Peripheral arterial insufficiency is a product of progressive arterial degenerative disease. Further arterial insufficiency is associated with an increased morbidity and mortality in the suffering population. Usually this condition presents with decreases exercise tolerance and intermittent claudication.
Enhanced physical activity is one of the most effective means of improving the life of affected patients. Researchers tried to answer how enhanced physical activity helps in this regards?
They found following answer to that:
Exercise training-induce vascular adaptations to ischemic muscle. Vascular remodeling assumes an important means for improved oxygen exchange and blood flow delivery. Relevant exercise-induced signals stimulate angiogenesis, within the active muscle (e.g. hypoxia), and arteriogenesis (enlargement of pre-existing vessels via increased shear stress) to increase oxygen exchange and blood flow capacity, respectively.
This above statement is supported by following evidences from pre-clinical studies:
1. There is increase in collateral blood flow over time as the exercise progresses.
2. This is accompanied by significant enlargement of isolated collateral vessels.
3. Increased production of angiogenic growth factors (e.g. VEGF, FGF-2) is seen.
Thus, enhanced physical activity can be an effective means of enlarging the structure and function of the collateral circuit.
However findings illustrate clear distinctions between the processes influencing angiogenesis and arteriogenesis. Further, sympathetic modulation of the collateral circuit does not eliminate the increase in collateral circuit conductance induced by exercise training. These findings indicate that structural enlargement of the collateral vessels is essential to realize the increase in collateral-dependent blood flow capacity caused by exercise training. This raises the potential that meaningful vascular remodeling can occur in patients with intermittent claudication who actively participate in exercise training.
Yang HT et al; J Physiol Pharmacol. 2008 Dec;59 Suppl 7:57-70.