Review Article - (2023) Volume 9, Issue 4
Breath training has been reported to be effective in the alleviation of sleep disturbed breathing. Yet, despite the attractiveness of low cost, non-invasive therapies there is limited adoption resulting from perceived lack of supporting clinical data and a sound scientific theory. A multidisciplinary literature review was undertaken covering clinical outcomes, apnea co-morbidities, dysfunctional breathing, neuro-physiology of breathing control, brain neuroplasticity, intermittent hypoxic therapy, Functional Magnetic Resonance Imaging (fMRI), neuromuscular control of upper airway muscles, and anthropology. The results were crosscorrelated to formulate a coherent theory for the efficacy of neuroplastic breath training in the alleviation of sleep disturbances. The analysis suggests that such training should be considered as an adjunct therapy for patient phenotypes presenting elevated ventilatory loop gain.
Sleep apnea • Snoring • Breath training • Dysfunctional breathing • Neurophysiology of breathing • Neuro-plasticity • Intermittent hypoxia
There is some evidence that breath training and regular practice of activities requiring high degrees of breath control may alleviate snoring and other symptoms of sleep apnea [1]. However, until now, use of such treatments has not entered the mainstream of therapies for two main reasons. First, proposed and observed breathing protocols are heterogeneous and have not been extensively tested for clinical efficacy. Second, no clear scientific theory has been proposed that could explain the link between conscious breathing modulation in the waking state and alleviation of sleep apnea. However, in reviewing the scientific literature in several different and seemingly unconnected fields, we suggest that indeed there is sufficient scientific and clinical evidence to support coherent hypotheses regarding potential mechanisms by which breathing training could assist certain patients with sleep apnea.
The impact of sleep apnea
Sleep-Disordered Breathing (SDB) is a classification of sleep abnormalities that includes Obstructive Sleep Apnea (OSA) and Central Sleep Apnea (CSA). OSA is characterized by repeated episodes of events while asleep including apneas (complete airway obstruction lasting at least 10 seconds), hypopneas (partial airway obstruction lasting at least 10 seconds), and respiratory-event-related arousals (lasting less than 10 seconds). These disturbances result in recurring arousals from sleep, sympathetic nervous system activation, and in some cases, hypoxemia. Depending upon varying definitions, the minimum significant frequency of these events may be 5 times-15 times per hour and may occur up to 100 times per hour or more. By far the most common type of SDB is OSA, where mechanical obstruction of the airway occurs due to sleep-related loss of upper airway dilator muscle tone. It is often associated with common physical characteristics such as obesity, retrognathia, and redundant tissue crowding the posterior pharynx. CSA, less frequently seen, is caused by abnormalities in the control of breathing, with episodes of under-ventilation leading to arousals from sleep. Although OSA and CSA are caused by different processes, they occur simultaneously in some individuals. Indeed, even the simplified split between OSA and CSA has come under scrutiny and a more complex categorization of SDB causes based on phenotypical classes is suggested [2].
Current treatments for sleep apnea; Advantages and disadvantages
There are a number of treatment options available for the management of OSA, each associated with various advantages and disadvantages. The most commonly deployed intervention, particularly for moderate or severe OSA, is nasal positive airway pressure, of which Continuous Positive Airway Pressure (CPAP) is the most common version. Controlled administration of pressurized air through a sealed nasal or nasal/oral interface can open the collapsed airway and regularize breathing while asleep, abolishing the airway collapse that leads to SDB and its associated arousals. One improvement to CPAP is Automatic Positive Airway Pressure (APAP). While CPAP has one continuous pressure setting, APAP is able to respond to changing pressure needs by constantly measuring how much resistance is present in breathing. The technology in an APAP machine allows it to remain on a low pressure setting until a change in breathing is detected and more airflow required. Advantages to nasal positive airway pressure devices include easy accessibility, high efficacy and good quality data reporting. Disadvantages include variable and often poor user compliance, inconvenience associated with travel and other lifestyles, and in some cases, poor efficacy. Additionally, the treatment is only effective when it is used – it does not cure the condition. Oral appliances are also commonly utilized for the treatment of OSA. Mandibular Advancement Splints (MAS) advance the mandible, maintaining enhanced airway patency by reducing airway collapse that is caused by the lower jaw drifting posteriorly during sleep. Customized devices administered by trained dental practitioners may be beneficial for selected OSA patients, particularly those with milder forms of the disease. Advantages include portability and convenience. Disadvantages to MAS include variable efficacy, no data reporting, discomfort, and dental side effects. Again, this treatment is non-curative and only effective when used.
