Chapter VIII (2)

When giving reasons for the belief that the vertebrate skeleton is mechanically originated, one of the facts put in evidence was, that in the vertebrate series the transition from the cartilaginous to the osseous spine begins peripherally (§ 257): each vertebra being at first a ring of bone surrounding a mass of cartilage. And it was pointed out that this peripheral ossification is ossification at the region of greatest pressures. Now it is not vertebræ only that follow this course of development. In a cylindrical bone, though it is differently circumstanced, the places of commencing ossification are still the places on which the severest stress falls. Let us consider how such a bone that has to bear a longitudinal pressure is mechanically affected. If the end of a walking-cane be thrust with force against the ground, the cane bends; and partially resuming its straightness when relieved, again bends, usually towards the same side, when the thrust is renewed. A bend so caused acts on the fibres of the cane in nearly the same way as does a bend caused by supporting the cane horizontally at its two ends and suspending a weight from its middle. In either case the fibres on the convex side are extended and the fibres on the concave side compressed. Kindred actions occur in a rod that is so thick as not to yield visibly under the force applied. In the absence of complete homogeneity of its substance, complete symmetry in its form, and an application of a force exactly along its axis, there must be some lateral deflection; and therefore some distribution of tensions and pressures of the kind indicated. And then, as the fact which here specially concerns us, we have to note that the strongest tensions and pressures are borne by the outer layers of fibres. Now the shaft of a long bone, subject to mechanical actions of this kind, similarly has its outer layer most strained. In this layer, therefore, on the mechanical hypothesis, ossification should commence, and here it does commence--commences, too, midway between the ends, where the bends produce on the superficial parts their most intense effects. But we have not in this place simply to observe that ossification commences at the places of greatest stress, but to ask what causes it to do this. Can we trace the physical actions which set up this deposit of dense tissue? It is, I think, possible to indicate a “true cause” that is at work; though whether it is a sufficient cause may be questioned. We concluded that in certain other cases, the formation of dense tissue indirectly results from the alternate squeezing and relaxation of the vessels running through the part; and the inquiry now to be made is, whether, in developing bone, the same actions go on in such ways as to produce the observed effects. At the outset we are met by what seems a fatal difficulty--cartilage is a non-vascular tissue: this substance of which unossified bones consist is not permeated by minute canals carrying nutritive liquid, and cannot, therefore, be a seat of actions such as those assigned. This apparent difficulty, however, furnishes a confirmation. For cartilage that is wholly without permeating canals does not ossify: ossification takes place only at those parts of it into which the canals penetrate. Hence, we get additional reason for suspecting that bone-formation is due to the alleged cause; since it occurs where mechanical strains can produce the actions described, but does not occur where mechanical strains cannot produce them. Let us consider more closely what the several factors are. It will suffice for the argument if we commence with the external vascular layer as already existing, and consider what will take place in it. Cartilage is elastic--is somewhat extensible, and spreads out laterally under pressure, but resumes its form when relieved. How, then, will the minute channels traversing it in all directions be affected at the places where it is strained by a bend? Those on the convex side will be laterally squeezed, in the same way that we saw the sap-vessels on the convex side of a bent branch are squeezed; and as exudation of the sap into the adjacent prosenchyma will be caused in the one case, so, in the other, there will be caused exudation of serum into the adjacent cartilage: extra nutrition and increase of strength resulting in both cases. The parallel ceases here, however. In the shoot of a plant, bent in various directions by the wind, the side which was lately compressed is now extended; and hence that squeezing of the sap-vessels which results from extension, suffices to feed and harden the tissue on all sides of the shoot. But it is not so with a bone. Having yielded on one side under longitudinal pressure, and resumed as nearly as may be its previous shape when the pressure is taken off, the bone yields again