Energy supply

This article deals with the supply of energy in the muscle cell, a special case of energy metabolism . For the technical processes for supplying the population with energy see energy supply , for the way living beings eat see material and energy change .

In physiology, energy supply (also energy metabolism or metabolism ) is understood as the mobilization, transport and degradation of energy-rich substrates with ATP production (resynthesis) in the muscle cells of animals. It is used to perform muscle work . A distinction is made between different types of energy supply, differentiated according to energy carrier ( creatine phosphate , carbohydrates , fats or proteins ) and metabolic pathway ( aerobic (oxidative), anaerobic lactic acid (with lactate) or anaerobic alactic acid (without lactate)). The metabolic processes that occur in connection with oxygen and take place in the mitochondria are called aerobic . The anaerobic metabolism, however, takes place outside the mitochondria in the cytoplasm . If this takes place with an increased lactate production, one speaks of a lactic energy supply, otherwise of an alactic metabolism.

introduction

In order for a muscle to perform contraction work, it needs energy , which comes from exothermic chemical reactions . In this case, chemical into mechanical energy converted. The energy requirement of the organism therefore increases with physical work. Most of the energy required for muscle contraction is provided by hydrolysis (water retention) of adenosine triphosphate (ATP) into adenosine diphosphate (ADP) and phosphate (P _i ). The ATP is thus the direct energy supplier of the muscles. However, since its supply is very limited, the muscles have to (re) produce ATP during exercise, for example, in order to be able to maintain activity. The energy required for the reconstruction ( resynthesis ) of ATP is in turn obtained through the gradual oxidation of the nutrients sugar (carbohydrates), fats or fatty acids and proteins (amino acids). You have three fundamentally different mechanisms at your disposal. There is the anaerobic-alactacid energy supply, which runs anaerobically (without the aid of oxygen) and alactacid, i.e. without (significant) lactic acid production (lactate production). The second resynthesis path is the anaerobic-lactacide , which is also anaerobic, but is associated with lactate production. In contrast, with aerobic energy provision, the energy is released with the consumption of oxygen.

history

As early as 1841 Berzelius and 1877 Du Bois-Reymond observed that there was a close connection between muscle contraction and metabolism , and they showed that the work of contracting muscle cells is linked to the formation of lactate . In 1914, these observations led Parnas and Wagner to see the lactate formation underlying the breakdown of the muscle's glycogen depot as a direct energy source for the work of contraction. This statement was supported by the fact that the formation of lactate from glycogen is associated with a release of energy. However, the experiments by Hoett and Marks in 1926 questioned the dependence of the contraction process on lactate formation, and Clark and Eggleton in 1932 proved that lactate formation, which clearly exceeds lactate utilization, only occurs after prolonged muscle work. (Since the lactate utilization was not paid much attention to for a long time, it was assumed at the time that lactate was only formed after prolonged muscle work).

After the substance creatine phosphate was discovered in the muscle, a connection between the creatine phosphate metabolism and the contraction processes in the muscle cells was established, since a decrease in creatine phosphate was observed during the contraction process and an increase in creatine phosphate during the recovery phase. While these and other findings raised doubts about the dependence of the contraction process and lactate formation and revealed an important role for creatine phosphate, Lundgaard in 1931 clearly refuted the lactate theory of muscle contraction. By means of a suitable experiment with the aid of a muscle that he had poisoned with a special substrate which prevents lactate formation, but which was still contractible and the work performed was proportional to the breakdown of creatine phosphate, he irrevocably stopped the lactate theory. An anaerobic resynthesis path for creatine phosphate was thus seen in lactate formation . Furthermore, it was found that lactate formation does not occur under aerobic conditions and the resynthesis of creatine phosphate takes place through oxidative reactions.

