Controlled breathing during transient hypoxia did not significantly alter the heart rate response compared to spontaneous breathing (-0.71 vs -0.62; P≥0.22).
Does controlled breathing compared to spontaneous breathing alter the heart rate response to transient hypoxia in healthy volunteers?
Hypoxic tachycardia in humans is not secondary to hyperpnoea, as voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response.
Absolute Event Rate: -0.71% vs -0.62%
p-value: p=≥ 0.22
New Findings What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Abstract Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation Hyp‐VI; in liters per minute per percentage of blood oxygen saturation ( ), tidal volume Hyp‐VT; in litres per , heart rate Hyp‐HR; in beats per minute per , systolic Hyp‐SBP; in millimetres of mercury per and mean blood pressure Hyp‐MAP; in millimetres of mercury per and systemic vascular resistance Hyp‐SVR; in dynes seconds (centimetres) −5 per was calculated as the slope of the regression line relating the variable to , including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR ( r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique ( r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
Paleczny et al. (Thu,) conducted a other in Healthy subjects (n=17). Controlled breathing vs. Spontaneous breathing was evaluated on Heart rate response to hypoxia (Hyp-HR) (p=≥ 0.22). Controlled breathing during transient hypoxia did not significantly alter the heart rate response compared to spontaneous breathing (-0.71 vs -0.62; P≥0.22).