Stikkordarkiv: Pustemønster

A CLASSIFICATION-BASED COGNITIVE FUNCTIONAL APPROACH FOR THE MANAGEMENT OF BACK PAIN

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Denne beskriver et ganske så komplett opplegg for behandling og undervisning av klienter med nesten alle typer muskel og leddplager.

Klikk for å få tilgang til OSullivanIFOMPT-Oct2012.pdf

Pathoanatomical factors: F.eks. funn på røntgen og MRI, som spiller liten rolle i kroniske muskel og leddplager.

Physical factors: muskelspenning og bevegelsesmønster endres ved smertetilstander. F.eks. kjermuskulatur spenner seg mer i bevegelser hos smertepasienter.

Lifestyle factors: interessant at mat og kosthold er det eneste av livsstilsfaktorer som ikke nevnes på denne listen. Ellers er trening, stress, søvn, røyk, overvekt, m.m. med.

Cognitive and psychosocial factors: angst, depresjon, frykt, katastrofering, og særlig ideen om at (f.eks.) ryggen må beskyttes pga smertene.

Social factors: trivsel i jobb, familie, forhold, og livssituasjon.

Neurophysiological factors: endringer i hjernen, som f.eks. mindre går materie, økt hjerneaktivitet i hvile, endres kroppsbilde, mindre nedregulering av smerte.

Individual factors: mål med behandling, forventninger, grunnleggende helsekunnskap, m.m.

Genetic factors: Visse gener gir økt disponering for smertetilstander.

Jeg likte spesielt dette sitatet:

Manual therapy is only used as a window of opportunity to change behaviors where movement impairments are present.

Systemic inflammation impairs respiratory chemoreflexes and plasticity

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Denne studien beskriver hvordan systemisk betennelse påvirker pustefunksjonen og gjør at det blir vanskeligere å endre pustemønser, f.eks. å gjøre pusteøvelser, eller å tilpasse pusten til aktivitetsnivå. Spesielt den kjemiske og motoriske delen av pustefysiologien blir dårligere. Noe som viser seg i laver CO2 sensitivitet (kjemisk) og svakere pustemuskler (Motorisk).

Nevner spesielt at det er mikroglia celler i CNS som påvirkes av betennelse, og som kan oppretthodle betennelse siden de sender ut cytokiner, m.m. Astrosytter kan også bidra mye siden de aktiverer NFkB. Den gode nyheten her er at økt CO2 nedregulerer NFkB. TLR-4 (Toll-like receptor) aktiveres av patogener og problemer i cellene, og aktiverer NFkB, og nedreguleres av økt CO2.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172820/

Abstract

Many lung and central nervous system disorders require robust and appropriate physiological responses to assure adequate breathing. Factors undermining the efficacy of ventilatory control will diminish the ability to compensate for pathology, threatening life itself. Although most of these same disorders are associated with systemic and/or neuroinflammation, and inflammation affects neural function, we are only beginning to understand interactions between inflammation and any aspect of ventilatory control (e.g. sensory receptors, rhythm generation, chemoreflexes, plasticity). Here we review available evidence, and present limited new data suggesting that systemic (or neural) inflammation impairs two key elements of ventilatory control: chemoreflexes and respiratory motor (vs. sensory) plasticity. Achieving an understanding of mechanisms whereby inflammation undermines ventilatory control is fundamental since inflammation may diminish the capacity for natural, compensatory responses during pathological states, and the ability to harness respiratory plasticity as a therapeutic strategy in the treatment of devastating breathing disorders, such as during cervical spinal injury or motor neuron disease.

Most lung and CNS disorders are associated with systemic and/or neural inflammation, including chronic lung diseases (Stockley, 2009), traumatic, ischemic and degenerative neural disorders (Teeling and Perry, 2009) and obstructive sleep apnea.

Systemic inflammation affects sensory receptors that modulate breathing, but can also trigger inflammatory responses in the central nervous system (CNS) through complex mechanisms. The primary CNS cells affected during systemic inflammation are microglia, the resident immune cells of the CNS, and astrocytes (Lehnardt, 2010).

