1. Check for reverse breathing: "Take a normal breath, hold it, and then exhale." Wait 30 seconds. "Take another normal breath and then exhale." (Watch the screen for evidence of reverse breathing and shoulder use) (1 min)
   
   
2. Resting baseline: "Inhale and exhale through your nostrils for the next three minutes" (3 min)
   
   
3. Peak flow meter: "This is a peak flow meter. It measures how much air you can exhale with a single breath. Take a deep breath and exhale as forcefully as you can. We will record two measurements. "Take your first breath when you are ready." Record the first value. "Take your second breath when you are ready." Record the second value. (2 min)
   
   
4. Incentive inspirometer: "This is an incentive inspirometer. It measures how much air you can inhale with a single breath. Inhale as deeply as you can through the mouthpiece and then remove the mouthpiece and exhale normally into the air. We will record three volumes. Practice a few times and then tell me when you are ready." Patient signals readiness. "Take your first inhalation." Record the first volume. "Take your second inhalation." Record the second volume. "Take your third inhalation." Record the third volume. (4 min)
   
   
5. Serial-7s stressor: "Mentally count backward from 1000 by 7s until I stop you and ask for the number you are on. Inhale and exhale through your nostrils for the next three minutes." (3 min)
   
   
6. Recovery 1: "Stop subtracting and inhale and exhale through your nostrils for the next three minutes." (3 min)
   
   
7. Visualize a recently upsetting experience: "Use all your senses to vividly recreate a recently upsetting experience. Raise a finger when you are re-experiencing the event and continue for the next three minutes. Inhale and exhale through your nostrils." (3 min)
   
   
8. Recovery 2: "Stop your visualization and inhale and exhale through your nostrils for the next three minutes." (3 min)
   
   
9. Inspirometer challenge: "Watch the piston rise in the inspirometer. The top edge of the piston marks the volume you have inhaled. Inhale a volume of 500 ml and then exhale through your nose. Repeat this." Use this procedure for 1000, 1500, 2000, 2500, and 3000-ml challenges. (3 min)
   

Clinicians should watch for startle response or senile postures, holding the stomach in, tight clothing, use of accessory muscles, and abnormal breathing behaviors (gasping, sighing, and stopping). A therapist should breathe effortlessly because there can be a modeling effect where a therapist's breathing behaviors influences the patient's breathing.

The patient should allow the jaw, neck, and shoulders to relax. Breathing should be effortless (the notch in the throat should not drop). This idea is captured by the autogenic phrase, "It breathes me." Attention should settle below the waist. Where attention is directed can affect breathing pattern. The stomach should extend (plop out) during inspiration. The patient should exhale completely. The stomach should contract before inhaling. The patient should pause longer after exhalation than following inhalation.

Your patient should passively increase tidal volume (air moved in and out of lungs with each breath), not slow down respiration rate. Remember that lungs are ventilated by moving volumes of air, not respiration rate. When tidal volume increases, respiration rate should decrease.

Below is a BioTrace+ / NeXus-10 training screen designed to teach effortless breathing. The bottom trace displays the respiration sensor's rhythmic expansion and contraction.





You can help your patient learn effortless breathing using five strategies.

First, ask the patient to lie supine (on the back) with palms up, legs apart, and head supported. Place a book (or rice sack) on the patient's stomach. Ask the patient to watch the book's rise and fall during breathing. Move your patient to a seated position with back straight and legs uncrossed for generalization. Have the patient gently place a hand over the stomach. Ask the patient to observe the hand's rise and fall during breathing.

Second, train the patient using an incentive inspirometer. The spirometer should be level with the patient's mouth to allow a healthy upright posture. The goal should be to effortlessly increase tidal volume. The piston in the incentive spirometer provides tidal volume feedback from breath to breath.

Third, augment the patient's proprioception of movement during breathing. Instruct the patient to breathe effortlessly while sitting upright. Place your hands above the patient's hips. The patient will feel expansion against the hands during inspiration and reduced pressure during expiration.

