Biofeedback Has Therapeutic Effects on Asthma,Although Additional Research Is Needed to Document Specificity

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Biofeedback to increase heart rate variability and decrease muscle tension improves asthma and allows a decrease in steroid medication. Large-scale studies deserve funding, as does research on specificity and pathway of effects. Insurance reimbursement and standard use are warranted.

Key Points

Asthma is a widespread disease, affecting 8.4% of the population in the United States (Loftus & Wise, 2016), with an estimated worldwide prevalence of 100 million people by 2025 (Masoli et al., 2004). Asthma's economic impact is growing yearly: over $80 billion in 2013 (Nurmagambetov et al., 2018). Triggers for asthma exacerbations can include exposure to allergens or viral infection, as well as exercise and exposure to cold air (National Heart, Lung and Blood Institute, 2020).

Asthma is typically diagnosed by a combination of symptoms and lung function tests. It is usually accompanied by inflammation of tissues of the lung, but it is also characterized by the tightening of smooth muscles in the central airways, called “bronchoconstriction” (National Heart Lung and Blood Institute, 2007). The inflammatory and autonomic ¹ systems work synergistically in asthma. When the airways are inflamed, they become more reactive to various aggravating stimuli, including exposure to cold air, virus infection, and pollution, which can cause both increased inflammation and bronchoconstriction.

Autonomic nervous system reactivity also may trigger asthma symptoms (Ohno, 2017). Many asthma patients appear to be “parasympathetically tuned” to stress, with stress-induced increases in parasympathetic ² activity, causing bronchoconstriction. In one of our studies, we presented asthma patients with a series of mild psychological stress tasks. Some of the study participants scored high on the psychological trait of defensiveness, where people do not admit to having common faults that most of us do have. This characteristic is usually related to greater autonomic reactivity to stress. In our study, defensive asthma patients showed evidence of both bronchoconstriction and elevated parasympathetic activity. Defensive individuals without asthma, however, tended to show decreased parasympathetic activity (a typical stress response) with minimal effects on the airways (Feldman et al., 2002). This is the “fight flight reaction,” characterized by a decrease in parasympathetic and an increase in sympathetic activity. ³

The fight-flight response ordinarily would dilate the airways, allowing oxygen to enter the system more easily, thus promoting muscular activity. This might be expected to improve asthma condition (Matera et al., 2020). Indeed, we found that laboratory stressors, such as mental arithmetic, that lead to an active coping response appear to produce bronchodilation (widening of the airways), both in asthma patients and in healthy people. This improves airway function in the short run (Lehrer et al., 1996). Nevertheless, the overall impact of stress on asthma appears to be negative. Contributing to this may be a peculiar pattern of autonomic stress response in many people with asthma: a blunted sympathetic stress response with a tendency toward an augmented parasympathetic response (Feldman et al., 2002; Lemanske & Kaliner, 1990; Miller & Wood, 1997). Also, sympathetic stress reactions can trigger “parasympathetic rebound” effects when sympathetic activity subsides. Gellhorn (1959) found that stimulating the sympathetic system causes the parasympathetic system to become more easily reactive to stimulation. This can cause an increase in parasympathetic activity, which, in turn, can lead to bronchoconstriction (Lehrer et al., 1997).

Additionally, levels of anxiety and depression tend to be higher among patients with asthma (Kulikova et al., 2021; Ye et al., 2021). They are often accompanied by increased inflammation and some autonomic changes that can exacerbate asthma (Bratek et al., 2015; Miller et al., 2009; Paine et al., 2019). The greater prevalence of panic symptoms in asthma (Carr, 1999; Vazquez et al., 2017) can be particularly problematic because symptoms of panic and asthma can overlap, causing people to treat the wrong condition, with occasionally disastrous consequences (Tietz et al., 1975). Symptoms of hyperventilation ⁴ are common in both conditions, with anxiety causing an increase in respiratory effort as part of an emergency activation process (Masaoka & Homma, 2001). Increased breathing, a common accompaniment of anxiety (Guyon et al., 2020; Masaoka et al., 2004), can lead to hyperventilation symptoms, which mimic symptoms both of asthma and panic. It also occurs during exercise, which is a common asthma trigger (Gerow & Bruner, 2021).

This paper reviews evidence that two biofeedback methods reduce stress and improve asthma condition, and reviews indications for pathways by which these effects occur. We enumerate gaps in evidence that warrant further investigation but conclude that there is sufficient empirical support from a number of modest-sized studies to warrant widespread adoption of the method, as well as support for large-scale studies and continued research on populations for whom the method might be most effective. Currently, biofeedback is usually treated as an investigational intervention by medical insurance companies, with consequent denial of benefits (Blue Cross Blue Shield of Massachusetts, 2022), and no large-scale studies have been funded for definitive proof of effectiveness.