towards the same side when again longitudinally pressed. Hence the substance of its concave side, never rendered convex by a bend in the opposite direction, would not receive any extra nutrition did no other action come into play. But if we consider how intermittent pressures must act on cartilage, we shall see that there will result extra nutrition of the concave side also. Squeeze between two pieces of glass a thin bit of caoutchouc which has a hole through it. While the caoutchouc spreads out away from the centre, it also spreads inwards, so as partially to close the hole. Everywhere its molecules move away in directions of least resistance; and for those near the hole, the direction of least resistance is towards the hole. Let this hole stand for the transverse section of one of the minute canals or channels passing through cartilage, and it will be manifest that on the side of the unossified bone made concave in the way described, the compressed cartilage will squeeze the canals traversing it; and, in the absence of perfect homogeneity in the cartilage, the squeeze will cause extra exudation from the canals into the cartilage. Thus every additional strain will give to the cartilage it falls upon, an additional supply of the materials for growth. So that presently the side which, by yielding more than any other, proves itself to be the weakest, will cease to be the weakest. What further will happen? Some other side will yield a little--the bends will take place in some other plane; and the portions of cartilage on which repeated tensions and pressures now fall will be strengthened. Thus the rate of nutrition, greatest at the place where the bending is greatest, and changing as the incidence of forces changes, will bring about at every point a balance between the resistances and the strains. Thus, too, there will be determined that peripheral induration which we see in bones so circumstanced. As in a shoot we saw that the woody deposit takes place towards the outside of the cylinder, where, according to the hypothesis, it ought to take place; so, here, we see that the excess of exudation and hardening, occurring where the strains are most intense, will form a cylinder having a dense outside and a porous or hollow inside. These processes will be essentially the same in bones subject to more complex mechanical actions, such as sundry of the flat bones and others that serve as internal fulcra. Be the strains transverse or longitudinal, be they torsion strains or mixed strains, the outer parts of the bone will be more affected by them than its inner parts. They will therefore tend everywhere to produce resisting masses having outer parts more dense than their inner parts. And by causing most growth where they are most intense, they will call out reactive forces adequate to balance them. There are doubtless obstacles in the way of this interpretation. It may be said that the forces acting on the outer layers in the manner described, would compress the canals too little to produce the alleged effects; and if evenly distributed along the whole lengths of the layers, they would probably do so. But it needs only to bend a flexible mass and observe the tendency to form creases on the concave surface, to feel assured that along the surface of an ossifying bone, the yielding of the tissue when bent will not be uniform. In the absence of complete homogeneity, the interstitial yielding will take place at some points more than others, and at one point above all others. When, at the weakest point--the centre of commencing ossification--an extra amount of deposit has been caused, it will cease to be the weakest; and adjacent points, now the weakest, will become the places of yielding and induration. It may be further objected that the hypothesis is incompatible with the persistence of cartilage for so long a time between the epiphysis of bones and the bony masses which they terminate. But there is the reply that the places occupied by this cartilage being places at which the bone lengthens, the non-ossification is in part apparent only--it is rather that new cartilage is formed as fast as the pre-existing cartilage ossifies; and there is the further reply that the slowness of the ultimate ossification of this part, is due to its non-vascularity, and to mechanical conditions which are unfavourable to its acquirement of vascularity. Once more, there is the demurrer that in the epiphyses ossification does not begin at the surface but within the mass of the cartilage. Explanation of this implies ability to follow out the mechanical actions in a resilient substance which, like india-rubber, admits of being distorted in all ways by pressure and recovering its form, and it seems impossible to say how the more superficial and more deep-seated canals traversing it will be respectively affected.

