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FRIMED2-FRIPRO forskerprosjekt, medisin og helse

Mechanisms for a Novel Muscle Memory

Alternative title: Mekanismer for en cellulær muskelhukommelse

Awarded: NOK 9.0 mill.

It is part of training studio folklore that if you have once been strong you can easily get strong again, even if you have neglected exercise for a long time. Previously this has been attributed to motor learning and technical skills. We have however provided a proof-of principle for a cellular muscle memory related to muscle mass building in the muscle cells themselves. This project shows that muscle cells are DNA-poore, and that the DNA content limits the cell size. We show that the the DNA content limits the cell size and potential for growth, and that muscle memory might rely partly in the number of cell nuclei and partly on epigenetic mechanisms regulating the accessibility of the genes.

Det viktigste er at prosjektet har etablert muskelhukommelse som et viktig forskningsfelt i idrettsfysiologien. Forskningen har hatt betydelig innflytelse både vitenskapelig, men high impact publikasjoner, men er også svært hyppig omtalt og diskutert i idrettsmiljøer med en stor mengde omtaler i mane land og på mange språk i ulike idrettsfora. Prosjektet påirker måten man tenker om trening i ulike deler av livtsløpet.

The muscle fibres are the largest cells in the body, and the size generally determines the force. While almost all other cells contain only one nucleus, muscle fibres have several hundred, and it is believed that each of them support a certain volume of cytoplasm. The textbook understanding is that during strength exercise fibres hypertrophy and new nuclei are added to pre existing fibres from fusing stem cells, while during disuse, fibres shrink and loose nuclei by apoptosis. We have developed in vivo imaging techniques where single nuclei can be followed in the animal with time-lapse microscopy. These techniques have suggested that the textbook model is wrong and that nuclei are not lost from muscle fibres during atrophy. Since we confirm that nuclei are added during hypertrophy, we suggest that the permanent increase in the number of nuclei after an hypertrophy episode could represent a form of cellular "memory". Our main goal is to provide convincing data for the existence of a "muscle memory", such that an elevated number of nuclei is beneficial in aiding later strength training. The ability to generate new muscle nuclei is impaired in the elderly; thus, the demonstration of a muscle memory should lead to a health advice for early exercise in order to counteract weakness in the elderly. We have observed that anabolic steroids generate new muscle nuclei in animals, similar experiments will be performed in humans, and might lead to changes in the worlds anti doping rules. In patients we will investigate muscle wasting with improved histological methods in order to find out if our new model also applies to humans, thus demonstrating that muscle wasting is not a degenerative disease. In animal models we will investigate the cellular dynamics of myonuclei and the molecular mechanisms underlying centronuclear myopathies. In addition to nucleic number as a novel memory mechanism we will investigate if genome imprinting also plays a role for the "memory.

Publications from Cristin

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Funding scheme:

FRIMED2-FRIPRO forskerprosjekt, medisin og helse

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