Skeletal muscle calcium movement

The first molecule, the Ca2+ channel, is required for coupling at the triad. Skeletal muscle contains higher concentrations of this L-type Ca2+ channel that can be accounted for on the basis of measured voltage-dependent Ca2+ influx because much of the Ca2+ channel protein in the T-tubular membrane does not actively gate calcium ion movement but, rather, acts as a voltage transducer that links depolarization of the T-tubular membrane to Ca2+ release through a receptor protein in the SR membrane. The ryanodine receptor mediates sarcoplasmic reticulum Ca2+ release. The bar-like structures that connect the terminal elements of the SR with the T-tubular membrane in the triad are formed by a large protein that is the principal pathway for Ca2+ release from the SR. This protein, which binds the... 

Fig. 47.3. Events leading to sarcoplasmic reticulum calcium release in skeletal muscle. 1. Acetylcholine, released at the synaptic cleft, binds to acetylcholine receptors on the sar-colemma, leading to a change of conformation of the receptors such that they now act as an ion pore. This allows sodium to enter the cell and potassium to leave. 2. The membrane polarization that results from these ion movements is transmitted throughout the muscle fiber by the T-tubule system. 3. A receptor in the T-tubules (the dihydropyridine receptor, DHPR) is activated by membrane polarization (a voltage-gated activation) such that activated DHPR physically binds to and activates the ryanodine receptor in the sarcoplasmic reticulum (depolarization-induced calcium release). 4. The activation of the ryanodine receptor, which is a calcium channel, leads to calcium release from the SR into the sarcoplasm. In cardiac muscle, activation of DHPR leads to calcium release from the T-tubules, and this small calcium release is responsible for the activation of the cardiac ryanodine receptor (calcium-induced calcium release) to release large amounts of calcium into the sarcoplasm.

Fig. 10-23 Calcium movement across the sarcoplasmic reticulum in skeletal muscle. Note the potential futile cycle.

Winegrad, S. 1968. Intracellular calcium movements of frog skeletal muscle during recovery from tetanus. J. Gen. Physiol. 51 65-83. 

Adult osteomalacia often has an insidious presentation. " " The underlying disorder may be more apparent than skeletal defects (e.g., diarrhea in sprue). Diffuse skeletal pain, bony tenderness, and proximal muscle weakness may occur. Pain on movement and muscle weakness may result in a characteristic waddling gait. Hypophosphatemia and secondary hyperparathyroidism may contribute to these symptoms. Tetany can result from sufficiently depressed serum ionized calcium. Skeletal deformities (infrequent in adults) include leg bowing, pigeon chest, scoliosis, kyphosis, and shortening of the spine. 

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