title: Exercise-induced muscle damage and inflammation: fact or fiction?
abstract: Physical exercise is necessary for maintaining normal function of skeletal muscle. The mechanisms governing normal muscle function and maintenance are vastly unknown but synergistic function of hormones, neurosignalling, growth factors, cytokines and other factors, is undoubtedly important. Because of the complex interaction among these systems the lack of complete understanding of muscle function is not surprising. The purpose of exercise-induced changes in muscle cell function is to adapt the tissue to a demand of increased physical work capacity. Some of the approaches used to investigate changes in skeletal muscle cell function are exercise and electrical stimulation in animals and human models and isolated animal muscle. From these models, it has been concluded that during physical exercise, in an intensity and duration dependent manner, skeletal muscle is damaged and subsequently inflamed. The purpose of the inflammation would be to repair the exercise-induced damage. Because of the design and methods used in a majority of these studies, concerns must be raised, and the question asked whether the paradigm of exercise-induced muscle inflammation in fact is fiction. In a majority of conducted studies, a non-exercising control group is lacking and because of the invasive nature of the sampling methods used to study inflammation it does not appear impossible that observed inflammatory events in human skeletal muscle after physical exercise are methodological artefacts.
authors: Department of Physiology and Pharmacology, Karolinska Institute, and Stockholm University College of Physical Education Sports, Stockholm, Sweden.
authors: C
authors: C
authors: Malm
mesh_terms: D000222:Adaptation, Physiological / Q000276:immunology; D000818:Animals; D015444:Exercise; D006801:Humans; D007107:Immune System / Q000502:physiology; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000276:immunology / Q000293:injuries*; D009220:Myositis / Q000209:etiology* / Q000276:immunology