Fourth, monitor accessory muscles like the trapezius to insure that your patient does not use excessive effort. A trapezius-scalene placement is shown below.




 

Shaffer, Bergman, and White (1997) found that accessory muscle SEMG provided a sensitive index of breathing effort. A BioGraph ® Infiniti accessory muscle training screen is shown below.





Fifth, confirm your patient's success by measuring end-tidal CO2 with a capnometer. The main objective of effortless breathing is to normalize end-tidal CO2 to about 5% (36 torr). Unless the mechanical changes in your patient's breathing accomplish this goal, training may be of limited value.

Shaffer, Bergman, and Dougherty (1998) demonstrated that end-tidal CO2 is the best indicator of breathing effort.






Your patient may feel uncomfortable shifting to an effortless breathing pattern. You can minimize discomfort by cognitive preparation (educational talks and materials), encouraging use of loose-fitting clothes, reminding the patient that breathing should be effortless (no use of accessory muscles and no oxygen starvation), and assigning daily practice.

Remember that part of breathing training is to not suspend breathing (apnea) during daily activities. Shaffer, Sponsel, Knight, Belcher, et al. (1993) reported that videogame playing promoted dysfunctional breathing. Training should generalize continuous effortless breathing when performing activities like talking, writing checks, or reaching for objects (Peper, 1989).



Hyperventilation syndrome (HVS) has been increasingly reconceptualized as a behavioral breathlessness syndrome in which hyperventilation is the consequence and not the cause of the disorder. The traditional model that hyperventilation results in reduced arterial CO2 levels has been challenged by the finding that many HVS patients have normal arterial CO2 levels during attacks.

While HVS and panic disorder are separate conditions, their symptoms greatly overlap. About 50% of patients diagnosed with panic disorder and 60% of those diagnosed with agoraphobia hyperventilate, while only 25% of HVS patients experience panic disorder (Newton, 2005).

Phobia provides the best model of hyperventilation. Breathing is predominantly thoracic. These patients breathe over 20 breaths per minute using accessory muscles (the sternum moves forward and upward) and restricting diaphragm movement.

Peper (1989) has observed that normal breathers find imitating hyperventilators' chest movements difficult. Shallow breathing is punctuated with effortless sighs and gasps. Hyperventilators interrupt breathing (apnea) when surprised, writing checks, talking, or moving (Fried, 1990; Peper, 1989).

The BioGraph ® Infiniti display below shows the shallow rapid breathing that characterizes hyperventilation.







The prevalence of HVS in the United States may be as high as 6%. The male-to-female ratio is about 1 to 7 (Newton, 2005).



Rapid breathing is associated with shallow breathing due to incomplete contraction of the diaphragm. The lungs have less chest cavity space for expansion during inspiration. The respiratory system tries to maintain minute volume (air moving in and out of the lungs in one minute) through faster breathing. This may reduce tidal volume (air moved in and out with each breath) below a normal 500 milliliter (ml) value and expel CO2. Hyperventilators may show shallow, rapid breathing, increased minute volume, decreased tidal volume, and loss of CO2 (Fried, 1990).

In some patients, hyperventilation may decrease blood CO2 from a normal 5% to 2.5% (since CO2 is more permeable than oxygen). CO2 loss elevates blood pH above 7.4 (increases alkalinity) and reduces tissue uptake of oxygen due to the Bohr effect.

In the Bohr effect, elevated blood pH causes hemoglobin to tightly bind oxygen, slowing oxygen release to body tissues and reducing the partial pressure of oxygen (PO2).





A capnometer, which measures end-tidal CO2, is shown below. This is the partial pressure of carbon dioxide in expired air measured by a capnometer at the end of expiration. The average value is 5% (36 torr) for a resting adult (Fried, 1987).

