Muscles require energy to perform their functions. Energy provision can be provided through various pathways by the breakdown and conversion of nutrients.
What is energy provision?
Muscles need energy to perform their functions. Energy provision can be ensured through various pathways. Energy provision for activities of the muscle is possible in 4 different ways. They differ in terms of the speed and the amount with which they can provide energy. The intensity of the muscle activity determines which of these processes is used to provide energy. Often the different processes run side by side. In the anaerobic (without oxygen involvement) alactacid (without lactate attack) process, the ATP (adenosine triphosphate) store and the creatine phosphate store provide energy for a short time. However, this lasts only for 6-10 seconds, in well-trained athletes for up to 15 seconds, and is retrieved during maximal, high-speed power and speed performances. All other processes require the presence of glucose or fatty acids. They provide ATP (adenosine triphosphate) in various amounts through a complete or incomplete breakdown. In anaerobic lactic energy production, glycogen, the storage form of glucose, is incompletely cleaved. Therefore, this process is also called anaerobic glycolysis. Lactate and little energy is produced, which is sufficient for 15 – 45 second, in top athletes for 60 second intensive performances. For long-duration, low-intensity exercise, energy is derived from the complete combustion of glucose or fatty acids in aerobic (using oxygen) energy production processes that occur in the mitochondria of muscle cells.
Function and task
Muscles need energy to perform their functions. They convert it into mechanical work to move joints or stabilize areas of the body. However, mechanical efficiency is very low because only about one-third of the energy provided is used for kinetic needs. The rest is burned in the form of heat, which is either released to the outside or used to maintain body temperature. Athletes for whom fast or high effort movements over short periods of time are important draw their energy from the energy stores located in the plasma of the muscle cells. Typical disciplines that meet these requirements include the 100-meter sprint, weightlifting, or high jump. Typical sporting activities that have a duration of 40 – 60 seconds under maximum possible power are the 400 meter run, 500 meter speed skating or 1000 meter track cycling, but also a long final sprint at the end of an endurance race. The muscles obtain the energy for these activities from anaerobic lactic energy metabolism. In addition to lactate, hydrogen ions are also produced, which gradually overacidify the muscle and thus represent the limiting factor for this type of sporting activity. In long-duration, low-intensity sporting activities, energy must be constantly replenished without producing substances that cause the muscle to break down. This happens through the complete combustion of glucose and fatty acids, which are obtained from carbohydrates and fats. In the end, after various stages of degradation, both energy sources end up as acetyl-coenzyme A in the citrate cycle, where they are degraded with oxygen consumption and provide significantly more energy than anaerobic glycolysis. Significantly, the body’s fat reserves can provide energy significantly longer than carbohydrate stores, but at low intensity. Therefore, if endurance athletes do not replenish their carbohydrate stores in between training sessions, they may experience a significant drop in performance.
Diseases and ailments
All diseases that affect the breakdown, transport, and absorption of fatty acids and glucose have negative consequences for energy provision. In diabetes, primarily the uptake of glucose from the blood into the cells is impaired, for which insulin is needed. Depending on the severity, this can lead to a reduced supply in the muscle cells, which reduces performance.The consequence of this absorption disturbance is the rise in blood glucose levels, a signal for the pancreas to produce even more insulin to break down this excess. In addition to the long-term organ damage caused by the change in blood composition, this process directly affects the ability of the liver to mobilize fat and glucose reserves. There, the increased presence of insulin promotes the conversion of glucose into its storage form glycogen and the formation of storage fat, inhibiting the mobilization of these substances for energy delivery. Liver diseases such as fatty liver, hepatitis, hepatic fibrosis, and cirrhosis have similar effects on fat mobilization, although the mechanisms of action are different. The balance between fat uptake and storage on the one hand and degradation and transport on the other is disturbed in these diseases due to enzymatic defects, with effects on overall performance. There are some rare diseases that take place directly in the muscle cells, some of which have significant consequences for the affected individuals. These genetic diseases are grouped under the term metabolic myopathies. There are 3 basic forms with different variants:
In mitochondrial diseases, the gene defects cause disturbances in the respiratory chain, which is important for the aerobic breakdown of glucose. As a result, either no or only a small amount of ATP is formed and made available as an energy carrier. In addition to muscular symptoms, neuronal degeneration is prominent. In glycogen storage disease (the best known form is Pompe disease), the conversion of glycogen into glucose is disturbed by the gene defects. The earlier this disease occurs, the worse the prognosis. Lipid storage disease behaves similarly, but here there are problems with fat conversion. A wide range of symptoms occur in all diseases. Muscularly, there are sometimes considerable reductions in performance, rapid fatigue, the occurrence of muscle cramps, muscle hypotonia and, with prolonged progression, muscle atrophy.