Sources of energy for muscle work
During striated muscle fiber working ATP breaks down and forms ADP and inorganic phosphate. Resynthesis of ATP is carried out in reactions that take place without oxygen (anaerobic mechanisms) or with inhaled oxygen (aerobic).
Creatine kinase mechanism (alaktate, anaerobic).
Creatine phosphate is on the contractile filaments of myofibrils and reacts quickly in rephosphorylation reaction:
Creatine
phosphate + ADF 
Creatine + ATP
This mechanism is first included in the resynthesis of ATP at the beginning of muscular work and runs at maximum rate until it runs out of creatine phosphate in the muscles. It plays a crucial role in short-term exercise (100 m run). Creatine phosphokinase system works in fast-twitch muscle fibers, and therefore forms the basis of speed and endurance.
Miokinase mechanism is the resynthesis of ATP at the expense of rephosphorylation between two molecules of ADP with miokinase participation:
2 ADP = ATP + AMP
It occurs in the muscles by increasing the concentration of ADP in the sarcoplasm, i.e. during muscle fatigue.
Glycolytic mechanism (lactate, anaerobic) is resynthesis of ATP in the anaerobic breakdown of muscle glycogen or blood glucose to form lactic acid. It is activated after the 20-second intense work of creatinekinasephosphorylation, reaching a peak after 40-80 seconds.
Aerobic ATP resynthesis mechanism (oxidative phosphorylation) in normal conditions gives a 90% resynthesized ATP. The energy is produced by oxidation (in the Krebs cycle) of the breakdown products of carbohydrates, fatty acids, acetate and acetoacetate. It is implemented during prolonged physical work.
For cardiac muscle the main pathway of resynthesis of ATP is oxidative phosphorylation, and oxidation of non-carbohydrate substances provides 65-70% of myocardial energy requirements. The main substrate of respiration of heart muscle is fatty acids.
9.2. Mechanism of muscle contraction and its regulation
1. The contraction begins with a nerve impulse. In the synapse, acetylcholine is released. It stimulates sarcolemma, depolarizes the membrane and generates action potential at its surface.
2. The action potential spreads deep into the muscle fiber reaches the sarcoplasmic reticulum and promotes the release of calcium ions from the reticulum in the sarcoplasm.
3. Calcium ions activate ATPase centers in the heads of myosin. ATP is cleaved, ADP, and Pi remain on myosin. Interaction site of the myosin heads is blocked by troponin.
4. Calcium ions bind to troponin and unlock the myosin heads. Myosin head is free to rotate and when it reaches the desired position it is associated with F-actin, forming with the axis the fibril angle of 90.
5. Myosin heads and the active sites of actin form crosslinking adhesions – an actin-myosin complex.
6. ADP and Pi are split off from the heads of myosin; the released energy is used for the conformational changes of contractile proteins.
7. Myosin heads are bent. The angle the myosin with the axis of fibrils is changed from 90 to 45. Tension is created between thick and thin filaments. Thin filament moves to the direction of the sarcomere.
8. The new molecule of ATP binds to the myosin – F-actin complex.
9. Myosin – F-actin complex has a low affinity for actin, and myosin head is separated from the F-actin. There is relaxation of the muscle (Fig. 10).
Fig. 10. The mechanism of muscle contraction
The overall contraction process is the result of summing a large number of adhesion formation along the entire length of myofibrils involved in the process of contraction the excited muscle. Calcium ions play a key regulatory role. Myofibrils interact with ATP and contracts at C(Ca) = 10-6-10-5 M. If the excitation ceases, the concentration of calcium ions in the sarcoplasm is decreased, and the heads of the myosin filaments stop to attach actin filaments. In the presence of ATP, the muscle relaxes, and its length reaches the initial phase. If there isn’t ATP synthesis (anoxia, death, gassing), the muscle stiffness is developed. The myosin cross bridges attached to actin filaments, resulting in immobility of the muscles.