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Nutrition and post-exercise mitochondrial biogenesis

  • Research type

    Research Study

  • Full title

    Effect of nutrition on novel regulators of post-exercise mitochondrial biogenesis

  • IRAS ID

    189642

  • Contact name

    Andrew Philp

  • Contact email

    a.philp@bham.ac.uk

  • Sponsor organisation

    University of Birmingham

  • Duration of Study in the UK

    0 years, 11 months, 31 days

  • Research summary

    Mitochondria are often referred to as 'the powerhouses of the cell' for their role in energy production. Mitochondria are the site of aerobic energy production in the cell and are therefore crucial in the utilisation of carbohydrates and fats to produce energy. The content and function of skeletal muscle mitochondria declines during ageing and with inactivity. Importantly, this occurs concurrently with the development of chronic diseases such as type II diabetes, which is partially due to reduced mitochondrial capacity for fat utilisation for energy production.

    Encouragingly, mitochondrial content and function increases following endurance exercise training. However, the adaptive mechanisms responsible for increasing mitochondrial content and function in skeletal muscle remains poorly understood, while the elucidation of these mechanisms holds great therapeutic potential. Additionally, there is some evidence that manipulating nutrition prior to exercise (i.e. eating before (fed-state) or exercising following an overnight fast (fasted-state)) may influence the exercise-training induced increase in mitochondrial content and function and therefore utilisation of fat as a fuel. Importantly, increased utilisation of intramuscular fat as a fuel for exercise is important in increasing insulin sensitivity, and thus opposing the development of type II diabetes, following exercise training. Therefore, elucidating the effect of pre-exercise nutrition on these post-exercise adaptive mechanisms will provide important insight into the optimal integration of nutrition and exercise to improve mitochondrial function.

    In this respect, we will investigate the hypothesis that exercising in the fasted-state will increase molecular processes important in increasing mitochondrial content and function such as the signalling, localisation, interactions, activity and gene expression of proteins related to increasing mitochondrial content and function. The expected outcomes will help determine if exercising in the fasted state could be used to optimise the increase in skeletal muscle mitochondrial content and function following exercise.

  • REC name

    West Midlands - Black Country Research Ethics Committee

  • REC reference

    16/WM/0058

  • Date of REC Opinion

    4 Apr 2016

  • REC opinion

    Further Information Favourable Opinion