Publications by authors named "Camilla T Schytz"
Article Synopsis
- In skeletal muscle, glycogen is stored in different locations, and this affects how quickly it can be used during exercise.
- A study tested how varying exercise durations (1 min vs. 15 min) and carbohydrate intake impact glycogen use; it found that different glycogen pools are preferentially used based on the duration of the exercise.
- Lowering carbohydrate and energy intake after depleting glycogen reduces the availability and size of glycogen particles, particularly affecting the intramyofibrillar and subsarcolemmal pools.
The impact of training status and sex on intrinsic skeletal muscle mitochondrial respiratory capacity remains unclear. We examined this by analysing human skeletal muscle mitochondrial respiration relative to mitochondrial volume and cristae density across training statuses and sexes. Mitochondrial cristae density was estimated in skeletal muscle biopsies originating from previous independent studies.
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- * Strength athletes show distinct mitochondrial features, including denser cristae, smaller size, and a higher surface-to-volume ratio compared to untrained individuals, despite similar overall mitochondrial volume.
- * Resistance exercise is linked to mild mitochondrial stress and increased expression of genes involved in mitochondrial growth and stress responses, suggesting that strength training influences mitochondrial adaptations.
Performance in short-duration sports is highly dependent on muscle glycogen, but the total degradation is only moderate and considering the water-binding property of glycogen, unnecessary storing of glycogen may cause an unfavorable increase in body mass. To investigate this, we determined the effect of manipulating dietary carbohydrates (CHO) on muscle glycogen content, body mass, and short-term exercise performance. In a randomized and counterbalanced cross-over design, twenty-two men completed two maximal cycle tests of either 1-min (n = 10) or 15-min (n = 12) duration with different pre-exercise muscle glycogen levels.
View Article and Find Full Text PDFMitochondrial dysfunction has been implicated as a central mechanism in the metabolic myopathy accompanying critical limb ischemia (CLI). However, whether mitochondrial dysfunction is directly related to lower extremity ischemia and the structural and molecular mechanisms underpinning mitochondrial dysfunction in CLI patients is not understood. Here, we aimed to study whether mitochondrial dysfunction is a distinctive characteristic of CLI myopathy by assessing mitochondrial respiration in gastrocnemius muscle from 14 CLI patients (65.
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