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Division of Sleep Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA. khu@bidmc.harvard.edu
Heartbeat fluctuations in mammals display a robust temporal structure characterized by scale-invariant/fractal patterns. These scale-invariant patterns likely confer physiological advantage because they change with cardiovascular disease and these changes are associated with reduced survival. Models of physical systems imply that to produce scale-invariant patterns, factors influencing the system at different time scales must be coupled via a network of feedback interactions. A similar cardiac control network is hypothesized to be responsible for the scale-invariant pattern in heartbeat dynamics, although the essential network components have not been determined. Here is shown that scale-invariant cardiac control occurs across time scales from minutes to approximately 24 h, and that lesioning the mammalian circadian pacemaker (suprachiasmatic nucleus; SCN) completely abolishes the scale-invariant pattern at time scales>or approximately 4 h. At time scales<or approximately 4 h, the scale invariance persisted following SCN lesion but with a different pattern. These results indicate previously unrecognized multiscale influences of the SCN on heart rate fluctuations that cannot be explained by a simple pacemaker of 24-h rhythmicity. The conclusion is that the SCN serves as a major node in the cardiac control network and imparts scale-invariant cardiac control across a wide range of time scales with strongest effects between approximately 4 and 24 h. These results demonstrate that experimental manipulations (e.g., SCN lesion) can be used to begin to model and understand the origin of scale-invariant behavior in a neurophysiological system.
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