The ability of cells to develop force and to shorten are commonly associated with skeletal muscles. These processes are not limited to skeletal muscles, however, but extend to cardiac muscles that pump blood, the smooth muscles that both maintain forces for extended durations and empty the contents of cavities, and in the migration of individual cells such as leukocytes around the body. All of these processes rely on the interaction of actin and myosin, the primary components of thin and thick filaments, respectively. The structure of the filaments converts the scalar myosin ATPase into vectorial force and shortening. Individual differences produce the diverse mechanical activities in the body. With experimental observations going back hundreds of years, the technical details known about contraction rival those of any other biophysical system, details that are covered below.

The skeletal length–tension relation

It was only with the discovery of the overlapping filaments of striated muscle in 1954 (Huxley and Niedergerke, 1954; Huxley and Hanson, 1954) that the molecular basis for muscle contraction was formed. This restriction did not keep previous scientists, certainly going back to Pugh, from observing the behavior of muscle. His description of the length–tension curve, although not by that name, is clear to us today. Extend a muscle, and its force increases, but stretch it too far, and it weakens: accurate, and even perhaps implying the damage that occurs if muscles are overstretched. We do have the advantage of having considerably more information than Pugh had.