Of course it is not meant that this osseous development by direct equilibration takes place in the individual. Though it is a corollary from the argument that in each individual the process must be furthered and modified by the particular actions to which the particular bones are exposed; yet the leading traits of structure assumed by the bones are assumed in conformity with the inherited type. This, however, is no difficulty. The type itself is to be regarded as the accumulated result of such modifications, transmitted and increased from generation to generation. The actions above described as taking place in the bone of an individual, must be understood as producing their total effect little by little in the corresponding bones of a long series of individuals. Even if but a small modification can be so wrought in the individual, yet if such modification, or a part of it, is inheritable, we may readily understand how, in the course of geologic epochs, the observed structures may arise in the assigned way.

Here may fitly be added a strong confirmation. If we find cases where individual bones, subject in exceptional degrees to the actions described, present in exceptional amounts the modifications attributed to them, we are greatly helped in understanding how there may be produced in the race that aggregate of modifications which the hypothesis implies. Such cases occur in ricketty children. I am indebted to Mr. Busk for pointing out these abnormal formations of dense tissue, that are not apparently explicable as results of mechanical actions and reactions. It was only on tracing out the processes here at work, that there suggested itself the specific interpretation of the normal process, as above set forth. When, from constitutional defect, bones do not ossify with due rapidity, and are meanwhile subject to the ordinary strains, they become distorted. Remembering how a mass which has been made to yield in any direction by a force it cannot withstand, is some little time before it recovers completely its previous form, and usually, indeed, undergoes what is called a “permanent set;” it is inferable that when a bone is repeatedly bent at the same time that the liquid contained in its canals is poor in the materials for forming dense tissue, there will not take place a proportionate strengthening of the parts most strained; and these parts will give way. This happens in rickets. But this having happened, there goes on what, in teleological language, we call a remedial process. Supposing the bone to be one commonly affected--a femur; and supposing a permanent bend to have been caused in it by the weight of the body; the subsequent result is an unusual deposition of cartilaginous and osseous matter on the concave side of the bone. If the bone is represented by a strung bow, then the deposit occurs at the part represented by the space between the bow and the string. And thus occurring where its resistance is most effective, it increases until the approximately-straight piece of bone formed within the arc, has become strong enough to bear the pressure without appreciably yielding. Now this direct adaptation, seeming so like a special provision, and furnishing so remarkable an instance of what, in medical but unscientific language, is called the _vis medicatrix naturæ_, is simply a result of the above-described mechanical actions and reactions, going on under the exceptional conditions. Each time such a bent bone is subject to a force which again bends it, the severest compression falls on the substance of its concave side. Each time, then, the canals running through this part of its substance are violently squeezed--far more squeezed than they or any other of the canals would have been, had the bone remained straight. Hence, on every repetition of the strain, these canals near the concave surface have their contents forced out in more than normal abundance. The materials for the formation of tissue are supplied in quantity greater than can be assimilated by the tissue already formed; and from the excess of exuded plasma, new tissue arises.[50] A layer of organizable material accumulates between the concave surface and the periosteum; in this, according to the ordinary course of tissue-growth, new vessels appear; and the added layer presently assumes the histological character of the layer from which it has grown. What next happens? This added layer, further from the neutral axis than that which has thrown it out, is now the most severely compressed, and its vessels are the most severely squeezed. The place of greatest exudation and most rapid deposit of matter, is therefore transferred to this new layer; and at the same time that active nutrition increases its density, the excess of organizable material forms another layer external to it: the successive layers so added, encroaching on the space between the concave surface of the bone and the chord of its arc. What limits the encroachment on this space?--what stops the process of filling it up? The answer to this question will be manifest when observing that there comes into play a cause which gradually diminishes the forces falling on each new layer. For the transverse sectional area is step by step increased; and an increase of the area over which the weight borne is distributed, implies a relatively smaller pressure upon each part of it. Further, as the transverse dimensions of the bone increase, the materials composing its convex and concave layers, becoming further from the neutral axis, become better placed for resisting the strains to be borne. So that both by the increased quantity of dense matter and by its mechanically more-advantageous position, the bendings of the bone are progressively decreased. But as they are decreased, each new layer formed on the concave surface has its substance and its vessels less compressed; and the resulting growth and induration are rendered less rapid. Evidently, then, the additions, slowly diminishing, will eventually cease; and this will happen when the bone no longer bends. That is to say, the thickening of the bone will reach its limit when there is equilibrium between the incident forces and the forces which resist them. Here, indeed, we may trace with great clearness the process of direct equilibration--may see how an unusual force, falling on the moving equilibrium of an organism and not overthrowing it, goes on working modifications until the reaction balances the action.

That, however, which now chiefly concerns us, is to note how this marked adaptation supports the general argument. Unquestionably bone is in this case formed under the influence of mechanical stress, and formed just where it most effectually meets the stress. This result, not otherwise explained, is explained by the hypothesis above set forth. And when we see that this special deposit of bone is accounted for by actions like those to which bone-formation in general is ascribed, the probability that these are the actions at work becomes very great.[51]

Of course it is not alleged that osseous structures arise in this way alone. The bones of the skull and various dermal bones cannot be thus interpreted. Here the natural selection of favourable variations appears the only assignable cause--the equilibration is indirect. We know that ossific deposits now and then occur in tissues where they are not usually found; and such deposits, originally abnormal, if they occurred in places where advantages arose from them, might readily be established and increased by survival of the fittest. Especially might we expect this to happen when a constitutional tendency to form bone had been established by actions of the kind described; for it is a familiar fact that differentiated types of tissue, having once become elements of an organism, are apt occasionally to arise in unusual places, and there to repeat all their peculiar histological characters. And this may possibly be the reason why the bones of the skull, though not exposed to forces such as those which produce, in other bones, dense outer layers including less dense interiors, nevertheless repeat this general trait of bony structure. While, however, it is beyond doubt that some bones are not due to the direct influence of mechanical stress, we may, I think, conclude that mechanical stress initiates bone-formation.

§ 302. What is the origin of nerve? In what way do its properties stand related to the properties of that protoplasm whence the tissues in general arise? and in what way is it differentiated from protoplasm simultaneously with the other tissues? These are profoundly interesting questions; but questions to which positive answers cannot be expected. All that can be done is to indicate answers which seem feasible.

That the property specially displayed by nerve, is a property which protoplasm possesses in a lower degree, is manifest. The sarcode of a Rhizopod and the substance of an unimpregnated ovum, exhibit movements that imply a propagation of stimulus from one part of the mass to another. We have not far to seek for a probable origin of this phenomenon. There is good reason for ascribing it to the extreme instability of the organic colloids of which protoplasm consists. These, in common with colloids in general, assume different isomeric forms with great facility; and they display not simply isomerism but polymerism. Further, this readiness to undergo molecular re-arrangement, habitually shows itself in colloids by the rapid propagation of the re-arrangement from part to part. As Prof. Graham has shown, matter in this state often “pectizes” almost instantaneously--a touch will transform an entire mass. That is to say, the change of molecular state once set up at one end, spreads to the other end--there is a progress of a stimulus to change; and this is what we see in a nerve. So much being understood, let us re-state the case more completely.

