Dette er et svar på en studie hvor de viser at HRV er høyest ved 0.1 Hz (6 pust/min).
http://journal.publications.chestnet.org/article.aspx?articleid=1082860
we determined that the phase relationship between heart rate and respiration was 0° only at a respiratory frequency of approximately 0.1 Hz, in which the target frequency heart rate variability also was highest (Fig 1 ).
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
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.
I medisinsk sammenheng benyttes ofte elektrisk stimuli i øret for å styrke vagusnerven gjennom dens forbindelse til huden i øret. I denne studien viser de at vagus nerven stimuleres best om man synkroniserer stimulien med utpust. Denne kobler altså medisinsk stimuli med pustens stimuli. Men de har ingen oppmerksomhet på mulighetene ved å senke pustefrekvens samtidig.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376238/
Chronic pain disorders such as CPP are in great need of effective, non-pharmacological options for treatment. RAVANS (Respiratory-gated Auricular Vagal Afferent Nerve Stimulation) produced promising anti-nociceptive effects for QST outcomes reflective of the noted hyperalgesia and central sensitization in this patient population. Future studies should evaluate longer-term application of RAVANS to examine its effects on both QST outcomes and clinical pain.
The analgesic mechanisms of VNS have not been fully elucidated, but are likely mediated by afferent (not efferent) input to supraspinal brain regions [16]. Vagal afference is relayed to the nucleus tractus solitarious (NTS) in the medullary brainstem. Importantly, the NTS also receives somatosensory afference via the auricular branch of the vagus (ABV) nerve from specific portions of the auricle [17]. ABV afference is transmitted to both the NTS [17] and the spinal trigeminal nucleus (SpV) [18], by neurons located in the superior (jugular) ganglion of the vagus nerve. Respiration can modulate NTS activity directly (the lungs are innervated by the vagus nerve) and indirectly. In regard to the latter, inspiration increases venous return to the thorax, which increases arterial pressure, and hence vagal (and glossopharyngeal n.) afference to the NTS via aortic and carotid baroreceptors, respectively [19]. The NTS then inhibits efferent vagal outflow to the heart [20, 21], leading to a transient inspiratory tachycardia with every breath. This feedback loop is termed “respiratory sinus arrhythmia” [22]. Hence, the dorsal medullary vagal system operates in tune with respiration, and we propose that supplying vagal afferent stimulation gated to the exhalation phase of respiration (i.e. when thoracic baroreceptor afference does not enter the NTS), will optimize t-VNS therapy (see Figure 1 for schematic). Furthermore, such intermittent, irregular stimulation (i.e., varying with respiration) will also mitigate classical neuronal adaptation/accomodation, which can occur with continuous stimulation of NTS neurons [23].
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
Nevner at 6 pust i minuttet gir beste respons på HRV og vagusnerven. I tillegg til å dempe blodtrykk markant. Studien ga disse resultatene med en bare 4 minutters pustesession.
http://circ.ahajournals.org/content/105/2/143.full
Background— It is well established that a depressed baroreflex sensitivity may adversely influence the prognosis in patients with chronic heart failure (CHF) and in those with previous myocardial infarction.
Methods and Results— We tested whether a slow breathing rate (6 breaths/min) could modify the baroreflex sensitivity in 81 patients with stable (2 weeks) CHF (age, 58±1 years; NYHA classes I [6 patients], II [33], III [27], and IV [15]) and in 21 controls. Slow breathing induced highly significant increases in baroreflex sensitivity, both in controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) and in CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025), which correlated with the value obtained during spontaneous breathing (r=+0.202, P=0.047). In addition, systolic and diastolic blood pressure decreased in CHF patients (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02).
Conclusions— These data suggest that in patients with CHF, slow breathing, in addition to improving oxygen saturation and exercise tolerance as has been previously shown, may be beneficial by increasing baroreflex sensitivity.
Breathing at 6 breaths/min, compared with spontaneous breathing, slightly increased overall spontaneous fluctuations in RR interval, reduced fluctuations in blood pressure, and significantly increased the baroreflex sensitivity in both CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025) and controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) (Figure 1).
The slow breathing rate in the CHF group also produced an increase in mean RR interval of 20 ms and a decrease in both systolic and diastolic blood pressure (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02) (Figure 2).
Elektrisk stimuli av vagusnerven er en effektiv behandling ved blodforgiftning, i mus.
http://www.ncbi.nlm.nih.gov/pubmed/17901837
Abstract
OBJECTIVE:
Electrical vagus nerve stimulation inhibits proinflammatory cytokine production and prevents shock during lethal systemic inflammation through an alpha7 nicotinic acetylcholine receptor (alpha7nAChR)-dependent pathway to the spleen, termed the cholinergic anti-inflammatory pathway. Pharmacologic alpha7nAChR agonists inhibit production of the critical proinflammatory mediator high mobility group box 1 (HMGB1) and rescue mice from lethal polymicrobial sepsis. Here we developed a method of transcutaneous mechanical vagus nerve stimulation and then investigated whether this therapy can protect mice against sepsis lethality.
DESIGN:
Prospective, randomized study.
SETTING:
Institute-based research laboratory.
SUBJECTS:
Male BALB/c mice.
INTERVENTIONS:
Mice received lipopolysaccharide to induce lethal endotoxemia or underwent cecal ligation and puncture to induce polymicrobial sepsis. Mice were then randomized to receive electrical, transcutaneous, or sham vagus nerve stimulation and were followed for survival or euthanized at predetermined time points for cytokine analysis.
