If the fasciae provide the sacks for the muscles, and the bones provide the rigidity needed for an erect posture, then it is the muscle bulk (along with other connective tis- sue) that gives the body its final shape. In addition, mus- cles provide stability to the bones. The skeleton cannot stand erect by itself. It is the muscles that give us our posture—our stance toward life. This stance relies on both mechanical (gravitational) and emotional contribu- tions. It is the muscles that give us the dynamic move- ment we associate with life itself.
The recruitment of muscle would not happen were it not for the nervous system. The motor unitis the final common pathway of the alpha motor system’s outflow to the end plates located on the muscle fibers. The lower motor neuron associated with the motor unit resides in the ventral horn of the spinal cord. Hundreds or even thousands of interneuronal connections converge upon that motor neuron (see Figure 2–1). The segmental in- terplay of the spinal reflexes is driven by excitatory and inhibitory potentials: The stretch receptors of the muscle spindle place an excitatory valence on the lower motor neuron, while the Golgi tendon organs provide the re- flex-driven inhibitory potentials. These two inputs func- tion as sensory motor integrators that deal with gravity, the mass of everyday life, and our efforts to interact with the world. They keep us up and moving and inform the rest of the nervous system of the instantaneous length of each muscle and the force it is exerting.
The lower motor neuron is also regulated by upper motor neurons. Some of these come directly from the cortex, carrying out fine motor intentions. The thought behind a movement originates in the frontal lobes. It then passes through the prefrontal cortex to pick up the general body position in space needed for the move- ment. Then it goes through the motor strip to pick up the final details of any fine motor aspects of the move- ment. Some of the cortical outflow goes directly to the lower motor neuron via the pyramidal tracts. Some travel via the extrapyramidal tract, which synapses with lower centers of the brain. Here the intended move- ment is integrated with the internal (kinesthetic) and external senses, and is blended with motor patterns as- sociated with given and acquired reflexes. The cerebellum monitors the whole affair, fine-tuning the final act.
When examining muscles, clinicians tend to study each compartment for its own function. Manual muscle testing is routinely taught as a method to isolate the strength of a given muscle. To test muscles correctly, one must know how to position the limb, where to resist it, how to coach the subject to exert effort, and how to floor, unable to do any work. Muscles are affected by
asymmetrical growth patterns in the bones. Leg-length discrepancies of more than one-half inch, for example, cause faulty posture. Ligaments, another type of con- nective tissue, secure bone to bone. They also provide the needed limitations in range of motion, while adding stability to the bones themselves. In fact, all of the bones in the body are knit together with ligaments. This lends a certain coherence to the support that the bones provide. The spine and pelvis are very clear examples of this phenomenon.
Mother Nature would much prefer that we rest on our bones and ligaments as the means of holding ourselves erect in the neutral posture against the gravitational field, thereby sparing the metabolic consequences of using muscle to do the same task. But what happens to our muscles when we habitually defy the well-aligned posture? In essence, they overwork and often eventually ache. It is as if Mother Nature is using the ache to beckon us back into stacking our weight on our bones and ligaments.
What happens if we fall or otherwise tear the connec- tive tissue from around the bones? Such microtears are not uncommon in spinal flexion/extension injuries asso- ciated with motor vehicle accidents. This ligament laxity may create disorder in associated muscles. The muscles tend to increase their tonus around the injured joint, as if to provide an internal splint to the bones. Although this splinting may provide an effective short-term solution to a weakened joint, the long-term consequence is usu- ally pain.
If there is asymmetry in the nature of connective tissue associated with a particular joint, this imbalance usually leads to an asymmetrical recruitment of the muscles as- sociated with that joint. For example, if the left temporo- mandibular joint (TMJ) has ligament laxity while the right aspect of the joint has normal ligamental support, an asymmetrical recruitment of motor units will be seen in surface electromyography (SEMG) recordings from ho- mologous muscles during a symmetrical movement (e.g., opening the mouth). Surface EMG monitoring can help clinicians interpret information about the joints (end range of motion or joint play) and can help manual therapists demonstrate the effects of mobilization of the joint. The postmanipulation effects on SEMG should yield normalized recruitment patterns (±20%) during symmetrical dynamic movements. In addition, feedback and retraining of the newly mobilized joint may help prevent the movements and postures of life from creating the same limitation in the future.
grade the strength of the resulting effort. These tests are far from natural movement patterns. Rather, they are more like slices of unique movement patterns, taken out of a normal muscle contraction context and frozen in time. They are relevant only to the extent that the infor- mation gained can be placed within a more functional context.
A single, discrete muscle rarely works on its own in a real and varied life situation. The nervous system has more than 600 muscles from which to choose and an area as large as the human form with which to work.
