Stikkordarkiv: Pustemønster

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Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

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Nevner hvordan 6 pust i minuttet øker HRV og vagus nervens effekt på hjertet. Nevner også hvordan CO2 synker ved 15 pust i minuttet og holdes normalt ved 6 pust i minuttet. De med hjerteproblemer har mye større reaksjon på CO2 enn andre, og generelt lavere nivå.

http://hyper.ahajournals.org/content/46/4/714.full

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4±1.9 years) and in 26 controls (52.3±1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and “alpha angle” method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7±3.7 to 141.1±4 mm Hg, P<0.05; and from 82.7±3 to 77.8±3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8±3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and controls (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

However, breathing at 6 breaths/min significantly increased the baroreflex sensitivity in hypertensive (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and control subjects (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001;Figure 2).

Hypertensive subjects showed a significantly higher resting respiratory rate (14.55±0.82 versus 11.76±1.00; P<0.05) and a significantly lower CO2-et values compared with control subjects (Figure 3). During controlled breathing at 6/min, there were no significant changes in CO2-et and in Vm. The lack of change in Vm, despite lower breathing rate, was attributable to a significant increase in Vt in hypertensives and controls. Controlled breathing at 15/min induced a marked decrease in CO2-et, particularly in hypertensive subjects, and a marked relative increase in Vm and Vt (Figure 3).

We found that paced breathing, and particularly slow breathing at 6 cycle/min, reduces blood pressure in hypertensive patients. The reduction in blood pressure during slow breathing is associated with an increase in the vagal arm of baroreflex sensitivity, indicating a change in autonomic balance, related to an absolute or relative reduction in sympathetic activity.

This demonstrated that slow breathing is indeed capable of inducing a modification in respiratory and cardiovascular control, and that appropriate training could induce a long-term effect. In subjects with chronic congestive heart failure, a condition known to induce sympathetic and chemoreflex activation, slow breathing induced a reduction in chemoreflexes and an increase in baroreflex.10,25 We have also shown that in these patients, 1-month training in slow breathing could induce prolonged benefits, even in terms of exercise capacity.25

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Understanding the rhythm of breathing: so near yet so far

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Nevner mange interessante prinsipper om pusten og hvordan dens rytmiske egenskaper regulerer kroppsfunksjoner.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671763/

Abstract
Understanding the mechanisms leading from DNA to molecules to neurons to networks to behavior is a major goal for neuroscience, but largely out of reach for many fundamental and interesting behaviors. The neural control of breathing may be a rare exception, presenting a unique opportunity to understand how the nervous system functions normally, how it balances inherent robustness with a highly regulated lability, how it adapts to rapidly and slowly changing conditions, and how particular dysfunctions result in disease. Why can we assert this? First and foremost, the functions of breathing are clearly definable, starting with its regulatory job of maintaining blood (and brain) O2, CO2 and pH; failure is not an option. Breathing is also an essential component of many vocal and emotive behaviors including, e.g., crying, laughing, singing, and sniffing, and must be coordinated with such vital behaviors as suckling and swallowing, even at birth. Second, the regulated variables, O2, CO2 and pH (and temperature in non-primate mammals), are continuous and are readily and precisely quantifiable, as is ventilation itself along with the underlying rhythmic motor activity, i.e., respiratory muscle EMGs. Third, we breathe all the time, except for short breaks as during breath-holding (which can be especially long in diving or hibernating mammals) or sleep apnea. Mammals (including humans) breathe in all behavioral states, e.g., sleep-wake, rest, exercise, panic, or fear, during anesthesia and even following decerebration. Moreover, essential aspects of the neural mechanisms driving breathing, including rhythmicity, are present at levels of reduction down to a medullary slice. Fourth, the relevant circuits exhibit a remarkable combination of extraordinary reliability, starting ex utero with the first air breath – intermittent breathing movements actually start in utero during the third trimester – and continuing for as many as ~109 breaths, as well as considerable lability, responding rapidly (in less than one second) and with considerable precision, over an order of magnitude in metabolic demand for O2 (~0.25 to ~5 liters of O2/min). Breathing does indeed persist! Finally, breathing is genetically determined to work at birth, with a well-defined developmental program underlying a neuroanatomical organization with apparent segregation of function, i.e., rhythmogenesis is separate from motor pattern (burst shape and coordination) generation. Importantly, single human gene mutations can affect breathing, and several neurodegenerative disorders compromise breathing by direct effects on brainstem respiratory circuits (See below).

