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Neue-Aspekte zur durchblutungssteigernden und insulinähnlichen Wirkung der Muskelarbeit: Mögliche Beteiligung des Kallikrein-Kinin-Prostaglandin Systems

New aspects of the blood flow-augmenting and insulin-like activity of muscle exercise: Possible involvement of the kallikrein-kinin-prostaglandin system

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Summary

Adaptations of energy metabolism, as they occur during contractions of skeletal muscle besides by anaerobic glycolysis are achieved via changes in capillary blood flow providing substrates and oxygen for combustion. Since, initially, oxygen supply is restricted in the working muscle, glucose would seem to be the adequate fuel as it may be used anaerobically and yields more energy per mole of oxygen than fatty acids under such circumstances. Besides glucose, amino acids are also required for accelerated proteosynthesis according to the work load. Therefore, an enlargement of the capillary net has to be accompanied by an amplification of the action of insulin, which is often present in only small amounts, e.g., after an overnight fast. This aim is met in three ways: (1) enlargement of the capillary net with accelerated blood flow increasing the supply of insulin and the number of receptor sites for insulin binding; (2) accelerated transport of insulin through the capillary wall, providing more insulin in the interstitial space and at the plasma membranes; (3) a molecular mechanism directly involving the insulin-receptor-messenger complex, localized at the plasma membrane of the working muscle cell.

These mechanisms resemble a self-regulatory process, set in motion by the release of metabolites from the working tissue. From recent studies there is accumulating evidence that kinins liberated from their precursors are involved as tissue hormones by carrying the signal across the interstitial space to the smooth muscle cells of the capillary vessels. Concomitantly, prostaglandins are released intracellulary to bring about, in cooperation with kinins, the various adaptive mechanisms.

Amplifying systems of this kind may play a role not only in muscle but also in other tissues where adequate kinin or prostaglandin release would appear beneficial under several clinical conditions such as shock, coronary infarction, would healing, etc.

Zusammenfassung

Anpassungen des Energiestoffwechsels wie sie im kontrahierenden Skelettmuskel auftreten, werden im Anschluß an die Phase der anaeroben Glycolyse über Änderungen des kapillaren Blutflusses vorgenommen, der Substrate und Sauerstoff für die Energiegewinnung heranträgt. Da zu Beginn der Leistung die Sauerstoffversorgung limitiert ist, scheint Glucose das geeignete Substrat, da sie sowohl anaerob zur Energiegewinnung benützt werden kann als auch pro Molekül Sauerstoff mehr Energie als Fettsäuren liefert. Neben der Glucose werden auch Aminosäuren für eine beschleunigte Proteosynthese und Muskelhypertrophie benötigt. Aus diesem Grunde muß die Erweiterung des kapillaren Gefäßnetzes von einer Modulation der Wirkung von Insulin begleitet sein, das häufig z.B. nach einem Übernachtfasten nur in niedrigen Konzentrationen vorliegt. Dieses Ziel wird auf dreierlei Weise erreicht: 1. Durch Erweiterung des kapillaren Gefäßnetzes, was zu einer verbesserten Versorgung mit Insulin und zu einem größeren Angebot an Insulinrezeptoren führt, 2. durch einen beschleunigten Transport von Insulin durch die kapillaren Gefäßwände, so daß mehr Insulin im interstitiellen Raum und an den Plasmamembranen des Gewebes vorhanden ist. 3. durch einen Effekt auf molekularer Ebene am „Insulin-Rezeptor-Messenger“-Mechanismus. Diese Adaptationen sind Teile eines selbstregulatorischen Prozesses, der durch die Freisetzung von Metaboliten aus dem arbeitenden Muskel in Gang gesetzt wird. Aus neueren Studien gibt es zunehmend Hinweise, daß Kinine und Prostaglandine beteiligt sind. Die ersteren werden bei Bedarf aus ihrem Präkursorprotein Kininogen proteolytisch freigesetzt und tragen als Gewebshormone das Signal des arbeitenden Muskelgewebes über den interstitiellen Raum zur glatten Gefäßmuskelzelle der Kapillaren. Daraufhin werden Prostaglandine aus Plasmamembranlipiden freigesetzt, die als Zellmediatoren zusammen mit den Kininen die verschiedenen Adaptationsmechanismen hervorrufen.

Verstärkersysteme dieser Art dürfen nicht nur im Muskel, sondern auch in anderen Geweben eine Rolle spielen, in denen eine adäquate Kinin- und Prostaglandin-Freisetzung unter den verschiedensten klinischen Bedingungen, z.B. im Schock, beim Herzinfarkt, bei Wundheilung etc. für die adäquate Bereitstellung von Sauerstoff, energiereichen Substraten und Aminosäuren als Bausteinen sorgt.

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  1. Forschergruppe Diabetes und III. Medizinische Klinik (Stoffwechsel- und Endokrinologie) des Krankenhauses Schwabing, Akademisches Lehrkrankenhaus der Ludwig-Maximilians-Universität München, Germany

    Günther Dietze

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Anläßlich des Weltkongresses „Kinin 1981“ vom 2.–5.11.81 in München

Mit Unterstützung der Deutschen Forschungsgemeinschaft, SFB 51

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Dietze, G. Neue-Aspekte zur durchblutungssteigernden und insulinähnlichen Wirkung der Muskelarbeit: Mögliche Beteiligung des Kallikrein-Kinin-Prostaglandin Systems. Klin Wochenschr 60, 429–444 (1982). https://doi.org/10.1007/BF01720357

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