In our physiological laboratories we stimulate muscle by chemical, thermal, mechanical, and electrical means, but generally by electrical, and preferably by the faradic current, if we wish to study other than single muscle twitchings. It is the opening or closing of the current, the change, which produces contraction. With one stimulus we obtain only one twitch (after a "latent period" of at most 1/100 second after the stimulus reaches the muscle); by means of a series of such stimuli we get longer contractions, i.e., movements; with stimuli following closely upon one another we obtain strong, continuous cramp called tetanus, which is more easily produced, and by weaker stimuli, in a tired than in a rested muscle. We stimulate the muscle either indirectly by allowing the current to pass through its motor nerve, or directly by letting it pass through the muscle.

It has been found that irritability is different in different muscles - different, for example, in the flexors and extensors; the former are usually more irritable, and respond to a stimulus which is too weak to produce a contraction of the extensors.

Different muscles contract in response to the same stimulus with different strength and speed according to slight differences of histological structure Without regard to their sectional area. The poorer a striated muscle is in the inter-fibrous homogeneous mass called "sarcoplasm," and consequently the richer it is in striated muscle fibres, the quicker, and I suppose the stronger, is its contraction, all other things being equal.

As for the weakening influence of the fatigued motor nerve itself, we may say that in all probability it is to be looked for in the ganglion cells, and in the end plates, but not in the nerve fibres. By stimulating a motor nerve (by means of an induction current) one can keep the corresponding muscle in tetanus for hours. But as soon as the stimulus passes through a ganglion cell - as, for example, in the case when reflex movement is produced by stimulation of a sensory nerve - one notices, after the stimulation has continued some time, distinct symptoms of nerve fatigue, which, as we remarked in passing, must be distinguished from fatigue of the muscle itself (see below).

Central or peripheral changes of pathological nature in the neurons which have to do with our movements {whether these neurons are motor or sensory) bring about various changes in our movements, and may cause involuntary movements and abnormally weak or exhausted motor power, just as they may produce abnormally strong or in other ways disturbed movements.

Thus we see pareses and paralysis arise as the result of tumours or of cerebral or spinal haemorrhage, hysteria, acute anterior poliomyelitis, and certain poisonings, traumata, etc. In meningitis, hysteria, epilepsy, spastic diseases of the spinal cord, tetanus infections, hydrophobia, strychnine poisoning, etc., we see tonic or clonic cramp. In tetanus the muscles may contract with such force that, e.g., sterno-cleido-mastoid wrenches the clavicle from its articulation with the sternum. In traumatic or rheumatic or degenerative processes in the peripheral nerves we have similar motor symptoms - sometimes hypertonic, usually hypotonic. If the sensory nerve elements (see below), on which to a certain extent our movements depend, are injured, various motor symptoms are apt to arise.

If, for example, the posterior roots of the peripheral nerves, which only contain sensory fibres, are cut in a mammal, extensive functional motor disturbances arise, with symptoms which are purely paralytic. In certain nervous diseases, especially tabes, disturbances of co-ordination arise *; the movements become swaying and uncertain in form and consequently weaker in strength.

The strength of our movements, other things being equal, depends to a certain extent on the thickness of our muscles, or rather of the muscle fibres. Measurement is easy only on muscles with parallel fibres, which fibres are usually (by the way) 3 to 4 cm. long, but may be even 12 cm. In measuring, the section must always be made at right angles to the muscle fibres, and examination is consequently more difficult in muscles with diagonal, e.g., with penniform, fibres. Henke reckoned that a muscle at the beginning of its contraction is able to lift 7 to 8 kg. per square cm. of its sectional area; others have given the larger number of 10 kg. A muscle which has become atrophied owing to a bandage, inactivity, or lack of nourishment for one reason or another, is therefore, other things being equal, necessarily weaker than a normally thick muscle.

But the power of a muscle does not only depend upon the quantity of its protoplasm, but also on its quality. I have already mentioned the difference in power, even within normal limits, between different muscles according to their richness in fibre or sarcoplasm. Degenerative and inflammatory changes in muscles of all kinds weaken them. Fatty degeneration, granular albuminoid degeneration ("Trubeschwellung"), myomalacia often greatly lower the strength of muscles. Acute and chronic myositis have the same effect, the former more particularly by tension in the tissues and pain, the latter frequently also by increasing the interstitial connective tissue and its encroachment upon the fibres. Alcoholism and senility are common causes of muscular weakness.

* Co-ordination is understood most easily by the student, according to my experience, if it is defined as the correct relation during movement between the different parts of the nervous system innervating the working muscles.

According to Schwann's law, a muscle contracts more forcibly theless it is previously contracted. The flexors of the arm, for example, are strongest at the point of maximum extension, weakest at extreme flexion. It is worth noting that a muscle is not at its maximum strength during that part of its contraction in which it is using up the greatest amount of oxygen and producing most C02, namely, during the greatest shortening. The blood vessels of the muscle are also fully distended during its greatest shortening.