Even when in their “resting state,” microglia are highly active, surveying their environment (Raivich, 2005,Parkhurst and Gan, 2010). When confronted with pathological conditions, such as neuronal injury/degeneration or bacterial/viral/fungal infection, they become “activated,” shifting from a stellate, ramified phenotype to an amoeboid shape (Kreutzberg, 1996). Activated microglia can be phagocytic, or they can release toxic and protective factors, including cytokines, prostaglandins, nitric oxide or neurotrophic factors (e.g. BDNF) (Kreutzberg, 1996, Graeber, 2010). Despite the importance of microglia in immune function, they are diffuse in the CNS (~70-90% of CNS cells are glia; microglia are ~5-10% of those cells).

Astrocytes, on the other hand, contribute to the overall inflammatory response since they release cytokines, triggering nuclear factor-kappa B (NFκB) signaling elsewhere in the CNS. Further, they express many TLRs, including TLR-4, capable of eliciting an inflammatory response (Li and Stark, 2002, Farina et al., 2007,Johann et al., 2008). Given their relative abundance, astrocytes may play a key role in CNS inflammatory responses.

TLR-4 receptors are cytokine family receptors that activate transcription factors, such as NFκB (Lu et al., 2008). NFκB regulates the expression of many inflammatory genes, including: IL-1β, -6 and -18, TNFα, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) (Ricciardolo et al., 2004, Nam, 2006). Endogenous molecules known to activate TLR-4 receptors include (but are not limited to) heat shock proteins (specifically HSP60, Ohashi et al., 2000, Lehnardt et al., 2008), fibrinogen, surfactant protein-A, fibronectin extra domain A, heparin sulfate, soluble hyaluronan, β-defensin 2 and HMGB1 (Chen et al., 2007).

The role of inflammation (and specifically microglia) in chronic pain has been studied extensively (reviewed in Woolf and Salter, 2000, Trang et al., 2006, Mika, 2008, Abbadie et al., 2009, Baumbauer et al., 2009). A remarkable story has emerged, demonstrating the interplay between neurons, microglia, inflammation and plasticity in this spinal sensory system. In short, inflammation induces both peripheral and central sensitization, leading to allodynia (hypersensitivity to otherwise non-painful stimuli) and hyperalgesia (exaggerated or prolonged responses to a noxious stimulus) (Mika, 2008).

An important aspect of ventilatory control susceptible to inflammatory modulation is the chemoreflex control of breathing. Chemoreflexes are critical for maintaining homeostasis of arterial blood gases viaclassical negative feedback (Mitchell et al., 2009), or acting as “teachers” that induce plasticity in the respiratory control system (Mitchell and Johnson, 2003). Major chemoreflexes include the hypoxic (Powell et al., 1998) and hypercapnic ventilatory responses (Nattie, 2001), arising predominantly from the peripheral arterial and central chemoreceptors (Lahiri and Forster, 2003).

To date, no studies have reported the impact of systemic inflammation on hypercapnic responses. However, increased CO2 suppresses NFκB activation, possibly suppressing inflammatory gene expression (Taylor and Cummins, 2011). In fact, hypercapnia has been used to treat ischemia/reperfusion injury to decrease inflammation and reduce lung tissue damage (Laffey et al., 2000, O’Croinin et al., 2005, Curley et al., 2010, Li et al., 2010).

Further work concerning the influence of systemic inflammation on hypercapnic ventilatory responses is warranted, particularly since impaired CO2 chemoreflexes would allow greater hypercapnia and minimize the ongoing inflammation; in this sense, impaired hypercapnic ventilatory responses during inflammation may (in part) be adaptive.

