title: Aging alteration of cardiac vagosympathetic balance assessed through the tone-entropy analysis.
abstract: BACKGROUND
  Age-associated alterations of cardiac autonomic functions have been investigated intensively through heart rate variability analyses. However, changes with age in cardiac vagosympathetic balance remain to be elucidated.
  
  
  METHODS
  We studied 142 male subjects (30-69 yr) at a health care center in Kyoto, Japan. Electrocardiographic data were collected from subjects in a recumbent position for 10 min in the morning. Analysis was done by classifying the subjects into four age groups. In a pharmacological experiment carried out in December 1996, tone was verified to reflect the cardiac vagosympathetic balance, and entropy the total autonomic neural efferent activity. We assessed the heart rate variability through the tone-entropy (T-E) analysis that was described previously. In essence, two indexes, tone and entropy, were defined on a distribution of successive variations of heart period.
  
  
  RESULTS
  No significant differences were detected in clinical conditions among the four age groups. Tone increased and entropy decreased significantly with age. The aging process was expressed as a curvilinear path in T-E space. Compared to the pharmacological experiment, it was observed that aging degenerated the heart function from an ordinary to a denervated one. The same aging path was superimposed in the opposite direction on the heart recovery path after dynamic exercise in which cardiac vagosympathetic balance tended toward vagus division, corresponding with restoration of total autonomic activity.
  
  
  CONCLUSIONS
  An age-related reduction in cardiac autonomic function was consistent with previous reports. The vagosympathetic balance was altered with this reduction: vagal predominance was impaired significantly in proportion to the withdrawal of total cardiac autonomic activity.
authors.affiliation: Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Oida
authors.forename: T
authors.initials: T
authors.lastname: Kannagi
authors.forename: T
authors.initials: T
authors.lastname: Moritani
authors.forename: Y
authors.initials: Y
authors.lastname: Yamori
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000502:physiology; D004525:Efferent Pathways / Q000502:physiology; D004562:Electrocardiography; D015444:Exercise / Q000502:physiology; D006321:Heart / Q000502:physiology; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009476:Neurons, Efferent / Q000502:physiology; D010276:Parasympatholytics / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D016683:Supine Position; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*
chemical_list: D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics; D013565:Sympatholytics; D001285:Atropine; D011433:Propranolol