Why does inspiration increase heart rate

Exaggerating conditions during RSA amplifies this effect as we demonstrated in this study but only during maximum inspiration, during maximum expiration HR also increased instead of decreasing like it normally does during regular expiration. It is very well established that the sinoatrial node SA node is the dominant pacemaker of the heart and regulates the frequency of heartbeat [20] and this was established a very long time ago [21].

However, one does not fail to attribute the faster heart rate to the intense physical activity just because it is the SA node that sets the beating rhythm and pace of the heart. In similar fashion and reasoning we have designed our study to investigate the effects of breathing pattern manipulations on RSA. Bouairi and coworkers [22] stated that RSA in humans and in animals is mediated almost entirely through changes in parasympathetic cardiac vagal tone and this has been reported by many other studies [].

While fully cognizant of the fact that RSA is controlled by cardiac vagal tone, we wanted to investigate what happens to RSA when a person takes maximum inspiration and holds for 15 seconds and similarly when a person expires maximally and holds for 15 seconds.

Indeed, we found that the normal RSA observations where HR increases during inspiration and decreases during expiration were not fully observed in our study in that HR increased significantly during maximum expiration held for 15 seconds. We certainly feel that this is a novel and in fact exciting observation and we have put forward some plausible explanations for this observation. Our study demonstrated that indeed the RR Interval is significantly shortened during sustained maximum inspiration resulting in higher HR compared to normal breathing RR interval with lower HR.

This is in agreement with our first hypothesis about sustained inspiration resulting in shorter RR intervals hence higher HR. However, we did not observe longer RR Intervals during sustained maximum expiration as expected based on our second hypothesis for sustained expiration.

In fact, we observed significantly shorter RR Intervals hence higher HR during maximum expiration which was the exact opposite of our second hypothesis. This may be because HR is influenced more by the amount of blood that is returned to the heart following the principles of Frank- Starling Law of the heart which states that during systole, the heart pumps out the volume of blood returned to it during diastole [ 29] rather than the mere physical mechanics of sub-atmospheric thoracic pressure during inspiration and supra-atmospheric thoracic pressure during expiration directly on the heart itself.

That is, the more stretching that occurs to the myocardium during ventricular filling, the greater the pressure generated by the heart, and thus the greater the stroke volume. Simply put; the heart beats faster when more blood is returned to it as the higher thoracic pressure during maximum expiration compresses the venae cavae and the pulmonary veins causing more blood to be deposited into the atria.

Furthermore, this may be a survival mechanism in which the body attempts to provide more O2 to the cells by pumping more blood from the heart during expiration, a time when the body is not taking in more O2. This suggests that during the cardiac cycle there are more urgent matters to be addressed than the mere direct physical mechanics of intra-thoracic pressure on the heart during the respiratory cycle. This study confirmed that sustained maximum inspiration held for at least 15 seconds does indeed shorten the RR Interval which results in higher HR compared to normal breathing inspiration which confirms our first hypothesis.

We observed the opposite results contrary to our second hypothesis for sustained maximum expiration held for at least 15 seconds where the RR interval was in fact shortened resulting in faster HR compared to expiration during normal breathing. Contrary to observations during normal breathing expiration and our second hypothesis, maximum expiration sustained for 15 seconds shortened the RR Interval thus also resulting in higher HR which was similar to results observed during sustained maximum inspiration.

This is exactly opposite to what is observed during normal breathing expiration. Further studies of sustained maximum expiration are required to determine possible reasons behind this observation.

We are very grateful to the Heritage University Institutional Review Board for its work in reviewing, monitoring, and regulating experimental studies involving human subjects or animal models. We would also like to thank Dr. Alexander Alexiades, our colleague in the Biology Department here at Heritage University for his assistance with statistical analysis methods.

Abstract This study investigated the physical effects of the respiratory cycle on heart rate by exaggerating the conditions under which Respiratory Sinus Arrhythmia RSA occurs. There was a significant difference in the longest RR interval during normal breathing versus the longest RR interval during expire-hold or inspire-hold treatments; P values ranged from P Keywords: Heart Rate; RR Interval; Respiratory Sinus Arrhythmia; Maximum Inspiration; Maximum Expiration Introduction It is well established that heart rate variability in synchrony with the respiratory cycle, known as Respiratory Sinus Arrhythmia RSA , is regulated through cardiac vagal control [].