Recently devices to improve the tone of the upper airway muscles and tongue to prevent tissues from collapsing into the upper airway have shown some success in improving mild OSA [3]. The regimen of Neuromuscular Electrical Stimulation (NMES) therapy is usage for 20 minutes daily for several weeks, followed with occasional usage to maintain the benefit of the muscle training. Surgical options for SDB are much less frequently deployed for treatment of OSA than in the past. Tonsillectomies can be performed in selected children with good efficacy, but in adults, upper airway procedures have been largely abandoned because they do not result in long-term improvement. Jaw reconfiguration procedures in a small number of carefully selected individuals with severe OSA and retrognathia may be effective, but these are complicated, painful, and expensive procedures. More recently, some patients with significant OSA unable to use nasal positive pressure devices have undergone surgical procedures to implant upper airway hypoglossal nerve stimulators to treat the condition, and while can be effective, it is expensive and has limited application [4]. Anatomically based treatments for obstructive sleep apnoea OSA such as CPAP and MAS often do not completely resolve OSA or, as mentioned above, are poorly tolerated with non-compliance in a significant proportion of patients. In the case of CPAP, the gold standard of OSA treatment, 46% to 83% of patients have been reported to be non-adherent to treatment [5], Compliance from MAS is higher but reduction of the Apnea Hypopnea Index (AHI) is lower and side effects including craniofacial changes can occur [6-8]. These disadvantages have resulted in interest in treatments that address physiological traits found to contribute to instability of breathing control during night-time breathing such as hypersensitivity of the chemoreflex or loop gain, poor responsiveness of upper airway dilating muscles and low arousal threshold during sleep [2,9].
Unstable breathing control
In humans with dysfunctional breathing, automatic breathing control mechanisms that normally preserve respiratory homeostasis with normal breathing rate, volume, rhythm and carbon dioxide levels being maintained, can become chronically disordered [10, 11]. This occurs in part as a result of increases in chemo-receptor sensitivity occurring due to chronic stress, the elevated respiratory drive found in patients with heart disease and chronic respiratory diseases such as asthma and COPDi as well as long term dysregulation of the brain stem and central autonomic networks [12-17]. Abnormalities in physiological indices of breathing control are widespread, triggered by situations that increase ventilation and are sustained during wakefulness and sleep [18, 19]. OSA events may be triggered by one or more of at least four different causes [2].
•In many instances, mechanical restriction of the upper airways is present, particularly in obese individuals.
•These restrictions may be exacerbated by weak upper airway musculature leading to airway collapse while asleep.
•A third cause is a propensity to wake easily, referred to as ‘low arousal threshold’ where disturbances including breathing irregularities may trigger an apnea event.
• A fourth cause is high Loop Gain (LG) in the breathing control system.