Many muscles need to serve the three functions of pos- ture, emotions, and motions. To think of testing one muscle is entirely too simplistic. Instead, the only way in which muscle testing works is to have a theory of dys- function that involves areas of effort up and down the kinetic chain of movement. Then, in the process of de- termining which muscles are weak or strong in that chain, all or part of the chain might be tested.
When testing muscles, the clinician should assess muscle grouping such as agonists (prime movers), syn- ergists (helpers), and antagonists (opposing muscle groups). In addition, as the tests move toward real and varied life activities, it becomes necessary to address is- sues of timing. Surface EMG as an assessment tool, like muscle testing, begins to make sense only when it is viewed in a much broader perspective. Along with mus- cle testing, SEMG can be used to monitor the muscles
involved or suspected to be involved in a particular movement. In this way, clinicians can assess not only the muscles’ strength, but also their synergy with other muscles.
This type of thinking is illustrated by simple abduction of the left arm. Imagine that the subject is standing with arms at his or her sides. The intention is to raise the left arm out from the side to a horizontal 90-degree posture.
The muscle fibers of the middle deltoid act as the pri- mary mover. The anterior and posterior aspects of the deltoid assist in a synergistic fashion. The upper fibers of the trapezius, along with the deeper supraspinatus, also assist in this movement. The middle and lower fibers of the trapezius, serratus anterior, and others stabilize the scapula to anchor the weight of the 15-pound arm against the chest wall. Because this is an asymmetrical ac- tion, the erector spinae muscles on the contralateral (right) side begin to activate to stabilize the cantilevered effect of gravity’s pull on the torso. This places a strain on the pelvis, which is stabilized by the gluteus medius and tensor fasciae latae. The left leg bears a greater weight, and muscles are slightly activated in various aspects of the thigh, calf, and foot. In addition, it is necessary to super- impose the waves of respiration in the abdominal and intercostal area upon this holding pattern. Place a little bit of emotional arousal into the situation, and the over- all tone is increased by, say, 10%. Place a 10-pound weight in the outstretched hand, and the recruitment Figure 2–1 A reconstructed model of a spinal motor neuron showing the large number of small presynaptic knobs from other neurons terminating on it.
Source:Reproduced from J. Mishlove. The Roots of Consciousness.Random House, 1975. Illustration by Sherry Hogue. Scan provided courtesy of Jeffrey Mishlove.
overlaps the actin fibers (Abands). The Aband is where all of the work of the cross-bridging takes place.
The actin filament is a thin fiber with two negatively charged molecules that spiral around each other. The myosin filament is a much thicker filament with “globu- lar heads” on it. These filaments are also negatively charged. In the resting state, these two filaments lie next to each other, mutually repelled by their negative charges. In the 1950s, Huxley8proposed a “ratchet” or sliding filament model that describes the generation of active tension. In this model, each globular head of the myosin fiber has one ATP molecule attached to it, which is negatively charged.
The nerve action potential from the lower motor neu- ron causes a release of acetylcholine (ACh) at the neuro- muscular junction. This sends a charge through the transverse tubules (Figure 2–3) that, when it reaches the sarcoplasmic reticulum, allows pores to be opened and calcium ions to flood the space where the myosin and actin fibers are located. Each calcium ion has a very strong positive charge to it, and it bonds instantly with the actin filament. At this point, the negatively charged myosin filament with its ATP molecule is strongly at- tracted to the now positively charged actin filament (Figure 2–4). As these two filaments are pressed against each other by the chemically induced electromagnetic attraction, the globular heads are forced to flatten out;
the resulting ratchet effect forces the two filaments to move past each other. The force of the bending of the globular heads, however, causes the ATP molecule to be released. The energy associated with this release pro- vides the energy needed to free the calcium ion from the actin fiber and pumps it back to the sarcoplasmic reticulum. Simultaneously, the myosin and actin fila- ments separate from each other, being held slightly apart by the two negative charges. Immediately, an- other ATP molecule attaches to the globular head on the myosin filament and the cycle is ready to begin all over again. Thus, the globular heads of the myosin act as cross-bridges for the actin chains. Through successive activations and cross-bridging, the muscle twitches while it shortens and work is done.
The metabolized ATP molecule, now known as adeno- sine diphosphate (ADP), is reconstituted in the mito- chondria. Using the Krebs cycle, the mitochondrion rebuilds the ADP back into ATP, using the glucose and oxygen provided by the circulation system. The by- products of this process include lactic acid, free hydrogen ions, and carbon dioxide. These by-products need to be pattern along the entire kinetic chain increases dramati-
cally. Such a weight can be held at this height for only a short period of time, because the more distal muscles begin to fatigue much faster than the more proximal postural muscles. Within the first minute, the volley of activity to the middle deltoid has increased and synchro- nized to counter the fatigue factor. Within 4 minutes the failure point is reached, the arm gives way to the gravita- tional pull, and the posture is recalibrated.