How does Physical Activity Exert Beneficial Effects on Atherosclerosis and Coronary Artery Disease?

This post describes an update seminar delivered by Harold Laughlin, Professor at the University of Missouri at the 2017 HAPS Annual Conference in Salt Lake City.


Update Seminar VII was given by Harold Laughlin.  In this talk, the benefits of exercise on cardiovascular health were clearly documented.  I’m sure we’ve all heard the sobering stats before.  Cardiovascular disease, largely due to atherosclerosis, is the leading cause of death in the USA, accounting for ~ 1/3rd of all deaths.  As our President-Elect Ron Gerrits announced, we were all left feeling very inspired to getting fit for the HAPS conference Fun Run next year!  

For those interested in a great review article on the regulation of coronary blood flow during exercise, Harold mentioned the Physiology Review article by Duncker and Bache (2008).   In particular, here is list of some of the things we know so far regarding coronary blood flow during exercise:

  • During exercise, heart rate and myocardial contraction increase to meet the increased oxygen demands of the body and heart itself.
  • In order to meet increased metabolic demand, coronary blood flow increases (~5 fold) and there is also a small increase in oxygen extraction.
  • An increase in heart rate, will increase the relative time spent in systole, which affects (impedes) coronary blood flow.
  • There are many factors which regulate coronary vessel dilation (neurohormones, endothelial factors, and myocardial factors)
  • During exercise, coronary vasodilation appears to be induced by many factors including: exercise-induced ischemia, shear stress, increased arterial pressure, tangential wall stress, higher levels of endogenous NO, and β-adrenergic activity.
  • Exercise training results in coronary microvascular adaptations including: the formation of new capillaries, increased arteriolar diameters, increased adrenergic receptor responsiveness, and increased endothelium-dependent vasodilation (as a result of increased expression of endothelial NO synthase (eNOS), increased NO production, and increased Kv (potassium voltage) channel activity).

In his talk, Harold brought up some current data from his experiments with swine vasculature (Simmons et al., 2012).  He noted that healthy individuals typically have good vasomotor tone, and express low levels of the inflammatory markers and adhesion molecules (e.g. E-selectin and vascular cell adhesion molecule-1, VCAM-1) that are associated with atherosclerosis.  It has been previously found that endothelial cells located at bifurcations and other points of turbulence, are more at risk for developing atherosclerotic plaques than straight conduit arteries (Davies et al. 2010).  Laughlin et al. (2012) decided to investigate the straight conduit arteries and veins in six different regions of the swine to determine whether there were any differences in susceptibility to the development of atherosclerosis.  Overall, they found conduit arteries expressed higher levels of both pro- and anti-atherogenic markers than veins.  Also as one might expect, vessels of healthy individuals that lack atherosclerosis, are the most responsive to exercise.

In this talk, the improvements in vasculature as a result of exercise training were specifically addressed (Green et al. 2017).  The exercise-induced effects on vasculature is actually remarkable.  It is estimated that physical activity increases longevity, and reduces the risk of cardiovascular mortality by 42-44%.  The positive effect of exercise is noted to have dose-dependent curve and exercise training has been found to be on par with contemporary drug interventions (Green et al. 2017).  Exercise induces structural and functional adaptations in the vascular walls that reduce the risk of atherosclerotic plaque formation.  In addition increased capillary density and formation of additional collateral circulation is observed, as exercise induces the release of VEGF (Vascular Endothelial Growth Factor) (Green et. al. 2017).  Also, exercise was found to increase endothelial progenitor cell (EPC) activity which contributes to the growth of new vessels as well as repair.

It is important to note that exercise training increases cardiac output and oxygen uptake, without increasing mean arterial pressure.  This is because as cardiac output increases, peripheral vasodilation occurs (reducing afterload).  Exercise training improves vasodilation capabilities through structural changes.  During exercise, the increased systolic pressure stimulates vascular endothelial and smooth muscle cells to grow and align in response to stress, allowing for greater vasodilation.  In addition, vessel wall stretching induces vasodilation through increased eNOS activity (which produces the vasodilator NO) and activation of Kv channels (which causes smooth muscle cells to hyperpolarize and relax).  In addition, increased blood flow, has been found to increase both acetylcholine and prostacyclin levels which have been shown to induce vasodilation.  Conversely, low levels of shear stress, has been found to increase expression of adhesion molecules (ICAM-1 and VCAM-1) and reduce levels of the endogenous vasodilator NO (Green et al. 2017).

Thankfully for those of us looking to improve vasodilatory function in our conduit arteries and increase our capillary density, improvements through exercise can be seen in as little as 1-4 weeks of exercise and of course continue with longer training sessions.  So with that in mind, I’ll be sure to grab my running shoes and sign my kids up for sports, as fewer than 30% of females and 50% of males get the recommended 60 minutes 5-7 days/ week of exercise!  Yikes-arama!  Time to unplug and play…

A big thank you to Harold Laughlin for a highly motivating talk!


Post from Dr. Zoë Soon, School of Health and Exercise Sciences, University of British Columbia Okanagan, BC, Canada


Davies, P.F., Civelek, M., Fang, Y., Guerraty, M.A. Passerini, A.G. (2010). Endothelial heterogeneity associated with regional athero-susceptiblity and adaptation to disturbed blood flow in vivo. Semin. Thromb. Hemost. 36, 265-275.

Duncker, D.J. and Bache, R.J. (2008). Regulation of coronary blood flow during exercise. Physiol. Rev. 88, 1009-1086.

Green, D.J., Hopman, M.T.E., Padilla, J., Laughlin, M.H., Thijssen, D.H.J. (2017). Vascular adaptation to exercise in humans: role of hemodynamic stimuli. Phsiol. Rev. 97, 495-528.

Simmons, G.H., Padilla, J., and Laughlin, M.H. (2012). Heterogeneity of endothelial cell phenotype within and amongst conduit vessels of the swine vasculature. Exp. Physiol. 97(9), 1074-1082.

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