Hypothesis 1: Inspiration During maximum inspiration the pressure in the thoracic cavity is at its lowest sub-atmospheric level and therefore exerts much less compression around the heart resulting in shorter RR intervals and thus faster heart rate. Chess, G. Influence of cardiac neural inputs on rhythmic variations of heart period in the cat.

Cohen, M. Short-term cardiovascular oscillations in man: measuring and modeling the physiologies. Cole, C. Heart rate recovery immediately after exercise as a predictor of mortality. Heart rate recovery after submaximal exercise testing as a predictor of mortality in a cardiovascularly healthy cohort. Collins, M. Autonomic response to coronary occlusion in animals susceptible to ventricular fibrillation. Cooley, J. An algorithm machine for the calculation of complex Fourier series.

Cyon, E. Davies, C. Sinus arrhythmia in man at rest. De Jong, M. Heart rate variability analysis in the assessment of autonomic function in heart failure.

Denton, T. Fascinating rhythm: a primer on chaos theory and its application to cardiology. Denver, J. Methodological issues in the quantification of respiratory sinus arrhythmia.

Donders, F. Zur Physiologie des nervus vagus. Eckberg, D. Human sinus arrhythmia as an index of vagal cardiac outflow. Sympathovagal balance: a critical appraisal. Circulation 96, — The human respiratory gate. Einthoven, W. Eppinger, H. Ewing, D. The value of cardiovascular autonomic function tests: 10 years experience in diabetes.

Diabetes Care 8, — New method for assessing cardiac parasympathetic activity using 24 hour electrocardiograms. Farrell, T. Risk stratification for arrhythmic events in postinfarction patients based upon heart rate variability, ambulatory electrocardiographic variables and the signal-averaged electrocardiogram. Fleisher, L. Approximate entropy of heart rate as a correlate of postoperative ventricular dysfunction. Anesthesiology 78, — Floyer, S. Smith and B.

Walford London , The Pulse Watch. Published by J. Nicholson, W. Taylor and J. Clements London. Fouad, F. Assessment of parasympathetic control of heart rate by a noninvasive method. Paris 3, 55— Gleick, J. Chaos: Making of a New Science. New York: Viking Press. Goldberger, A. Nonlinear dynamics, fractals, and chaos: applications to cardiac electrophysiology.

Applications of nonlinear dynamics to clinical cardiology. Grossman, P. Toward understanding respiratory sinus arrhythmia: relations to cardiac vagal tone, evolution and biobehavioral functions. A comparison of three quantification methods for estimation of respiratory sinus arrhythmia. Psychophysiology 27, — Guevara, M. Phase-locking, period-doubling bifurcations and irregular dynamics in periodically stimulated cardiac cells.

Guyton, A. Pressoreceptor-autonomic oscillation: a probable cause of vasomotor waves. Hainsworth, R. Circulatory responses from lung inflation in anesthetized dogs. Hales, S. Published by W. Innys and R. Manby, London. Halliwill, J. Effect of a vagomimetic atropine dose on canine cardiac vagal tone and susceptibility to sudden cardiac death.

Hamlin, R. Autonomic control f heart rate in the horse. Sinus arrhythmia in the dog. Hayano, J. Respiratory sinus arrhythmia. A phenomenon improving pulmonary gas exchange and circulatory efficiency. Circulation 94, — Hedman, A. Hering, E. Abteilung 60, — Abteilung 64, — Hering, H. A functional test of heart vagi in man. Hirsch, J. Respiratory sinus arrhythmia in humans: how breathing pattern modulated heart rate. Ho, K. Predicting survival in heart failure case and control subjects by use of fully automated methods for deriving nonlinear and conventional indices of heart rate dynamics.

Hohnloser, S. Heart rate variability used as an arrhythmia risk stratifier after myocardial infarction. Pacing Clin. Holter, N. New method for heart rate studies continuous electrocardiography of active subjects. Hon, E. Electronic evaluations of fetal heart rate patterns preceding fetal death, further observations. Hopf, H. Low-frequency spectral power of heart rate variability is not a specific marker of cardiac sympathetic modulation.