Finally, in 1931 , Lohmann discovered adenosine triphosphate (ATP). As a result of this discovery, creatine phosphate as a direct energy source for muscle work has now also been called into question, since in the following period the ATP was ascribed a very important role as a coenzyme , regulating factor in cell metabolism , energy carrier and direct energy source. When it was found out which high energy content the ATP actually has, it was recognized as the direct energy source of muscle contraction and Lohmann formulated the quantitative reactions on which it is based:

Creatine phosphate + ADP ↔ creatine + ATP ( creatine kinase ),

ATP + H ₂ O → ADP + P + energy ( myosin ATPase )

Energy storage

While the energy-rich phosphates ATP and creatine phosphate (KrP) can be used within the muscle cell, glycogen, fats and proteins can also be used from other depots. The various energy stores differ significantly in terms of the amount available and the maximum possible energy flow rate.

Substrate	approximate amount in phosphate residues (-P) in mmol / kg muscle	maximum duration of use (in competition)
ATP adenosine triphosphate	6th	2 - 3 s (theoretical, since resynthesis is immediate)
KrP creatine phosphate	20-25	7 - 10 s (theoretical, since resynthesis is immediate)
Total phosphate storage (phosphages)	30th	7 - 10 s (20 s)
glucose	270	45 - 90 s (anaerobic degradation)
Glycogen	3000	45 - 90 min (aerobic breakdown)
Fats (triglycerides)	50,000	several hours
Proteins (amino acids)	?	only with extreme endurance

Adenosine triphosphate (ATP)

The directly available ATP storage is only sufficient under strong muscular stress to provide energy for about one to two seconds, i.e. one to three muscle contractions. Even under the condition that ATP is split up to AMP, the resting muscle only has an ATP supply of approx. 6 µmol / g = 6 mmol / kg. When you consider the fact that humans use as much ATP every day as their body weight corresponds, it is all the more astonishing that ATP, which is so important for muscle contraction and the only immediate source of energy, is only so limited is present in the muscle cell.

Creatine phosphate (KrP)

Since the ATP supply in the muscle is only sufficient for one to three muscle contractions (about two seconds of exercise), the body must constantly strive to resynthesize ATP as a vital substance. This is where creatine phosphate comes into play, which is an energy-rich chemical compound made up of creatine (Kr) and a phosphate residue. The existing bond between the phosphate and the creatine has an energy potential corresponding to the ATP. Due to the quick reaction:

ADP + creatine phosphate ↔ ATP + creatine

the ATP is resynthesized by splitting off the phosphate residue and transferring it to ADP. In addition, creatine phosphate is available in about three to four times the amount (20–30 µmol / g) of ATP in the muscle cell. The creatine phosphate store is therefore of great importance for the performance of the skeletal muscles, as it is able to provide the necessary energy for around ten seconds (untrained people approx. 6 s, highly trained people approx. 12–20 s) with strong concentration work. It is also the source of energy that can resynthesize the ATP immediately, until other reaction pathways are activated at a later point in time.

In creatine phosphate, a decisive role is also seen as an energy gradient, which enables high substrate throughputs. It is also clear that the creatine phosphate content depends on the amount and duration of the work done. If the stress is extremely high, the creatine phosphate store can be almost completely exhausted and quickly refilled after the stress is over. If, however, the subsequent delivery of the energy-rich phosphates does not take place, the muscle's ability to contract will cease to exist.

glucose

In healthy people, the blood contains a certain amount of glucose within a range of concentrations (see also blood sugar ) . If this energy is converted, there is a constant replacement from the two next-named energy sources.

Glycogen

This is a form of glucose, the "storable form" so to speak. Glycogen can be stored as muscle glycogen in the skeletal muscles (approx. 1.5 g glycogen / 100 g muscular tissue) and in the liver . Liver glycogen (75–90 g) is used to keep the blood sugar level constant (80–100 mg% ) and thus helps to maintain the functionality of the central nervous system (CNS). Since the CNS is dependent on a constant supply of glucose from the blood and itself has low glycogen reserves, up to 60% of the glucose released by the liver into the blood ensures the brain metabolism . In the case of long-lasting submaximal loads (long-term endurance), the glucose uptake of the muscle from the blood flowing through and thus the liver glycogen plays an important role. Studies by Coggan (1990) show that after 90 minutes of exposure to about 60% of the VO ₂ max, the oxidation of plasma glucose is about one third of the total carbohydrate oxidation.