Morning attenuation in cerebrovascular CO2 reactivity in healthy humans is associated with a lowered cerebral oxygenation and an augmented ventilatory response to CO2

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Denne beskriver hvordan blodkarenes respons på CO2 er dårligere om morgenen, og det er derfor det skjer flere slag og slikt om morgenen. Den nevner mange interessante prinsipper. Bl.a. at lavere vasomotor respons (på CO2) gir mindre oksygen til hjernen. Og at i opptil 20 sekunder etter en 20 sekunder holdning av pust (etter utpust) øker fortsatt oksygenmengden og blodgjennomstrømningen i hjernen. Nevner også at siden blodkarene i hjernen reagerer dårligere på CO2 om morgenen blir det lett at pusten over- eller underkompenserer, så pustemønsteret blir uregelmessig om morgenen. Spesielt om man har underliggende faremomenter som hjerte/karsykdommer.

http://jap.physiology.org/content/102/5/1891

 

Furthermore, our results suggest that morning cerebral tissue oxygenation might be reduced as a result of a decreased cerebrovascular responsiveness to CO2 or other factors, leading to a higher level of desaturation.

Our data indicate that the cerebrovascular reactivity to CO2 in healthy subjects is significantly reduced in the morning and is strongly associated with an augmented ventilatory response to CO2. It is likely that this reduction in MCAV CO2 reactivity, by reducing blood flow through medullary respiratory control centers, increases both the arterial-brain tissue PCO2 difference and the H+ concentration presented to the central chemoreceptor(s) (11, 44). In effect, it appears the brain tissue is more susceptible in the morning to changes in arterial PCO2, which could increase the likelihood of ventilatory overshoots and undershoots.

However, as was the case with the hypercapnic challenge, subjects holding their breath in the morning experienced a significantly blunted increase in MCAV compared with evening, likely a result of a reduced cerebrovascular responsiveness to CO2.

In conclusion, our results suggest that early morning reductions in cerebrovascular CO2 reactivity strongly influence the magnitude of the ventilatory response to CO2. This may have significant implications for breathing stability, increasing the chances of periodic breathing in the morning in patients with additional risk factors. The early morning reduction in cerebral oxygenation with hypercapnic challenge, mild hypoxemia, or during apnea may be a contributing factor in the high prevalence of early morning stroke. Whether differences in the responses of CBF, oxygenation, or V̇E to CO2challenge are associated with other risk factors for stroke, such as gender or age, remains to be elucidated.

Respiratory effects on experimental heat pain and cardiac activity.

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Her viser de hvordan HRV pust (6 bpm) resuserer smerte og påvirker hjerterytmen. De sammenlignet med hvordan distraksjon reduserer smerte of fant at pusten fungerer litt bedre. De nevner at pustens smertereduserende effekt virker gjennom andre mekanismer enn distraksjon.

http://www.ncbi.nlm.nih.gov/pubmed/19671085

http://www.researchgate.net/publication/26732610_Respiratory_effects_on_experimental_heat_pain_and_cardiac_activity

Abstract

OBJECTIVE:

Slow deep breathing has been proposed as an effective method to decrease pain. However, experimental studies conducted to validate this claim have not been carried out.

DESIGN:

We measured thermal pain threshold and tolerance scores from 20 healthy adults during five different conditions, namely, during natural breathing (baseline), slow deep breathing (6 breaths/minute), rapid breathing (16 breaths/minute), distraction (video game), and heart rate (HR) biofeedback. We measured respiration (rate and depth) and HR variability from the electrocardiogram (ECG) output and analyzed the effects of respiration on pain and HR variability using time and frequency domain measures of the ECG.

RESULTS:

Compared with baseline, thermal pain threshold was significantly higher during slow deep breathing (P = 0.002), HR biofeedback (P < 0.001), and distraction (P = 0.006), whereas thermal pain tolerance was significantly higher during slow deep breathing (P = 0.003) and HR biofeedback (P < 0.001). Compared with baseline, only slow deep breathing and HR biofeedback conditions had an effect on cardiac activity. These conditions increased the amplitude of vagal cardiac markers (peak-to-valley, P < 0.001) as well as low frequency power (P < 0.001).

CONCLUSION:

Slow deep breathing and HR biofeedback had analgesic effects and increased vagal cardiac activity. Distraction also produced analgesia; however, these effects were not accompanied by concomitant changes in cardiac activity. This suggests that the neurobiology underlying respiratory-induced analgesia and distraction are different. Clinical implications are discussed, as are the possible cardiorespiratory processes responsible for mediating breathing-induced analgesia.