 

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Insects breathe discontinuously to avoid oxygen toxicity

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Veldig spennende artikkel fra Nature om hvordan insekter puster for å unngå oksygenforgftning.

http://www.nature.com/nature/journal/v433/n7025/abs/nature03106.html

http://www.brocku.ca/researchers/glenn_tattersall/research/discussionpapers/Insects%20breathe%20periodically.pdf

The respiratory organs of terrestrial insects consist of tracheal tubes with external spiracular valves that control gas exchange. Despite their relatively high metabolic rate, many insects have highly discontinuous patterns of gas exchange, including long periods when the spiracles are fully closed. Two explanations have previously been put forward to explain this behaviour: first, that this pattern serves to reduce respiratory water loss1, and second, that the pattern may have initially evolved in underground insects as a way of dealing with hypoxic or hypercapnic conditions2. Here we propose a third possible explanation based on the idea that oxygen is necessary for oxidative metabolism but also acts as a toxic chemical that can cause oxidative damage of tissues even at relatively low concentrations. At physiologically normal partial pressures of CO2, the rate of CO2 diffusion out of the insect respiratory system is slower than the rate of O2 entry; this leads to a build-up of intratracheal CO2. The spiracles must therefore be opened at intervals to rid the insect of accumulated CO2, a process that exposes the tissues to dangerously high levels of O2. We suggest that the cyclical pattern of open and closed spiracles observed in resting insects is a necessary consequence of the need to rid the respiratory system of accumulated CO2, followed by the need to reduce oxygen toxicity.

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Effect of short-term practice of breathing exercises on autonomic functions in normal human volunteers

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Nevner hvordan sakte pust bedrer tilstanden i det autonome nervesystem. De bruker 6 sek inn og 6 sek ut i denne studien, som stimulerer vagusnerven best.

Klikk for å få tilgang til 0807.pdf

Background & objectives: Practice of breathing exercises like pranayama is known to improve autonomic function by changing sympathetic or parasympathetic activity. Therefore, in the present study the effect of breathing exercises on autonomic functions was performed in young volunteers in the age group of 17-19 yr.

Methods: A total of 60 male undergraduate medical students were randomly divided into two groups: slow breathing group (that practiced slow breathing exercise) and the fast breathing group (that practiced fast breathing exercise). The breathing exercises were practiced for a period of three months. Autonomic function tests were performed before and after the practice of breathing exercises.

Results: The increased parasympathetic activity and decreased sympathetic activity were observed in slow breathing group, whereas no significant change in autonomic functions was observed in the fast breathing group.

Interpretation & conclusion: The findings of the present study show that regular practice of slow breathing exercise for three months improves autonomic functions, while practice of fast breathing exercise for the same duration does not affect the autonomic functions.

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You cannot wash off blood with blood: entering the mind through the body.

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The old Zen saying, «You cannot wash off blood with blood,» refers to the conviction that it is difficult to control thoughts with other thoughts.

This saying implies that the way to control the mind is through the body. In Zen meditation (zazen), this is accomplished through the regulation of breathing and posture. The purpose of this article is to examine the relationship between breathing, posture and concentration in one tradition of Zen. I will explore how this relationship may be relevant to the practice of psychotherapy and the healing arts, as well as its implications for future research in these fields.

http://www.ncbi.nlm.nih.gov/pubmed/22742675

http://www.explorejournal.com/article/S1550-8307(12)00076-6/fulltext

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Zazen and Cardiac Variability