If the glycogen deposits in the liver are heavily emptied, the blood sugar level falls and, at less than 70 mg%, can already cause coordinative disorders. Normally, however, an overly intensive glucose metabolism to the detriment of the brain metabolism is prevented by protective mechanisms. The plasma insulin concentration, which regulates the permeability of glucose through the cell membrane, drops to up to 50% of the initial value when the glycogen reserves decrease due to long-term muscular work. In addition, the liver can partially regenerate glucose from substrates such as alanine and glycerine ( gluconeogenesis ) during prolonged stress .

With intensive continuous performance (competition), the body's glycogen reserves are sufficient for around 60 to 90 minutes to maintain the glucose supply.

Fats

Body fat is in the subcutaneous fat tissue (skin depot) and in the muscle cells in the form of triglycerides . Triglycerides consist of three fatty acids bound to glycerine. The free fatty acids (FFA) can be oxidized in almost all organs. In the muscle cell it is converted into so-called “C2 body” acetyl-CoA and introduced into the citric acid cycle . However, the chemical reaction is very slow, so that this form of energy supply delivers a decreasing relative proportion of the energy provided as the load increases. As the intensity continues to grow, their absolute share also decreases. The intramuscular triglyceride content is 0.3-0.8% by volume. The free fatty acids are released from the triglycerides with absorption of water ( hydrolysis ). The lipolysis (Triglyceridspaltung) is determined by the load-induced release of catecholamines epinephrine and norepinephrine priority and on prolonged exposure to the growth hormone somatropin stimulated. It is inhibited by the blood lactate concentration. Blood lactate values ​​of 5 - 8 mmol / l lead to a significant reduction in the plasma level of fatty acids.

The use of fat oxidation depends on various factors such as the duration of exercise, exercise intensity and intramuscular glycogen supply. The fat deposits of the subcutaneous fat tissue are mainly used for long-lasting low and medium intensity loads and already reduced glycogen reserves; mobilization only begins after a 15 to 30 minute load period. The level of endurance training plays a major role here, as the percentage of fatty acids burned in the energy supply increases with the increasing level of performance, thus conserving carbohydrate deposits.

Blood fats are an intermediate form of energy. In addition to metabolizing sugar, muscle cells are also able to mobilize energy directly from fat.

Egg whites

→ See also amino acid metabolism

Since proteins are normally broken down into amino acids in the building metabolism, they are only metabolized during long periods of stress (from 90 minutes) and reduced intramuscular glycogen stores, and can then cover 5 - 15% of the total energy metabolism. An oxidation of amino acids can be demonstrated by the increase in urea in the blood serum, for example after long-term endurance exercise. The concentration of leucine , isoleucine and valine in the blood also falls , which indicates that they are involved in the oxidative metabolism in the skeletal muscles. In extreme situations such as staying at high altitudes, the organism is also able to break down muscle protein indirectly, i.e. to metabolize itself.

Energy metabolism

→ See also energy metabolism

The energy required for the resynthesis of ATP can be mobilized in different ways. There are four types of energy supply , differentiated according to energy carrier and metabolic pathway. Based on the provision of energy forms that occur in competition in a specific proportional and temporal structure, takes place in the sports science-based training theory the performance structural derivation of the training areas .

ATP as the basis of energy metabolism

The breakdown of ATP releases energy

The basis for every muscle contraction is the breakdown of adenosine triphosphate into adenosine diphosphate (ADP) and phosphate (P). The ATP is a high-energy compound, consisting of adenine with ribose and three phosphates. It is the only source of energy that the cell can use directly. The so important ATP enables not only mechanical work, but also very important energy-demanding transformations, the activation of the free fatty acids and the maintenance of the labile protein structures. The reaction of the ATP to the myosin ATPase, which is important for muscle contraction, is:

ATP → ADP + P (+ energy).

