you treat anyone or anything that walks...

Ia afferents

You remember them, large diameter afferent (sensory) fibers coming from muscle spindles and appraising the nervous system of vital information like length and rate of change of length of muscle fibers, so we can be coordinated. They act like volume controls for muscle sensitivity. Turn them up and the muscle becomes more sensitive to ANY input, especially stretch (so they become touchy…maybe like you get if you are hungry and tired and someone asks you to do something); turn them down and they become less or unresponsive.

Their excitability is governed by the sum total (excitatory and inhibitory) of all neurons (like interneuron’s) acting on them (their cell bodies reside in the anterior horn of the spinal cord).

If we slow things down, the rate of change of length slows as well and excitability decreases, like we see in this study (3-6% slower). We also notice that the length of contraction increases; hmmm, why doesn’t it decrease?

Remember these folks are on a treadmill. The treadmill is constantly moving, opposite the direction of travel. With the foot on the ground, this provides a constant rate of change of length of the gastroc/soleus (ie, it is putting it through a slow stretch); so , once the muscle is activated, it contracts for a longer period of time because of the treadmill putting a slow stretch on the gastroc (and soleus).

This article also talks about people with upper motor neuron lesions. An important set of inhibitory neurons come from higher centers of the brain, in the motor cortex. These tend to attenuate the signals affecting the Ia afferents, and keep us stable. When we have an upper motor neuron lesion (like a brain lesion or stroke), we lose this “attenuation” and the stretch reflexes (and muscle tone) becomes much more active (actually hyperactive), making the muscle more sensitive to stretch. This loss of attenuation, along with differing firing patterns of the gastroc are important to remember in gait rehab.

The soleus and medial gastroc begin firing in the first 10% of the gait cycle (at the beginning of loading response) and fire continuously until pre swing (peaking just after midstance). The lateral head begins firing at midstance; both heads (along with soleus) decelerate the forward momentum of the tibia, flex the knee at midstance, and the medial head assists in adducting the calcaneus to assist in supination.

Making sure these muscles fire appropriately is important and needling is just one way of helping them to function better. Don’t overlook the tricep surae on your next patient that has a “hitch in their giddyup”.

Effects of treadmill walking speed on lateral gastrocnemius muscle firing.

by Edward A Clancy, Kevin D Cairns, Patrick O Riley, Melvin Meister, D Casey Kerrigan

American journal of physical medicine rehabilitation Association of Academic Physiatrists (2004) Volume: 83, Issue: 7, Pages: 507-51 PubMed: 15213474

Abstract

OBJECTIVE: To study the electromyographic profile-including ON, OFF, and peak timing locations-of the lateral gastrocnemius muscle over a wide range of walking speeds (0.5-2.1 m/sec) in healthy young adults. DESIGN: We studied gastrocnemius muscle-firing patterns using an electromyographic surface electrode in 15 healthy subjects ambulating on a treadmill at their normal walking speed and at three paced walking speeds (0.5, 1.8, and 2.1 m/sec). Initial heel contact was determined from a force-sensitive switch secured to the skin over the calcaneous. RESULTS: For all speeds, the gastrocnemius firing pattern was characterized by a main peak, occurring 40-45% into the gait cycle, that increased in amplitude with walking speed. Speeds of > or =1.3 m/sec produced a common electromyographic timing profile, when the profile is expressed relative to the stride duration. However, at 0.5 m/sec (a speed typical of individuals with upper-motor neuron lesions), the onset of gastrocnemius firing was significantly delayed by 3-6% of the gait cycle and was prolonged by 8-11% of the gait cycle. CONCLUSION: Many patients with upper motor neuron lesions (e.g., stroke and traumatic brain injury) walk at speeds much slower than those commonly described in the literature for normal gait. At the slow walking speed of 0.5 m/sec, we have measured noticeable changes in the electromyographic timing profile of the gastrocnemius muscle. Given the importance of appropriate plantar flexor firing patterns to maximize walking efficiency, understanding the speed-related changes in gastrocnemius firing patterns may be essential to gait restoration.

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.

More thoughts on stretching

   We get a lot of interest in our posts on stretching. Seems like this is a pretty hot subject and there is a lot of debate as to whether it is injury preventative or not. Are you trying to physically lengthen the muscle or are you trying to merely bring it to its physiological limit?  There’s a big difference in what you need to do to accomplish each of these goals. Lets take a look at each, but 1st we need to understand a little about muscles and muscle physiology.

 Muscles are composed of small individual units called sarcomeres. Inside of these “sarcomeres” there are interdigitating fibers of actin and myosin (proteins) which interact with one another like a ratchet when a muscle contracts.  Sarcomeres can be of various lengths, depending on the muscle, and are linked and together from one end of the muscle to the other. When a muscle contracts concentrically (the muscle shortening while contracting) the ends of the sarcomere (called Z lines or Z discs) are drawn together, shortening the muscle fiber over all (see the picture above).
 
 Signals are sent from the brain (actually the precentral gyrus of the cerebral cortex areas 4, 4s and 6) down the corticospinal tract to the spinal cord to synapse on motor neurons there.  These motor neurons (alpha motor neurons) then travel through peripheral nerves to the muscles to cause them to contract (see picture above).

   The resting length of the muscle is dependent upon two factors:
The physical length of the muscle
2. The “tone” of the muscle in question.

The physical length of the muscle is determined by the length of the sarcomeres and the number of them in the muscle.   The “tone” of the muscle determined by an interplay of neurological factors and the feedback loops between the sensory (afferent) receptors in the muscle (Ia afferents, muscle spindles, Golgi tendon organs etc.), relays in the cerebellum and basal ganglia as well as input from the cerebral cortex.

 If you’re trying to “physically lengthen” a muscle, then you will need to actually add sarcomeres to the muscle. Research shows that in order to do this with static stretching it must be done 20 to 30 minutes per day per muscle.

 If you were trying to “bring a muscle to its physiological limit” there are many stretching methods to accomplish this.  Pick your favorite whether it be a static stretch, contract/ relax, post isometric relaxation etc. and you’ll probably be able to find a paper to support your position.

  Remember with both not to ignore neurological reflexes (see above). Muscle spindle loops are designed to provide feedback to the central nervous system about muscle length and tension. Generally speaking, slow stretch activates the Ia afferent loop which causes causes physiological contraction of the muscle (this is one of the reasons you do not want to do slow, steady stretch on a muscle in spasm). This “contraction” can be fatigued overtime, causing the muscle to be lengthened to it’s physiological limit.  Do this for an extended period of time (20-30 mins per day) and you will physically add sarcomeres to the muscle.

 Next time you are stretching, or you were having a client/patient stretch, think about what it is that you’re actually trying to accomplish  because there is a difference.

We are and remain The Gait Guys.  Bald, good-looking, and above-average intelligence. Spreading gait literacy with each post we publish.

thanks to scienceblogs.com for the corticospinal tract image