Chest Breathing Promotes COPD and Dyspnea

By Dr. Artour Rakhimov (www.NormalBreathing.com)

Chest breathing is very common in people with COPD even during quiet breathing at rest or during physical exercise. What are the effects? First of all, let us focus on effects of chest breathing on the most important COPD problem: low oxygen in body cells.

The diaphragm allows you to provide increased O2 transport in the lungs and more effective CO2 (carbon dioxide) removal from the blood. Normal breathing during rest has little tidal volume (only about 550 ml for just one breath for a 70-kg person), but it provides hemoglobin in the arterial blood with around 98-99% O2 saturation due to the major role of the diaphragm in the respiratory process.

The textbook, Respiratory Physiology (written by Dr. West, 2000), claims that the lower 10% of the lungs transports more than 40 ml of O2 per minute, while the upper 10% of the lungs transports less than 6 ml of O2 per minute. Hence, the lower parts of our lungs are about 6-7 times more effective in O2 transport than the top of the lungs due to better blood supply mostly caused by gravity.

Hence, chest breathing is the fundamental abnormality leading to hypoxemia (low blood oxygenation), dyspnea, shortoness of breath, and many other symptoms of COPD.

Further, decreased oxygen transport to body tissues will certainly enhance almost any other chronic illness. Indeed, think of healthcare research. A variety of published scientific articles have realized that cell hypoxia (low oxygen levels in tissues) is the main factor that promotes most cancers. Cardiovascular disease or angina pain is based on decreased amount of o2 inside heart muscle groups. Diabetes, bronchitis, cystic fibrosis, asthma, arthritis, GI ailments, and psychological disorders, they're all associated with decreased level of O2 within the body organs. Therefore, when these diseases grow to be acute and people are hospitalized or perhaps in critical treatment because of episodes or serious exacerbations, emergency professionals usually utilize 100 % pure o2 in order to save lives of people. Why? It is because for all those these ailments O2 concentrations in body tissues becomes dangerously small.

For this reason, chest respiration promotes COPD and other chronic ailments because of decreased O2 delivery to body organs.

Second, diaphragmatic breathing causes natural massage of the lymphatic nodes to be found just below the diaphragm, while the chest breathing prevent this. The lymphatic system, or the sewage system of the human body, doesn't employ a pump and for that reason, the lymph nodes can be found around those regions of one's body exactly where normal compression is actually created. By way of example, we have substantial number of lymph nodes on our neck. Throughout the day, most people do countless movements of our head. Subsequently, the lymphatic liquid will be pushed via valves out developing normal drainage of the lymphatic system. In the same manner, we have a large number of lymph nodes under arms and surrounding regions, to ensure that once we move our arms, the lymph nodes receive normal massage to eliminate unwanted substances. Inside groin region, you can find an additional set of lymph nodes which can be massaged by movements of our legs. You will discover no lymph nodes within all those locations of the body which do not experience natural massage.

Nonetheless, the lymph nodes from your stomach, kidneys, liver, spleen, pancreas, both colons, as well as other organs can be found just underneath your diaphragm.

For this reason, nature wants us all to be able to inhale using the diaphragm during rest. In case we have chest breathing, we increase bodily pollution along with accumulation of waste products within abdominal vital organs. For this reason, it's not at all a big surprise that seriously sick persons, people with COPD included, frequently develop and even die from multiple organ malfunction.

The diaphragm can help you to inhale with less effort and to utilize less energy.

Most contemporary people have got just close to 20-25 seconds for the body oxygen test (stress-free breath holding examination conducted immediately after natural exhale and only until initial stress) because their breathing is about two times bigger compared to the current medical norm. Indeed, one hundred years ago, according to published studies, ordinary people had about two times more body oxygen. Why? This is due to the fact their breathing had been diaphragmatic, slower and lighter.