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Endelig en studie som nevner noen effekter av Zen meditasjon hvor fokus er på å puste veldig sakte, helt ned til 1 pust/min, bl.a. varme. Viser hvordan HRV påvirkes forskjellig, hvor hos noen økes hjerterytmen betraktelig i små perioder, noe som kan være en effekt av ting som skjer under meditasjonen. Desverre innser de at de burde ha målt kroppstemperatur, CO2, blodsirkulasjon og flere parametere for å se tydeligere hva som skjer i kroppen under så sakte pust.

http://www.psychosomaticmedicine.org/content/61/6/812.long

Figure 3 shows pre-Zazen rest period data from a Zen master (KS). This individual breathed close to 6 breaths/min throughout the rest period. Note the comparative absence of high-frequency cardiac variability and the major low-frequency peak at 0.1 Hz. A very-low-frequency peak also is notable. Note the periodic occurrence of irregularities in cardiac rhythm, superimposed on the sinus rhythm, each with a short R-R interval followed by a long one.

Figure 4 shows the last 5-minute period of Zazen from KS. During this period, respiration rate was slowed to less than 1 breath/min. Cardiac variability at this time occurred almost exclusively within the very-low-frequency range (Figure 4), with a power of more than 13 times greater than at rest.

Feelings of Warmth

The participants’ experiences of warmth during Zazen suggest that the body’s thermoregulatory system may have been affected by practice of this discipline. Subject KS, whose very-low-frequency wave amplitudes particularly increased, specifically remarked on his feelings of increased warmth during Zazen. Perhaps breathing at this very slow rate stimulated sympathetic reflexes that affect oscillations in HR within this very-low-frequency range. The meaning of these observations remains ambiguous, however, because we did not specifically examine thermoregulation, vascular tone, blood pressure, or any index of sympathetic activity. Although increases in HR occurred among some Rinzai subjects, these changes were small and not significant. Additional data are required on vascular and body temperature changes during Zazen and their possible relationship with increased sympathetic arousal and HR very-low-frequency wave activity. Previous observations of experienced Indian Yogis have similarly shown significant increases in body temperature during practice of yoga (58).

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Influence of breathing frequency on the pattern of respiratory sinus arrhythmia and blood pressure: old questions revisited

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Mer om hvordan pustefrekvens styrer HRV, eller RSA (Respiratory Sinusoid Arrythmia) som de kaller det i denne studien. Nevner at 0,1 Hz (6 pust i minuttet) gir bedre HRV enn 0,2 Hz (12 pust i minuttet). Den viser også at 0,1 Hz gir høyest CO2 i utpusten. Og den bekrefter at det er vagus som styrer HRV siden blokkade av et hormon ikke påvirket HRV.

http://ajpheart.physiology.org/content/298/5/H1588

Respiratory sinus arrhythmia (RSA) is classically described as a vagally mediated increase and decrease in heart rate concurrent with inspiration and expiration, respectively. However, although breathing frequency is known to alter this temporal relationship, the precise nature of this phase dependency and its relationship to blood pressure remains unclear. In 16 subjects we systematically examined the temporal relationships between respiration, RSA, and blood pressure by graphically portraying cardiac interval (R-R) and systolic blood pressure (SBP) variations as a function of the respiratory cycle (pattern analysis), during incremental stepwise paced breathing. The principal findings were 1) the time interval between R-R maximum and expiration onset remained the same (∼2.5–3.0 s) irrespective of breathing frequency (P = 0.10), whereas R-R minimum progressively shifted from expiratory onset into midinspiration with slower breathing (P < 0.0001); 2) there is a clear qualitative distinction between pre- versus postinspiratory cardiac acceleration during slow (0.10 Hz) but not fast (0.20 Hz) breathing; 3) the time interval from inspiration onset to SBP minimum (P = 0.16) and from expiration onset to SBP maximum (P = 0.26) remained unchanged across breathing frequencies; 4) SBP maximum and R-R maximum maintained an unchanged temporal alignment of ∼1.1 s irrespective of breathing frequency (P = 0.84), whereas the alignment between SBP minimum and R-R minimum was inconstant (P > 0.0001); and 5) β1-adrenergic blockade did not influence the respiration-RSA relationships or distinct RSA patterns observed during slow breathing, suggesting that temporal dependencies associated with alterations in breathing frequency are unrelated to cardiac sympathetic modulation. Collectively, these results illustrate nonlinear respiration-RSA-blood pressure relationships that may yield new insights to the fundamental mechanism of RSA in humans.