The triggers (b, c, and d) each have a probability of about 35% of being present during an OSA episode. Specifically, LG is a parameter that quantifies the stability of the negative feedback chemoreflex or ventilatory control system. The overall LG of this system reflects the ratio of the ventilatory response to the disturbance that triggered the response. When breathing deviates from a state in which ventilatory activity matches metabolic demand, e.g., during hypopnea, ventilation will normally correct blood gas concentrations to re-establish homeostatic levels. This occurs when LG is ≤1. However, if the ventilatory response is disproportionately larger than the disturbance, ventilation will not only correct the disturbance in blood gases but will overshoot. This is more likely to occur when LG>1. In this case the partial pressure of carbon dioxide in arterial blood (PaCO2) will be reduced resulting in hypoventilation, upper airway muscle slackness and a secondary airway obstruction such that respiratory events become self-perpetuating in a vicious circle. The higher LG, the less stable is ventilatory chemoreflex control and the greater the likelihood of SDB. Unstable breathing control can be modeled using standard engineering control loop theory [20], in which there are both ‘controller’ and ‘plant’ components, with a delay time between the two. The system, when functioning correctly maintains a balance between breathing performance and metabolic needs in both sleep and awake modes. The controller senses CO2 and O2 blood gas concentrations from centrally and peripherally located chemo-sensors and determines appropriate stimulus signals taking into account prevailing upper airway geometry. The muscles used for breathing i.e., the plant, are activated to return CO2 and O2 in the blood to normal values. There is an inherent delay before the system can reach equilibrium. Both chemoreceptor sensitivity and the effectiveness of the lungs to alter blood gases reflect controller and plant gain respectively. The product of these is the overall LG of the system. Because there is a circulation delay between when ventilation begins to modify blood gases and when the chemoreceptors sense the change, if the gain of either or both of the controller or the plant are too high, there is potential for ventilatory overshoot producing sustained breathing fluctuations in the system. If LG ≤ 1, these dampen out and stabilize. If LG>1, they will increase in amplitude and instability resulting in a self-perpetuating repetition of apneic or hypopnea events observed in SDB both during sleep and in the wakened state. There are a number of methods for determining the value of LG which can help in determining whether therapies designed to reduce LG might be appropriate. These include using data derived in a polysomnographic sleep study, modifying CPAP pressures, and monitoring breath-holding parameters in the awakened state [21-24].
Autonomous and volitional breathing control
There is an important additional factor. It is possible to modify breathing patterns when conscious, for example by voluntarily stopping breathing, breathing more slowly, deeper etc. These volitional actions are controlled within the motor cortex located at the top of the brain. However, when asleep, or not voluntarily modifying breathing patterns, the autonomous control system takes over; humans continue to breathe naturally to maintain homeostasis. Autonomous breathing is controlled primarily from the medulla oblongata, a primitive part of the brain located at the brain stem. This ability is unique to humans and is believed to have evolved with the development of complex language skills [25]. There is experimental evidence [26], that voluntary breathing modulations provide a mechanism for humans to re-program autonomous breathing cycles through neuroplastic modification. This suggests that disordered and dysfunctional breathing patterns such as exist in SDB may be amenable to Breathing Retraining (BR).
Review of breath training for dysfunctional breathing and chronic disease mitigation
Dysfunctional breathing is a condition that occurs as a result of dysregulated breathing control. It can manifest as inappropriate hyperventilation and various types of neuromuscular breathing pattern disorders affecting the lower and upper airway [27]. While dysfunctional breathing is most often observed in daytime breathing behaviors there is likely to be a bidirectional relationship between daytime and night-time breathing dysfunction. There are many studies reporting therapeutic efficacy of breath training for a range of chronic conditions complicated by the presence of dysfunctional breathing These conditions include asthma [28, 29]. Chronic Obstructive Pulmonary Disease (COPD) [30], functional cardiac disturbance, chronic anxiety and panic disorder [31, 32]. Dysfunctional breathing has also been reported in patients with somatic and medically unexplained physical symptoms [33, 34]. Breathing therapy has been found to be effective in such patients, helping to restore normal breathing parameters. The correction of dysfunctional breathing is associated with better disease control as evidenced by a reduction in medication needs [35], reduction in panic attacks, reduced symptoms and improved general health and in the case