Molecular change, implying as it does motion of molecules, communicates motion to adjacent molecules; be they of the same kind or of a different kind. If the adjacent molecules, either of the same kind or of a different kind, be stable in composition, a temporary increase of oscillation in them as wholes, or in their parts, may be the only result; but if they are unstable there are apt to arise changes of arrangement among them, or among their parts, of more or less permanent kinds. Especially is this so with the complex molecules which form colloidal matter, and with the organic colloids above all. Hence it is to be inferred that a molecular disturbance in any part of a living animal, set up by either an external or internal agency, will almost certainly disturb and change some of the surrounding colloids not originally implicated--will diffuse a wave of change towards other parts of the organism: a wave which will, in the absence of perfect homogeneity, travel further in some directions than in others. Let us ask next what will determine the differences of distance travelled in different directions. Obviously any molecular agitation spreading from a centre, will go furthest along routes that offer least resistance. What routes will these be? Those along which there lie most molecules that are easily changed by the diffused molecular motion, and which yet do not take up much molecular motion in assuming their new states. Molecules which are tolerably stable will not readily propagate the agitation; for they will absorb it in the increase of their own oscillations, instead of passing it on. Molecules which are unstable but which, in assuming isomeric forms, absorb motion, will not readily propagate it; since it will disappear in working the changes in them. But unstable molecules which, in being isomerically transformed, do not absorb motion, and still more those which, in being so transformed, give out motion, will readily propagate any molecular agitation; since they will pass on the impulse either undiminished, or increased, to adjacent molecules. If then we assume, as we are not only warranted in doing but are obliged to do, that protoplasm contains two or more colloids, either mingled or feebly combined (since it cannot consist of simple albumen or fibrin or casein, or any allied proximate principle); it may be concluded that any molecular agitation set up by what we call a stimulus, will diffuse itself further along some lines than along others, if the components of the protoplasm are not quite homogeneously dispersed, and if some of them are isomerically transformed more easily, or with less expenditure of motion, than others; and it will especially travel along spaces occupied chiefly by those molecules which give out molecular motion during their metamorphoses, if there should be any such. But now let us ask what structural effects will be wrought along a tract traversed by this wave of molecular disturbance. As is shown by those transformations which so rapidly propagate themselves through colloids, molecules that have undergone a certain change of form, are apt to communicate a like change of form to adjacent molecules of the same kind--the impact of each overthrow is passed on and produces another overthrow. Probably the proneness towards isochronism of molecular movements necessitates this. If any molecule has had its components re-arranged, and their oscillations consequently altered, there result movements not concordant with the movements in adjacent untransformed molecules, but which, impressing themselves on the parts of such untransformed molecules, tend to generate in them concordant movements--tend, that is, to produce the re-arrangements involved by these concordant movements. Is this action limited to strictly isomeric substances? or may it extend to substances that are closely-allied? If along with the molecules of a compound colloid there are mingled those of some kindred colloid; or if with the molecules of this compound colloid there are mingled the components out of which other such molecules may be formed; then there arises the question--does the same influence which tends to propagate the isomeric transformations, tend also to form new molecules of the same kind out of the adjacent components? There is reason to suspect that it does. Already when treating of the nutrition of parts (§ 64), it was pointed out that we are obliged to recognize a power possessed by each tissue to build up, out of the materials brought to it, molecules of the same type as those of which it is formed. This building up of like molecules seems explicable as caused by the tendency of the new components which the blood supplies, to acquire movements isochronous with those of the like components in the tissue; which they can do only by uniting into like compound molecules. Necessarily they must gravitate towards a state of equilibrium; such state of equilibrium--moving equilibrium of course--must be one in which they oscillate in the same times with neighbouring molecules; and so to oscillate they must fall into groups identical with the groups around them. If this be a general principle of tissue-growth and repair, we may conclude that it will apply in the case before us. A wave of molecular disturbance passing along a tract of mingled colloids closely-allied in composition, and isomerically transforming the molecules of one of them, will be apt at the same time to form some new molecules of the same type, at any place where there exist the proximate components, either uncombined or feebly combined in some not very different way. And this will be most likely to occur where the molecules of the colloid that are undergoing the isomeric change, predominate, but have scattered through them the other molecules out of which they may be formed, either by composition or modification. That is to say, a wave of molecular disturbance diffused from a centre, and travelling furthest along a line where lie most molecules that can be isomerically transformed with facility, will be likely at the same time to further differentiate this line, and make it more characterized than before by the easy-transformability of its molecules. One additional step, and the interpretation is reached. Analogy shows it to be not improbable that these organic colloids, isomerically transformed by slight molecular impact or increase of molecular motion, will some of them resume their previous molecular structures after the disturbance has passed. We know that what are stable molecular arrangements under one degree of molecular agitation, are not stable under another degree; and there is evidence that re-arrangements of an inconspicuous kind are occasionally brought about by very slight changes of molecular agitation. Water supplies a clear case. Prof. Graham infers that water undergoes a molecular re-arrangement at about 32°--that ice has a colloid form as well as a crystalloid form, dependent on temperature. Send through it an extra wave of the molecular agitation we call heat, and its molecules aggregate in one way. Let the wave die away, and its molecules resume their previous mode of aggregation. And obviously such transformations may be repeated backwards and forwards within narrow limits of temperature. Now among the extremely unstable organic colloids, such a phenomenon is far more likely to happen. Suppose, then, that the nerve-colloid is one of which the molecules are changed in form by a passing wave of extra agitation, but resume their previous form when the wave has passed: the previous form being the most stable under the conditions which then recur. What follows? It follows that these molecules will be ready again to undergo isomeric transformation when there again occurs the stimulus; will, as before, propagate the transformation most along the tract where such molecules are most abundant; will, as before, tend to form new molecules of their own type; will, as before, make the line along which they lie one of easier transfer for the molecular agitation. Every repetition will help to increase, to integrate, to define more completely, the course of the escaping molecular motion--extending its remoter part while it makes its nearer part more permeable--will help, that is, to form a line of discharge, a line for conducting impressions, a nerve.

