2018 Vanguard Grant

Years funded: 2019-2020

Until recently it was thought that all of an individual's heart cells were present at birth and that changes during the lifespan in heart size and function were related to adaptation in heart cell size. In the past decade it has become apparent that, in fact, the heart has an intrinsic ability to grow new cells, although it remains unclear in humans whether this capacity lasts into adulthood.

A recent Australian study in rats showed that doing lots of exercise whilst juvenile led to a larger heart in adulthood, with more heart cells present, than if a similar amount of exercise was started later in life. In fact, exercise training whilst juvenile resulted in around 20 million more heart cells being present in adulthood, than if training started later in life. The implications of these findings, if they prove to be true in humans, are very important as they would provide further impetus for concerns regarding the high prevalence of inactivity in childhood, and new hope regarding the potential for long term prevention of cardiovascular disease across the lifespan.

A key question remains: is it true, in humans, that early life physical activity (and perhaps the impact of other CV risk factors) can modify heart size, function and health much later in life?

This project will take advantage of unparalleled information available from a large and richly characterized longitudinal study (the Western Australian Pregnancy Cohort “Raine” Study) of ~2000 participants in whom detailed phenotypic and lifestyle data, including repeated measures of physical activity and other major risk factors are available throughout childhood, adolescence and into early adulthood. By collecting sophisticated measures of heart wall function at age 30, utilising novel 4D tissue Doppler strain rate imaging (ie cardiac mechanics), alongside measures of heart size and volumes, we will establish the extent to which early life habits and risk exposure impact upon adult heart health.