 

In conclusion, this is the first experimental study to systematically control for breathing frequency and distraction effects and to show that respiratory-induced analgesia reduces pain in healthy subjects. The combined cardiorespiratory and antinociceptive effects observed during slow deep breathing suggest that the modulation of HR and pain share a common neurophysiological pathway. Our results, therefore, support the use of slow deep breathing as an inexpensive and valuable adjunct to the current treatment of pain.

Respiration-induced hypoalgesia: exploration of potential mechanisms.

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Denne beskriver hvordan sakte pust demper smerteopplevelse. Men i denne studen puster de kun 50% fra normal pustefrekvens. Om man puster 16 pust i minuttet blir dette 8 pust i minuttet. Det er fortsatt litt igjen til 6 pust i minuttet (autonom pust) som gir maksimal effekt på vagus nerven.

http://www.ncbi.nlm.nih.gov/pubmed/22770894

Respiration-Induced Hypoalgesia: Exploration of Potential …

The present study asked 30 healthy participants (M(age) = 21 years, M(education) = 15 years, 80% white non-Hispanic) to breathe at normal, slow (50% normal), and fast (125% normal) rates while constant-intensity, suprathreshold electric stimulations were delivered to the sural nerve to elicit pain and the nociceptive flexion reflex (NFR, a measure of spinal nociception).

Slow breathing reduced pain relative to normal and fast breathing. This respiration-induced hypoalgesia does not appear to be due to gating of spinal nociception or changes in parasympathetic activity.

Breathing at a rate of 5.5 breaths per minute with equal inhalation-to-exhalation ratio increases heart rate variability.

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Denne nevner at 5.5 pust i minuttet gir best HRV, og at innpust og utpust skal være lik lengde.

http://www.ncbi.nlm.nih.gov/pubmed/24380741

Abstract

OBJECTIVES:

Prior studies have found that a breathing pattern of 6 or 5.5 breaths per minute (bpm) was associated with greater heart rate variability (HRV) than that of spontaneous breathing rate. However, the effects of combining the breathing rate with the inhalation-to-exhalation ratio (I:E ratio) on HRV indices are inconsistent. This study aimed to examine the differences in HRV indices and subjective feelings of anxiety and relaxation among four different breathing patterns.

METHODS:

Forty-seven healthy college students were recruited for the study, and a Latin square experimental design with a counterbalance in random sequences was applied. Participants were instructed to breathe at two different breathing rates (6 and 5.5 breaths) and two different I:E ratios (5:5 and 4:6). The HRV indices as well as anxiety and relaxation levels were measured at baseline (spontaneous breathing) and for the four different breathing patterns.

RESULTS:

The results revealed that a pattern of 5.5 bpm with an I:E ratio of 5:5 produced a higher NN interval standard deviation and higher low frequency power than the other breathing patterns. Moreover, the four different breathing patterns were associated with significantly increased feeling of relaxation compared with baseline.

CONCLUSION:

The study confirmed that a breathing pattern of 5.5 bpm with an I:E ratio of 5:5 achieved greater HRV than the other breathing patterns. This finding can be applied to HRV biofeedback or breathing training in the future.

 

Behavioural modification of the cholinergic anti-inflammatory response to C-reactive protein in patients with hypertension

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Denne beskriver hvordan regulering av pusten kan påvirke vagus nerven til å dempe betennelser og redusere CRP (en betennelsesmarkør) i blodet.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2012.02523.x/full

Objectives.  A central hypothesis of the cholinergic anti-inflammatory reflex model is that innate immune activity is inhibited by the efferent vagus. We evaluated whether changes in markers of tonic or reflex vagal heart rate modulation following behavioural intervention were associated inversely with changes in high-sensitivity C-reactive protein (hsCRP) or interleukin-6 (IL-6).

