[Questioning the mechanism behind slow breathing and heart coherence training]. / Vraagtekens bij het werkingsmechanisme van slow-breathing en hartcoherentietraining.

BACKGROUND: Slow breathing and heart coherence training are being offered increasingly as treatments for anxiety, depression and stress-related mental and somatic complaints. Both of these interventions are aimed at influencing (i.e. increasing or optimising) heart rate variability and the mechanism involved is described in terms such as heart coherence, resonance breathing and heart-brain communication. AIM: To find out whether treatment effects are indeed based on the optimisation of heart rate variability. METHOD: Our literature search focused on 1) the assumption that poor mental health is definitely linked to deviant heart rate variability, and 2) the assumption that optimising heart rate variability leads specifically to a reduction of complaints and symptoms. RESULTS: There is insufficient evidence to support these two assumptions. CONCLUSION: Slow breathing and heart coherence training probably achieve their effects as a result of non-specific psychological mechanisms.

Double-blind placebo-controlled study of the hyperventilation provocation test and the validity of the hyperventilation syndrome.

BACKGROUND: Hyperventilation syndrome (HVS) describes a set of somatic and psychological symptoms thought to result from episodic or chronic hyperventilation. Recognition of symptoms during the hyperventilation provocation test (HVPT) is the most widely used criterion for diagnosis of HVS. We have investigated the validity of the HVPT and of the concept of HVS. METHODS: In a randomised, double-blind, crossover design, the ability of 115 patients with suspected HVS to recognise symptoms during the HVPT was compared with the ability to recognise symptoms during a placebo test (isocapnic overbreathing, with carbon dioxide levels maintained by manual titration). 30 patients who had positive results on the HVPT underwent ambulatory transcutaneous monitoring of pCO2 to ascertain whether they hyperventilated during spontaneous symptom attacks. FINDINGS: Of the 115 patients who underwent the HVPT and the placebo test, 85 (74%) reported symptom recognition during the HVPT (positive diagnosis HVS). Of that subset, 56 were also positive on the placebo test (false-positive), and 29 were negative on the placebo test (true-positive). False-positive and true-positive patients did not differ in symptom profile or in physiological variables. During ambulatory monitoring (15 true-positive, 15 false-positive) 22 attacks were registered. Transcutaneous end-tidal, pCO2 decreased during only seven. The decreases were slight and apparently followed the onset of the attack, which suggests that hyperventilation is a consequence rather than a cause of the attack. There were no apparent differences between false-positive and true-positive patients. INTERPRETATION: The HVPT is invalid as a diagnostic test for HVS. Hyperventilation seems a negligible factor in the experience of spontaneous symptoms. The term HVS should be avoided.