More on weak muscles. Just WHY are they weak? Know before you activate!

Dr Allen’s post last week on chronic ankle instability (click here for post) served as an inspiration for many of us. It brings to mind the many reasons muscles can become “weak”.

So why does a muscle become weak? We like to categorize the causes as follows:

• local
• segmental
• long loop/cortical

Local causes include muscle injury and muscle pathologies, like muscular dystrophy and neuromuscular endplate disorders like myasthenia gravis. Segmental causes are largely due to reflexes which occur at the spinal cord level. Long loop and cortical causes ae due to an increased inhibition or lack of drive from higher centers, such as the motor cortex and cerebellum.

Lets examine local causes in more detail. To understand causes we must understand what makes a muscle contract.

Muscles are composed of many proteins, 2 of which are actin and myosin (see above). Actin has 2 forms, F (filamental) and G (globular) actin. Imagine 2 grapefruits side by side (G actin) held together in the middle by small filaments (F actin). Now imagine these another set immediately below, in a repeating pattern. These groups of 2 are held together at the sides by an additional protein called tropomyosin. This whole complex looks a little like train tracks. Along the strands of tropomyosin, at regular intervals is yet another protein called troponin. We like to think of troponin as a triangular shaped protein and each part of the triangle has a particular binding site: one for tropomyosin, one for actin and another for calcium ions.

Myosin is another component of muscle, that looks similar to a bunch of golf clubs. The head of the club will, under the right circumstances, interact with actin, the body (tail) of the club interacts with other myosin bodies.

Globular actin and myosin heads are like 2 teenagers and like to interact with one another. Normally, in a resting state, troponin protein covers the active site of myosin binding on G actin. In the presence of calcium, there is a change in shape of the troponin molecule, moving it off of the active site of actin, allowing myosin to bind there. When this happens, the head ratchets and muscle contraction occurs. In the presence of adequate fuel (ie ATP) the myosin head detaches from actin and “recocks”, ready for another contraction cycle (see 2nd picture above).

So where does the calcium come from? It is stored in areas of the muscle called the terminal cisterns. It is released when an action potential fires the peripheral nerve to the neuromuscular endplate of a muscle.

Can calcium be released any other way? Sure it can. How about if the terminal cisterns are damaged, from an injury to the muscle? How about if they are damaged from a disease process?

So, when calcium is released, no matter how it is released, muscles contract. If calcium is not released, then muscles do not contract.

From a local cause, If a muscle is weak, one of the following are usually causing the weakness:

• there is physical damage to the muscle causing fewer of the working units of the muscle (called sarcomeres) contract
  

this is by far the most common, due to overuse or trauma

• there is a problem with the connection of the nerve to the muscle
  

Disruption of nerve to muscle connections can be also be due to trauma or disease. Weakness that is becoming progressive and worsening, needs to be evaluated further and may be the signal for a progressive muscular or neurological disorder (muscular dystrophy, myasthenia gravis, Gullian Barre, etc)

• there is insufficient neurotransmitter at the neuromuscular end plate to fire the muscle
  

this is usually due to a disease process

• Insufficient calcium could theoretically hamper a muscles contraction, but since calcium is involved with nerve transmission as well, tetany (ie sustained contraction and spasm) would most likely occur due to other reasons that we will not explore at this juncture.
  

OK, so that sums up local causes. Look for a follow up post about segmental causes next…

We are: The Gait Guys

Neuromechanics Weekly: Pain Matters

We know that joint swelling (and thus inflammation) inhibits the contraction of the muscle which crosses the joint from the landmark work of Iles and Stokes back in the late 80’s. Now here is a paper stating that pain does the same thing. 

This tells us that there is an axon collateral from the primary pain neuron (the “C” fiber) that somehow inhibits the alpha moto neuron, similar to a flexor reflex, as pictured. his is most likely through affecting the gamma moto neuron (which goes to the spindles) rather than the alpha motoneuron; so the “sensitivity” of the muscle is changed (remember, spindles detect length changes, golgi’s tension).

So what does this mean to us and gait? It tells us that pain will inhibit the activity (voluntary and involuntary) of the ability for one to use their muscles, especially those crossing the joint in questions. Be aware of inflammation (painful or non painful) or the painful joint, which can contribute to a compensation pattern.