Design.  Subjects diagnosed with hypertension (n = 45, age 35–64 years, 53% women) were randomized to an 8-week protocol of behavioural neurocardiac training (with heart rate variability biofeedback) or autogenic relaxation. Assessments before and after intervention included pro-inflammatory factors (hsCRP, IL-6), markers of vagal heart rate modulation [RR high-frequency (HF) power within 0.15–0.40 Hz, baroreflex sensitivity and RR interval], conventional measures of lipoprotein cholesterol and 24-h ambulatory systolic and diastolic blood pressure.

Results.  Changes in hsCRP and IL-6 were not associated with changes in lipoprotein cholesterol or blood pressure. After adjusting for anti-inflammatory drugs and confounding factors, changes in hsCRP related inversely to changes in HF power (β =−0.25±0.1, P = 0.02), baroreflex sensitivity (β = −0.33±0.7, P = 0.04) and RR interval (β = −0.001 ± 0.0004, P = 0.02). Statistically significant relationships were not observed for IL-6.

Conclusions.  Changes in hsCRP were consistent with the inhibitory effect of increased vagal efferent activity on pro-inflammatory factors predicted by the cholinergic anti-inflammatory reflex model. Clinical trials for patients with cardiovascular dysfunction are warranted to assess whether behavioural interventions can contribute independently to the chronic regulation of inflammatory activity and to improved clinical outcomes.

Chronic low-grade inflammation contributes to the development of experimental and clinical hypertension [1–3], and it increases the risk for myocardial infarction, stroke and sudden cardiac death [4]. C-reactive protein (CRP) is an established index of systemic inflammation. It is produced chiefly by hepatocytes under the regulation of a cascade of pro-inflammatory cytokines [tumour necrosis factor-α (TNF-α), interleukin-1ß [IL-1ß] and IL-6] that are expressed in response to conditions that include vascular injury and infection. In addition, CRP is produced by human coronary artery smooth muscle cells following exposure to pro-inflammatory cytokines [5], which suggests that it may contribute independently to endothelial dysfunction and atherogenesis [6].

Clinical trials that have attempted to modify vagal efferent activity by means of aerobic exercise [17, 18], resistance exercise [19] or device-guided vagal nerve stimulation [20–22] have yet to demonstrate consequent reduction in pro-inflammatory activity that is independent of confounding factors such as anti-inflammatory medications.

Subjects received four weekly and two biweekly 1-h sessions of behavioural neurocardiac training or autogenic relaxation, as described previously [23]. Home practice sessions complemented the laboratory-based training. All sessions began with a 10-min review of cognitive-behavioural guidelines for managing daily stress [25].

At the completion of each task, subjects were trained to cognitively disengage from negative or aroused affect and to focus attention on slowing respiration (within their comfort zone) to 10-s cycles (6 breaths min−1). During each countering exercise, subjects were guided by the use of biofeedback to increase RR spectral power at approximately 0.1 Hz, as shown on a biofeedback display of the RR power spectrum (0.003–0.5 Hz) and breaths min−1.

The major finding of this study is that following an 8-week protocol of behavioural neurocardiac training or autogenic relaxation amongst patients with hypertension, change in hsCRP was associated independently and inversely with changes in tonic and reflex vagal heart rate modulation as measured by RR high-frequency power (ms2 per Hz), baroreflex sensitivity (ms per mmHg) and lengthening of the RR interval (ms). A statistical trend in the data suggested a similar inverse association between changes in IL-6 and RR high-frequency power.

A central hypothesis of the cholinergic anti-inflammatory reflex model is that the innate immune response is regulated, in part, by rapid and localized efferent activity of the vagus nerve. Previous reviews have identified the functional anatomy and neural mechanisms of this model [10, 29, 30]. In brief, efferent fibres of the vagus nerve comprise a neural anti-inflammatory pathway that culminates in the release of acetylcholine in proximate sites where pro-inflammatory factors have been expressed. Acetylcholine has been shown to bind to subunit α7 of nicotinic acetylcholine receptors on cytokine-producing immune cells [30]. This inhibits the activation of NF-κB and the subsequent expression of a pro-inflammatory cascade that includes TNF-α, IL-6 and CRP [10].