The changes associated with reduced PC02 (percentage Of C02 in arterial blood) may constrict blood vessels in the brain (linked to transient ischemic attacks in stroke) and the heart (low PC02 levels may cause angina). Further, increased blood pH raises neuronal excitability which may contribute to grand mal seizures (Fried, 1990).



Hyperventilation increases heart rate, cardiac output, and blood pressure. Hypertensives gasp and pull down their shoulders when inhaling. They often cannot talk and breathe at the same time. Their blood pressures rise when they talk, gasping for air. The disruption of breathing when talking is probably a factor in cases of essential hypertension.

Hyperventilation removes normal, chaotic, variability in heart rate. In healthy patients, heart rate varies with the breathing cycle. Heart rate increases with inspiration and decreases with expiration. Hyperventilation suppresses this healthy variability called the respiratory sinus arrhythmia (RSA). The RSA is replaced with a nonvarying heart rate that is less adaptive when workload changes. Normal parasympathetic control over the heart is replaced with sympathetic control. The absence of RSA is predictive of coronary heart disease (Peper, 1989).



Fried (1989) contends that hyperventilation accompanies or is a factor in 50-70% of medical complaints.




          


Many symptoms treated using biofeedback are associated with hyperventilation. Where hyperventilation causes or worsens these symptoms, training patients to breathe effortlessly should be part of the treatment plan.




 

Postural evaluation and correction should precede breathing instruction. Both the startle response and senile posture mechanically restrict breathing and produce hyperventilation. Unless the chest cavity can normally expand and the diaphragm completely descend, healthy effortless breathing will be impossible.

In the startle response, contraction of the rectus abdominis produces thoracic breathing, which may escalate to hyperventilation. Abdominal muscle contraction depresses the rib cage and abdominal cavity, and pressures the viscera (large internal organs). During normal inhalation, the diaphragm muscle descends toward the abdominal cavity to produce a vacuum in the thoracic cavity to pull in air. But when the startle response constricts the viscera, it interferes with the diaphragm's downward movement, suddenly stopping breathing (Hanna, 1988).






In the senile posture, the muscles at your center of gravity "simultaneously pull the pelvis and hips up toward the trunk, yet pull the trunk and shoulder girdle down toward the pelvis" (Hanna, 1988, p. 70). The senile posture produces chronic shallow breathing and hyperventilation by immobilizing the chest (your entire rib cage is pulled down).







The relationship between hyperventilation and psychological state is bidirectional. Psychological disorders can produce hyperventilation; and hyperventilation can produce psychological symptoms in vulnerable patients. Psychological causes of hyperventilation include anxiety, depression, fight-or-flight response, panic attacks, phobic reactions, and suppressing anger. Maladaptive learned responses also contribute to hyperventilation. These responses include gasping, holding breaths, holding the stomach in, and sighing. These breathing behaviors may be habits or responses to self-generated or environmental stimuli (Fried, 1990).



Tight corsettes produced fainting in the 19th century (Peper, 1989). In the 2000s, tight clothing, especially designer jeans and panty hose, can contribute to hyperventilation. How does this happen? When clothing holds the stomach in, this constricts the viscera and interferes with the diaphragm's downward movement during inspiration. This reduces lung ventilation and the respiratory system compensates by breathing more rapidly.

Shaffer, Mayhew, Bergman, Dougherty, and Irwin (1999) demonstrated that wearing tight jeans increased minute volume 11% and oxygen uptake per kg of body weight, 6%, compared with wearing loose jeans.

A BioGraph ® Infiniti display of thoracic breathing is shown below. Note the minimal abdominal excursion (red trace) and rapid respiration rate.







Hyperventilation results whenever blood pH drops below 7.0 (acid). The body compensates for increased acidity by raising respiration rate and expelling more C02. The lungs account for 85% of this adjustment; the kidneys 15% (Fried, 1990).

Several medical conditions can produce hyperventilation.






