The cross-sectional cycle can continue as long as there are sufficient amounts of ATP and Ca2+ in the cytoplasm.  Discontinuation of the Crossbridge cycle may occur when Ca2+ is actively pumped into the sarcoplasmic reticulum. When Ca2+ is no longer present on the thin filament, tropomyosin returns the conformation to its previous state to block the binding sites again. The myosin stops binding to the thin filament and the muscle relaxes. Ca2+ ions leave the troponin molecule to maintain the concentration of Ca2+ ions in the sarcoplasm. The active pumping of Ca2+ ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils. This causes ca2+ ions to be removed from troponin. Thus, the tropomyosin-troponin complex again covers the binding sites at the actin filaments and the contraction stops. In both situations, the force generated by the muscle is not sufficient to keep the biceps brachii in a completely contracted state.
This causes the vigorous lengthening of the muscle fibers, which is called eccentric contraction. The word “contraction” could be confusing because the biceps lengthen brachii, so what`s really going on? During an eccentric contraction, the muscle tries to shorten itself by creating tension, but it actually lengthens. Indeed, the external force exerted on the muscle overwhelms the force generated by the concentric contraction. Eccentric contraction is not a simple passive stretch of the muscle, but a tension stretch designed to slow down and smooth the repositioning of the heavy load. The end of the crossbridge cycle (and the exit of the muscle in the latch state) occurs when the light-chain phosphatase of myosin removes phosphate groups from myosin heads. Phosphorylation of 20 kDa myosin light chains is well correlated with the speed of shortening of smooth muscles. Meanwhile, there is a rapid eruption of energy consumption, measured by oxygen consumption. A few minutes after their appearance, calcium levels drop significantly, phosphorylation of 20 kDa myosin light chains decreases, and energy consumption decreases; However, the strength of the tonic smooth muscles is preserved. During muscle contraction, rapidly changing transverse bridges form between activated actin and phosphorylated myosin, creating strength. He hypothesizes that force maintenance results from dephosphorylated “locking bridges” that circulate slowly and maintain force.
A number of kinases such as rhokinase, DAPK3 and protein kinase C are thought to participate in the prolonged phase of contraction, and the flow of Ca2+ may be significant. Unlike skeletal muscle, smooth muscle and heart muscle contractions are myogenic (meaning they are initiated by the smooth muscle or heart cells themselves, rather than being stimulated by an external event such as nerve stimulation), although they can be modulated by stimuli from the autonomic nervous system. The contraction mechanisms in these muscle tissues are similar to those of skeletal muscle tissue. After systole, intracellular calcium is reabsorbed into the sarcoplasmic ATTiculum pump (SERCA) of the sarco/endoplasmic reticulum, ready for the next cycle. Calcium is also expelled from the cell, mainly through the sodium-calcium exchanger (NCX) and, to a lesser extent, through an ATPase calcium plasma membrane. Some of the calcium is also absorbed by the mitochondria.  An enzyme, phospholamban, serves as a brake on SERCA. At low heart rate, phospholamban is active and slows down ATPase activity, so Ca2+ doesn`t have to leave the cell completely.
At high heart rates, phospholamban is phosphorylated and deactivated, resulting in the absorption of most of the Ca2+ from the cytoplasm into the sarcoplasmic reticulum. Also this fall, calcium buffers moderate themselves in the concentration of Ca2+, which allows a relatively small decrease in the concentration of free Ca2+ in response to a significant change in total calcium. The decrease in the concentration of Ca2+ allows the troponin complex to dissociate from the actin filament and thus end the contraction. The heart relaxes so that the ventricles can fill with blood and start the heart cycle again. The force-speed relationship refers to the speed at which a muscle changes its length (usually regulated by external forces such as tension or other muscles) with the amount of force it generates. The force decreases hyperbolically relative to the isometric force as the shortening rate increases, and eventually reaches zero at maximum speed. The opposite is true when the muscle is stretched – the force increases beyond the isometric maximum until an absolute maximum is finally reached. This intrinsic property of active muscle tissue plays a role in the active cushioning of joints operated by simultaneously active counter-muscles. In such cases, the force-speed profile amplifies the force generated by the lengthening muscle at the expense of the shortening muscle. This favor of the muscle, which balances the joint, effectively increases the cushioning of the joint. In addition, the strength of the cushioning increases with muscle strength. The motor system can thus actively control joint damping via the simultaneous contraction (co-contraction) of opposing muscle groups.
 The length-tension relationship refers to the strength of an isometric contraction at the length of the muscle where the contraction occurs. Muscles work with the greatest active tension when they approach an ideal length (often their length at rest). In addition, if stretching or shortening is carried out (whether due to the action of the muscle itself or an external force), the maximum active tension generated decreases.  This decrease is minimal for small deviations, but the voltage decreases rapidly as the length continues to deviate from the ideal. Due to the presence of elastic proteins in a muscle cell (such as titin) and the extracellular matrix, when the muscle is stretched beyond a certain length, there is a completely passive tension that counteracts the elongation. In combination, there is a strong resistance to the elongation of an active muscle well beyond the peak of active tension. During a concentric contraction, a muscle is stimulated to contract according to the sliding wire theory. This happens along the entire length of the muscle, creating strength at the origin and beginning, shortening the muscle and changing the angle of the joint. As for the elbow, a concentric contraction of the biceps would cause the arm to bend to the elbow when the hand passes from the leg to the shoulder (a bicepslock). A concentric contraction of the triceps would change the angle of the joint in the opposite direction, stretching the arm and moving the hand towards the leg. The strength of skeletal muscle contractions can be roughly divided into contractions, summations and tetanus.