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Low-frequency muscle contraction inc...
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Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states./
作者:
Inyard, April Corinne.
面頁冊數:
121 p.
附註:
Adviser: Eugene Barrett.
Contained By:
Dissertation Abstracts International69-04B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3312144
ISBN:
9780549599913
Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states.
Inyard, April Corinne.
Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states.
- 121 p.
Adviser: Eugene Barrett.
Thesis (Ph.D.)--University of Virginia, 2008.
Insulin and exercise each increase skeletal muscle microvascular blood volume (MBV) and glucose uptake. One effect of contraction-mediated microvascular recruitment is expansion of endothelial surface area to potentially enhance nutrient exchange within muscle. In studies described here, we first sought to define whether muscle contraction increases MBV, whether this process is separable from the effect of contraction on total femoral blood flow (FBF), whether contraction-induced increases in MBV (like those provoked by insulin) are blocked by inhibition of nitric oxide (NO) synthase, and finally whether increasing MBV increases the exchange of macromolecules between plasma and muscle interstitium. We showed that brief, low-frequency isometric contraction more than doubled MBV in a NO-independent manner without affecting FBF. Furthermore, this MBV response was associated with significantly enhanced movement of both albumin and iodinated insulin into muscle. The effects of combined insulin and contraction on MBV were additive, and this brief contractile stimulus further increased insulin-mediated glucose uptake (IMGD), in agreement with previous studies. We then studied whether the model of insulin resistance provoked by raising plasma FFAs (which blunts both IMGD and increases in MBV) affects contraction-induced increases in MBV and transport of proteins into muscle. Acute FFA elevation alone had no effect on MBV and did not blunt the response to contraction. However, combination of FFAs and insulin elicited a paradoxical decrease in MBV and FBF, where the former was restored to baseline by contraction. Contraction still effectively, although not significantly, increased protein movement into skeletal muscle. We conclude that low-frequency contraction recruits muscle microvasculature by a NO-independent pathway and facilitates muscle uptake of insulin in the absence of increases in blood flow. Acute increases in plasma FFAs that produce systemic insulin resistance prevent insulin- but not contraction-induced increases in MBV. The decline in MBV seen with FFA and insulin infusion can be rescued, suggesting that muscle contraction acts on the microvasculature by a mechanism distinct from that of insulin and this is preserved in FFA-induced insulin resistance. This microvascular response with increased access of insulin to muscle interstitium may, in part, explain enhanced insulin action in exercising insulin-resistant muscle.
ISBN: 9780549599913Subjects--Topical Terms:
1017835
Biology, Animal Physiology.
Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states.
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Insulin and exercise each increase skeletal muscle microvascular blood volume (MBV) and glucose uptake. One effect of contraction-mediated microvascular recruitment is expansion of endothelial surface area to potentially enhance nutrient exchange within muscle. In studies described here, we first sought to define whether muscle contraction increases MBV, whether this process is separable from the effect of contraction on total femoral blood flow (FBF), whether contraction-induced increases in MBV (like those provoked by insulin) are blocked by inhibition of nitric oxide (NO) synthase, and finally whether increasing MBV increases the exchange of macromolecules between plasma and muscle interstitium. We showed that brief, low-frequency isometric contraction more than doubled MBV in a NO-independent manner without affecting FBF. Furthermore, this MBV response was associated with significantly enhanced movement of both albumin and iodinated insulin into muscle. The effects of combined insulin and contraction on MBV were additive, and this brief contractile stimulus further increased insulin-mediated glucose uptake (IMGD), in agreement with previous studies. We then studied whether the model of insulin resistance provoked by raising plasma FFAs (which blunts both IMGD and increases in MBV) affects contraction-induced increases in MBV and transport of proteins into muscle. Acute FFA elevation alone had no effect on MBV and did not blunt the response to contraction. However, combination of FFAs and insulin elicited a paradoxical decrease in MBV and FBF, where the former was restored to baseline by contraction. Contraction still effectively, although not significantly, increased protein movement into skeletal muscle. We conclude that low-frequency contraction recruits muscle microvasculature by a NO-independent pathway and facilitates muscle uptake of insulin in the absence of increases in blood flow. Acute increases in plasma FFAs that produce systemic insulin resistance prevent insulin- but not contraction-induced increases in MBV. The decline in MBV seen with FFA and insulin infusion can be rescued, suggesting that muscle contraction acts on the microvasculature by a mechanism distinct from that of insulin and this is preserved in FFA-induced insulin resistance. This microvascular response with increased access of insulin to muscle interstitium may, in part, explain enhanced insulin action in exercising insulin-resistant muscle.
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http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3312144
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