Dynamic interactions between musical, cardiovascular, and cerebral rhythms in humans.

BACKGROUND: Reactions to music are considered subjective, but previous studies suggested that cardiorespiratory variables increase with faster tempo independent of individual preference. We tested whether compositions characterized by variable emphasis could produce parallel instantaneous cardiovascular/respiratory responses and whether these changes mirrored music profiles. METHODS AND RESULTS: Twenty-four young healthy subjects, 12 musicians (choristers) and 12 nonmusician control subjects, listened (in random order) to music with vocal (Puccini's "Turandot") or orchestral (Beethoven's 9th Symphony adagio) progressive crescendos, more uniform emphasis (Bach cantata), 10-second period (ie, similar to Mayer waves) rhythmic phrases (Giuseppe Verdi's arias "Va pensiero" and "Libiam nei lieti calici"), or silence while heart rate, respiration, blood pressures, middle cerebral artery flow velocity, and skin vasomotion were recorded.Common responses were recognized by averaging instantaneous cardiorespiratory responses regressed against changes in music profiles and by coherence analysis during rhythmic phrases. Vocal and orchestral crescendos produced significant (P=0.05 or better) correlations between cardiovascular or respiratory signals and music profile, particularly skin vasoconstriction and blood pressures, proportional to crescendo, in contrast to uniform emphasis, which induced skin vasodilation and reduction in blood pressures. Correlations were significant both in individual and group-averaged signals. Phrases at 10-second periods by Verdi entrained the cardiovascular autonomic variables. No qualitative differences in recorded measurements were seen between musicians and nonmusicians. CONCLUSIONS: Music emphasis and rhythmic phrases are tracked consistently by physiological variables. Autonomic responses are synchronized with music, which might therefore convey emotions through autonomic arousal during crescendos or rhythmic phrases.

Interval hypoxic training improves autonomic cardiovascular and respiratory control in patients with mild chronic obstructive pulmonary disease.

OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is associated with cardiac autonomic nervous system dysregulation. This study evaluates the effects of interval hypoxic training on cardiovascular and respiratory control in patients with mild COPD. METHODS: In 18 eucapnic normoxic mild COPD patients (age 51.7 +/- 2.4 years, mean +/- SEM), randomly assigned to either training or placebo group, and 14 age-matched healthy controls (47.7 +/- 2.8 years), we monitored end-tidal carbon dioxide, airway flow, arterial oxygen saturation, electrocardiogram, and continuous noninvasive blood pressure at rest, during progressive hypercapnic hyperoxia and isocapnic hypoxia to compare baroreflex sensitivity to hypoxia and hypercapnia before and after 3 weeks of hypoxic training. In double-blind fashion, both groups received 15 sessions of passive intermittent hypoxia (training group) or normoxia (placebo group). For the hypoxia group, each session consisted of three to five hypoxic (15-12% oxygen) periods (3-5 min) with 3-min normoxic intervals. The placebo group inhaled normoxic air. RESULTS: Before training, COPD patients showed depressed baroreflex sensitivity, as compared with healthy individuals, without evident chemoreflex abnormalities. After training, in contrast to placebo group, the training group showed increased (P < 0.05) baroreflex sensitivity up to normal levels and selectively increased hypercapnic ventilatory response (P < 0.05), without changes in hypoxic ventilatory response. CONCLUSION: Eucapnic normoxic mild COPD patients already showed signs of cardiovascular autonomic abnormalities at baseline, which normalized with hypoxic training. If confirmed in more severe patients, interval hypoxic training may be a therapeutic strategy to rebalance early autonomic dysfunction in COPD patients.

Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control.

We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO(2)), and to normoxic hypercapnia. Oxygen saturation (SaO(2)), end-tidal CO(2) (et-CO(2)), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O(2): -0.33 +/- 0.05, -0.74 +/- 0.02 and -1.59 +/- 0.3, p < 0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO(2), whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO(2). We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.

Slow breathing improves arterial baroreflex sensitivity and decreases blood pressure in essential hypertension.

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.