The latch state is believed to occur when the cross-bridge cycle slows down, causing the myosin heads to stay in contact with the actin filament for a longer period of time. This allows tension to be maintained in smooth muscle at a low energy cost. It is important to note that the intracellular concentration of calcium ions (Ca++) decreases during the tonic phase of contraction, although it remains higher than the resting/basal level. The mechanism behind smooth muscle's ability to maintain force at a low intracellular Ca++ concentration during tonic contraction involves the dephosphorylation of the myosin regulatory light chain while the myosin cross-bridge is attached to the actin filament. This results in a slower dissociation rate of the myosin from the actin, allowing the myosin to spend more time in an attached, force-generating conformation. The relaxation of smooth muscle after tonic contraction occurs when the intracellular Ca++ concentration decreases to a level that prevents the net phosphorylation of the regulatory light chain by MLCK. It has also been suggested that caldesmon may play a role in the transition to the latch state. 

As mentioned before, the latch state reduces ATP consumption. In this state, smooth muscle utilizes 300 times less ATP compared to skeletal muscle to generate the same amount of force. Smooth muscle, like skeletal muscle, requires ATP for ion transport to maintain the resting membrane potential, store Ca++ in the sarcoplasmic reticulum (SR), and remove Ca++ from the cell. These metabolic needs are easily met by oxidative phosphorylation. Fatigue in smooth muscle only occurs if the cell is deprived of oxygen. However, even in the presence of sufficient oxygen, aerobic glycolysis with lactic acid production supports the functioning of membrane ion pumps.

The regulation of myoplasmic calcium concentration in smooth muscle involves two sources of calcium ions: the sarcolemma and the SR. The sarcolemma controls the influx and efflux of calcium ions from the extracellular pool. On the other hand, the SR membranes determine the movement of calcium ions between the myoplasm and the SR pool. Unlike skeletal muscle contraction, extracellular calcium ions are necessary for smooth muscle contraction. Therefore, the regulation of myoplasmic calcium concentration involves both the SR and the sarcolemma. Various factors can influence the myoplasmic concentration of calcium ions.
The latch state is thought to reflect a slowing of the cross-bridge cycle, so that the myosin heads remain in contact with the actin filament for a longer time, thereby maintaining tension at low energy cost. Note that the intracellular [Ca++] falls to a low level during the tonic phase of contraction, though it is still above the resting/ basal [Ca++]. The mechanism contributing to the ability of smooth muscle to maintain force at a low intracellular [Ca++] during tonic contraction is thought to involve dephosphorylation of the myosin regulatory light chain while the myosin cross-bridge is attached to the actin filament, resulting in slowing of the rate of dissociation of the myosin from the actin, allowing the myosin to spend more time in an attached, force-generating conformation. Relaxation of smooth muscle following tonic contraction occurs when intracellular [Ca++] decreases to a level that prevents a net phosphorylation of the regulatory light chain by MLCK. It has also been proposed that caldesmon may participate in the transition to the latch state.
As already noted, ATP consumption is reduced during the latch state. Under this condition, smooth muscle uses 300fold less ATP than would be required by skeletal muscle to generate the same force. Smooth muscle, like skeletal muscle, requires ATP for ion transport to maintain the resting membrane potential, sequester Ca++ in the SR, and extrude Ca++ from the cell. All these metabolic needs are readily met by oxidative phosphorylation. Fatigue of smooth muscle does not occur unless the cell is deprived of oxygen. However, aerobic glycolysis with lactic acid production normally supports membrane ion pumps even when oxygen is plentiful.
Regulation of Myoplasmic Calcium Concentration
The mechanisms that couple activation to contraction in smooth muscle involve two Ca++ sources: one involving the sarcolemma and the other involving the SR. The sarcolemma regulates Ca++ influx and efflux from the extracellular Ca++ pool. The SR membranes determine Ca++ movement between the myoplasm and the SR pool. Skeletal muscle contraction does not require extracellular Ca++ (see ). In contrast, extracellular Ca++ is important for smooth muscle contraction. Thus regulation of myoplasmic [Ca++] involves not only the SR but also the sarcolemma (
Fig. 14.10). A number of factors can alter the myoplasmic
Na+-K+ pump 2K+ 3 Na+ Ca++ MLCK off CaCM CM ATP Receptor-activated CaCM*MLCK ATP G G Sarcoplasmic reticulum Time IP3 PIP2 3Na Cell Ca++ Neurotransmitter or hormone Neurotransmitter or hormone Ca++ channel Refilling ATP ?