The maintenance of CD with increases in fiber size in that study suggests that angiogenesis occurred in skeletal muscle and that diabetes-associated capillary rarefaction may be reversible.
In addition to atherosclerosis in larger blood vessels, TSP-1 may play a role in capillary rarefaction in skeletal muscles, as has been observed in obese Zucker rats [ 42] and in type 1 diabetic mice [ 4].
The reduced capability of diabetic compared to healthy endothelial cells to increase VEGF-A production in response to exercise stimulus may be related to the impaired vascular function and capillary rarefaction in diabetic skeletal muscle.
The current study shows that despite the capillary rarefaction found in the skeletal muscle of sedentary, older adults with IGT, AEX+WL significantly increases skeletal muscle capillarization.
This occurs especially in capillaries, which could be a direct cause to capillary rarefaction seen in diabetic muscles.
Cytokines [ 18], capillary rarefaction [ 19], and other processes create insulin resistance by decreasing skeletal muscle substrate delivery.
Therefore, despite impaired angiogenesis and capillary rarefaction in sedentary people with insulin resistance and IGT, the ability to increase capillarization in skeletal muscle is maintained and likely contributes to AEX+WL-induced improvements in insulin sensitivity in older adults at risk for type 2 diabetes.
If this is also the case in skeletal muscle, it may lead to excess accumulation of extracellular matrix components and endothelial cell death, leading to dysfunctional capillaries and capillary rarefaction.
Capillary rarefaction and the concomitant resistance artery remodeling increase peripheral resistance and capillaries stiffness occurring in hypertensive individuals increases their central systolic and pulse pressures4.
Kida, Y., Ieronimakis, N., Schrimpf, C., Reyes, M. & Duffield, J.S. EphrinB2 reverse signaling protects against capillary rarefaction and fibrosis after kidney injury.
