Historical experiments: In 1883, Ringer observed that contraction of isolated frog heart ceases when CaCl2 was omitted from the bathing solution. This was reversible.
Fifty years later, Heilbrunn and Wiercinsky showed that injection of CaCl2 directly into skeletal muscle fibers causes contraction and no other cation duplicated this effect. They concluded that "Calcium might be an activator of muscle."
A.V. Hill, the founder of muscle physiology, predicted that the activator of muscle must come from an internal source, since membrane depolarization is quickly followed by mechanical response, e.g., a skeletal muscle can be fully activated within a few milliseconds. Diffusion of an activator from the surface to the interior of a fiber would take a much longer time.
In the 1960s it was shown that sarcoplasmic reticulum (SR) preparations exhibit Ca2+-ATPase activity. That is, the SR membrane contains Ca2+ pump that transports Ca2+ from the sarcoplasm into the SR lumen at the expense of ATP. Furthermore, it was established that the SR contains large amounts of calcium salts.
The experiments of Huxley and Taylor (1958): These authors raised the question, which part of the sarcomere is involved in activation of contraction? They mounted a single frog fiber under the microscope, immersed in physiological salt solution. Electrical pulse was applied through a very narrow pipette to the fiber, so that the tip of pipette was placed either to the center of A band or I band. The I band shortened when the pipette was applied to I band, whereas no response was obtained when the pipette was applied to A band (Fig. CA1). It was shown later that in frog muscle the junction of transverse tubules and SR are located in the I band, thus these experiments supported the concept that electrical stimulation of the tubules in muscle releases Ca2+ from SR.
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