Ivo and Shawn…The Gait Guys. Making your life less painful and more functional….

Muscle Nerve. 2000 Aug;23(8):1219-26.

Inhibition of motor unit firing during experimental muscle pain in humans.

Sohn MK, Graven-Nielsen T, Arendt-Nielsen L, Svensson P.

Source

Center for Sensory-Motor Interaction, Orofacial Pain Laboratory, Aalborg University, Denmark.

Abstract

Electromyographic activity was recorded in the masseter muscle to investigate whether the firing characteristics of single motor units (SMUs) were affected by muscle pain. Capsaicin was injected into the masseter to induce pain. The interspike interval (ISI) and recruitment threshold of SMUs were measured while subjects performed isometric contractions at 5, 7.5, 10, 15, and 20% of maximum voluntary contraction. All subjects were able to maintain a stable isometric force during pain, but the mean ISI was significantly increased without changing the recruitment threshold. In all the experimental conditions, the firing frequency increased with increasing force, and SMUs recruited at low force fired at higher rates for all force levels. These results suggest that acute stimulation of nociceptive muscle afferents inhibits SMU activity without changing recruitment order in the homonymous muscle.

Copyright 2000 John Wiley & Sons, Inc.

Its a great day to be a neuro geek

So if the receptors on the bottom of the foot aren’t involved aren’t involved in 2 joint muscles staying coordinated (like the hamstring and rectus femoris in this study), how do we determine the appropriate muscle length and ratios? How about our built in muscle length receptors? Lets hear it for muscle spindles! Hooray for Ia and type II afferents!

Sifting through the science so you don’t have to. We are The Gait Guys…

Exp Brain Res. 1998 Jun;120(4):479-86.

Coordination of two-joint rectus femoris and hamstrings during the swing phase of human walking and running.

Prilutsky BI, Gregor RJ, Ryan MM.

Source

Department of Health and Performance Sciences, Center for Human Movement Studies, The Georgia Institute of Technology, Atlanta 30332-0110, USA.

Abstract

It has been hypothesized previously that because a strong correlation was found between the difference in electromyographic activity (EMG) of rectus femoris (RF) and hamstrings (HA; EMG(RF)-EMG(HA)) and the difference in the resultant moments at the knee and hip (Mk-Mh) during exertion of external forces on the ground by the leg, input from skin receptors of the foot may play an important role in the control of the distribution of the resultant moments between the knee and hip by modulating activation of the two-joint RF and HA. In the present study, we examined the coordination of RF and HA during the swing phase of walking and running at different speeds, where activity of foot mechanoreceptors is not modulated by an external force. Four subjects walked at speeds of 1.8 m/s and 2.7 m/s and ran at speeds of 2.7 m/s and 3.6 m/s on a motor-driven treadmill. Surface EMG of RF, semimembranosus (SM), and long head of biceps femoris (BF) and coordinates of the four leg joints were recorded. An inverse dynamics analysis was used to calculate the resultant moments at the ankle, knee, and hip during the swing phase. EMG signals were rectified and low-pass filtered to obtain linear envelopes and then shifted in time to account for electromechanical delay between EMG and joint moments. During walking and running at all studied speeds, mean EMG envelope values of RF were statistically (P<0.05) higher in the first half of the swing (or at hip flexion/knee extension combinations of joint moments) than in the second half (or at hip extension/knee flexion combinations of joint moments). Mean EMG values of BF and SM were higher (P<0.05) in the second half of the swing than in the first half. EMG and joint moment peaks were substantially higher (P<0.05) in the swing phase of walking at 2.7 m/s than during the swing phase of running at the same speed. Correlation coefficients calculated between the differences (EMG(RF)-EMG(HA)) and (Mk-Mh), taken every 1% of the swing phase, were higher than 0.90 for all speeds of walking and running. Since the close relationship between EMG and joint moments was obtained in the absence of an external force applied to the foot, it was suggested that the observed coordination of RF and HA can be regulated without a stance-specific modulation of cutaneous afferent input from the foot. The functional role of the observed coordination of RF and HA was suggested to reduce muscle fatigue.

This week on Neuromechanics Weekly:

The necessary factors for muscle contraction. Stay tuned for what controls muscle tone next week.

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Shawn and Ivo