Hyperventilation is a side effect of several medications:






Fried (1990) contends that diet can produce hyperventilation directly or indirectly. The main culprits include foods that contain or create tyramine, trigger allergic reactions, and dietary mineral and vitamin deficiencies.

Tyramine, an amino acid, produces components of the fight-or-flight response. These are the same foods that a small percentage of headache patients should avoid and include aged cheese, alcohol, and chocolate. Since tyramine in circulating blood constricts vessels, this substance may contribute to vasoconstrictive disorders. The main conditions include: angina, hypertension, idiopathic epilepsy, migraine, and Raynaud's.

Allergic reactions to food can trigger hyperventilation to maintain blood oxygen levels. The vasoconstrictor, histamine, is often released during allergic reactions. Histamine reduces blood oxygen by constricting vessels (reducing blood flow) and directly affecting red blood cell transport of oxygen.

Mineral deficiencies directly and indirectly produce hyperventilation. These include low levels of: calcium, iron, magnesium, potassium, and zinc. Vitamin deficiencies in B6, C, and folic acid are also implicated in hyperventilation.




Asthma involves episodic reversible airway obstruction, chronic airway inflammation and hypersensitivity to stimuli (like allergens, cold air, exercise, and viral infection). Chronic inflammation may scar the airway resulting in obstruction that does not reverse with medication.

While allergens, exercise, and drugs like aspirin can trigger asthma attacks, both acute and chronic stress can also precipitate asthma attacks in children diagnosed with this disorder. Attacks by bullies, family conflict, and academic difficulties can increase the risk of asthma attacks eight times (Sandberg et al., 2000).







Estimates of asthma prevalence in the United States range from 3-10% (Kussin & Fulkerson, 1995; Tortora & Derrickson, 2006). While both asthma prevalence and mortality have recently increased for both European and African Americans, poor urban African Americans are disproportionately affected (Weil et al., 1999).



Tortora and Derrickson (2006) identify the following asthma symptoms:

• difficult breathing (dyspnea)
  
• coughing
• wheezing
• chest tightness
• heart rate over 100 beats-per-minute (tachycardia)
• fatigue
• moist skin
• anxiety

The early phase response features smooth muscle spasm and excessive mucus secretion, which obstruct the airways. The late phase response involves inflammation, scar tissue formation, fluid accumulation, and death of the epithelial cells that line the bronchioles. Mast cells and eosinophils in the bronchioles of the lungs release several chemical mediators. The most important mediators include histamine, immunoglobulin E (IgE), leukotrienes, prostaglandins, thromboxane, and platelet-activating factor (Tortora & Derrickson, 2006; Fox, 2006).



HRV biofeedback can train clients to increase the power of a specific frequency band. The optimal training protocol for both asthma and cardiovascular health teaches clients to increase power in the low frequency (LF) band.

Evgeny Vaschillow hypothesizes that each individual has an intrinsic resonant frequency that maximizes overall health. For most persons, this frequency is located around 0.1 Hz and can be produced by creating a “relaxed mental state, with a positive emotional tone, breathing diaphragmatically at a rate of about 4.5-7.5 breaths per minute” (Moss, 2004).

Breathing generates respiratory sinus arrhythmia (RSA), heart rate speeding and slowing across each respiratory cycle. RSA depends on parasympathetic (vagus nerve) regulation of the heart. While disruption of vagal signals to the heart almost completely ends RSA, interference with sympathetic signals does not affect it (Papillo & Shapiro, 1990).

Since 0.1 Hz means one-tenth of a cycle per second, 0.1 Hz equals 6 cycles per minutes. A respiration rate of six breaths (respiratory cycles) per minute paces the heart so that maximum heart rate variability develops at 0.1 Hz within the low frequency range. Heart rate variability is highest at this resonant frequency because it combines HRV due to slow breathing, parasympathetic activity, and blood pressure regulation.

