ARTERIAL STIFFNESS & AGE--EFFECTS ON CIRCULATORY CONTROL
ARTERIAL STIFFNESS & AGE--EFFECTS ON CIRCULATORY CONTROL
批准号:
6016816
负责人:
J ANDREW TAYLOR
金额:
$9.57万
依托单位国家:
美国
项目类别:
财政年份:
1997
资助国家:
美国
项目状态:
已结题
起止时间:
1997-06-01 至 2002-05-31
中文摘要
描述(改编自申请人的摘要):这第一个奖项将
研究心血管功能下降与心血管功能增加的关系。
血管硬度随着年龄的增长,并响应于1995年国家研究所
关于老化计划公告(PA-95-074)。 相关硬化
颈动脉压力感觉区将有效地使压力感受器反射脱敏,
压力感受器对压力相关的拉伸有反应。 动脉
压力感受性反射是迷走神经和交感神经的平均水平的关键决定因素。
交感神经流出;因此,下迷走神经和大交感神经流出
与心血管疾病相关的压力感受性反射减弱
这是由于血管硬度增加。 虽然动脉硬化增加
随着年龄的增长,它与有氧能力呈负相关,而与年龄无关。
因此,慢性有氧训练可能有助于维持压力反射自主神经
通过减轻与年龄相关的动脉硬化来控制循环。 的
该提案的具体目标是确定:1)与年龄有关的
迷走神经和交感神经流出的压力反射控制的减少是
与更大的颈动脉僵硬度有关,2)压力感受性反射的年龄相关下降
迷走神经和交感神经流出的控制被颈动脉小动脉
僵硬与有氧健身,和3)一个程序,定期
老年人的有氧运动训练增加了压力反射控制,
迷走神经和交感神经流出由于颈动脉硬度降低。 是
假设年龄相关的压力反射循环减少
对照组与颈动脉僵硬度增加和基底动脉硬化度改变相关
自主神经外流可以通过运动训练逆转。 满足这些
目的,最先进的神经生理学和超声检查措施将
评估自主神经流出的压力反射增益相对于真实的
压力感受器激活的刺激改变颈动脉尺寸。 年轻
(20-30岁)及以上(60-80岁)男性和女性将被严格筛选
为了确定老化过程本身的影响(与
疾病、不活动等)压力反射功能,基础自主神经流出,
和颈动脉僵硬 与年龄相关的衰退可能逆转,
有氧运动训练将进行评估,
纵向。 研究者表示这些研究是独特的;
没有数据表明气压传感器的尺寸变化与
人类心血管自主神经流出的并发变化。 他觉得
尽管有数据表明颈动脉硬度在
在压力感受性反射功能中,尚不清楚压力感受性反射的僵硬度是否增加,
最终导致压力反射增益的年龄相关性降低
减少迷走神经和增加交感神经流出。 此外,他认为,
尚不清楚有氧健身是否调节这些与年龄相关的影响。 他
指出,这一信息是至关重要的,以了解是否钝化压力感受器反射,
继发于血管硬化的功能是老化的管道,
损害自主循环控制并增加心血管
发病率
英文摘要
DESCRIPTION (Adapted from the Applicant's Abstract): This FIRST award will
investigate the relation of decreased cardiovascular function to increased
vascular stiffness with age and is responsive to a 1995 National Institute
on Aging program announcement (PA-95-074). Age-related stiffening of
carotid barosensory areas would effectively desensitize the baroreflex since
baroreceptors are responsive to pressure-related stretch. The arterial
baroreflex is a key determinant of the mean level of both vagal and
sympathetic outflows; thus, the lower vagal and greater sympathetic outflows
associated with cardiovascular diseases may result from blunted baroreflexes
due to increased vascular stiffness. Though arterial stiffness increases
with age, it is negatively related to aerobic capacity regardless of age.
Thus, chronic aerobic training may help to maintain baroreflex autonomic
circulatory control by mitigating age-related arterial stiffening. The
specific aims of this proposal are to determine if: 1) age-related
decreases in baroreflex control of vagal and sympathetic outflows are
related to greater carotid stiffness, 2) age-related declines in baroreflex
control of vagal and sympathetic outflows are reduced by lesser carotid
stiffness associated with aerobic fitness, and 3) a program of regular
aerobic exercise training in older humans increases baroreflex control of
vagal and sympathetic outflows due to decreased carotid stiffness. It is
hypothesized that the age-related reductions in baroreflex circulatory
control associated with increased carotid stiffness and altered basal
autonomic outflow can be reversed by exercise training. To fulfill these
aims, state-of-the-art neurophysiologic and ultrasonographic measures will
be made to assess baroreflex gain of autonomic outflow relative to the true
stimulus for baroreceptor activation changes in carotid dimensions. Young
(20-30 yr.) and older (60-80 yr.) men and women will be rigorously screened
to determine the influence of the aging process per se (as opposed to
disease, inactivity, etc.) on baroreflex function, basal autonomic outflow,
and carotid stiffness. The possible reversal of age-related declines by
aerobic exercise training will be assessed both cross-sectionally and
longitudinally. The investigator indicates that these studies are unique;
that there are no data which relate changes in barosensory dimensions to
concurrent changes in cardiovascular autonomic outflow in humans. He feels
that despite data indicating that carotid stiffness plays a significant role
in baroreflex function, it is unknown if increased stiffness in barosensory
areas results in the age-related reduction in baroreflex gain, ultimately
decreasing vagal and increasing sympathetic outflow. Further, he feels that
it is unknown if aerobic fitness modulates these age-related effects. He
states that this information is crucial to understand if blunted baroreflex
function secondary to vascular stiffening is the conduit by which aging
compromises autonomic circulatory control and increases cardiovascular
morbidity.
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