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Normal Breathing Defeats Chronic Diseases

Diaphragm Function | Diaphragmatic Breathing Benefits

Diaphragm Function and RespirationThe diaphragm, in normal health, does over 75% of the work of breathing at rest (Ganong, 1995; Castro, 2000). Most modern people, as it is easy to observe, have predominantly chest breathing. Does chest breathing interfere with the health of humans and the normal functioning of the diaphragm? What are the benefits of diaphragmatic breathing?

Two Main Functions of the Diaphragm and Benefits of diaphragmatic breathing

- To regulate efficient O2 delivery and (partial) CO2 elimination. (Note that, while the majority of modern people believe in the deep breathing myth and the poisonous nature of CO2, medical science has found dozens of benefits of CO2 in the human body.)

Respiratory Physiology, by John West, documents that the upper 7% of the lung delivers 4 ml of oxygen per minute, while the lower 13% of the lung brings in 60 ml of oxygen every minute (West, 2000). Therefore, lower parts of the lungs are about 7 times more productive in oxygen transport. While normal breathing at rest has a small tidal volume (only about 500 ml for a 70-kg person), it provides hemoglobin in the arterial blood with up to 98-99% O2 saturation due to the leading role of the diaphragm in the respiratory process.

In contrast, chest breathing is usually larger and deeper (up to 12-18 L/min for minute ventilation, 700-900 mL for tidal volume, and 18-25 breaths/minute in mild forms of heart disease, diabetes, asthma and so forth). But during thoracic breathing, blood oxygen levels are actually reduced due to inhomogeneous gas exchange: lower the parts of the lungs do not get fresh air supply during chest breathing. In certain cases, this pathology (chest breathing) can greatly contribute to or even lead to pneumoperitoneum, emphysema, chronic respiratory fatigue, severe asthma, bronchitis, cystic fibrosis, heart disease, diabetes, cancer tumor growth, and other pathologies.

- To perform lymphatic drainage of the lymph nodes from the visceral organs. The diaphragm is a lymphatic pump, since about 60% of all lymph nodes in the human body are located just under the diaphragm. Dr. Shields, in his study, "Lymph, lymph glands, and homeostasis" (Shields, 1992), reported that diaphragmatic breathing stimulates the cleansing of the lymph nodes by creating a negative pressure pulling the lymph through the lymphatic system. This increases the rate of toxic elimination by about 15 times.

Chest breathing at rest causes lymphatic stagnation in the stomach, pancreas, spleen, liver, kidneys, large and small colon, and other organs. Hence, effective lymphatic drainage is also among the benefits of diaphragmatic breathing. This may sound as confusing as trying to explain how does an annuity work to someone who has never heard of one, but simply each function works off each other to create the bigger picture.

Other functions and benefits of using the diaphragm (not related to breathing)

- To help in defecation, urination, and vomiting by increasing the intra-abdominal pressure. All these processes are mainly reflexive in their nature and the contribution of the diaphragm to these processes, in health, is small but valuable.

However, alveolar hyperventilation (or elevated minute ventilation rates, due to thoracic breathing) can lead to spasm in the muscles of the lower digestive tract, causing constipation. People with constipation strain themselves too much (in the elderly, this often results in the formation of diverticula). But with regular, gentle diaphragmatic breathing, bowel movements occur more easily - and it becomes unnecessary to use the diaphragm forcefully (which creates high intra-abdominal pressure) to make the bowel movement.

- To help in the production of speech (with one's voice) and other sounds (e.g., laughter) by changing the intra-abdominal pressure. In normal health, high CO2 levels dilate the airways, making air movements easier, while the diaphragm naturally remains relaxed. In this case, the diaphragm plays a main role in the generation of speech sounds and voice sounds.

When we switch to thoracic breathing (as during unnoticeable hyperventilation), this function of the diaphragm is taken over by the chest muscles. The resulting hypocapnia constricts bronchi and bronchioles, leading to a tenser voice and a higher pitch of the voice. This effect is especially noticeable during singing, so it is not a surprise that singing teachers encourage diaphragmatic breathing in their students.

Causes of the diaphragm dysfunction and chest breathing in modern people

Hyperventilation is the main, and generally the only, cause of chest breathing in modern people and their inability to enjoy the diaphragmatic breathing benefits. Why? Because alveolar hypocapnia, regardless of the presence of the ventilation-perfusion mismatch, leads to hypoxia in body cells, including the muscle cells of the diaphragm. As a result, the diaphragm gets into a state of spasm. If breathing gets slower or closer to the norm (e.g., due to breathing retraining), the oxygen level in the diaphragm will increase and it will be again the main respiratory muscle used for breathing at rest.

How to restore function to the diaphragm

Diaphragm function can be improved using simple Diaphragmatic Breathing Exercises, Techniques and Instructions. In order to achieve constant abdominal breathing, it is necessary to use more special techniques. Medical research and numerous clinical trials suggest that resistive breathing (e.g., pursed lip breathing and western respiratory sport trainers) improves diaphragm function and lung function results. However, there are faster and better ways to restore the functioning of the diaphragm and enjoy the benefits of diaphragmatic breathing. These include breathing exercises and techniques and the use of breathing devices (e.g., the Frolov device, Samozdrav, and the Amazing DIY breathing device).

