Skeletal muscle glycogen manipulation and adaptation to exercise
Research type
Research Study
Full title
The role of skeletal muscle glycogen manipulation on substrate utilisation and adaptation to endurance exercise
IRAS ID
189620
Contact name
Andrew Philp
Contact email
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. As the site of aerobic energy production in the cell, mitochondria are therefore crucial in the utilisation of carbohydrates and fats for the production of 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 a reduced capacity of mitochondria to breakdown fat for energy production.
Encouragingly, mitochondrial content and function is enhanced 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. There is some evidence that the signal transduction pathways involved in increasing mitochondrial content and function are heightened following exercise performed with low skeletal muscle carbohydrate stores (glycogen). Furthermore, exercise training conducted in glycogen-depleted states augments the increase in mitochondrial content and function and therefore capacity to use 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, interpreting the effect of pre-exercise glycogen content on these post-exercise adaptive mechanisms, and fat utilisation during exercise, will provide important insight into the optimal integration of nutrition and exercise to improve mitochondrial function. Furthermore, whether there is an ‘all or nothing’ or a ‘graded’ effect of glycogen depletion on skeletal muscle adaptation remains undetermined.
In this respect, we will investigate the hypothesis that molecular signal transduction pathways involved in expanding mitochondrial content and improving mitochondrial function will be augmented with decreasing pre-exercise muscle glycogen content. Secondly, we will determine how utilisation of fats for energy production during exercise is affected by graded degrees of pre-exercise glycogen depletion. The expected outcomes will help determine if exercising while at different degrees of glycogen depletion 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/0059
Date of REC Opinion
8 Apr 2016
REC opinion
Further Information Favourable Opinion