Anesthesiology 82, — Houle, M. Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity. Huikuri, H. Power-law relationship of heart rate variability as a predictor of mortality in the elderly. Circulation 97, — Fractal correlation properties of R-R interval dynamics and mortality inpatients with depressed left ventricular function after an acute myocardial infarction. Circulation , 47— Measurement of heart rate variability by methods based upon on nonlinear dynamics.

Abnormalities in beat-to-beat dynamics of heart rate before the spontaneous onset of life-threatening ventricular tachyarrhythmias in patients with prior myocardial infarction. Hurst, J. Naming the waves in the ECG, with a brief account of their genesis. Circulation 98, — Hyndman, B. The role of rhythms in homeostasis.

Kybernetik 15, — Spectral Analysis of sinus arrhythmia during mental loading. Ergonomics 18, — Spontaneous rhythms in physiological control systems. Nature , — Iyengar, N. Age-related alterations in the fractal scaling of cardiac interbeat interval dynamics.

Jokinen, V. Temporal changes and prognostic significance of measures of heart rate dynamics after acute myocardial infarction in the beta-blocking era. Jouven, X. Heart rate profile during exercise as a predictor of sudden death.

Karakaya, O. Acute effect of cigarette smoking on heart rate variability. Angiology 58, — Katona, P. Respiratory sinus arrhythmia: noninvasive measure of parasympathetic control.

Cardiac vagal efferent and heart period in the carotid sinus reflex. Katz, L. Fishman and D. Kay, S. Spectrum analysis: a modern perspective. IEEE 6, — Kiilavuori, K. Reversal of autonomic derangement by physical training in chronic heart failure assessed by heart rate variability.

Kingwell, B. Heart rate spectral analysis, cardiac norepinephrine spillover, and muscle sympathetic nerve activity during human sympathetic nervous activation and failure. Circulation 90, — Kleiger, R. Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. Koepchen, H.

Koh, J. Human autonomic rhythms: vagal cardiac mechanisms in teraplegic subjects. Kollai, M. Respiratory sinus arrhythmia is a limited measure of cardiac parasympathetic control in man. La Rovere, M. Baroreflex sensitivity and heart rate variability in prediction of total cardiac mortality after myocardial infraction. Lancet , — Baroreflex sensitivity, clinical correlates and cardiovascular mortality among patients with a first myocardial infarction: a prospective study.

Circulation 78, — Laito, T. Long-term alterations of heart rate dynamics after coronary artery bypass surgery. Lanza, G. Prognostic role of heart rate variability in patients with recent acute myocardial infarction. Laude, D. Spectral analysis of systolic blood pressure and heart rate oscillations related to respiration. Lombardi, R. Linear and nonlinear dynamics of heart rate variability after acute myocardial infraction with normal and reduced left ventricular ejection fraction.

Lorenz, E. Deterministic nonperiodic flow. Atmospheric Sci. Ludwig, C. Madwell, J. Low frequency oscillations in arterial pressure on heart rate: a simple computer model. Fractal analysis of heart rate dynamics as a predictor of mortality in patients with depressed left ventricular function after acute myocardial infarction. Heart rate dynamics before and after spontaneous onset of ventricular fibrillation inpatients with healed myocardial infarcts.

Fractal analysis o and time- and frequency-domain measures of heart rate variability as predictors of mortality in patients with heart failure. Prediction of sudden cardiac death by fractal analysis of heart rate variability in elderly subjects. Dynamic analysis of heart rate may predict subsequent ventricular tachycardia after myocardial infarction. Malik, M. Heart rate variability in relations to prognosis after myocardial infarction: selection of optimal processing techniques.

Influence of the recognition artefact in the automatic analysis of long-term electrocardiograms on time domain measurements of heart rate variability. Malliani, A. Cardiovascular neural regulation explored in the frequency domain. Circulation 84, — Mancia, G. Smoking impairs baroreflex sensitivity in humans. Maule, S. Prolonged QT interval and reduced heart rate variability in patients with uncomplicated essential hypertension.

Mayer, S. Sber Akd Wiss. Math-naturwiss Klasse 3. Abeitlung 74, — Mayer-Kress, G. Dimensional analysis of nonlinear oscillations in brain, heart and muscle. Mazzuero, G. Long-term adaptation of h heart rate variability after myocardial infarction. Significant variability of the breathing and heart rates was observed in the experiments see Fig.

