Blood pressure and heart rate are tightly regulated by the autonomic nervous system through dynamic interactions between respiratory and cardiovascular control centers. Alterations in respiratory patterning — particularly slow, paced, or deep breathing — produce rapid changes in heart–lung interactions, baroreflex function and heart-rate variability (HRV), mechanisms that underlie short-term modulation of heart rate and blood pressure [1].
A growing body of experimental work indicates that voluntary slow or paced breathing reliably increases vagal indices of HRV and respiratory-sinus-arrhythmia while reducing markers of sympathetic drive; these changes are associated with improved baroreflex sensitivity and altered central autonomic network activity that plausibly mediate acute reductions in heart rate and arterial pressure [1,2].
Clinical and population-level studies and reviews have examined whether breathing exercises translate into clinically meaningful blood-pressure lowering. Recent systematic reviews and scoping analyses report modest but statistically significant reductions in systolic and diastolic blood pressure and small decreases in resting heart rate after breathing-based interventions, with effect sizes varying by breathing protocol, session duration and population studied. However, heterogeneity in methods (breathing rates, inhalation:exhalation ratios, training duration) and the short follow-up intervals in many trials limit definitive conclusions about optimal prescriptions and durability of effect [3,4].
Mechanistic work suggests an optimal or “resonance” breathing frequency (commonly near 5–6 breaths per minute) that maximizes cardiovagal gain and HRV; breathing at or near this frequency appears to produce the largest immediate autonomic shifts in healthy subjects and is therefore commonly used in physiological experiments and biofeedback protocols [5,6].
Despite this background, many prior investigations differ in sample size, the exact breathing instructions used and the timing of outcome assessment, and relatively few studies report detailed, time-resolved trajectories of heart rate and blood pressure immediately before, during and after a single standardized deep-breathing session in a healthy adult sample. To address this gap, the present physiological assessment quantified acute changes in heart rate, systolic and diastolic blood pressure, and respiratory rate in a cohort of healthy volunteers undergoing a brief, supervised paced deep-breathing exercise. The study aims were to (1) characterize immediate cardiovascular responses to a 5-minute paced deep-breathing episode and (2) describe short-term recovery over the subsequent five minutes
Study Design and Setting: A prospective, controlled, physiological assessment was conducted in a tertiary-care medical institute. The study aimed to quantify acute cardiovascular responses to a structured deep-breathing exercise performed under standardized laboratory conditions.
Study Population and Sample Size: A total of 60 healthy adult volunteers were enrolled. Sample size was determined pragmatically to provide adequate precision for detecting short-term changes in heart rate and blood pressure within individuals. Participants were recruited and were evaluated for eligibility by a trained investigator.
Inclusion Criteria
Exclusion Criteria
Baseline Assessment
Participants reported to the laboratory in the morning after avoiding caffeine, strenuous physical activity, and heavy meals for at least 2 hours. Following 10 minutes of seated rest, baseline measurements were recorded:
All measurements were taken twice, one minute apart, and the mean values were used for analysis.
Deep Breathing Protocol: Participants performed a guided deep-breathing exercise consisting of:
A metronome and verbal cues ensured uniform pacing. The procedure was supervised by a physiology person to maintain consistency.
Post-Intervention Measurements: Immediately after completing the breathing exercise, HR and BP were measured again using the same instruments and protocol. Measurements were repeated after 5 minutes to assess short-term recovery patterns.
Outcome Measures
Primary outcomes included:
Secondary outcome:
Statistical Analysis
Data were entered into a spreadsheet and analyzed using standard statistical software. Continuous variables were expressed as mean ± standard deviation. Pre- and post-intervention values were compared using paired-sample t-tests. A p-value <0.05 was considered statistically significant. Effect sizes were calculated to determine the magnitude of physiological change.
A total of 48 healthy adults were included in the final analysis. The baseline characteristics of the study population are summarized in Table 1. Participants had a mean age of 26.8 ± 4.9 years and an average BMI of 23.4 ± 2.8 kg/m². Baseline cardiovascular parameters were within the normal physiological range, with a mean resting heart rate of 78.6 ± 6.7 beats/min, systolic blood pressure of 118.9 ± 7.8 mmHg, and diastolic blood pressure of 76.4 ± 6.1 mmHg. The mean resting respiratory rate was 15.2 ± 1.9 breaths/min.
Following the deep-breathing exercise, significant reductions were observed across all primary outcomes (Table 2). Heart rate showed a marked decrease from 78.6 ± 6.7 to 69.8 ± 6.1 beats/min (p < 0.001). Systolic blood pressure declined by an average of 5.8 mmHg, while diastolic pressure decreased by 3.6 mmHg, both with strong statistical significance (p < 0.001). Respiratory rate also demonstrated a notable drop from 15.2 ± 1.9 to 12.7 ± 1.6 breaths/min (p < 0.001).
Assessment at five minutes after the intervention revealed partial reversal of these effects (Table 3). Heart rate increased to 72.4 ± 6.3 beats/min, though values remained lower than baseline. Systolic blood pressure rose modestly to 115.2 ± 7.6 mmHg, and diastolic pressure to 74.2 ± 6.0 mmHg. Respiratory rate increased to 13.9 ± 1.7 breaths/min. The return toward baseline was statistically significant for heart rate and respiratory rate, whereas the recovery in diastolic pressure did not reach the threshold for significance (p = 0.07). All changes are shown in Figure 1.
