Key result
Acute device-guided slow breathing in normal subjects did not change blood pressure or pulse interval, but significantly increased pulse interval variability and baroreflex sensitivity (P<0.05).
Why the study?
Does acute device-guided slow breathing improve cardiovascular parameters and baroreflex sensitivity in normal subjects?
Does acute device-guided slow breathing improve cardiovascular parameters and baroreflex sensitivity in normal subjects?
Acute device-guided slow breathing increases baroreflex sensitivity and cardiac vagal modulation in normal subjects, suggesting a potential mechanism for its blood pressure-lowering effects in hypertension.
May support vagal mechanisms for breathing interventions; leaves open efficacy and BP effects in hypertensive patients.
Repeatedly performed slow breathing (SLB) exercise has been reported to reduce blood pressure (BP) in hypertension. Among the possible mechanisms responsible for such an effect, an increased baroreflex sensitivity has been suggested to play a role. Aim of our study was to explore whether acute performance of SLB obtained with a device-guided breathing exercise (RESPeRATE, InterCure) has any influence on BP, pulse interval (PI, 1/HR) and spontaneous sensitivity of baroreflex control of HR (BRS) in normal subjects. In supine normal volunteers (n=15; age 39.9±8.4 yrs, 10 males) finger BP, PI, respiratory rate (RR), ETCO2 and SaO2 were continuously recorded for 3 periods of 15 min each: baseline (BAS), SLB, and resumption of spontaneous breathing (SB). Beat-by-beat systolic (S)BP and PI values were averaged during each period. SD was used as an index of variability of SBP and PI. BRS was quantified as the αLF and αHF coefficient (squared ratio of the spectral powers of PI and SBP at 0.1 and 0. 3 Hz, respectively) and by the slope of +PI/+SBP and -PI/-SBP sequences. RR was 12.5 breath/min during BAS and SB and fell to 5.2 breath/min during SLB (p<0.01). ETCO2 and SaO2 did not change throughout the study. BAS SBP and PI were 124.3±13.5 mm Hg and 0.951±0.134 sec, respectively, with no change during SLB or SB. PI SD was 0.064±0.026 sec in BAS and increased to 0.074±0.028 and 0.082±0.030 sec during SLB and SB respectively (p<0.01). SBP SD showed a tendency to increase in parallel (NS). αLF was 12.6±6.5, 14.9±7.2 and 14.7±7.5 msec/mm Hg during BAS, SLB, and SB respectively (p<0.05 vs BAS). The corresponding values of -PI/-SBP slope were 13.0±7.8, 15.6±6.7 and 16.3±6.4 msec/mm Hg (p<0.05 vs BAS). αHF and +PI/+SBP slope also showed a tendency to increase vs BAS. The number of +PI/+SBP and -PI/-SBP sequences was 7.7±6.6 and 8.4±5.7, respectively, during BAS, increased to 23.2±16.9 and 32.3±16.0 during SLB (p<0.01) and returned to 10.2±6.9 and 12.4±5.2 during SB (NS vs BAS). In summary, acute SLB has no effect on BP and PI in normal subjects, but increases PI variability and BRS in the LF region and with baroreceptor deactivation during and after SLB exercise. We conclude that the favourable effects of repeatedly performed SLB exercise on cardiovascular parameters may be at least partially mediated by an increased BRS and by improved cardiac vagal modulation.
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Gianfranco Parati (2002) studied Normal subjects (n=15). Device-guided slow breathing (RESPeRATE) vs. Baseline and spontaneous breathing was evaluated on Blood pressure, pulse interval, and baroreflex sensitivity (p=<0.05). Acute device-guided slow breathing in normal subjects did not change blood pressure or pulse interval, but significantly increased pulse interval variability and baroreflex sensitivity (P<0.05).
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