By Abigail Cook, University of Leeds, @abbycook94
Exercise is good for you. We see this statement daily in one form or another, whether it’s on social media, as advice from medical professionals or making headlines in the news. We know it’s good for our hearts, keeping our weight under control and is even beneficial for our mental health. A question I am often asked is: why is exercise so good for us? My research focuses on the effect of exercise on human arteries and the cells lining these arteries.
Helping blood vessels saves the heart
Cardiovascular disease (CVD) is one of the leading causes of death in the Western world and is responsible for 25% of all deaths in the UK (BHF, 2017). Only 60% of CVD cases, however, can be explained by traditional risk factors such as fat, high blood pressure, and diabetes (Mora et al., 2007). Of the rest, changes to blood vessels appears to play a major part.
Thus, targeting blood vessels appears to be an attractive way to reduce poor functioning of the blood vessels and CVD. As exercise directly impacts blood pressure, heart rate and the quantity of blood leaving the heart per beat, it provides a method of reaching this target without using drugs.
This is especially important given that physical inactivity is the fourth highest risk factor for mortality worldwide. Also physical fitness, when assessed by aerobic capacity (the maximum oxygen consumption in an exercise session), is the strongest predictor of death in populations with and without CVD.
The scene inside our blood vessels
For the appropriate amount of blood to be delivered to our organs and tissues, arteries need to widen appropriately. One of the key molecules that tells the arteries to widen is nitric oxide (NO). NO is produced by the inner lining of the blood vessel. Its release is controlled by the force, which I study in the lab, called shear stress, applied by blood to this lining.
Shear stress can be characterised in different ways, with each form resulting in different responses from the inner lining of the vessels. High levels of unidirectional shear stress occur in the straight sections of blood vessels. This is associated with the production of molecules that fight inflammation, which protect the cell from abnormal growth and proliferation, and even cell death. Low levels of bidirectional shear stress are most often found at curvatures and at branches of blood vessels. This type of shear stress generates molecules that are associated with inflammation.
The areas that are exposed to low levels bidirectional shear stress are at the greatest risk of developing atherosclerosis (a type of CVD), the disease where an artery becomes narrowed due to the build-up of plaques. Prolonged exposure to this type of shear stress can lead to dysfunction of the inner lining of blood vessels, which is an early indicator of CVD.
Exercise lends a helping hand
The ideal shear stress throughout the vasculature to minimise the likelihood of developing CVD such as atherosclerosis would be high levels of unidirectional shear stress. One way of increasing shear stress is by exercising.
Exercise increases heart rate, cardiac output, blood flow, and thus shear stress. Undertaking regular exercise has been shown to be protective against atherosclerosis and slow down the progression of CVD. It is unclear, however, what type of exercise training is most beneficial to the blood vessels. Continuous exercise may provide steady levels of shear stress, whereas interval exercise may allow shear stress to vary throughout exercise from a low to a high level.
My research uses ultrasound and MRI technology to understand the patterns and levels of shear stress applied to arteries during differing exercise protocols. The arteries of interest are both are susceptible to developing atherosclerosis (the aorta and the common femoral artery), and they can be monitored during an exercise protocol.
This is especially important in the common femoral artery as it is directly supplying blood to the working muscle during exercise. Then, I am examining what happens when these patterns and levels are replicated in cells grown in the laboratory, in order to see which type of exercise enhances cell function most effectively.
BHF. (2017). Cardiovascular Disease Statistics 2017. BHF.
Mora S, Cook N, Buring JE, Ridker PM & Lee IM. (2007). Physical activity and reduced risk of cardiovascular events: potential mediating mechanisms. Circulation 116, 2110-2118.