of heart disease patients decreasing the number of cardiac events by 30% [36-39]. Conditions shown to be successfully treated by breathing therapies include those with common co-morbidities with SDB, e.g., asthma and chronic airway obstruction, nasal obstruction and mouth breathing, heart disease and hypertension, Vocal Cord Dysfunction (VCD) and autonomic nervous system dysfunction [40- 47]. Prevalence rates for VCD range from 2.8% to 22% in patients presenting with symptoms of dyspnea, This abnormality is in the posterior aspect of the upper airway, and reliable therapeutic approaches include controlled breathing and breath-holding. It has been reported that individuals who undertake breathing exercises for asthma, chronic rhinitis, anxiety or other conditions experience reduction of SDB symptoms [48]. It has also been proposed that some common mechanisms link these conditions [49]. Signs of dysfunctional breathing related to disordered automatic breathing control with a tendency to breathing instability and hyperventilation have also been observed in individuals with CSA and OSA during normal waking state [50, 51]. Increased tendency to hyperventilate as evidenced by heightened central chemo-sensitivity is a common finding in CSA and also in OSA where the extent of this increased chemo-sensitivity is positively related to the severity of OSA. It has been shown that respiratory instability contributes to collapsibility of the airways in OSA [52, 53]. Several researchers have suggested that increasing the robustness of neurochemical control of breathing in patients with OSA could reasonably be expected to decrease the number of obstructions in patients with moderate OSA [54, 55]. Summarizing this section, there is considerable evidence that BR undertaken for several weeks on a daily basis can mitigate the effects of several respiratory, cardiovascular and psychophysiological disorders and diseases and correct dysfunctional breathing. The effects of BR in SDB have not been rigorously explored. However, the evidence that does exist covers the continuum from case study reports to randomized controlled trials. Breath training regimens that show positive outcomes include playing the didgeridoo [56], and double reed wind instruments [57], daily practice of singing exercises [58, 59], breathing pattern and diaphragm training [60, 61], inspiratory resistance training [62, 63], and voluntary hypoventilation combined with breath holding [64, 65].
Observations supporting a theory to explain how breath training may alleviate SDB
In this section we describe several diverse observations that are relevant in supporting our theory.
Physiological traits and neurological triggers: Based on the observations reported above, it is suggested that the severity of sleep apnea is strongly affected by the efficiency of the body’s ability to compensate for anatomical deficits. OSA may be triggered by various combinations of anatomical limitations and physiological traits and “one size-fits-all” therapies are inappropriate [2]. The fact that the body routinely compensates for anatomical deficits explains why
• OSA is not always observed in obese subjects,
• OSA does not occur in the awakened state,
• OSA episodes are intermittent and may appear and disappear during sleep even if the subject maintains a constant sleep posture.
According to Eckert [2], although all, if not most, OSA patients have some degree of impairment in upper airway anatomy the extent to which anatomical deficits correlate with severity of OSA symptoms varies widely between sufferers. Approximately 19% of OSA sufferers have mild anatomical impairment and upper airway collapsibility and have similar impairments to many people who do not have OSA. As stated above, there are also at least three other physiological traits that contribute to OSA pathogenesis and are collectively present in almost 70% of OSA patients. These are
• Ineffective activation of upper-airway dilator muscles,
• Low arousal threshold and
• Unstable ventilatory control resulting from high respiratory loop-gain.
All three can result from neurophysiological dysfunction.
Sleep related instability of breathing control and increased LG persist in awake states: A high respiratory LG is a sign of breathing instability. If LG is high, after a breathing disturbance for any reason such as upper airway collapse, an asthma attack, or a CPAP malfunction, return to normal breathing and homeostasis does not easily occur. Breathing remains disturbed as control may over-correct and trigger further interruptions. Recent research [24], reports that high loop gain associated with OSA patients correlates closely with respiratory loop gain measured in the awakened state using self-imposed breathing disturbances via breath holding sequences. Subjects with high LG when awake, indicated by low breath holding capability and a tendency to hyperventilate post breath holding are strong indicators of OSA occurrence. High levels of breathing instability have been observed in both daytime and during sleep in patients with panic disorder and dysfunctional breathing. This instability can manifest as excessive sighing with irregular and chaotic breathing patterns in daytime breathing [16, 17], and excessive sensitivity to raising carbon dioxide levels during sleep [66, 67].
