#stretch reflex

Hello fellow sports scientists. I will be informing myself and anyone interested regarding certain topics related to sports science that I have researched and picked up from university. I will also try my best in sharing the latest interesting research in this field and others alike. It would make me very happy if anyone could share their knowledge so that we can learn from one another and prove that upon closer examination, sports science isn't as simple as many people think it is. Without further ado, this week I will be writing about motor units.

Different motor neurones innervate certain types of muscle. Alpha motor neurons are the largest in diameter, while also having the fastest conduction velocity and innervate extrafusal muscle, which refers to skeletal muscles used to perform conscious movements that originate from the motor cortex in the brain. On the other hand, beta motor neurons innervate intrafusal muscles (also called muscle spindles), which prevent damage to the skeletal muscles by preventing over-lenghtening under great tension/load (helps produce stretch reflex). These spindles are found in the muscle belly and are embedded in extrafusal fibres, while being covered with connective tissue. Lastly, Gamma motor neurons sense whether the surrounding extrafusal muscle is lengthening or shortening and accordingly sends sensory information to intrafusal muscle to undergo the same movements. All of these act to create fine movements and to prevent the skeletal muscles from over stretching. 

Next, innervation ratio will be explained and how this determines functionality of muscles. Innervation ratio refers to the number of muscle cells that can be excited/innervated by a single motor unit. Muscles that require finer movements, such as the lateral rectus (an eye muscle) have a lower innervation ratio. In this case, one motor unit (a number of motor neurons connecting onto different strands of muscle fibres, which are controlled by one motor unit) innervates 9 muscle fibres, however there a total of 2970 motor units in total. On the contrary, the medial gastrocnemius (a muscle in the lower leg) has 579 motor units, but each unit innervates 1934 muscle fibres. It seems that muscles that require greater force production, but less specificity have a higher innervation ratio with a lower number of units and vice versa for muscles requiring finer movements.  Below are a few more examples.

Now, the origins and layout of motor neurons will be examined closer. Motor neurons originate from the spinal cord and tend to be clustered within close proximity to one another. The soma (cell body) of motor neurons are found in the ventral horn of the spinal cord, which is covered by grey matter and their axons travel all the way to an effector (muscle or gland) to produce an effect via electrical impulse. An interesting aspect is that certain areas of the ventral horn will consist of motor neuron clusters responsible for a activating flexer or extensor muscles. Others will activate the proximal and axial muscles, as well as distal muscles as well. 

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?

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Perform the Myotatic Crunch This area reflex is the contraction relative to a muscle involuntary caused by its own stretching. For to illustrate, this reflex allows the spile to contract when the doctor taps your knee with a spank. In fact, this reflex exists for almost every muscle in the body and generates a contraction much stronger unless any that could be achieved with conventional studying. That is also known inasmuch as the myotatic snore.<\p>

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