Coronary collateral vessels supply blood to areas of myocardium at risk after arterial occlusion.
Flow through these channels is driven by a pressure gradient between the donor and the
occluded artery. Concomitant with increased collateral flow is an increase in shear force, a potent
stimulus for collateral development (arteriogenesis). Arteriogenesis is self-limiting, often ceasing
prematurely when the pressure gradient is reduced by the expanding lumen of the collateral vessel.
After the collateral has reached its self-limited maximal conductance, the only way to drive further
increases is to re-establish the pressure gradient.
During exercise, the myocardial oxygen demand is increased, subsequently increasing coronary
flow. Therefore, exercise may represent a means of driving augmented arteriogenesis in patients
with stable coronary artery disease. Studies investigating the ability of exercise to drive collateral
development in humans are inconsistent. However, these inconsistencies may be due to the heterogeneity
of assessment methods used to quantify change. This article summarises current evidence
pertaining to the role of exercise in the development of coronary collaterals, highlighting areas of