Table 1. Baseline Characteristics of Participants (n = 48)
|
Variable |
Mean ± SD |
|
Age (years) |
26.8 ± 4.9 |
|
BMI (kg/m²) |
23.4 ± 2.8 |
|
Resting Heart Rate (beats/min) |
78.6 ± 6.7 |
|
Resting SBP (mmHg) |
118.9 ± 7.8 |
|
Resting DBP (mmHg) |
76.4 ± 6.1 |
|
Resting Respiratory Rate (breaths/min) |
15.2 ± 1.9 |
Table 2. Cardiovascular Parameters Before and Immediately After Deep Breathing
|
Parameter |
Pre-intervention (Mean ± SD) |
Post-intervention (Mean ± SD) |
Mean Change |
p-value |
|
Heart Rate (beats/min) |
78.6 ± 6.7 |
69.8 ± 6.1 |
−8.8 |
<0.001 |
|
SBP (mmHg) |
118.9 ± 7.8 |
113.1 ± 7.4 |
−5.8 |
<0.001 |
|
DBP (mmHg) |
76.4 ± 6.1 |
72.8 ± 5.9 |
−3.6 |
<0.001 |
|
Respiratory Rate (breaths/min) |
15.2 ± 1.9 |
12.7 ± 1.6 |
−2.5 |
<0.001 |
Table 3. Cardiovascular Parameters Five Minutes After the Deep-Breathing Exercise
|
Parameter |
Immediate Post-intervention |
5-min Post-intervention |
Mean Difference |
p-value |
|
Heart Rate (beats/min) |
69.8 ± 6.1 |
72.4 ± 6.3 |
+2.6 |
<0.01 |
|
SBP (mmHg) |
113.1 ± 7.4 |
115.2 ± 7.6 |
+2.1 |
<0.05 |
|
DBP (mmHg) |
72.8 ± 5.9 |
74.2 ± 6.0 |
+1.4 |
0.07 |
|
Respiratory Rate (breaths/min) |
12.7 ± 1.6 |
13.9 ± 1.7 |
+1.2 |
<0.01 |
Figure 1: Changes in Physiological parameters following deep breathing
The present study demonstrated that a single session of paced deep breathing elicited prompt reductions in heart rate and blood pressure, and that these changes began to revert toward baseline during the five-minute recovery period. This pattern aligns with existing evidence showing that slow or deep breathing prompts rapid autonomic adjustments through enhanced parasympathetic activity and modulation of baroreflex sensitivity [7,8].
One plausible mechanism is that deep breaths engage pulmonary stretch receptors and augment cardiovagal reflexes, thereby increasing baroreflex sensitivity and reducing sympathetic output. In a study of healthy adults, slow-paced breathing at approximately six breaths per minute increased baroreflex gain and cardiovagal activity compared with rapid breathing, supporting this mechanistic interpretation [9,10]. In the context of our findings, the magnitude of heart rate reduction (≈ 8.8 beats/min) and systolic blood-pressure drop (≈ 5.8 mmHg) are consistent with the short-term responsiveness reported in similar physiological assessments.
Comparative interventions in hypertensive populations have reported larger absolute blood-pressure reductions over multiple sessions, for example reductions in systolic pressure by ~8–9 mmHg after several weeks of breathing exercises [11]. Although our healthy volunteer cohort and brief intervention differ in paradigm and baseline risk, our observed acute effect reinforces the notion that even a singular breathing bout can engage cardiovascular regulatory processes. The partial recovery of parameters within five minutes observed in our data is similarly recorded in other short-term breathing studies, which note that the effect attenuates unless the practice is repeated or sustained [12].
The tempo of breathing is likely a critical determinant of response magnitude. According to a recent systematic investigation, breathing at or near “resonance” frequency (~5–6 breaths/min) produces maximal heart-rate variability and baroreflex coupling, thus optimizing cardiovascular impact [13]. Our study protocol used a 6-breath/min pace (4-s inhalation, 2-s hold, 4-s exhalation) which aligns with that resonance range; the results therefore support the application of resonance-paced breathing for immediate autonomic modulation.
Despite these supportive findings, certain limitations should be acknowledged. First, our study involved a healthy, young adult cohort rather than individuals with elevated cardiovascular risk; thus, generalizability to hypertensive or older populations remains uncertain. Second, we assessed only very short-term cardiovascular responses and did not evaluate sustained or long-term effects of regular breathing practice. Third, although measurements were taken post-intervention and at five minutes, there was no continuous monitoring during the breathing session or extended recovery period, which may omit dynamic transitional behaviours. Future research might incorporate continuous recording of heart rate variability and blood pressure waves during and after breathing interventions, extend the monitoring window, and include diverse participant populations such as hypertensive or diabetic subjects.
This physiological assessment demonstrates that a brief session of paced deep breathing produces immediate and meaningful reductions in heart rate, systolic blood pressure, diastolic blood pressure, and respiratory rate in healthy adults. Although partial recovery occurs within five minutes, post-intervention values remain lower than baseline, indicating a sustained short-term autonomic benefit. These findings highlight the potential of simple, structured breathing practices as a non-pharmacological approach to transient cardiovascular modulation. Further studies incorporating longer follow-up intervals, diverse populations, and repeated breathing sessions could provide deeper insights into the therapeutic utility of controlled respiration techniques.