Lehrer and colleagues (2000) have pioneered cardiovascular resonant frequency biofeedback for asthma. Their Smetankin protocol combines HRV biofeedback with abdominal pursed-lips breathing. They train patients to breathe at their individual resonant frequency.




             



Gevirtz (2005) has reported that while asthma does not affect an individual's heart rate resonant frequency, it does reduce HRV at this frequency. Conversely, breathing at the heart rate resonant frequency (0.1 Hz) improves asthma symptoms.




           


Moss has conceptualized HRV biofeedback “as a process of training an active balancing between the sympathetic and parasympathetic branches’ effects on the heart rhythm” (Shaffer & Moss, 2006). Increasing the percentage of heart rate variability within the low frequency range and breathing at 5-7 breaths per minute to produce a dominant HRV spike at 0.1 Hz are important HRV biofeedback training objectives (Moss, 2004).




            


The BioGraph ® Infiniti screen below teaches clients to increase heart rate variability indexed by SDNN (the standard deviation of the interbeat interval) through rhythmic breathing and positive emotion.
 

Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for asthma at level 2 efficacy, possibly efficacious. The criteria for level 2 efficacy include "At least one study of sufficient statistical power with well identified outcome measures, but lacking randomized assignment to a control condition internal to the study" (p. 10). A level 2 rating was awarded due to mixed results.

Lehrer et al. (1997) reported a controlled study that showed that RSA biofeedback produced large-scale within-session decreases in respiratory impedance in adults diagnosed with asthma. When Lehrer and colleagues (1997) compared RSA biofeedback, neck/trapezius SEMG biofeedback, and incentive inspirometry biofeedback, only the RSA biofeedback group decreased pulmonary impedance (resistance of the bronchioles to air flow).

Kern-Buell, McGrady, Conran, and Nelson (2000) reported that SEMG biofeedback may have reduced inflammation and reduced asthma symptoms.

Lehrer, Smetankin, and Potapova (2000) reported that the Smetankin method of respiratory sinus arrhythmia biofeedback reduced asthma symptoms and airway resistance in 20 unmedicated children.

Huntley, White, and Ernst (2002) surveyed controlled studies of relaxation procedures, including SEMG biofeedback, and found no evidence of improved pulmonary function or symptom improvement.

Song and Lehrer (2003) instructed 5 female volunteers to breathe at respiratory rates of 3, 4, 6, 8, 10, 12, and 14 breaths per minute while they measured heart rate variability (HRV) amplitude. Slower respiration rates produced higher HRV amplitudes. HRV amplitude peaked at 4 breaths per minute and declined at 3 breaths per minute. These authors proposed that these results may be due to more complete acetylcholine inactivation as breathing slows, a negative resonance between baroreflex effects and HRV, or some interaction between these two processes.

Lehrer and colleagues (2004) examined the clinical efficacy of heart rate variability (HRV) biofeedback in a study of 94 adult asthma patients. After prestabilization with controller medication, they randomly assigned these patients to HRV biofeedback with abdominal breathing training, HRV biofeedback alone, placebo EEG biofeedback, or a waiting list control. Subjects in the two HRV conditions were prescribed less steroid medication and showed improved pulmonary function (measured by forced oscillation pneumography) than control subjects. The two HRV groups did not significantly differ in clinical outcome. All groups showed improved asthma symptoms and did not differ in the frequency of severe asthma flares. The authors concluded that HRV biofeedback shows promise as an adjunctive treatment for asthma that could reduce reliance on steroid medication.

Below is a BioTrace+ / NeXus-10 screen that shows three different components of heart rate variability (HRV), the variability in beats/min, the percentage of activity in the low-frequency (LF) zone, and the level of coherence/correlation between the respiration (RSP) and heart rate (HR) signals.







While chronic obstructive pulmonary disease (COPD) is mainly caused by smoking tobacco, additional causes include cystic fibrosis, alpha-1 antitrypsin deficiency, bronchiectasis (chronic abnormal bronchiole dilation), and rare bullous lung diseases (featuring thin-walled sacs that contain air) (Kleinschmidt, 2005).