MEASUREMENTS AND MAIN RESULTS:
Transcutaneous vagus nerve stimulation dose-dependently reduced systemic tumor necrosis factor levels during lethal endotoxemia. Treatment with transcutaneous vagus nerve stimulation inhibited HMGB1 levels and improved survival in mice with polymicrobial sepsis, even when administered 24 hrs after the onset of disease.
CONCLUSIONS:
Transcutaneous vagus nerve stimulation is an efficacious treatment for mice with lethal endotoxemia or polymicrobial sepsis.
Mer om vagusnerven og betennelsesdemping
http://www.ncbi.nlm.nih.gov/pubmed/22913335
Abstract
BACKGROUND:
The immune system protects the host against dangerous pathogens and toxins. The central nervous system is charged with monitoring and coordinating appropriate responses to internal and external stimuli. The inflammatory reflex sits at the crossroads of these crucial homeostatic systems. This review highlights how the vagus nerve-mediated inflammatory reflex facilitates rapid and specific exchange of information between the nervous and immune systems to prevent tissue injury and infection.
METHODS:
Review of the pertinent English-language literature. Nearly two decades of research has elucidated some of the essential anatomic, physiologic, and molecular connections of the inflammatory reflex. The original descriptions of how these key components contribute to afferent and efferent anti-inflammatory vagus nerve signaling are summarized.
RESULTS:
The central nervous system recognizes peripheral inflammation via afferent vagus nerve signaling. The brain can attenuate peripheral innate immune responses, including pro-inflammatory cytokine production, leukocyte recruitment, and nuclear factor kappa β activation via α7-nicotinic acetylcholine receptor subunit-dependent, T-lymphocyte-dependent, vagus nerve signaling to spleen. This efferent arm of the inflammatory reflex is referred to as the «cholinergic anti-inflammatory pathway.» Activation of this pathway via vagus nerve stimulation or pharmacologic α7 agonists prevents tissue injury in multiple models of systemic inflammation, shock, and sepsis.
CONCLUSIONS:
The vagus nerve-mediated inflammatory reflex is a powerful ally in the fight against lethal tissue damage after injury and infection. Further studies will help translate the beneficial effects of this pathway into clinical use for our surgical patients.
Veldig spennende studie som nevner at HRV trening av pusten har langtids virkninger på hjerte/kar sykdommer og at det aktiverer nevroplastisitet, altså vari endring i nervesystemet. Bekrefter at pustefrekvensen på 6x /min (5 sek inn, 5 sek ut), gir en opptrening vagusnerven. Viser også at man får effekt uten biofeedback, men nervesystemet resonderer bedre med biofeedback.
http://www.ncbi.nlm.nih.gov/pubmed/14508023
http://www.psychosomaticmedicine.org/content/65/5/796.long
Abstract
OBJECTIVE: We evaluated heart rate variability biofeedback as a method for increasing vagal baroreflex gain and improving pulmonary function among 54 healthy adults.
METHODS: We compared 10 sessions of biofeedback training with an uninstructed control. Cognitive and physiological effects were measured in four of the sessions.
RESULTS: We found acute increases in low-frequency and total spectrum heart rate variability, and in vagal baroreflex gain, correlated with slow breathing during biofeedback periods. Increased baseline baroreflex gain also occurred across sessions in the biofeedback group, independent of respiratory changes, and peak expiratory flow increased in this group, independently of cardiovascular changes. Biofeedback was accompanied by fewer adverse relaxation side effects than the control condition.
CONCLUSIONS: Heart rate variability biofeedback had strong long-term influences on resting baroreflex gain and pulmonary function. It should be examined as a method for treating cardiovascular and pulmonary diseases. Also, this study demonstrates neuroplasticity of the baroreflex.
The resonant HRV frequency usually is ∼0.1 Hz (6 cycles/min). At this frequency, we previously found that HR and BP oscillate 180° out of phase (20), while HR and respiration oscillate in phase with each other (0° phase relationship, with inhalation coinciding with HR accelerations and exhalation with decelerations). Thus, when people breathe at their resonant frequency, respiratory effects on HRV stimulate baroreflex effects (ie, as the individual inhales, HR rises, BP falls, and the consequent baroreflex response produces a further increase in HR, with corresponding effects during exhalation). The consequent resonance effects produce very large increases in both HRV and baroreflex gain, which can be obtained only when subjects try to increase HRV at this particular frequency (20).
Biofeedback acutely increased both HRV and baroreflex gain, and chronically increased baroreflex gain and peak expiratory flow even among healthy individuals, in whom these measures ordinarily are thought to be stable. Other interventions known to increase baroreflex gain, including β-adrenergic blockade (30) and exercise training (31), also prevent sudden death in high-risk populations. Further research may show that HRV biofeedback training may have similar salutary effects, without the side effects that medication often causes.
The acute baroreflex effects are consistent with our hypothesis that stimulation of HRV at its resonant frequency by respiratory activity involves amplification of the vagal baroreflex response, and that this “exercises” the baroreflex.
However, the cumulative changes in baroreflex gain, both within and, more importantly, across sessions, were not simple effects of slow breathing. The effects of biofeedback on baroreflex gain, both within and between sessions, remained significant, after factoring out the effects of respiration rate. Thus, although breathing at participants’ resonant frequencies produced immediate baroreflex augmentation, over time (both within individual sessions and over weeks of practice) the baroreflex became intrinsically more responsive, an effect that no longer depended on breathing rate and volume. Thus, the intrinsic resting baroreflex increased.
Verkstedet Bodywork & Breathing System 