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Vøddaglykogen og vøddavirkni undir hørðum intervalarbeiði við denti á kaliumregulering.


Magni Mohr

Deildini fyri Heilsu og Sjúkrarøkt, Fróðskaparsetrið

Aðrir luttakarar:
Thomas Bull Andersen and Kristian Overgaard

01.08.2020 - 01.08.2021

Samlaður kostnaður:
kr. 840.000

Stuðul úr Granskingargrunninum:
kr. 200.000

Muscle glycogen is stored in different compartments in skeletal muscle andi s a major fuel source during exercise. Accordingly, a close temporal relationship has been demonstrated between muscle glycogen content and exercise tolerance during both prolonged and high intersity intermittet exercise. Muscle glycogen stores are therefore important for our ability to sustain a given exercise intensity, which is of relevancy during work tasks, exercise and possibly even daily physical activities. The effert of low muscle glycogen on exercise tolerence is likely to be related to several mechanisms. Thus, except the role as an important energy substrate, resulting in a reduced rate of glycolysis in a glycogen depleted state, lowered muscle glycogen content has also been demonstrated to affect muscle excitation-contraction coupling in terms of altered calcium kinetics. In addition, the sodium-potassium pumps which are the main regulators of the muscle excitability and contractility may be adversely influenced by the muscle glycogen depletion due to their preferential use of glycogen as a substrate. In addition, it has been demostrated, that despite whole-muscle glycogen still being above critical leves, specific sub-groups of skeletal muscle fibers and compartments within the muscle cell may be a low glycogen state. Lowered muscle glycogen content may therefore impair muscle function even at moderately reduced levels, which has been suggested in several previous studies. In athletic populations this is crucial for performance, but for the general population this may also have important implications. For example, untrained persons, elderly or certain patients groups, such as type 2 diabetics, may have low initial glycogen concentrations in their muscles due to a low training state and/or an impaired capacity for glucose uptake. For these peaple, exercise is a key element to counteract reductions in cardiovascular – and skeletal muscle health, as well as in the management of type 2 diabetes. However, the iowered initial muscle glycogen stores in these individual already at the onset of exercise may advance fatigue development and reduce their abiliity to tolerate exercise, especially of higher intensities. Therefore, a better understanding of mechanisms related to muscle glycogen and muscle function and fatigability is critical in order to target training, dietary and/or pharmacological interventions. Thus, the aim of the present project is to study the relationship between muscle glycogen content and muscle function, with special emphasis on skeletal muscle potassium regulation. This will be accomplished in a dual project with the use of an exercise protocol and subsequent diet intervention with concomplished measures of muscle glycogen content, muscle function, potassium regulation and exercise tolerence. In addition, an animal model will be applied in order to be able to obtain more direct measures of potential underlying mechanistic regulators of muscle function in association with lowered muscle glycogen content.

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