title: The effect of sham feeding on neurocardiac regulation in healthy human volunteers.
abstract: BACKGROUND
  Distension and electrical stimuli in the esophagus alter heart rate variability (HRV) consistent with activation of vagal afferent and efferent pathways. Sham feeding stimulates gastric acid secretion by means of vagal efferent pathways. It is not known, however, whether activation of vagal efferent pathways is organ- or stimulus-specific.
  
  
  OBJECTIVE
  To test the hypothesis that sham feeding increases the high frequency (HF) component of HRV, indicating increased neurocardiac vagal activity in association with the known, vagally mediated, increase in gastric acid secretion.
  
  
  METHODS
  Continuous electrocardiography recordings were obtained in 12 healthy, semirecumbent subjects during consecutive 45 min baseline, 20 min sham feeding (standard hamburger meal) and 45 min recovery periods. The R-R intervals and beat-to-beat heart rate signal were determined from digitized electrocardiography recordings; power spectra were computed from the heart rate signal to determine sympathetic (low frequency [LF]) and vagal (HF) components of HRV.
  
  
  RESULTS
  Heart rate increased during sham feeding (median 70.8 beats/min, 95% CI 66.0 to 77.6; P<0.001), compared with baseline (63.6, 95% CI 60.8 to 70.0) and returned to baseline levels within 45 min. Sham feeding increased the LF to HF area ratio (median: 1.55, 95% C.I 1.28 to 1.77; P<0.021, compared with baseline (1.29, 95% CI 1.05 to 1.46); this increase in LF to HF area ratio was associated with a decrease in the HF component of HRV.
  
  
  CONCLUSIONS
  Sham feeding produces a reversible increase in heart rate that is attributable to a decrease in neurocardiac parasympathetic activity despite its known ability to increase vagally mediated gastric acid secretion. These findings suggest that concurrent changes in cardiac and gastric function are modulated independently by vagal efferent fibres and that vagally mediated changes in organ function are stimulus- and organ-specific.
authors.affiliation: Department of Medicine, McMaster University, Hamilton, Canada.
authors.forename: M V
authors.initials: MV
authors.lastname: Kamath
authors.forename: R
authors.initials: R
authors.lastname: Spaziani
authors.forename: S
authors.initials: S
authors.lastname: Ullal
authors.forename: G
authors.initials: G
authors.lastname: Tougas
authors.forename: J C
authors.initials: JC
authors.lastname: Guzman
authors.forename: C
authors.initials: C
authors.lastname: Morillo
authors.forename: J
authors.initials: J
authors.lastname: Capogna
authors.forename: Mohammed
authors.initials: M
authors.lastname: Al-Bayati
authors.forename: David
authors.initials: D
authors.lastname: Armstrong
mesh_terms: D000328:Adult; D004435:Eating / Q000502:physiology*; D004525:Efferent Pathways / Q000502:physiology; D004562:Electrocardiography; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D006321:Heart / Q000294:innervation*; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D009928:Organ Specificity; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010919:Placebos; D014630:Vagus Nerve / Q000502:physiology*
chemical_list: D010919:Placebos