Reference pages: Breathing norms and the DIY body oxygen test:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test

References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in body tissues
- Nerve stabilization: Carbon dioxide has powerful calmative and sedative effects on brain neurons and nerve cells


Castro M. Control of breathing. In: Physiology, Berne RM, Levy MN (eds), 4-th edition, Mosby, St. Louis, 1998.

Ganong WF, Review of medical physiology, 15-th ed., 1995, Prentice Hall Int., London.

Shields JW, MD, Lymph, lymph glands, and homeostasis, Lymphology, Dec. 1992, 25, 4: 147.

West JB. Respiratory physiology: the essentials. 6th ed. Philadelphia: Lippincott, Williams and Wilkins; 2000.

Poole DC, Sexton WL, Farkas GA, Powers SK, Reid MB, Diaphragm structure and function in health and disease, Med Sci Sports Exerc. 1997 Jun;29(6):738-54.
Department of Kinesiology, Kansas State University Manhattan 66506, USA.
The diaphragm is the primary muscle of inspiration, and as such uncompromised function is essential to support the ventilatory and gas exchange demands associated with physical activity. The normal healthy diaphragm may fatigue during intense exercise, and diaphragm function is compromised with aging and obesity. However, more insidiously, respiratory diseases such as emphysema mechanically disadvantage the diaphragm, sometimes leading to muscle failure and death. Based on metabolic considerations, recent evidence suggests that specific regions of the diaphragm may be or may become more susceptible to failure than others. This paper reviews the regional differences in mechanical and metabolic activity within the diaphragm and how such heterogeneities might influence diaphragm function in health and disease. Our objective is to address five principal areas: 1) Regional diaphragm structure and mechanics (GAF). 2) Regional differences in blood flow within the diaphragm (WLS). 3) Structural and functional interrelationships within the diaphragm microcirculation (DCP). 4) Nitric oxide and its vasoactive and contractile influences within the diaphragm (MBR). 5) Metabolic and contractile protein plasticity in the diaphragm (SKP). These topics have been incorporated into three discrete sections: Functional Anatomy and Morphology, Physiology, and Plasticity in Health and Disease. Where pertinent, limitations in our understanding of diaphragm function are addressed along with potential avenues for future research.

Darnley GM, Gray AC, McClure SJ, Neary P, Petrie M, McMurray JJ, MacFarlane NG, Effects of resistive breathing on exercise capacity and diaphragm function in patients with ischaemic heart disease, Eur J Heart Fail. 1999 Aug;1(3):297-300.
Institute of Biomedical and Life Sciences, Glasgow University, Scotland, UK.
BACKGROUND: Muscle weakness has been suggested to result from the deconditioning that accompanies decreased activity levels in chronic cardiopulmonary diseases. The benefits of standard exercise programs on exercise capacity and muscular strength in disease and health are well documented and exercise capacity is a significant predictor of survival in patients with chronic heart failure (CHF). Selective respiratory muscle training has been shown to improve exercise tolerance in CHF and such observations have been cited to support the suggestion that respiratory muscle weakness contributes to a reduced exercise capacity (despite biopsies showing the metabolic profile of a well trained muscle).
AIMS: This study aimed to determine the effects of selective inspiratory muscle training on patients with chronic coronary artery disease to establish if an improved exercise capacity can be obtained in patients that are not limited in their daily activities.
METHODS: Nine male patients performed three exercise tests (with respiratory and diaphragm function assessed before the third test) then undertook a 4-week program of inspiratory muscle training. Exercise tolerance, respiratory and diaphragmatic function were re-assessed after training.
RESULTS: Exercise capacity improved from 812+/-42 to 864+/-49 s, P<0.05, and velocity of diaphragm shortening increased (during quiet breathing from 12.8+/-1.6 to 19.4+/-1.1 mm s(-1), P<0.005, and sniffing from 71.9+/-9.4 to 110.0+/-12.3 mm s(-1), P<0.005). In addition, five from nine patients were stopped by breathlessness before training; whereas only one patient was stopped by breathlessness after training.
CONCLUSION: The major findings in this study were that a non-intensive 4-week training programmed of resistive breathing in patients with chronic coronary artery disease led to an increase in exercise capacity and a decrease in dyspnea when assessed by symptom limited exercise testing. These changes were associated with significant increases in the velocity of diaphragmatic excursions during quiet breathing and sniffing. Patients that exhibited small diaphragmatic excursions during quiet breathing were most likely to improve their exercise capacity after the training programmed. However, the inspiratory muscle-training programmed was not associated with any significant changes in respiratory mechanics when peak flow rate, forced expiratory volume and forced vital capacity were measured. The resistive breathing programmed used here resulted in a significant increase in the velocity of diaphragm movement during quiet breathing and sniffing. In other skeletal muscles, speed of contraction can be determined by the relative proportion of fiber types and muscle length (Jones, Round, Skeletal Muscle in Health and Disease. Manchester: University Press, 1990). The intensity of the training programmed used here, however, is unlikely to significantly alter muscle morphology or biochemistry. Short-term training studies have shown that there can be increases in strength and velocity of shortening that do not relate to changes in muscle biochemistry or morphology. These changes are attributed to the neural adaptations that occur early in training (Northridge et al., Br. Heart J. 1990; 64: 313-316). Independent of the mechanisms involved, this small, uncontrolled study suggests that inspiratory muscle training may improve exercise capacity, diaphragm function and symptoms of breathlessness in patients with chronic coronary artery disease even in the absence of heart failure.

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