To characterise the variability of signals, the mean and standard deviation of the rates were calculated, and stationarity and normality tests were conducted. Due to the relatively small data size around breaths or heart beats per interval , the Shapiro-Wilk normality test was implemented to categorise normality, as this test yields a high statistical power with small sample sizes Stationarity was described in terms of an underlying trend, using the KPSS null hypothesis test A significance level of 0.

To analyse the transient response of heart rate to the step change in breathing rate, a moving average technique was applied to extract a low-frequency trend in the heart rate time series. To illustrate the effect of phase synchronization, a synchrogram 6 was used. Respiratory rate was used as a slow signal and heart rate was used as a fast signal.

In the case of synchronization in a n :1 ratio, n parallel lines are visible on a synchrogram; a single line is an indicator of synchronization in a ratio. To quantify the existence of CRS and to calculate the durations of synchronization episodes during the intervals of high-rate breathing, the phase difference and synchronization index were calculated and analysed as functions of time. It can be calculated using the following equation 6 :. The angular brackets denote an average over a time window with its centre at time moment, t.

The width of the window was chosen to be 7 heart beats. Since both signals, respiratory and heart, are stochastic, the phase difference is not a constant and fluctuates with time.

Equipment, methods, and software used are available from the corresponding author. The datasets recorded and analysed during the current study are not publicly available due to constraints within the ethical approval concerning volunteer data protection.

Anonymised time series are available from the corresponding author on reasonable request. Hayano, J. Respiratory sinus arrhythmia: a phenomenon improving pulmonary gas exchange and circulatory efficiency. Circulation 94 , — Eckberg, D. Point: respiratory sinus arrhythmia is due to a central mechanism. Article Google Scholar. Karemaker, J. Counterpoint: Respiratory sinus arrhythmia is due to the baroreflex mechanism.

Farmer, D. Brainstem sources of cardiac vagal tone and respiratory sinus arrhythmia. Schafer, C. Synchronization in the human cardiorespiratory system. Heartbeat synchronized with ventilation. Nature , — Lotric, M. Synchronization and modulation in the human cardio-respiratory system. Riedl, M. Cardio-respiratory coordination increases during sleep apnoea. Penzel, T.

Modulations of heart rate, ECG, and cardio-respiratory coupling observed in polysomnography. Kralemann, B. In vivo cardiac phase response curve elucidates human respiratory heart rate variability. Bartsch, R. Phase transitions in physiologic coupling. USA , — Pikovsky, A. Schlafke, M. Cardiorespiratory control: an integrated view H. Koepchen in memoriam. Sleep Res. Runge, J. Quantifying the causal strength of multi variate cardiovascular couplings with momentary information transfer.

Kotani, K. Model for cardiorespiratory synchronization in humans. P hys. Pokrovskii, V. On the conscious control of the human heart. Integration of the heart rhythmogenesis levels. Potyagailo, E. Cardiorespiratory synchronization in evaluation of the functional status and regulatory adaptive resources in children. Cardiorespiratory Synchronism in Humans. New diagnostic potentialities of cardiorespiratory synchronization in children.

Khovanov, I. Intrinsic dynamics of heart regulatory systems on short timescales: from experiment to modelling. Theory Exp. Razali, N. Journal of Statistical Modelling and Analytics 2 1 , 21—33 Google Scholar. Ferrer-Perex, H. A comparison of two modified stationarity tests. A Monte Carlo study. Download references. We thank all volunteers who participated in experiments.

Sean Perry, Natasha A. You can also search for this author in PubMed Google Scholar. Experimental design, execution of experiments and computational simulations were performed by SP; conception and design of the work by N. All authors approved the final version of the manuscript. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. Correspondence to Natasha A. Reprints and Permissions. Perry, S.

Control of heart rate through guided high-rate breathing. Sci Rep 9, Download citation. Received : 16 August Accepted : 18 December Published : 07 February Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

Experimental Brain Research By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Advanced search. Skip to main content Thank you for visiting nature. Download PDF. Subjects Cardiology Nonlinear phenomena. Abstract Understanding the complex dynamics of cardio-respiratory coupling sheds light on the underlying mechanisms governing the communication between these two physiological systems.

Introduction The interaction between the cardiac and respiratory systems is important for effective and efficient gas exchange 1. Figure 1. Full size image. Figure 2.

Figure 3. Figure 4. Full size table. Figure 5. Figure 6. Figure 7.