Every tissue is supported by countless capillaries, the smallest vessels in the branching vascular network. Take a square cross-section of tissue a millimeter in each dimension and one finds hundreds of capillaries passing through it. This intricate branching network of vessels must be constantly maintained, but unfortunately the processes of maintenance decline with age, as is the case for all complex systems in the body. The resulting progressive loss of capillary density reduces the supply of oxygen and nutrients, and this is thought to provide a meaningful contribution to loss of tissue function and the onset of age-related disease.
What can be done about this? Manipulating some of the regulators and participants at various stages of angiogenesis seems promising. Angiogenesis is a multi-step process wherein a new branch from an existing blood vessel is constructed. It is an example of one of the better understood mechanisms involved in the maintenance of our biology, as it is extensively studied and the research community has a good understanding of how it works, but there is still room for exploration at the detail level. Studies have shown that upregulation of VEGF, an important signal in angiogenesis, can lead to greater angiogenesis. VEGF is involved in the creation of pathological, leaky blood vessels in macular degeneration, but no such issue is seen in the animal studies in which circulating VEGF is increased. Alternatively, strategies to mobilize hematopoietic progenitor cells from the bone marrow into circulation, such as CXCL12 upregulation, used when harvesting hematopoietic cells from a donor for transplantation, also promote angiogenesis.
Today's open access paper focuses on the more prosaic intervention of exercise. There is evidence for late life exercise to partially reverse loss of capillary density in muscle tissue. Exercise is in general beneficial for systems throughout the body, so this is perhaps not surprising. Relatively few of the manifestations of aging are completely immune to treatment via lifestyle choice, even though the degree of reversal that can be achieved is much smaller than desired.
Skeletal muscle aging is often accompanied by capillary rarefaction, which limits the effective delivery and distribution of hormones, nutrients, and growth factors within skeletal muscle. Furthermore, exercise is widely regarded as having the potential to improve microcirculation and delay skeletal muscle aging. This review aims to explore exercise-induced improvements in capillarization and related adaptations to mitigate the adverse changes that occur during the aging process of skeletal muscle.
Studies have shown that older adults still possess the capacity to improve skeletal muscle capillarization through exercise. Moderate-intensity aerobic exercise not only significantly enhances the level of capillarization but also induces effects that can be maintained even after cessation of training. Capillarization adaptations induced by resistance training exhibit marked inter-individual variability, which is primarily determined by each individual's baseline level of capillarization, thereby resulting in distinct patterns of adaptation. The studies also revealed that the regulation of capillarization depends on the synergistic action of VEGF and eNOS, and that different types of exercise may elicit adaptations through distinct molecular pathways.
In conclusion: during the aging process, exercise-induced improvements in capillarization can enhance nutrient delivery, metabolic efficiency, and regenerative capacity in skeletal muscle. To some extent, these adaptations help suppress degenerative changes in muscle function and provide a targeted foundation for anti-aging intervention strategies.
View the full article at FightAging
