The initial purpose of the present study was to find an explanation for the long time interval elapsing between the activation of the auricle and the ventricle. Considering the fact that the auriculo-ventricular (A.V.) node is a structure which the impulse coming from the auricle traverses on its way towards the ventricle, it seemed likely that an explanation for the A.V. latency could be found by studying its activity. It was also expected that the node should reveal its activity through an action potential which in turn could be registered by appropriate means.

Volumetric experiments on single fibers isolated from semiten-dinosus muscles of frogs, some performed in correlation with measurements of membrane potential, confirm the data obtained on whole muscles, but only for the specific range of conditions in which most of the latter experiments have been done. These conditions are restricted to media in which the anion ( Cl usually) is permanent and the K is 10 to 12.5 meqlliter, or four to five times above the normal level in Ringer's solution. When other ionic conditions are employed, phenomena are disclosed which have not previously been described. The findings throw doubt upon the validity of some generally accepted views regarding the permeability properties of the membrane of frog muscle fibers and regarding the nature of the mechanisms which regulate their volume.

In cross-sections of single fibers from the frog semitendinosus muscle the number of thick myofilaments per unit area (packing density) is a direct function of the sarcomere length. Our data, derived from electron microscopic studies, fit well with other data derived from in vivo, low-angle X-ray diffraction studies of whole semitendinosus muscles. The data are consistent with the assumption that the sarcomere of a fibril maintains a constant volume during changes in sarcomere length. The myofilament lattice, therefore, expands as the sarcomere shortens. Since the distance between adjacent myofilaments is an inverse square root function of sarcomere length, the interaction of the thick and the thin myofilaments during sarcomere shortening may occur over distances which increase 70 A or more. The "expanding-sarcomere, sliding-filament" model of sarcomere shortening is discussed in terms of the current concepts of muscle architecture and contraction.

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