Anabolic resistance in intensive care: a lecture
- Authors: Kochergin V.G.1,2, Sviridov S.V.1, Subbotin V.V.2
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Affiliations:
- The Russian National Research Medical University named after N.I. Pirogov
- Moscow Clinical Scientific Center named after A.S. Loginov
- Issue: Vol 6, No 3 (2025)
- Pages: 151-155
- Section: Lectures
- URL: https://journals.rcsi.science/2658-4433/article/view/363057
- DOI: https://doi.org/10.17816/clinutr696536
- EDN: https://elibrary.ru/QPZYKB
- ID: 363057
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Abstract
Muscle atrophy and metabolic disorders are serious clinical challenges that substantially worsen the prognosis and increase the mortality rates in critically ill patients. Despite being widespread, traditional nutritional support remains ineffective in intensive care units. Therefore, it is crucial to evaluate alternative pathophysiological mechanisms of muscle atrophy.
This review of current publications identified anabolic resistance as a key factor reducing the effectiveness of standard nutritional support regimens for critically ill patients. In this condition, muscle tissue loses its ability to adequately respond to anabolic stimuli, such as amino acids or protein substrates. Pathophysiologically, anabolic resistance involves systemic inflammation, insulin resistance, immobilization, and bioenergetic muscle dysfunction. A stable isotope analysis revealed that anabolic resistance develops directly in muscle tissue rather than in the gastrointestinal tract. This explains why increasing protein intake alone is ineffective.
Clinical studies have shown that critically ill patients reduce protein uptake into their skeletal muscles by 60% compared with healthy individuals. However, gastrointestinal absorption remains intact. In anabolic resistance, inflammation is a more important factor than insulin resistance. Intensive care unit–acquired weakness leads to long-term functional impairment and complicates patient rehabilitation.
The analysis suggests that the current approaches to maintaining muscle mass in critically ill patients should be fundamentally revised. Instead of just increasing protein intake, new therapeutic strategies are needed to address intramuscular inflammation and impaired substrate utilization.
About the authors
Vladimir G. Kochergin
The Russian National Research Medical University named after N.I. Pirogov; Moscow Clinical Scientific Center named after A.S. Loginov
Author for correspondence.
Email: asqwerty1@yandex.ru
ORCID iD: 0000-0002-4995-1048
SPIN-code: 8520-0376
MD, Cand. Sci. (Medicine)
Russian Federation, Moscow; MoscowSergey V. Sviridov
The Russian National Research Medical University named after N.I. Pirogov
Email: sergey.sviridov.59@mail.ru
ORCID iD: 0000-0002-9976-8903
SPIN-code: 4974-9195
MD, Dr. Sci. (Medicine), Professor
Russian Federation, MoscowValerii V. Subbotin
Moscow Clinical Scientific Center named after A.S. Loginov
Email: v.subbotin@mknc.ru
ORCID iD: 0000-0002-0921-7199
SPIN-code: 4089-9559
MD, Dr. Sci. (Medicine)
Russian Federation, MoscowReferences
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