Bone blood flow regulation in humans

Abstract

Bone is a highly vascularized organ with an extensive network of arteries, arterioles, and capillaries that is critical for bone development, maintenance, and repair. Despite the importance of bone circulation to bone health, the regulation of blood flow to bone is not well understood in humans. One of the potential factors controlling bone blood flow is the sympathetic nervous system, bone vasculature being innervated by a rich network of sympathetic nerves. While no human studies have been conducted, animal data suggests that sympathetic activation reduces bone blood flow. If this were not the case, bone vasculature would respond simply as a passive pressure system. Therefore, we characterized bone blood flow regulation in health young individuals (N=12 (8M; 4F), 23±0.7 years) in response to isometric handgrip to fatigue (IHE). Sustained IHE is a profound pressor stimulus, resulting in active vasoconstriction in the nonactive leg and progressive increases in blood pressure. During IHE at 30% of maximal voluntary contraction, we measured blood pressure, whole leg blood flow (via Doppler ultrasound), and tibial blood perfusion (via near infrared spectroscopy). Tibial blood perfusion was determined as changes from resting baseline in oxygenated and deoxygenated hemoglobin content. Data is presented as mean change from resting baseline ± standard error. To account for different IHE time courses, all variables were normalized to 100% duration and averaged across individuals. Blood pressure increased progressively to end of IHE (at 10%: 5.46 ± 1.30 mmHg; at 100%: 48.0 ± 4.32 mmHg). Whole leg blood flow decreased progressively throughout IHE, suggesting active sympathetic vasoconstriction in the leg (at 10%: −0.70 ± 0.28 cm/s; at 100%: −2.26 ± 0.50 cm/s). Similarly, tibial oxygenated hemoglobin decreased progressively throughout the test (at 10%: −0.21 ± 0.31 μM; at 100%: −1.19 ± 1.12 μM) whereas tibial deoxygenated hemoglobin did not change significantly throughout IHE (at 10%: 0.06 ± 0.07 μM; at 100%: −0.4 ± 0.32 μM). This indicates that arterial flow (oxygenated hemoglobin) declined while bone metabolism (deoxygenated hemoglobin) remained unchanged in response to IHE. It should be noted that the decline in oxygenated hemoglobin was slower and lesser than that in whole leg blood flow. This data suggests that sympathetic activity is involved in controlling bone circulation, but vasoconstrictor responses is not as fast or as robust in bone as it is in the whole leg.Support or Funding InformationParalyzed Veterans of America (AED)