Moreover, despite extensive research, it remains unclear as to whether RSA is driven by respiratory synchronous oscillations in blood pressure via the arterial baroreflex or whether RSA and blood pressure are independently related to respiration via nonbaroreflex mechanisms (4, 14, 17, 28, 41, 46). Clarification of these fundamental relationships is important for our understanding of how autonomic neural outflow is coupled with respiratory activity, especially given that RSA is considered a surrogate of cardiac parasympathetic modulation and is widely applied in the calculation of spontaneous baroreflex sensitivity (7, 24, 34, 36, 37, 39).

Following an initial 5-min stabilization period, paced breathing was commenced at 0.20, 0.15, and 0.10 Hz in randomized order for 5 min each, with 2-min rests between trials.

Table 1.

Effect of breathing frequency on baseline variables

Breathing Frequency, Hz
0.20 0.15 0.10 P
Respiratory sinus arrhythmia amplitude, ms 123 ± 44 167 ± 69∗ 227 ± 92∗† <0.0001
R-R interval, ms 954 ± 83 958 ± 85 976 ± 82 0.17
Systolic blood pressure amplitude, mmHg 6.6 ± 1.8 8.8 ± 3.4∗ 10 ± 3.1∗† <0.0001
Systolic blood pressure, mmHg 120 ± 14 119 ± 13 117 ± 14 0.40
Mean arterial blood pressure, mmHg 79 ± 8.2 78 ± 8.0 79 ± 9.6 0.81
Diastolic blood pressure, mmHg 62 ± 7.1 62 ± 7.2 61 ± 8.5 0.88
End-tidal CO2, % 5.04 ± 0.90 5.11 ± 0.93 5.20 ± 0.94 0.41

  • Values are means ± SD. No differences in R-R interval, systolic blood pressure, mean arterial blood pressure, diastolic blood pressure, or end-tidal CO2 were found across the breathing frequencies.

  • ↵* Statistically significant compared with 0.20 Hz;

  • ↵† statistically significant compared with 0.15 Hz.

The present investigation is the first to apply a pattern analysis approach to characterize nonlinearities in the temporal relationships between respiration, RSA, and blood pressure within the boundaries of the respiratory cycle. Under the conditions of this study the five major findings are: 1) the time interval between R-R maximum and expiration onset remained the same irrespective of breathing frequency, whereas R-R minimum progressively shifted from expiratory onset into midinspiration with slower breathing; 2) two qualitatively distinct stages of cardiac acceleration during slow 0.10-Hz breathing were observed in most subjects; 3) both the time intervals between inspiration onset and SBP minimum and between expiration onset and SBP maximum were unchanged by breathing frequency; 4) SBP maximum and R-R maximum maintained a fixed temporal alignment irrespective of breathing frequency, whereas, in contrast, the alignment between SBP minimum and R-R minimum varied according to breathing frequency; and 5) β1-adrenergic blockade did not influence the respiration-RSA relationships or distinct RSA patterns observed during slow breathing.

Finally, consistent with the established literature, we observed a clear relationship between breathing frequency and RSA amplitude (11, 23, 45, 49). In this study 0.10-Hz breathing was associated with a ∼1.8-fold higher RSA amplitude compared with 0.20-Hz breathing. This is most likely due to breathing frequency coinciding with, and thus significantly augmenting, low frequency R-R interval fluctuations. The mechanism(s) behind this resonance phenomenon is unclear, but one proposal is that the augmentation of cardiovascular oscillations associated with slow breathing is due to global enhancement of arterial baroreflex sensitivity (7).

