For both healthy adults and patients with cardiovascular disease (CVD), aerobic fitness (V̇O2max) is a stronger predictor of the risk of future chronic disease and premature death than other established risk factors such as hypertension, smoking, or Type 2 diabetes. It is important to improve the understanding of the regulation of V̇O2max to enable optimisation of interventions aimed at increasing V̇O2max in the current predominantly sedentary population. Currently, only exercise training is a viable method for increasing V̇O2max. However, \~10-20% of people who follow fully supervised, standardised training interventions do not demonstrate a measurable increase in V̇O2max. Low response to training is a clinically relevant concern, but the large variability in response to exercise training also provides an opportunity to dissect out the molecular mechanisms responsible for adaptations to V̇O2max by contrasting low vs. high responders to training. It has been previously demonstrated that low responders for VO2max fail to up regulate a number of genes that encode putative 'myokines', while the high responders demonstrated a significant increase in the expression of these genes, suggesting these myokines may play an important mechanistic role in modulating VO2max. The aim of the present study is to examine whether low responders for VO2max have an attenuated increase in the plasma levels of the previously identified myokines.
Age range
18 Years – 40 Years
Sex
MALE
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Training induced changes in VO2max
Timeframe: Pre-intervention and 3 days post-intervention
Training induced changes in plasma myokines
Timeframe: Pre-intervention and 3 days post-intervention