To our knowledge, the present proof of principle study involving hypertensive patients provides the most direct evaluation of whether augmentation of tonic or reflex vagal heart rate modulation, in this instance by a behavioural intervention, attenuates independently pro-inflammatory activity as assessed by hsCRP and IL-6. It is noteworthy that the present findings were observed following only modest changes in markers of vagal HR modulation. Previous behavioural trials of heart rate variability biofeedback or relaxation [32–34] have reported a small but statistically significant increase in vagal HR modulation. Similarly, behavioural training is associated with a modest, but statistically significant decrease in proinflammatory factors, including hsCRP and IL-6 [35], although heart rate variability biofeedback failed to reduce other inflammatory factors following experimental administration of an endotoxin (lipopolysaccharide) [36].

In sum, the present findings support the model of a cholinergic anti-inflammatory reflex when pro-inflammatory activity is measured by hsCRP. Clinical trial evidence has demonstrated that behavioural interventions can significantly augment vagal heart rate modulation or cardiovagal baroreflex gain through the use of relaxation training and biofeedback [32–34].

Kritikk til polyvagal teorien og mye viktig om vagus-pust forbindelsen

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Svært viktig studie som forteller om alle aspekter ved vagus nervens og pustens relasjon. Nevner at det ikke er en direkte relasjon, og at det blir ikke riktig å si at RSA/HRV er en direkte intdikasjon på vagus nervens funksjon. Mange faktorer spiller inn. Sier også at vagus fyrer av like mye, men når pustefrekvensen synker blir signalene sterkere i løpet av den lange utpusten. Nevner også at i individet er det tydelig sammenheng mellom pust og HRV, men mellom forskjellige individer er det store forskjeller. Nevner også at vagus nerven fyrer av når CO2 øker for øke gassutvekslingen mellom blod og luft.

http://www.ncbi.nlm.nih.gov/pubmed/17081672

Mer fra studien er her.

Abstract

Respiratory sinus arrhythmia (RSA, or high-frequency heart-rate variability) is frequently employed as an index of cardiac vagal tone or even believed to be a direct measure of vagal tone. However, there are many significant caveats regarding vagal tone interpretation:

1. Respiratory parameters can confound relations between RSA and cardiac vagal tone.

2. Although intraindividual relations between RSA and cardiac vagal control are often strong, interindividual associations may be modest.

3. RSA measurement is profoundly influenced by concurrent levels of momentary physical activity, which can bias estimation of individual differences in vagal tone.

4. RSA magnitude is affected by beta-adrenergic tone.

5. RSA and cardiac vagal tone can dissociate under certain circumstances.

6. The polyvagal theory contains evolution-based speculations that relate RSA, vagal tone and behavioral phenomena.

We present evidence that the polyvagal theory does not accurately depict evolution of vagal control of heart-rate variability, and that it ignores the phenomenon of cardiac aliasing and disregards the evolution of a functional role for vagal control of the heart, from cardiorespiratory synchrony in fish to RSA in mammals. Unawareness of these issues can lead to misinterpretation of cardiovascular autonomic mechanisms. On the other hand, RSA has been shown to often provide a reasonable reflection of cardiac vagal tone when the above-mentioned complexities are considered. Finally, a recent hypothesis is expanded upon, in which RSA plays a primary role in regulation of energy exchange by means of synchronizing respiratory and cardiovascular processes during metabolic and behavioral change.

Autonomic system modification in zen practitioners

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Nevner mye om hvordan pustefrekvens påvirker HRV og  andre faktorer. Og spesielt hvordan dette endrer den normale pusten på lang sikt.

http://www.ncbi.nlm.nih.gov/pubmed/24469560

http://www.indianjmedsci.org/article.asp?issn=0019-5359;year=2013;volume=67;issue=7;spage=161;epage=167;aulast=Fiorentini

