May 28, 1897.] 



SCIENCE. 



823 



As the matter now stands, it seems to 

 me that any satis factor j"^ explanation of the 

 cell growth causing work-hypertrophies 

 must start from physical or chemical 

 changes in the muscle- or gland-cell itself 

 directly connected with the increased func- 

 tion. These changes are the primum mobile, 

 and, however important increased supply of 

 blood or lymph may be in the subsequent 

 chain of events, it is not the determining 

 factor. The whole problem is part of the 

 general one of the causes of pathological 

 cell-growth, to which I shall have occasion 

 to refer again. 



It is interesting to note that not all kinds 

 of excess of functional activity lead to 

 hypertrophy. A heart may beat for years 

 faster than normal without becoming hyper- 

 trophied. Small movements of muscle, 

 often repeated, do not cause hypertrophy. 

 It would appear that the amount of work 

 done in each functional act must attain a 

 certain height in order to stimulate growth. 

 On the other hand, if the muscle be 

 stretched beyond certain limits, it does not 

 hypertrophy ; on the contrary, it may 

 atrophy, as may be seen in greatly dis- 

 tended canals and cavities with muscular 

 walls. This behavior is also in accordance 

 with physiological obsei-vations. 



The compensatory hypertrophy of muscle 

 seems to be due mainly to increase in the 

 size of cells, although there are observa- 

 tions indicating that they may also multi- 

 ply. That of most glands is referable to 

 increase both in number and size of cells. 

 "Within four or five days after extirpation 

 of a kidney, karyokinetic figures may be 

 found in increased number in the cells of 

 the remaining kidney. 



The general character of the adaptation 

 secured by compensatory hypertrophy of 

 the heart is sufficiently well known. I 

 wish to point out certain of its imperfec- 

 tions. I shall not dwell upon the well- 

 known abnormal conditions, with their re- 



mote consequences, of the systemic or pul- 

 monary circulation, which are present 

 during the stage of compensation, nor shall 

 I speak of the various circumstances which 

 may interfere with the establishment of 

 compensatory hypertrophy. 



The muscle of a hypertrophied heart is 

 sometimes compared to that of the black- 

 smith's arm, and the statement is made 

 that there is no reason inherent in the 

 muscle itself why the one should fail more 

 than the other. This may be true, but it is 

 not self-evident. Exercise may influence 

 in various ways the nutrition, function and 

 growth of muscle as well as of other parts. 

 Mere increase in bulk is a coarse effect. 

 Quality may be improved as well as 

 quantity. The biggest muscle is not neces- 

 sarily the best or the most powerful. As 

 every trainer knows, various conditions 

 under which work is done influence the re- 

 sult. Increase in the reserve energy of the 

 heart, secured by judicious exercise— and 

 this is the main factor in endurance — prob- 

 ably cannot be attributed mainly to hyper- 

 trophy ; indeed, enlargement of this organ 

 from exercise is often a serious condition. 

 Much more might be said in this line of 

 thought, but I have indicated why it seems 

 to me unjustifiable to assume, without 

 further evidence, that the condition of the 

 muscle in pathological hypertrophies is 

 necessarily identical in all respects with 

 that in physiological hypertrophies. 



There is an important difference in the 

 working conditions between most hyper- 

 trophied hearts and the normal heart. 

 Although the maximal available energy of a 

 hypertrophied heart during compensation is 

 greater than that of the normal heart, 

 clinical experience shows that in the ma- 

 jority of cases the energy available for un- 

 usual demands — that is, the so-called re- 

 serve force — is less in the former than in 

 the latter. Sometimes, especially when the 

 hypertrophj' has developed in early life, the 