Conclusion

In summary, this study revealed several previously undescribed nonlinearities in respiration-RSA-blood pressure relationships in conscious humans. In contrast to prior studies, we found R-R minimum was not temporally aligned to expiration, beginning in late inspiration with slower breathing. Similarly, the onset of R-R maximum was not fixed to inspiratory onset but occurred in late expiration at slower breathing frequiencies. We also found that R-R maximum consistently occured ∼2.5–3.0 s following expiratory onset irrespective of breathing frequency. We observed two qualitatively distinct stages of cardiac acceleration during slow 0.10-Hz breathing, whereby the rate of cardiac acceleration occurring before inspiration was consistently less than the rate of cardiac acceleration following inspiratory onset, which to the best of our knowledge has not previously been described. Since these temporal dependencies were unaltered by selective β1-adrenergic blockade, they are most likely due to vagally mediated mechanisms. Furthermore, SBP maximum and R-R maximum maintained a temporal alignment of ∼1.1 s irrespective of breathing frequency whereas the delay between SBP minimum and R-R minimum became longer with slower breathing. These results demonstrate that the application of pattern analysis to the study of heart rate and blood pressure variability has potential to yield new insights into fundamental relationships between breathing and autonomic regulation of cardiovascular function.

 

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Relative timing of inspiration and expiration affects respiratory sinus arrhythmia.

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Nevner at det er 3 variabler som styrer hva som gir høyest HRV: 1. pustefrekvens. 2. mengeden luft per pust. 3. forholdet mellom lengden av innpust og utpust. Nevner at en rask og tydelig innpust blokkerer vagus.

http://www.ncbi.nlm.nih.gov/pubmed/10901389

1. The effect of a variation in inspiration and expiration times on heart rate variability was studied in 12 healthy subjects (mean age 30+/-6 years; five females). 2. Two 2 min trials of controlled breathing, with either short inspiration followed by long expiration or long inspiration followed by short expiration, were compared. Average expiration/inspiration time ratios were 1.0 and 3.4, respectively. The respiration rate in both trials was approximately 10 cycles/min. 3. In trials with short inspiration followed by long expiration, respiratory sinus arrhythmia (RSA; as measured by mean absolute differences and by the high frequency band) was significantly larger than in trials with long inspiration followed by short expiration. This effect could not be accounted for by differences in respiration rate or respiratory amplitude. The higher RSA during fast/slow respiration is primarily due to a more pronounced phasic heart rate increase during inspiration, indicating that inspiratory vagal blockade is sensitive to the steepness of inspiration. 4. Respiration rate and tidal volume are respiratory variables known to modulate RSA. The results of the present study indicate that RSA can also be modulated by a third respiratory variable, the expiratory/inspiratory time ratio.

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PHASE RELATIONSHIP BETWEEN NORMAL HUMAN RESPIRATION AND BAROREFLEX RESPONSIVENESS

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Nevner hvordan forskjellige pustefrekvenser påvirker det autonome nervesystemet.

http://jp.physoc.org/content/304/1/489.full.pdf+html

1. We studied the influences of phase of respiration and breathing frequency upon human sinus node responses to arterial baroreceptor stimulation.

2. Carotid baroreceptors were stimulated with brief (0.6 sec), moderate (30 mmHg) neck suction during early, mid, and late inspiration or expiratin at usual breathing rates, or, during early inspiration and expiration at breathing rates of 3, 6, 12, and 24 breaths/min.

3. Baroreceptor stimuli applied during early and mid inspiration and late expiration provoked only minor sinus node inhibition; stimuli begun during late inspiration and early expiration provoked maximum sinus node inhibition.

4. At breathing rates of 3, 6 and 12 breaths/min, expiratory baroreflex responses were significantly greater than inspiratory responses; at 24 breaths/min, however, inspiratory and expiratory baroreceptor stimuli produced comparable degrees of sinus node inhibition.

5. Our results delineate an important central biological rhythm in normal man: human baroreflex responsiveness oscillates continuously during normal, quiet respiration. The phase shift of baroreflex responsiveness on respiration suggests that this interaction cannot be ascribed simply to gating synchronous with central inspiratory neurone activity. Regularization of heart rate during rapid breathing is associated with loss of the differential inspiratory-expiratory baroreflex responsiveness which is present at usual breathing rates.