Respiratory linked control systems to upper airway dilatory muscles: Effective compensation for anatomical deficits that trigger airway collapse in OSA is dependent on the body’s ability to maintain adequate tone and function of upper airway dilating muscles during sleep and to co-ordinate airway dilation with phase of respiration [68]. Several important control systems that regulate upper airway patency are dependent on respiratory related reflexes. For example, neural drive to the key upper airway muscles that keep the upper airway open during sleep is tied to phasic respiratory input and fluctuation in carbon and oxygen. In addition, mechano-receptor reflexes in the throat that sense airway pressure help to co-ordinate airway tone with respiratory linked airway pressure changes [69].
The role of Mild Intermittent Hypoxia, (MIH): This is a term that describes a series of hypoxic events that are below the level at which potential pathological impacts may arise. Of course, sleep apnea is known to give rise to a number of dangerous outcomes but typically sleep apnea events are well beyond the level and duration imposed with the levels of MIH that are used therapeutically. There is considerable evidence that the application of MIH in a controlled way can be highly beneficial to a range of chronic diseases including various forms of SDB, asthma, cardiovascular and even neuro-physiological pathologies [70]. It is important to ensure that the level of hypoxic stress is maintained at a level below which it could have a detrimental effect. This implies periodic rather than continuous imposition for a limited time daily [71, 72]. In a research environment, intermittent hypoxia is usually applied externally by, for example, modifying the gas mixture concentrations provided to the subject, but can be self-applied more safely and less intensively by the subject themselves through techniques such as breath holding and voluntary hypoventilation. A meta-study undertaken for the National Institute of Health in the United States, after reviewing extensive clinical evidence, concludes that these types of breathing techniques are both safe and effective in the treatment of asthma [73].
Asthma and apnea are related: There are at least 22 acceptably rigorous clinical trials that, taken together, show that breath training using breathing control methods including slow breathing and hypoventilation combined with breath holding can alleviate the symptoms of asthma while reducing the use of reliever inhalers by two or more uses per day [73]. Moreover, the quality of life of patients measured using standardized tests is improved significantly [73]. Further, practitioners in breath training using hypoventilation combined with breath holding methods have observed that such protocols can relieve the symptoms of sleep apnea [64, 65]. Although the reports are largely anecdotal and not within a rigorous clinical environment, there is a significant volume of such cases that, taken together, they provide a substantial body of evidence indicating that imposition of periods of hypercapnia and hypoxia for a short time daily, may reduce apnea symptoms [74]. In all the case reports and trials using breath training for apnea, benefits were equally observed for both OSA and CSA. Asthma attacks are much more likely to occur during early morning sleeping hours and those attacks are more likely to be dangerous or even fatal [75]. There is a statistically significant co-morbidity between apnea and asthma. High OSA risk is associated with poorly controlled asthma independent of known asthma aggravators. It is recommended that patients who have difficulty achieving adequate asthma control should be screened for OSA [76].
he role of neuroplasticity in BR: According to the principles of neuroplasticity, the brain is constantly changing in response to external stimuli. Many different specialized parts of the brain have been shown to exhibit neuroplastic changes in response to the manipulation of stimuli or particular behaviors, sometimes with remarkable results [77]. Neuroplastic interventions are now accepted into a wide range of clinical practices such as rehabilitation from stroke, trauma and spinal cord injuries, the treatment of psychiatric, pediatric and developmental disorders, and as help in dealing with aging and other neuro-degenerative symptoms [78].