In another chemical reaction (not typically associated with myosin-ATPase), ATP can be broken down into AMP (adenosine monophosphate):

ATP → AMP + PP (+ energy).

The latter reaction, however, plays a subordinate role in the production of energy. The development of tension in the muscle is heavily dependent on the available ATP content. Reductions in this level lead (from a critical threshold value) to a restriction of the development of tension and finally to the inability to contract when stimulated. The changes in the ATP content are thus associated with changes in the potential work performance of a muscle cell. Shrinking muscles that do not do any work show no or only an insignificant decrease in ATP. Muscles performing work, which are also under stress, show a reduced ATP level depending on this work performance and a corresponding heat generation . The heat development during muscle work is therefore associated with a change in the ATP level and can be explained as a consequence of entropy .

ADP

By breaking down the ADP produced by the myosin ATPase, a suitable reaction, the myokinase (2 mol ADP → 1 mol ATP + 1 mol AMP), can produce ATP under extreme emergency conditions (this reaction usually plays a role in the energy supply of the muscles but no relevant role) . This would make the important ATP immediately available for further contraction work. As a result of the high ADP concentrations from myosin ATPase and the sensitivity of myokinase to high ADP levels - i.e. H. their activity is increased by a high ADP level - the ADP concentration is the control variable for the supply of ATP from ADP. Thus the apparent end product ADP is not a negligible quantity, because its high-energy phosphate bond can at least theoretically still be used.

Anaerobic energy metabolism

Anaerobic alactacid (phosphate metabolism)

With the anaerobic-alactacid energy supply, no oxygen is required and no lactic acid is produced. It plays the decisive role in the first few seconds of physical activity and is only sufficient for a few seconds or a few maximum muscle contractions (e.g. short sprints, starts, some forms of strength training) because the creatine phosphate, which serves as an energy carrier, is only present in small amounts Muscle cells is present. The rate of ATP formation (more precisely: the resynthesis of ATP from ADP and the energy source per unit of time) is highest in the anaerobic-alactacid metabolism. After the existing ATP supply in the muscles has been used up after a few seconds, further ATP resynthesis takes place in the following ten to 30 seconds using creatine phosphate, which is also quickly available.

The energy-supplying anaerobic-alactacid reactions:

ATP + H ₂ O → ADP + P + energy

ADP + creatine phosphate ↔ ATP + creatine

Anaerobic lactacid

→ See also lactic acid fermentation

The anaerobic lactic acid metabolism does not require oxygen, but leads to the formation of lactic acid (lactate). It takes place very quickly (about half the rate of ATP formation of the anaerobic-alactacid metabolism) and lasts for 20 - 40 seconds at approximately the maximum load (95%). The energy carrier is the glucose present in the cytosol , from which ATP is obtained via glycolysis . Disadvantage: If the performance is increased or a high performance demand is maintained, the aerobic mechanisms of degradation and utilization of the lactate formed cannot prevent a sharp increase in the lactate concentration. Ultimately, there is a sudden increase in lactate, the performance must be discontinued or the intensity must be greatly reduced.

In the anaerobic lactic energy metabolism, lactate and ATP are produced through chemical reactions through the breakdown of grape sugar (glucose) or glycogen (a storage form of glucose):

Glycogen ↔ 2ATP + lactic acid.

This reaction is called glycolysis with subsequent lactic acid fermentation, which takes place in the sarcoplasm (cf. Weineck 2006, p. 101). Glucose (especially from glycogen) is used as an energy supplier. Intracellular glycogen is energetically more beneficial because it does not have to be brought about via the bloodstream. The breakdown of 1 mole of glucose to lactate produces 2 moles of ATP. If glycogen is used, that brings 3 moles of ATP in purely mathematical terms. The intermediate product pyruvic acid (pyruvate) is converted anaerobically to lactate during lactic acid fermentation.

