Baroreflex resetting during exercise: mechanisms and meaning.
Baroreflex resetting during exercise: mechanisms and meaning.
复制标题
运动期间压力反射重置:机制和意义。
DOI:
10.1152/ajpheart.01275.2005
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发表时间:
2006
期刊:
影响因子:
--
通讯作者:
Sheriff,DonD
中科院分区:
文献类型:
--
作者:
Sheriff,DonD
THE CARDIOVASCULAR ADJUSTMENTS to exercise constitute wellcoordinated responses throughout the body. Virtually every organ system is required to do more (eg, skeletal muscle, the respiratory pump, and the cardiac pump) or to do the same as at rest while receiving less blood flow. Of all the organ systems, perhaps only global brain activity and blood flow are not modulated in some manner. The enormous demands for skeletal muscle blood flow imposed by dynamic exercise with a large muscle mass likely constitute the greatest challenge that is regularly imposed on the cardiovascular control mechanisms. The challenge of graded dynamic exercise is met by graded increases in cardiac output that make more flow and oxygen delivery available to active tissues and by graded reduction in the blood flow to inactive regions, which frees up additional oxygen delivery for active sites. The increase in calculated total systemic conductance permitted by the cardiovascular control mechanisms is well matched to the rise in cardiac output such that arterial pressure is well maintained or rises modestly. Some responses to isometric exercise differ. Owing to the sustained mechanical impingement of the muscle vasculature imposed by sustained muscle contraction, the cardiovascular response to this form of exercise has been characterized by the failure of the cardiovascular control systems to secure adequate blood flow for the contracting muscle. The resultant progression of muscle fatigue requires progressive increments in volitional effort to maintain force output until output can no longer be sustained. Heart rate and cardiac output rise progressively throughout the period of activity. Because a concomitant rise in vascular conductance is lacking, arterial pressure rises progressively as well. Although there are long-recognized similarities and dissimilarities between static and dynamic exercise (2), the cardiovascular neuroregulatory systems that bring about these adjustments likely share the same neurophysiological substrates with the substrates being activated in different patterns and/or at different levels of stimulation between the two forms of exercise. A longstanding challenge to cardiovascular physiologists has been the unraveling of the signals that produce the cardiovascular responses to exercise. Two overall regulatory schemes with long, rich histories continue to dominate present day research: 1) classical, negative-feedback control provided by afferents from active muscle (eg, a fall in blood flow leads to an accumulation of metabolites that stimulate sensory nerve endings, which elicits a rise in arterial pressure in an effort to restore blood flow), and 2) feedforward control provided by motor outflow from the cerebral cortex. Zuntz and Gebbert (cited in Ref. 4) established the basic idea of the importance of a feedback regulatory scheme provided by afferent neural signals from the muscles themselves. Critical early work was contributed by Alam and Smirk (1), who employed the trapping of nerve-activating chemical substances within previously active muscle by postexercise circulatory arrest, a powerful investigative tool, the use of which persists to the present day. The reflex nature of the responses was later more broadly defined by Coote et al.(3) and by McCloskey and Mitchell (9), whereas identification and characterization of the afferent fiber types involved has been provided by Kaufman et al.(7).Zuntz and Geppert and also Johansson (all cited in Ref. 4) appear to be the first to postulate the importance of motor command signals in evoking cardiorespiratory responses to exercise. Krogh and Lindhard (8) wrote of “irradiation of impulses from the motor …
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DOI:
10.1113/jphysiol.1913.sp001616
发表时间:
1913-10
期刊:
The Journal of Physiology
影响因子:
--
作者:
A. Krogh;J. Lindhard
通讯作者:
A. Krogh;J. Lindhard
DOI:
--
发表时间:
1971
期刊:
Journal of Physiology
影响因子:
--
作者:
By J. G. Coote;S. Hilton;J. Perez
通讯作者:
J. Perez
影响因子:
20.1
作者:
E. Asmussen
通讯作者:
E. Asmussen
影响因子:
3.3
作者:
L. Rowell
通讯作者:
L. Rowell
影响因子:
5.5
作者:
GOODWIN, GM;MCCLOSKEY, DI;MITCHELL, JH
通讯作者:
MITCHELL, JH