Such seems to me a not unfair series of deductions from the known habitudes of colloids in general and the organic colloids in particular. And I think that the implied nature and properties of nerve correspond better with the observed phenomena than do the nature and properties implied by other hypotheses. Of course the speculation as it here stands is but tentative, and leaves much unexplained. It gives no obvious reply to the questions--what causes the formation of nerves in directions adapted to the needs? what determines their appropriate connexions?--questions, however, to which, when we come to deal with physiological integration, we may find not unsatisfactory answers. Moreover it says nothing about the genesis of ganglia. A ganglion, it is clear, must consist of a colloidal matter equally unstable, or still more unstable, which, when disturbed, falls into some different molecular arrangement, perhaps chemically simpler, and gives out in so doing a large amount of molecular motion--serves as a reservoir of molecular motion which may be suddenly discharged along an efferent nerve or nerves, when excitement of an afferent nerve has disengaged it. How such a structure as this results, the hypothesis does not show. But admitting these shortcomings it may still be held that we are, in the way pointed out, enabled to form some idea of the actions by which nervous tissue is differentiated.

§ 303. A speculation akin to, and continuous with, the last, is suggested by an inquiry into the origin of muscular tissue. Contractility as well as irritability is a property of protoplasm or sarcode; and, as before suggested (§ 22), is not improbably due to isomeric change in one or more of its component colloids. It is a feasible supposition that of the several isomeric changes simultaneously set up among these component colloids, some may be accompanied by change of bulk and some not. Clearly the isomeric change undergone by the colloid which we suppose to form nerve, must be one not accompanied by appreciable change of bulk; since change of bulk implies “internal work,” as physicists term it, and therefore expenditure of force. Conversely, the colloid out of which muscle originates, may be one that readily passes into an isomeric state in which it occupies less space: the molecular disturbance causing this contraction being communicated to it from adjacent portions of nerve-substance that are molecularly disturbed; or being otherwise communicated to it by direct mechanical or chemical stimuli: as happens where nerves do not exist, or where their influence has been cut off. This interpretation seems, indeed, to be directly at variance with the fact that muscle does not diminish in bulk during contraction but merely changes its shape. That which we see take place with the muscle as a whole, is said also to take place with each fibre--while it shortens it also broadens. There is, however, a possible solution of this difficulty. A contracting colloid yields up its water; and the contracted colloid _plus_ the free water, may have the same bulk as before though the colloid has less. If it be replied that in this case the water should become visible between the substance of the fibre and its sarcolemma or sheath, it may be rejoined that this is not necessary--it may be deposited interstitially. Possibly the striated structure is one that facilitates its exudation and subsequent re-absorption; and to this may be due the superiority of striated muscle in rapidity of contraction. Granting the speculative character of this interpretation, let us see how far it agrees with the facts. If the actions are as here supposed, the contracted or more integrated state of the muscular colloid will be that which it tends continually to assume--that into which it has an increasing aptitude to pass when artificial paralysis has been produced, as shown by Dr. Norris--that into which it lapses completely in _rigor mortis_. The sensible motion generated by the contraction can arise only from the transformation of insensible motion. This insensible motion suddenly yielded up by a contracting mass, implies the fall of its component molecules into more stable arrangements. And there can be no such fall unless the previous arrangement is unstable. From this point of view, too, it is possible to see how the hydro-carbons and carbo-hydrates consumed in muscular action, may produce their effects. For these non-nitrogenous elements of food, when consumed in the tissues, give out large amounts of molecular motion. They do this in presence of the muscular colloids which have lost molecular motion during their fall in the stable or contracted state. From the molecular motion they give out, may be restored the molecular motion lost by the contracted colloids; and these contracted colloids may thus have their molecules raised to that unstable state from which, again falling, they can again generate mechanical motion.