With the increasing resolution of fMRI brain scans using voxel-based morphometry [79], it is possible to map the brain non-invasively in considerable detail showing rather precisely where, and to what extent, physical changes in the brain take place during different “training” stimulations, such as navigation, music, second language,and intense studying [80-84]. In particular, a study on mindfulness meditation [85], centered on breath training 16 participants took part in an eightweek mindfulness-based stress reduction program. Brain images showed increased gray-matter density in the hippocampus, important for learning and memory, and in structures associated with self-awareness, compassion, and introspection. Reductions in stress correlated with decreased gray-matter density in the amygdala, known to play an important role in anxiety and stress. None of these changes were seen in a control group. There is evidence that the two breathing control centers in the brain, volitional and autonomous, can interact. For example, it has been shown that prompting small gradual changes in breathing rate are retained when the prompts are removed [26], demonstrating that volitional modifications altered subsequent autonomous control. Brain neuroplasticity in breathing control is also evident in so-called Respiratory Long-Term Facilitation (rLTF) whereby, after a series of hypoxic events such as those that occur during obstructive sleep apnea, there is a long-term (> one hour) enhancement of upper airway muscle tone and general respiratory muscle activity. This serves to reduce the possible pathological effects of repeated depletion of oxygen [86, 87]. In a further study, it has been shown that the beneficial effects of rLTF are reduced when sleep patterns are disturbed. That is, if OSA advances to a stage where there is significant sleep deprivation, the mitigating effect of rLTF is reduced thereby increasing the possible pathological impact [88]. The beneficial effects of intermittent hypoxia induced rLTF of upper airway and respiratory muscles’ function and therefore breathing stability, are not realized in cases where chemo-reflex sensitivity is excessive [73], Mitchell and co-workers conjecture on the possible therapeutic benefits of using neuroplasticity for the alleviation of OSA symptoms [89, 90]. “OSA is associated with inadequate neuro-modulation and hyper-excitable brainstem respiratory motor neurons. Inadequate motor output from these neurons predisposes to upper airway collapse and repetitive apneas during sleep. By harnessing respiratory plasticity, it may be possible to restore synaptic inputs thereby increasing respiratory motor output to upper airway muscles and protecting upper airway patency during sleep.”
And further: “Since repetitive intermittent hypoxia elicits respiratory motor neuron plasticity and meta-plasticity, it may be a viable means of restoring respiratory function in ventilatory control disorders. The critical issue is to develop a protocol of intermittent hypoxia that elicits the intended plasticity without unintended consequences associated with more chronic severe hypoxia.” In other words, imposing carefully designed hypoxia sequences that maintain normal carbon dioxide levels may invoke neuroplastic changes in the breathing control centers in the brain that can mitigate the periodic apneas that occur in OSA.
As evidence of Mitchell et. al.’s conjectures, a clinical study [74], showed that daily exposure to twelve four-minute periodic episodes of hypoxia and sustained hypercapnia during waking for 10 days, reduced AHI noticeably. The results were evident well beyond the time that the exposures took place. Summarizing this section, there is evidence that the breathing control centers in the brain have memory which can be altered via neuroplasticity. rLTF is one example of this. The breathing control centers may act to alleviate the symptoms of OSA via rLTF responding to the periodic reduction in oxygen saturation. However, this feedback mechanism may be compromised in OSA sufferers. Reprogramming the control centers by imposing regulated hypoxic sequences has been shown to alleviate OSA symptoms, the results lasting beyond the period of imposition. Dempsey [55], has also suggested that alternative treatments to minimize respiratory control loop gain and breathing instabilities need to be tested in OSA patients with upper airways only moderately susceptible to collapse. Controlled trials of didgeridoo playing, and aerobic and breathing exercises were all undertaken in populations with mild to moderate OSA. Mechanisms proposed by the majority of authors of these studies have tended to focus on the effects of these activities on upper airway muscle tone [56], and respiratory muscle strengthening [61-63], with some suggesting that the mechanisms were related to biochemical aspects of breathing control [64], or to metabolic and anti-inflammatory effects. We conjecture that individuals with increased chemo-sensitivity and signs of daytime respiratory instability such as high LG may be the most likely candidates for a positive therapeutic outcome from BR. However, given that possible mechanisms and therapeutic targets of BR could include improved neural drive to upper airway dilating muscles as well as reduction of chemoresponsiveness, improved breathing control and reduced hyperarousal research is needed to establish which OSA phenotypes are most likely to respond to breathing retraining.
