Gordon A M, Ridgway E B
Eur J Cardiol. 1978 Jun;7 Suppl:27-34.
Muscle contraction is initiated by an elevation in intracellular calcium. The transient change in free calcium to a brief depolarization, the calcium transient, can be recorded using a calcium luminescent protein, aequorin. The calcium transient precedes force, peaking while force is rising and returning to the resting level as peak force is achieved. In single barnacle muscle fibers microinjected with aequorin, shortening the muscle during the declining phase of the calcium transient produces an addition light signal, indicating extra free calcium in the sarcoplasm. The amount of additional light is larger with larger length changes. It is also larger if the shortening occurs early in the calcium transient rather than later. The amount of this extra calcium correlates well with the instantaneous level of the calcium transient and not with the instantaneous force level. It is argued in a speculative manner that this extra calcium is coming from the myofilaments. This supports the hypothesis that calcium binding to the myofilaments is rapid and reversible, that reaccumulation of calcium into the sarcoplasmic reticulum (SR) could occur long before relaxation begins and that relaxation of tension could occur by some process other than the mere removal of calcium from the myofilaments.