However, the lactate produced during lactic acid fermentation has effects on the entire metabolism, both locally and in general, as it is transported to other areas of the body via the lactate shuttle mechanism. After maximum exercise, lactate levels of up to 25 mmol / kg can be found in the muscle, and up to 20 mmol / kg in the blood. This is usually accompanied by extreme acidification in the local tissue and in the arterial blood, which is associated with acidosis (greatly reduced pH value ). The acidosis leads to an enzyme inhibition, which brings about a halt in the glycolytic metabolic processes. This interruption of the maximum load represents an important protective function for the organism. It prevents excessive acidification of the muscle, which would result in the destruction of intracellular protein structures.

Aerobic energy metabolism

Aerobic glycolytic

The aerobic glycolytic metabolism uses carbohydrates with the use of oxygen. It plays a role in the provision of energy for all loads that last longer than a minute. The energy is obtained according to the simplified formula dextrose + oxygen → water + carbon dioxide + energy . This path has the following characteristics: It is faster than fat metabolism (ATP formation rate about a quarter of the anaerobic-alactacid metabolism), the glycogen (the specific form of grape sugar) is stored in the muscle, does not have to be transported first and glucose can be transported through beverages containing carbohydrates be tracked. It uses the energy released during the further metabolism of the energy-rich intermediate products. These are primarily the lactate and pyruvate produced by the anaerobic lactic metabolism. In contrast to the anaerobic metabolic pathways, the sub-processes oxidative decarboxylation , citric acid cycle and respiratory chain do not take place in the cytoplasm , but in the mitochondria . The aerobic carbohydrate metabolism has the largest share of muscle work at medium and submaximal intensity. Disadvantage: The body's own glycogen reserves are limited to about 60 to 90 minutes of continuous stress, with hours of muscle work, the intestinal absorption capacity for carbohydrates limits the intensity of the performance.

The activated acetic acid (acetyl-CoA), which is created by oxidative decarboxylation , goes through the citric acid cycle and the respiratory chain for further degradation . With this type of energy supply, about 32 moles of ATP are obtained from 1 mole of glucose. If the intracellular glycogen is used for degradation, 34 moles of ATP are produced:

1 glucose + 6 O ₂ + 32 ADP + 32 P → 6 CO ₂ + 6 H ₂ O + 32 ATP

With the aerobic breakdown of glucose, around 15 times as much ATP can be obtained as with lactic acid fermentation. However, this high energy yield also has a decisive disadvantage. With the help of oxidative combustion, many moles of ATP are made available, but this energy supply takes place via long reaction chains, which is why it takes a longer time until this energy is available.

Aerobic lipolytic (aerobic lipolysis)

→ See also fat burning

The aerobic lipolytic metabolism uses fatty acids with the use of oxygen. The energy is obtained according to the simplified formula fat + oxygen → water + carbon dioxide + energy (lipolysis - 1 mol FFS results in approx. 130 mol ATP). The process also takes place to a large extent (ATP production) in the mitochondria ( beta-oxidation ) and, at low intensity, makes up the largest part of muscle work. Advantage: very large body's own reserves (sufficient for days of continuous stress), disadvantage: very slow (ATP formation rate only about a tenth of the anaerobic-alactacid metabolism).

This reaction sets in after about 20 minutes of endurance exercise. In addition, protein can also serve as an energy supplier in emergencies, whereby these two types of energy generation (FFS and protein) are particularly relevant for endurance exercise (low exercise intensity).

Combination of forms under real loads

Due to the fact that the contraction speed of the muscle is fastest with the high-energy phosphates and the slowest with the oxidative energy supply, due to different flow rates, a mixed form of the energy-supplying systems can often be observed at different stress intensities with different stress duration. Thus the intensity of the muscle work, i.e. the contraction speed of the muscle fiber, changes depending on the energetically possible flow rate.