The advantages of using BR for the alleviation of SDB include
• A minimally invasive, low-cost therapy,
• Limited time-frame for treatment, and
• Possible reduced use of CPAP and NMES devices when used as an adjunct therapy.
Disadvantages include:
• Being used as the only method of treatment in situations where the severity of the condition would demand a more established therapy,
• Regression of symptoms requiring repeat training,
• Need for un-supervised patient compliance over several weeks of BR.
A holistic theory to support the role of breath training to alleviate sleep apnea: Based on the above review of diverse publications in the fields of respiratory control, neuroplasticity, OSA, and clinical studies in a range of chronic diseases, we suggest a holistic theory of how breath training in an awakened state can alleviate the symptoms of sleep disturbed breathing in patients with elevated LG.
Summarizing:
•SDB is often a result, not only of a collapsed upper airway structure, but poor respiratory control. Poor respiratory control in the awakened state highly correlates with poor control in sleep and the occurrence of sleep apnea. For example, elevated LG results in low breath holding capability and poor breathing recovery when awake and is also associated with sleep apnea.
•Dysfunctional breathing and poor respiratory control can be improved using breathing exercises while awake providing long term benefits in controlling asthma, panic attacks, anxiety and improving outcomes in cardiovascular and other diseases.
•Neuroplastic changes in the brain occur as a result of mindful attention to breathing combined with breathing modifications. These changes occur both in the short-term and, with extended exercises, in a much longer term. Permanent neuroplastic changes require repetition of exercises typically daily for a few weeks.
•MIH impositions have shown benefits in apnea alleviation and can be applied using voluntary breath holding and hypoventilation.
•We therefore conjecture that:
•Poor breathing control as evidenced by high LG, reduced respiratory linked phasic activity of upper airway dilatory muscles (and possibly low arousal threshold) can be improved in the awakened state using BR which combine mild selfimposed hypoxic sequences with interspersed relaxed breathing.
•Repetition of these exercises results in permanent neuroplastic changes within the autonomous breathing control centers in the brain.
•Such changes, by reducing LG, improving neural regulation of upper airway dilating muscles, and possibly low arousal threshold, can alleviate SDB through improved respiratory motor stability and control in sleep.
Additional clinical research is required to assess
• The impact of breathing retraining (BR) alone on mild OSA/ and chronic snoring,
• The potential for improved outcomes and applicability to more severe OSA when BR is combined with NMES or MAS therapies,
• To determine which phenotypes may benefit most from BR.
fMRI tracking of the autonomic breathing control centers in the brain over a twelve-week BR protocol in patients presenting high ventilatory loop gain would provide additional support to the theories presented in this review.
Drs. Warren and Benton have an ownership interest in Halare Inc. a company researching neuroplastic breath training.
This research was supported in part by grants from the Ben Franklin Technology Partnership (BFTP) and the Life Sciences of Pennsylvania Greenhouse (LSPGA) in the Commonwealth of Pennsylvania, and the National Institutes of Health, (NIH) under the Qualifying Therapeutic Discovery Project.
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
[Google Scholar] [Cross Ref].
Citation: Warren, A. Alleviating Sleep Apnea Employing Neuroplastic Breath Training: A Review of the Science . 2023, 09 (04), 001-007
Received: 07-Apr-2023, Manuscript No. cep-23-94906; Editor assigned: 10-Apr-2023, Pre QC No. cep-23-94906 (PQ); Reviewed: 12-Apr-2023, QC No. cep-23-94906 (Q); Revised: 27-Apr-2023, Manuscript No. cep-23-94906(R); Published: 30-Apr-2023, DOI: 10.35248/2471-2701.22.9(4).339
Copyright: ©2023 Warren, A. C. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Sources of funding : This research was supported in part by grants from the Ben Franklin Technology Partnership (BFTP) and the Life Sciences of Pennsylvania Greenhouse (LSPGA) in the Commonwealth of Pennsylvania, and the Warren National Institutes of Health, (NIH) under the Qualifying Therapeutic Discovery Project
