Effect of aging on the structure and function of skeletal muscle microvascular networks.
Humans are active creatures, yet physical activity and activity tolerance decline over the life span. One prevailing theme in the literature to account for a portion of the reduced activity tolerance with aging is the observation that the capacity to augment blood flow to skeletal muscle may be impaired with advancing age. This dysfunction may be due to adaptations in the structure or function of their microvascular networks, which collectively determine blood flow resistance. The intent of this review is to present the current knowledge of structure and function of microvascular networks from skeletal muscle with special regard to how these may adapt to, or persist through, the aging process. Skeletal muscles are supplied by an intricate branching network of arterioles and venules. The consistency of findings among available studies suggests that the overall arteriolar and venular network branching topology establishes early in development and varies little, if at all, over the life span. Microvascular networks are not a series of functionally isolated segmental branches. Rather, these networks transmit and communicate vasomotor signals along their lengths and among their branches. Current evidence suggests that aging is associated with a decrement in the capacity of upstream vessels to respond to downstream vasodilation and signals transmitted cell-to-cell along the vascular wall.
Bearden
Shawn E
SE
Department of Biological Sciences, Idaho State University, Pocatello, Idaho 83209, USA. bearshaw@isu.edu
D000375:Aging / Q000502:physiology*; D000818:Animals; D001808:Blood Vessels / Q000294:innervation / Q000502:physiology; D002200:Capillary Resistance / Q000502:physiology; D004730:Endothelium, Vascular / Q000294:innervation / Q000502:physiology; D006801:Humans; D051379:Mice; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*; D014666:Vasomotor System / Q000502:physiology*