Heart Rate Variability Biofeedback to Treat Asthma

Heart rate variability (HRV) refers to the variability of between-heartbeat intervals. It is often used to assess autonomic nervous system function. One important source of variability is caused by breathing. Heart rate goes up during inhalation and down during exhalation. This is called “respiratory sinus arrhythmia” (or RSA). It helps the efficiency of breathing by having the highest heart rate at times when there is the most fresh air in the bottom of the lung, where oxygen is taken in and carbon dioxide is let out. RSA ordinarily occurs at the frequency of breathing, usually around 15 times a minute. Another source of HRV is the baroreflex. This reflex controls swings in blood pressure. When blood pressure goes up the baroreflex causes heart rate to go down, and when blood pressure goes down the baroreflex causes heart rate to go up. Changes in heart rate thus modulate changes in blood pressure, by changing the amount of blood flowing through the vasculature with every swing. In this way, the baroreflex thus causes an oscillation in heart rate at about six times a minute (i.e., the amount of time it takes blood pressure to cycle in response to heart rate cycles), although the speed varies among people.

HRVB trains people to breathe at the rate of the baroreflex. This causes RSA and the baroreflex to stimulate each other, such that the two reflexes resonate. The resonance causes very large oscillations in heart rate at the frequency of the baroreflex. The large-amplitude oscillations exercise and strengthen the baroreflex (Lehrer et al., 2003). This greatly improves respiratory efficiency while also controlling blood pressure swings.

However, the baroreflex is neurally connected to many other control processes throughout the body. It is controlled by a brain center (nucleus tractus solitarius) that controls homeostasis ⁵ in many organs throughout the body, including emotional control centers in the brain (Andresen et al., 2004; Mather & Thayer, 2018). The baroreflex feeds back to the nucleus tractus solitarius as well as being controlled by it. Thus, stimulating and strengthening the baroreflex may be expected to improve resilience throughout the body, presumably including the lung. This has a wide variety of beneficial effects, including decreases in anxiety and depression (Lehrer et al., 2020a).

Research on brain blood flow using the fMRI has found that regular practice of HRVB strengthens connectivity between limbic system activity (which is activated by stress and is involved in generating anxiety and depression) and centers in the medial prefrontal cortex that modulates these emotions (Nashiro et al., in press). ⁶ Hence, practicing this method has clinically significant effects in reducing depression, anxiety, and various symptoms of stress (Lehrer et al., 2020). The method also has been found to reduce inflammatory activity, including decreases in an inflammatory chemical in the blood, C-reactive protein (Nolan et al., 2012), and decreased airway inflammation in asthma (Lehrer et al., 2018).

Evidence for Heart Rate Variability Biofeedback as a Treatment of Asthma

Heart rate variability biofeedback (HRVB) as a treatment for asthma has been studied for two decades and has shown promising results. The results show a large and significant beneficial effect on asthma outcomes (Lehrer et al., 2000, 2004, 2006; Taghizadeh et al., 2019) and that HRVB may be specific for reducing airway inflammation (Lehrer et al., 2018). A meta-analysis of HRVB studies found large effect sizes for improvement in respiratory disorders, as well as for anger, anxiety, pain, and depression with HRVB (Lehrer et al., 2020). These findings highlight the large potential of HRVB as an adjunct treatment in asthma, including stress-induced asthma, and other conditions.

In summary, there is growing evidence that HRVB can be an effective adjunct to the medical treatment of asthma. It ameliorates the effects of stress that may trigger asthma exacerbations and can reduce reliance on steroid medication (Lehrer et al., 2004). Steroid medications are used to reduce airway inflammation, but they have a variety of known side effects, including greater susceptibility to infection and fracture (Manson et al., 2009). There is evidence that HRVB may reduce airway inflammation as a mechanism of action. The specificity of clinical effects requires additional study in patients with more severe asthma, and in comparisons with other approaches to respiratory regulation. Also, the specific components in the HRVB method that produce therapeutic asthma effects require further investigation.

Muscle Relaxation and Surface EMG Biofeedback to Treat Asthma

In the early to mid-20th century, Edmund Jacobson invented and evaluated a method that teaches people to relax their skeletal muscles to close to zero levels (Jacobson, 1938). To measure this effect, he devised the surface electromyography (sEMG) method. This measures muscle tension from minute electrical signals that can be detected from electrodes pasted to the skin.