COPD afflicts about 34 million Americans and is the fourth major cause of death. Men present with COPD more often than women and it is mainly seen in adults over the age of 40. COPD patients present with different combinations of chronic bronchitis, emphysema, and less frequently, asthma (Kleinschmidt, 2005).



Evidence-Based Practice in Biofeedback and Neurofeedback (2004) rates biofeedback for chronic obstructive pulmonary disease (COPD) at level 2 efficacy, possibly efficacious. The criteria for level 2 efficacy include "At least one study of sufficient statistical power with well identified outcome measures, but lacking randomized assignment to a control condition internal to the study" (p. 14). A level 2 rating was awarded because this application has not been sufficiently investigated.

Esteve and colleagues (1996) randomly assigned participants to either breathing pattern training or a control group. The group that received respiratory training increased FEV1 (forced expiratory volume in one second) 22% and FVC (forced vital capacity) 19%, while the control group did not improve.

Giardino and colleagues (2004) treated COPD with a combination of HRV biofeedback and exercise. Ten participants received five HRV biofeedback sessions to increase HRV combined with paced breathing instruction. They also walked four times a week, using their paced respiration skills to control breathing. They checked their oxygen levels using an oximeter. These patients improved on the six-minute walking distance test (6MWD), which measures functional capacity, and the St. George’s Respiratory Questionnaire (SGRQ), which assesses overall quality of life. Eight of these participants achieved clinically significant gains on these measures.



Effortless breathing could be hazardous if your patient suffers from diseases which produce metabolic acidosis, like diabetes and kidney disease. In these cases, hyperventilation is an attempt to compensate for abnormal acidbase balance and slower breathing could endanger health.

Patients with low blood pressure should be cautious since effortless breathing can further lower blood pressure.

Finally, if your patient takes anti-hypertensive medication, insulin, or a thyroid supplement, effortless breathing can produce a functional overdose. If adjustment appears necessary, the patient should consult with the supervising physician before reducing dosage (Fried, 1990).







Now that you have completed this module, describe how you assess breathing, the way you integrate breathing training with biofeedback, and your favorite training hints.




Del Pozo, J., Gevirtz, R., Scher, B., & Guarneri, E. (2004). Biofeedback treatment increases heart rate variability in patients with known coronary artery disease. American Heart Journal, 147, E11.

Esteve, F., Blanc-Gras, N., Gallego, J., & Benechetrit, G. (1996). The effects of breathing pattern training on ventilatory function in patients with COPD. Biofeedback and Self-regulation, 21(4), 311-321.

Fried, R. (1987). The hyperventilation syndrome: Research and clinical treatment. Baltimore: John Hopkins University Press.

Gevirtz, R. N. (2005). Heart rate variability biofeedback in clinical practice. AAPB Fall workshop.

Huntley, A., White, A. R., & Ernst, E. (2002). Relaxation therapies for asthma: A systematic review. Thorax, 57(2), 127-131.

Kern-Buell, C. L., McGrady, A. V., Conran, P. B., & Nelson, L. A. (2000). Asthma severity, psychophysiological indicators of arousal and immune function in asthma patients undergoing biofeedback-assisted relaxation. Applied Psychophysiology and Biofeedback, 25(2), 79-91.

Kleiger, R. E., Miller, J. P., Bigger, J. T., et al., and the Multicenter Post-Infarction Research Group (1987). Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. American Journal of Cardiology, 59, 256-262. 

Kleinschmidt, P. (2005). Chronic obstructive pulmonary disease and emphysema. eMedicine.

Lehrer, P., et al. (1997). Respiratory sinus arrhythmia versus neck/trapezius EMG and incentive inspirometry biofeedback for asthma: A pilot study. Applied Psychophysiology and Biofeedback, 22(2), 95-109).