This conception of the nature and mode of action of muscle, while it is suggested by known properties of colloidal matter and conforms to the recent conclusions of organic chemistry and molecular physics, establishes a comprehensible relation between the vital actions of the lower and the higher animals. If we contemplate the movements of cilia, of a Rhizopod’s pseudopodia, of a Polype’s body, or of the long pendant tentacles of a _Medusa_, we shall see great congruity between them and this hypothesis. Bearing in mind that the contractile substance of developed muscle is affected not by nervous influence only, but, where nervous influence is destroyed, is made to contract by mechanical disturbance and chemical action, we may infer that it does not differ intrinsically from the primordial contractile substance which, in the lowest animals, changes its bulk under other stimuli than the nervous. We shall see significance in the fact ascertained by Dr. Ransom, that various agents which excite and arrest nervo-muscular movements in developed animals, excite and arrest the protoplasmic movements in ova. We shall understand how tissues not yet differentiated into muscle and nerve, have this joint irritability and contractility; how muscle and nerve may arise by the segregation of their mingled colloids, the one of which, not appreciably altering its bulk during isomeric change, readily propagates molecular disturbance, while the other, contracting when isomerically changed, less readily passes on the molecular disturbance; and how, by this differentiation and integration of the conducting and the contracting colloids, the one ramifying through the other, it becomes possible for a whole mass to contract suddenly, instead of contracting gradually, as it does when undifferentiated.

The question remaining to be asked is--What causes the specialization of contractile substance?--What causes the growth of colloid masses which monopolize this contractility, and leave kindred colloids to monopolize other properties? Has natural selection gradually localized and increased the primordial muscular substance? or has the frequent recurrence of irritations and consequent contractions at particular parts done it? We have, I think, reason to conclude that direct equilibration rather than indirect equilibration has been chiefly operative. The reasoning that was used in the case of nerve applies equally in the case of muscle. A portion of undifferentiated tissue containing a predominance of the colloid that contracts in changing, will, during each change, tend to form new molecules of its own type from the other colloids diffused through it: the tendency of these entangled colloids to fall into unity with those around them, will be aided by every shock of isomeric transformation. Hence, repeated contractions will further the growth of the contracting mass, and advance its differentiation and integration. If, too, we remember that the muscular colloid is made to contract by mechanical disturbance, and that among mechanical disturbances one which will most readily affect it simultaneously throughout its mass is caused by stretching, we shall be considerably helped towards understanding how the contractile tissues are developed. If extension of a muscular colloid previously at rest, produces in it that molecular disturbance which leads to isomeric change and decrease of bulk, then there is no difficulty in explaining the movements of cilia; the formation of a contractile layer in the vascular system becomes comprehensible; each dilatation of a blood-vessel caused by a gush of blood, will be followed by a constriction; the heart will pulsate violently in proportion as it is violently distended; arteries will develop in power as the stress upon them becomes greater; and we shall similarly have an explanation of the increased muscularity of the alimentary canal which is brought about by increased distension of it.

That the production of contractile tissue in certain localities, is due to the more frequent excitement in those localities of the contractility possessed by undifferentiated tissue in general, is a view harmonizing with traits which the differentiated contractile tissue exhibits. These are the relations between muscular exercise, muscular power, and muscular structure; and it is the more needful for us here to notice them because of certain anomalies they present, which, at first sight, seem inconsistent with the belief that the functionally-determined modifications of muscle are inheritable.

Muscles disagree greatly in their tints: all gradations between white and deep red being observable. Contrasts are visible between the muscles of different animals, between the muscles of the same animal at different ages, and between different muscles of the same animal at the same age. We will glance at the facts under these heads: noting under each of them the connexion which here chiefly concerns us--that between the activity of muscle and its depth of colour. The cold-blooded _Vertebrata_ are, taken as a group, distinguished from the warmblooded by the whiteness of their flesh; and they are also distinguished by their comparative inertness. Though a fish or a reptile can exert considerable force for a short time, it is not capable of prolonged exertion. Birds and mammals show greater endurance along with the darker-coloured muscles. If among birds themselves or mammals themselves we make comparisons, we meet with kindred contrasts--especially between wild and domestic creatures of allied kinds. Barn-door fowls are lighter-fleshed than most untamed gallinaceous birds; and among these last the pheasant, moving about but little, is lighter-fleshed than the partridge and the grouse which are more nomadic. The muscles of the sheep are not on the average so dark as those of the deer; and it is said that the flesh of the wild-boar is darker than that of the pig. Perhaps, however, the contrast between the hare and the rabbit affords, among familiar animals, the best example of the alleged relation: the dark-fleshed hare having no retreat and making wide excursions, while the white-fleshed rabbit, passing a great part of its time in its burrow, rarely wanders far from home. The parallel contrast between young and old animals has a parallel meaning. Veal is much whiter than beef, and lamb is of lighter colour than mutton. Though at first sight these facts may not seem to furnish confirmatory evidence, since lambs in their play appear to expend more muscular force than their sedate dams; yet the meaning of the contrast is really as alleged. For in consequence of the law that the strains which animals have to overcome, increase as the cubes of the dimensions, while their powers of overcoming them increase only as the squares (§ 46), the movements of an adult animal cost much more in muscular effort than do those of a young animal: the result being that the sheep and the cow exercise their muscles more vigorously in their quiet movements, than the lamb and the calf in their lively movements. It may be added as significant, that the domestic animal in which no very marked darkening of the flesh takes place along with increasing age, namely the pig, is one which, ordinarily kept in a sty, leads so quiescent a life that the assigned cause of darkening does not come into action. But perhaps the most conclusive evidences are the contrasts which exist between the active and inactive muscles of the same animal. Between the leg-muscles of fowls and their pectoral muscles, the difference of colour is familiar; and we know that fowls exercise their leg-muscles much more than the muscles which move their wings. Similarly in the turkey, in the guinea fowl, in the pheasant. And then, adding much to the force of this evidence, we see that in partridges and grouse, which belong to the same order as our domestic fowls but use their wings as constantly as their legs, little or no difference is visible between the colour of these two groups of muscles. Special contrasts like these do not, however, exhaust the proofs; for there is a still more significant general contrast. The muscle of the heart, which is the most active of all muscles, is the darkest of all muscles.