The skeletal muscles are part of the sympathetic nervous system, and increased muscle tension is associated with increased sympathetic arousal (Donadio et al., 2012; Victor et al., 1988). Muscle relaxation reduces sympathetic arousal (Davidson et al., 1979; Green, 2011), and a reduction in stress-induced sympathetic arousal may help asthma. As mentioned above, sympathetic arousal is the most common autonomic pathway for stress effects, and increased sympathetic arousal can lead to a parasympathetic rebound, thus exacerbating asthma; and sympathetic arousal is also related to increases in inflammatory processes (Padro & Sanders, 2014; Rosenkranz et al., 2022).

Muscle relaxation, particularly when profound, reduces sympathetic arousal, as found both in human studies of stress reactivity (Lehrer, 1978) and in animal studies using curare (Gellhorn, 1958), a plant extract that blocks muscle tension at the neuromuscular junction. There also is evidence that training in progressive relaxation can produce decreases in pro-inflammatory cytokines (proteins that induce inflammation in various parts of the body) (Koh et al., 2008). Thus, training in muscle relaxation might be expected to improve asthma both by reducing sympathetic arousal and reactivity and by decreasing inflammation.

It is also possible that specific relaxation of the facial muscles may be beneficial for patients with asthma. There is a well-known interaction between the vagus nerve, the parasympathetic nerve whose activation can trigger bronchoconstriction, and the trigeminal nerve, which controls facial muscle tension. By this pathway, increased facial muscle tension may increase vagal activity, and thus exacerbate asthma (Mercante et al., 2018). There is evidence that relaxation training, accompanied by sEMG biofeedback to the facial muscles, therefore, helps asthma, possibly through this mechanism (Davis et al., 1973; Huntley et al., 2002; Kern-Buell et al., 2000; Kotses et al., 1991; Lehrer et al., 1986). Randomized controlled trials using general muscle relaxation training, without specific sEMG training but including training to relax the facial muscles, have also found significant beneficial effects as an adjunct to asthma treatment (Nickel et al., 2005, 2006).

However, the beneficial effects of muscle relaxation on asthma may not be immediate, and relaxation may not be beneficial as a rescue procedure during an acute asthma flare. Because acute decreases in sympathetic arousal can induce a parasympathetic rebound, acute bronchoconstriction can occur during the practice of cultivated relaxation (Lehrer et al., 1997). Although uncommon, we have seen one patient who showed a clinically significant exacerbation of asthma symptoms during a relaxation session. Nevertheless, muscle relaxation leads to improved pulmonary function over time (ibid) and can reduce susceptibility to asthma exacerbations through a general reduction in autonomic reactivity.

In summary, the existing research on muscle relaxation for the treatment of asthma is promising, though further research is needed to better specify results. Many of the studies only included nonsteroid-dependent asthmatics with mild to moderate asthma. Therefore, there is little information on how muscle relaxation, with or without biofeedback, would impact those with severe asthma. Results of a study by Davis et al. (1973) found that the treatment might not be as effective for this group. Also, studies are needed to determine the long-term effects of relaxation training, particular characteristics of asthma or asthma sufferers where relaxation training might be most helpful (e.g., age, asthma severity, and allergic vs. nonallergic asthma), the need for “booster” training to preserve skills and bolster motivation to continue practice, the relative incremental effectiveness of including facial sEMG biofeedback to general training in progressive muscle relaxation, and the specific pathways by which relaxation training helps asthma (reduction in sympathetic arousal vs. reduction in trigeminal nerve output).

Overall Conclusions

Although these methods may not substitute for medical treatment of asthma, they improve asthma condition, have few or no side effects, and may decrease reliance on steroid medication, the most common medicine for controlling asthma, which has known long-term deleterious side effects (Gani et al., 2020; Ip et al., 1994; Petri et al., 1991). Cost also is often a deterrent to acceptance of asthma medication (Tudball et al., 2019), while some biofeedback apps are free or of nominal cost, and sensors are inexpensive to purchase or rent. A few sessions of professional training in the use of the equipment is usually less expensive than years of medication.

Despite demonstrated effects as an adjunctive asthma treatment, additional evidence is needed (1) to confirm the mechanisms by which biofeedback methods work, (2) to ascertain the components of each method that most contribute to the effectiveness, and (3) to determine the specific asthma populations for which they are most helpful (e.g., for various ages and levels of asthma severity). Additionally, a general limitation of evidence supporting biofeedback for asthma treatment is the lack of outcome data from well-controlled large-scale studies. Evidence thus far is from numerous smaller studies. Given the consistency of positive effects, support for large-scale clinical trials is warranted to confirm these results. However, not having the deep pockets of pharmaceutical companies, and without a major potential to generating financial windfalls, the only possible source of such funding is the government.