Lehrer, P., Smetankin, A., & Potapova, T. (2000). Respiratory sinus arrhythmia biofeedback therapy for asthma: A report of 20 unmedicated pediatric cases using the Smetankin method. Applied Psychophysiology and Biofeedback, 25(3), 193-200.

Lehrer, P. M., Vaschillo, E., & Vaschillo, B. (2000). Resonant frequency biofeedback training to increase cardiac variability: Rationale and manual for training. Applied Psychophysiology and Biofeedback, 25(3), 177-191.

Lehrer, P. M., Vaschillo, E., Vaschillo, B., Lu, S., Scardella, A., Siddique, M., & Habib, R. H. (2004). Biofeedback treatment for asthma. Chest, 126, 352-361.

Moss, D. (2004). Heart rate variability (HRV) biofeedback. Psychophysiology Today, 1, 4-11.

Newton, E. (2005). Hyperventilation syndrome. eMedicine.

Peper, E., Gibney, K. H., Tylova, H., & Harvey, R. (in press). Mastery through experience.

Peper, E., & Tibbetts, V. (1992). Fifteen-month follow-up with asthmatics utilizing EMG/incentive inspirometer feedback. Biofeedback and Self-Regulation, 17(2), 143-151.

Sandberg, S., Paton, J. Y., Ahola, S., McCann, D. C., McGuinness, D., Hillary, C. R., et al. (2000). The role of acute and chronic stress in asthma attacks in children. Lancet, 356, 982-987.

M. S. Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide (3rd ed.). New York: The Guilford Press.

Shaffer, F., Bergman, S., & Dougherty, J. (1998). End-tidal CO2 is the best Indicator of breathing effort [Abstract]. Applied Psychophysiology and Biofeedback, 23(2).

Shaffer, F., Bergman, S., & Henson, M. (1998). Description of the Truman breathing assessment protocol [Abstract]. Applied Psychophysiology and Biofeedback, 23(2).

Shaffer, F., Bergman, S., & White, K. (1997). Indicators of diaphragmatic breathing effort [Abstract]. Applied Psychophysiology and Biofeedback, 22(2), 145.

Shaffer, F., Knight, D., Sponsel, M., Belcher, J., et al. (1993). Vigilance reduces inhalation volume: Nintendo play may reinforce dysfunctional breathing [Abstract]. Biofeedback and Self-Regulation, 18(3).

Shaffer, F., Mayhew, J., Bergman, S., Dougherty, J., & Irwin, D. (1999). Designer jeans increase breathing effort [Abstract]. Applied Psychophysiology and Biofeedback, 24(2), 124-125.

Shaffer, F., & Moss, D. (2006). Biofeedback. In Y. Chun-Su, E. J. Bieber, & B. Bauer (Eds.). Textbook of complementary and alternative medicine (2nd ed.). Abingdon, Oxfordshire, UK: Informa Healthcare.

Song, H., & Lehrer, P. M. (2003) The effects of specific respiratory rates on heart rate and heart rate variability. Applied Psychophysiology and Biofeedback, 28(1), 13-23.

Stein,  P. K., Ehsani,  A. A., Domitrovich, P. P., Kleiger,  R. E., & Rottman, J. N. (1999). Effect of exercise training on heart rate variability in healthy older adults. Am Heart J., 138 (3 Pt 1), 567-76.

Tortora, G. J., & Derrickson, B. H. (2006). Principles of anatomy and physiology  (11th ed.). New York: John Wiley & Sons, Inc.

Weil. C. M., Wade, S. L., Bauman, L. J., Lynn, H., Mitchell, H., & LaVigne, J. (1999). The relationship between psychosocial factors and asthma morbidity in inner-city children with asthma. Pediatrics, 104, 1274-1280.

Yucha, C. B., & Gilbert, C. D. (2004). Evidence-based practice in biofeedback and neurofeedback. Wheat Ridge: AAPB.