74 THE PHYSIOLOGY OF MUSCLE AND NERVE. 



as having interfaces with the sarcoplasm along the lateral planes and with the 

 isotropic substance (light bands) at their ends, at which surface tension exists. 

 If the results of the chemical changes within the elements are such as to cause 

 a diminution in surface tension along the lateral walls, or an increase in this 

 energy at the end surfaces, the elements would tend to change from a cylinder 

 with straight to one with curved lateral walls, and this change, when multi- 

 plied by the total number of sarcous elements in the muscle, would account 

 for the shortening. The theory is deficient in not explaining how the surface 

 energy is changed, and also in failing to give an approximate quantitative 

 determination of the total amount of mechanical energy that might be obtained 

 in this way from the muscle. According to calculations made by Bernstein,* 

 the work energy exhibited by a contracting muscle is greater than can be 

 accounted for by probable changes in surface tension. 



Another theory has been adopted in recent years by an increasing number 

 of workers, and has been supported by many suggestive experiments. This 

 theory holds that the shortening of muscle in contraction is essentially a 

 phenomenon of imbibition. The instrument by which the shortening is 

 effected is the fibril, which is regarded as a coherent gel structure embedded in 

 a more liquid material, the sarcoplasm. When the muscle is stimulated, lactic 

 acid is formed in the fibril or in the sarcoplasm around it, and the effect of this 

 acid is to increase the power of imbibition of the fibril or of certain structures in 

 it, for example, the anisotropous discs. The swelling thus produced causes the 

 shortening of the muscle, and the subsequent relaxation is explained as due to 

 the removal of the acid by diffusion or by oxidation. The heat developed in 

 the muscle after the phase of shortening is past has been connected with this 

 latter process, namely, the oxidatiye destruction of the lactic acid, although 

 some authors contend that the lactic acid is not removed by oxidation to CO 2 

 and H 2 O, but is resynthesized to the sugar or the sugar-complex from which it 

 was derived. The theory has many variations as regards details, but the 

 central point is that the lactic acid is the agent which causes the contraction 

 by its action on the imbibition-properties of the fibril. The shortening in 

 rigor mortis is explicable in the same way as an acid effect. J 



* Bernstein-Pfliiger's "Archiv," 85, 271, 1901. See also Berg, "Biochem- 

 ical Bulletin," 2, 101, 1912. 



t For various expressions of this theory, consult McDougall, "Journal of 

 Anatomy and Physiology," 31, 410, 1897, and 32, 187, 1898. Meigs, "Amer- 

 ican Journal of Physiology," 26, 191, 1910, and 22, 477, 1908. Fletcher and 

 Brown, "Journal of Physiology," 48, 177, 1914. Hill, ibid., 46, 28, 1913. 

 Pauli, "Kolloid-chemie der Muskelkontraktion," 1912. 