Background: Meditation in its various forms is a traditional exercise with a potential benefit on well-being and health. On a psychosomatic level these exercises seem to improve the salutogenetic potential in man.Especially the cardiorespiratory interaction seems to play an important role since most meditation techniques make use of special low frequency breathing patterns regardless of whether they result from a deliberate guidance of breathing or other mechanisms, for example, the recitation of specific verse. During the different exercises of Zen meditation the depth and the duration of each respiratory cycle is determined only by the process of breathing. Respiratory manoeuvres during Zazen meditation may produce HR variability changes similar to those produces during biofeedback.Recognition that the respiratory sinus arrhythmia (RSA) was mediated by efferent vagal activity acting on the sinus node led investigators to attempt to quantify the fluctuations in R-R intervals that were related to breathing. Materials and Methods: Nine Zen practitioners with five years of experience took part in the study. Autonomic nervous system function was evaluated by heart rate variability (HRV) analysis during 24-hours ECG recording during zen meditation and at rest. Results: The data of this small observational study confirm that ZaZen breathing falls within the range of low frequency HR spectral bands. Our data suggest that the modification of HR spectral power remained also in normal day when the subject have a normal breathing. Conclusion: We suggest that the changes in the breathing rate might modify the chemoreflex and the continuous practice in slow breathing can reduce chemoreflex. This change in the automonic control of respiration can be permanent with a resetting of endogenous circulatory rhythms.

Figure 1: Power spectrum analysis of heart rate variability during zen meditation

Figure 2: Power spectrum analysis of heart rate variability to rest

In conclusion, repeated training to slow down breathing reduces the spontaneous breathing rate with long term effects on the cardiovascular control mechanisms. Indeed, when respiration slows to about 6 cycles/min, as in Zen practitioners and in the frequency range of the spontaneous LF oscillation, the cardiovascular fluctuations become maximal. The changes in the breathing rate might modify the chemoreflex and the continuous practice in slow breathing can reduce chemoreflex. This change in the autonomic control of respiration can be permanent with a resetting of endogenous circulatory rhythms.

Relationship between dysfunctional breathing patterns and ability to achieve target heart rate variability with features of «coherence» during biofeedback.

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Nevner hvordan en topp-pust relateres til lav HRV og problemer i hjerte/kar systemet.

http://www.ncbi.nlm.nih.gov/pubmed/22164811

Abstract

BACKGROUND:

Heart rate variability (HRV) biofeedback is a self-regulation strategy used to improve conditions including asthma, stress, hypertension, and chronic obstructive pulmonary disease. Respiratory muscle function affects hemodynamic influences on respiratory sinus arrhythmia (RSA), and HRV and HRV-biofeedback protocols often include slow abdominal breathing to achieve physiologically optimal patterns of HRV with power spectral distribution concentrated around the 0.1-Hz frequency and large amplitude. It is likely that optimal balanced breathing patterns and ability to entrain heart rhythms to breathing reflect physiological efficiency and resilience and that individuals with dysfunctional breathing patterns may have difficulty voluntarily modulating HRV and RSA. The relationship between breathing movement patterns and HRV, however, has not been investigated. This study examines how individuals’ habitual breathing patterns correspond with their ability to optimize HRV and RSA.

METHOD:

Breathing pattern was assessed using the Manual Assessment of Respiratory Motion (MARM) and the Hi Lo manual palpation techniques in 83 people with possible dysfunctional breathing before they attempted HRV biofeedback. Mean respiratory rate was also assessed. Subsequently, participants applied a brief 5-minute biofeedback protocol, involving breathing and positive emotional focus, to achieve HRV patterns proposed to reflect physiological «coherence» and entrainment of heart rhythm oscillations to other oscillating body systems.

RESULTS:

Thoracic-dominant breathing was associated with decreased coherence of HRV (r = -.463, P = .0001). Individuals with paradoxical breathing had the lowest HRV coherence (t(8) = 10.7, P = .001), and the negative relationship between coherence of HRV and extent of thoracic breathing was strongest in this group (r = -.768, P = .03).

CONCLUSION:

Dysfunctional breathing patterns are associated with decreased ability to achieve HRV patterns that reflect cardiorespiratory efficiency and autonomic nervous system balance. This suggests that dysfunctional breathing patterns are not only biomechanically inefficient but also reflect decreased physiological resilience. Breathing assessment using simple manual techniques such as the MARM and Hi Lo may be useful in HRV biofeedback to identify if poor responders require more emphasis on correction of dysfunctional breathing.