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Performing regular exercise is crucial for good health and wellbeing, whereas failing to perform sufficient exercise increases the risk of diseases such as cardiovascular disease, type 2 diabetes, cancer, etc. Various types of exercise are associated with health benefits, including for example moderate-intensity continuous exercise (MICT), resistance exercise, and sprint interval training (SIT). Although we have a good understanding of what health markers each of these types of exercise can improve, the molecular mechanisms responsible for these health benefits are often unclear. For example, considering the crucial importance of improvements in the health marker maximal aerobic capacity (VO2max, a key predictor of future morbidity and premature mortality) with MICT and SIT, it is remarkable that to date it remains uncertain whether this adaptation is due to central adaptations (e.g., stronger heart / increased blood volume) or peripheral adaptations (e.g., enhanced capillary density / increased mitochondrial content). Furthermore, our understanding of the signalling pathways involved in initiating the required adaptations is limited.
We have previously made some progress in this area by comparing low vs. high responders to training for VO2max (i.e., individuals with below and above average improvements), and contrasting differences between these groups for changes in gene expression from pre- to post training (Keller et al., 2011). The ~86 genes for which changes in expression following training were different between low vs. high responders are likely to be important mediators of adaptations to VO2max, making these genes important candidates for further study.
Apart from contrasting low vs. high responders to training, another promising approach is to contrast differences in signalling processes between effective vs. ineffective, but similar training programmes. For example, we have demonstrated that low volume SIT can be effective at improving VO2max with a minimal amount of sprint exercise (e.g., 2 x 20-s sprints in a 10-min low-intensity cycling session; Vollaard et al., 2017). Interestingly, performing more sprints in a training session does not increase the magnitude of adaptations, whereas performing a single sprint is insufficient. Thus, a testable hypothesis is that key signalling pathways will be activated to a similar extent with training protocols involving 2 or 6 sprints per session, but not with a single sprint.
The present PhD project aims to identify signalling pathways involved in adaptations to VO2max with exercise training. This will involve studies examining activation of signalling molecules following acute and chronic exercise, and identifying differences between low vs. high responders, and between effective vs. ineffective interventions. The PhD student will perform lab work involving testing of healthy human volunteers (supervision of exercise sessions, measurement of VO2max, venepuncture, cannulation, taking or assisting in taking muscle biopsies) as well as wet-lab work.
The PhD student will be based in the Physiology, Energy and Nutrition Research Group (PENRG) at the University of Stirling. The facilities and expertise within the team allow us to address fundamental and applied research questions at the cellular/molecular level using cell culture models through to molecular analysis of tissue samples obtained using tissue biopsy techniques, genetic and epigenetic analyses from tissue or blood samples, as well as whole body human physiological measurements of cardiovascular, respiratory, and metabolic function using a variety of techniques.
Entry Requirements
Applicants are expected to hold (or about to obtain) a minimum upper second class undergraduate honours degree (or equivalent) in a relevant Life Sciences or Medical Sciences subject such as Human Biology / Physiology / Exercise Physiology / Sport & Exercise Science, or similar.
How to Apply
Informal enquiries and expressions of interest may be made directly to the primary supervisor at n.vollaard@stir.ac.uk.
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