It shows the great usefulness of the different flow rates. If, for example, high intensities are to be achieved (high energy turnover), this is especially the case with high-speed loads, higher flow rates must be achieved. Consequently, the anaerobic-alactacide (ATP, PKr) as well as the lactacide energy production must be used. If lower work intensities are to be covered, such as long-distance runs, the aerobic energy supply processes inevitably predominate.

Oxygen deficit and EPOC

→ See EPOC and oxygen deficit

See also

• Anaerobic threshold
• Endurance training
• Training (sport)

Web links

• The muscular energy supply in sport - Dr. Kurt A. Moosburger, sports doctor and nutritionist from Austria (PDF; 189 kB)
• Energy supply - Dr. Peter Wastl, Institute for Sports Science, Heinrich Heine University Düsseldorf (PDF; 71 kB)

literature

• Bartl, Meinhard, Moisl: Abitur training in biology. Biology 1. Freising 1987.
• D. Cunningham, J. Faulkner: The effect of training on aerobic and anaerobic metabol-ism during short exhaustive run. In: Med. And Sci. in sports. 2 (1969), pp. 65-70.
• H. Heck, Trainer Academy Cologne eV (ed.): Energy metabolism and medical performance diagnostics. Schorndorf 1990, ISBN 3-7780-8081-4 .
• U. Helmich: Citric acid cycle. u-helmich.de , January 24, 2009.
• H. Senger, R. Donath: Regulating the oxidative substrate utilization in muscles with increased ATP turnover. In: Medicine and Sport. 12, pp. 391-400 (1977).

Individual evidence

1. ^ Fritz Zintl: Endurance training . blv, Munich 2009, ISBN 978-3-8354-0555-4 , p. 46 .
2. ↑ ^{a b c d} Fritz Zintl: Endurance training . blv, Munich 2009, ISBN 978-3-8354-0555-4 , p. 46-47 .
3. ^ ^{A b} T. Hettinger, W. Hollmann: Sports medicine, basics for work, training and preventive medicine. 4th edition. Stuttgart 2000, ISBN 3-7945-1672-9 , p. 62.
4. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 20.
5. ^ Andreas Hohmann, Martin Lames, Manfred Letzelter: Introduction to training science . Limpert, Wiebelsheim 2007, ISBN 978-3-7853-1725-9 , pp. 52 .
6. ↑ J. Weineck: Sports biology. 4th edition. Balingen 1994, ISBN 3-929587-43-2 , p. 101.
7. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 22.
8. ^ Andreas Hohmann, Martin Lames, Manfred Letzelter: Introduction to training science . Limpert, Wiebelsheim 2007, ISBN 978-3-7853-1725-9 , pp. 53 .
9. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 25.
10. ↑ ^{a b} Fritz Zintl: Endurance training . blv, Munich 2009, ISBN 978-3-8354-0555-4 , p. 48 .
11. ↑ ^{a b} Fritz Zintl: Endurance training . blv, Munich 2009, ISBN 978-3-8354-0555-4 , p. 48-49 .
12. ^ Fritz Zintl: Endurance training . blv, Munich 2009, ISBN 978-3-8354-0555-4 , p. 49 .
13. ↑ J. Weineck: Sports biology. 4th edition. Balingen 1994, ISBN 3-929587-43-2 , p. 38.
14. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 19.
15. ↑ J. Koolman et al. a .: Pocket Atlas of Biochemistry. Georg Thieme Verlag, 2002, ISBN 3-13-759403-0 , p. 336 ( books.google.de ).
16. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 32.
17. ↑ ^{a b} J. Weineck: Sports biology. 4th edition. Balingen 1994, ISBN 3-929587-43-2 , p. 39.
18. ↑ J. Keul, E. Doll, D. Keppler: Muscle Metabolism. The provision of energy in the skeletal muscle as the basis of its function. Munich 1969, DNB 457199261 , p. 38.
19. ^ J. Weineck, A. Weineck: Advanced course in sport. 3. Edition. Volume 1. Forchheim 2004, ISBN 3-00-013707-6 , p. 104.