The connexion of phenomena thus shown in so many ways, implies that the bulk of a muscle is by no means the sole measure of the quantity of force it can evolve. It would seem that, other things equal, the depth of colour varies with the constancy of action; while, other things equal, the bulk varies with the amount of force that has to be put forth upon occasion. These of course are approximate relations. More correctly we may say that the actions of pale muscles are either relatively feeble though frequent (as in the massive flanks of a fish), or relatively infrequent though strong (as in the pectoral muscles of a common fowl); while the actions of dark muscles are both frequent and strong. Some such differentiation may be anticipated by inference from the respective physiological requirements. A muscle which has upon occasion to evolve considerable force, but which has thereafter a long period of rest during which repair may restore it to efficiency, requires neither a large reserve of the contractile substance that is in some way deteriorated by action, nor highly developed appliances for bringing it nutritive materials and removing effete products. Where, contrariwise, an exerted muscle which has undergone much molecular change in evolving much mechanical force, has soon again to evolve much mechanical force, and so on continually; it is clear that either the quantity of contractile substance present must be great, or the apparatus for nutrition and depuration must be very efficient, or both. Hence we may look for marked unlikenesses of minute structure between muscles which are markedly contrasted in activity. And we may suspect that these conspicuous contrasts of colour between active and inactive muscles, are due to these implied differences of minute structure: partly differences between the numbers of blood-vessels and partly differences between the quantities or qualities of sarcous matter.

Here, then, we have a key to the apparent anomaly above hinted at--the maintenance of bulk by certain muscles which have been rendered comparatively inactive by changed habits of life. That the pectoral muscles of those domestic birds which fly but little, have not dwindled to any great extent, has been thought a fact at variance with the conclusion that functionally-produced adaptations are inheritable. It has been argued that if parts which are exercised increase, not only in the individual but in the race, while parts which become less active decrease; then a notable difference of size should exist between the muscles used for flight in birds that fly much, and those in birds of an allied kind that fly little. But, as we here see, this is not the true implication. The change in such cases must be chiefly in vascularity and abundance of contractile substance; and cannot be, to any great extent, in bulk. For a bird to fly at all, its pectoral muscles, bones of attachment, and all accompanying appliances, must be kept up to a certain level of power. If the parts dwindle much, the creature will be unable to lift itself from the ground. Bearing in mind that the force which a bird expends to sustain itself in the air during each successive instant of a short flight is, other things equal, the same as it expends in each successive instant of a long flight, we shall see that the muscles employed in the two cases must have something like equal intensities of contractile power; and that the structural differences between them must have relation mainly to the lengths of time during which they can continue to repeat contractions of like intensity. That is to say, while the power of flight is retained at all, the muscles and bones cannot greatly dwindle; but the dwindling, in birds whose flights are short or infrequent or both, will be in the reserve stock of the substance that is incapacitated by action, or in the appliances that keep the apparatus in repair, or in both. Only where, as in the struthious birds, the habit of flight is lost, can we expect atrophy of all the parts concerned in flight; and here we find it.

Are such differentiations among the muscles functionally-produced? or are they produced by the natural selection of variations distinguished as spontaneous? We have, I think, good grounds for concluding that they are functionally-produced. We know that in individual men and animals, the power of sustained action in muscles is rapidly adaptable to the amount of sustained action required. We know that being “out of condition,” is usually less shown by the inability to put out a violent effort than by the inability to continue making violent efforts; and we know that the result of training for prize-fights and races, is more shown in the prolongation of energy than in the intensification of energy. At the same time, experience has taught us that the structural change which accompanies this functional change, is not so much a change in the bulk of the muscles as a change in their internal state: instead of being soft and flabby they become hard. We have inductive proof, then, that exercise of a muscle causes some interstitial growth along with the power of more sustained action; and there can be no doubt that the one is a condition to the other. What is this interstitial growth? There is reason to suspect that it is in part an increased deposit of the sarcous substance and in part a development of blood-vessels. Microscopic observation tends to confirm the conclusions before drawn, that repetition of contractions furthers the formation of the matter which contracts, and that greater draughts of blood determine greater vascularity. And if the contrasts of molecular structure and the contrasts of vascularity, directly caused in muscles by contrasts in their activities, are to any degree inheritable; there results an explanation of those constitutional differences in the colours and textures of muscles, which accompany constitutional differences in their degrees of activity.

It may be added that if we are warranted in so ascribing the differentiations of muscles from one another to direct equilibration, then we have the more reason for thinking that the differentiation of muscles in general from other structures is also due to direct equilibration. That unlikenesses between parts of the contractile tissues having unlike functions, are caused by the unlikenesses of their functions, renders it the more probable that the unlikenesses between contractile tissue and other tissues, have been caused by analogous unlikenesses.

§ 304. These interpretations, which have already occupied too large a space, must here be closed. Of course out of phenomena so multitudinous and varied, it has been impracticable to deal with any but the most important; and it has been practicable to deal with these only in a general way. Much, however, as remains to be explained, I think the possibility of tracing, in so many cases, the actions to which these internal differentiations may rationally be ascribed, makes it likely that the remaining internal differentiations are due to kindred actions. We find evidence that, in more cases than seemed probable, these actions produce their effects directly on the individual; and that the unlikenesses are produced by accumulation of such effects from generation to generation. While for all the other unlikenesses, we have, as an adequate cause, the indirect effects wrought by the survival, generation after generation, of the individuals in which favourable variations have occurred--variations such as those of which human anatomy furnishes endless instances. Thus accounting for so much, we may not unreasonably presume that these co-operative processes of direct and indirect equilibration will account for what remains.

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[NOTE.--After having dismissed this revised chapter as done with, and sent it to the printer, further thought concerning those differentiations which produce bone, has reminded me of a fact of extreme and varied significance named in the first volume. I refer to the formation of adaptive structures round the ends of dislocated bones, and to the formation of “false joints.”

These are ontogenetic changes of which phylogeny yields no explanation. They do not repeat the traits of ancestral organisms, and they cannot be ascribed to either of the recognized evolutionary factors. If a humerus be broken across and, failing to set, presently comes to have its two loose ends so modified as in a measure to simulate the parts of a normal joint--the ends becoming smooth, covered with periosteum and supplied with fibrous tissue, and attached by ligaments in such ways as to allow of restrained movements--it is impossible to think that natural selection has had anything to do with the power of adjustment thus shown. No survival of individuals in which adaptations of this kind, now in one place and now in another, were better and better effected, could account for acquirement of the ability. Nor can it be supposed that the ability might result from a functionally-produced habit; since it is scarcely conceivable that the number of cases in which individuals profited by it (at first a little and gradually more) could be such (even did they survive) as to affect the constitution of the species. Both of the alleged causes of structural modifications are out of court. It is manifest, too, that the foregoing hypothesis respecting bone-formation yields us not the slightest help.

But on carefully considering the facts, certain phenomena of profound meaning may strike us. Here, in a part of the body where no such tissues ordinarily exist and to which no such structures are ordinarily appropriate, there arise tissues and structures adapted to the physical circumstances imposed on that part. Out of what do these abnormal but appropriate tissues arise? The substances around--osseous, cartilaginous, membranous--consist of differentiated elements too far specialized to allow of transformation. These new tissues, then, must originate from the undifferentiated protoplasm pervading the part. The units of this protoplasm, subject to the actions proper to an articulation, begin to assume the appropriate histological traits--are determined by local stimuli to form tissues ordinarily associated with such stimuli. What is the inevitable implication? These units--physiological or constitutional, as we may call them--must have possessed latent potentialities of falling into these special arrangements under stress of such conditions. At one point there arises periosteum and at another ligamentous tissue, while for the shaping of the ends of the bones--here into a rude hinged form and there into a rude ball-and-socket form, according to the habitual movements--there goes on some appropriate deposit of bone. Hence we must conclude that in the units of protoplasm which have not yet been organized into special tissues, there resides the ability to take on one or other type of histological structure according to circumstances; and, further, that there resides in each of them the still more marvellous ability to co-operate with kindred units dispersed around in developing that arrangement of the parts required to constitute a “false joint.” So that while these units have a general proclivity towards the structure of the organism as a whole, they have also proclivities towards structures proper to the local conditions into which they fall. There is latent in each unit the constitution of the entire organism and by implication the constitution of every organ; and each unit while co-operating with the aggregate is ready to take part in that particular arrangement proper to the position it has fallen into. If the reader will refer back to §§ 97_d_, 97_e_, in which it is shown that each member of a human society possesses a combination of potentialities like these, he will be the better enabled to believe that this thing _may be_ so while he is unable to conceive how it _is_ so.

And here, indeed, let it be pointed out how completely irrelevant is the test of conceivableness as applied to these ultimate physiological actions. For as here, from the un-united ends of the broken bone, there presently arises a rude joint with fit membranes, ligaments, and even synovial fluid, though we are absolutely unable to imagine the process by which the adjacent tissues produce this structure; so there may be from an organ enlarged by function, such reactive effect upon the system at large as eventually to influence the reproductive cells, though we may be absolutely unable to imagine how this can be done.]