Overbreathing lessens CO2 concentration in all muscle groups, including the diaphragm. Given that CO2 is a relaxant of muscles of the human body, hyperventilation produces a condition of spasm in the diaphragm. Moreover, deep breathing also predisposes us to slouching on account of stress around the shoulder blades, neck, and also other muscles in the top part of the body.

In the sick people, the problem is even worse. Their breathing is heavier during rest and they've got a lesser amount of O2 and CO2 in body cells. Hence, virtually they all are chest breathers.

On the list of techniques that are helpful for developing and learning diaphrgmatic breathing are the Frolov breathing device, Amazing DIY breathing device, Strelnikova respiratory gymnastic, and hatha yoga poses and breathing exercises.

Why Modern People Are Chest Breathers

Resources (www.NormalBreathing.com)

Dyspnea: Definition, Causes, and Treatment Options
Shortness of Breath: Causes Shortness of Breath and Easy Solution

www.NormalBreathing.com has hundreds of medical references, graphs, charts, analysis of breathing patterns, diagrams, free lifestyle modules, breathing exercises, and other resources to boost up cell oxygenation and enhance health.

References

Bianchi R, Gigliotti F, Romagnoli I, Lanini B, Castellani C, Grazzini M, Scano G, Chest wall kinematics and breathlessness during pursed-lip breathing in patients with COPD, Chest. 2004 Feb;125(2):459-65.
Fondazione Don C. Gnocchi IRCCS, Via Imprunetana 124, 50020 Pozzolatico, Florence, Italy.

Doucet M, Dubé A, Joanisse DR, Debigaré R, Michaud A, Paré MÈ, Vaillancourt R, Fréchette E, Maltais F, Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD, Thorax. 2010 Nov;65(11):963-70.
Centre de recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Québec, Canada.
These results indicate a greater susceptibility to a catabolic/anabolic imbalance favouring muscle atrophy in the quadriceps compared with the diaphragm in patients with COPD. The balance between the atrophy and hypertrophy signalling is inhomogeneous between respiratory and lower limb muscles, suggesting that local factors are likely to be involved in the regulation of muscle mass in COPD.

Caron MA, Debigaré R, Dekhuijzen PN, Maltais F, Comparative assessment of the quadriceps and the diaphragm in patients with COPD, J Appl Physiol. 2009 Sep;107(3):952-61.
Centre de Recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Quebec, Canada G1V 4G5.
... the oxidative metabolism varies in opposite directions, the diaphragm exhibiting increased resistance to fatigue while the quadriceps in COPD is characterized by premature fatigability. Differences in muscle phenotypic expression between the diaphragm and the quadriceps indicate that, in addition to systemic factors, the local microenvironment must participate in the reorganization seen in these two skeletal muscles in COPD.

Ottenheijm CA, Heunks LM, Dekhuijzen RP, Diaphragm adaptations in patients with COPD, Respir Res. 2008 Jan 24;9:12.
Dept. of Molecular and Cellular Biology, University of Arizona, Tucson, USA.
Inspiratory muscle weakness in patients with COPD is of major clinical relevance. For instance, maximum inspiratory pressure generation is an independent determinant of survival in severe COPD. Traditionally, inspiratory muscle weakness has been ascribed to hyperinflation-induced diaphragm shortening. However, more recently, invasive evaluation of diaphragm contractile function, structure, and biochemistry demonstrated that cellular and molecular alterations occur, of which several can be considered pathologic of nature. Whereas the fiber type shift towards oxidative type I fibers in COPD diaphragm is regarded beneficial, rendering the overloaded diaphragm more resistant to fatigue, the reduction of diaphragm fiber force generation in vitro likely contributes to diaphragm weakness. The reduced diaphragm force generation at single fiber level is associated with loss of myosin content in these fibers. Moreover, the diaphragm in COPD is exposed to oxidative stress and sarcomeric injury. This review postulates that the oxidative stress and sarcomeric injury activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force generating capacity of diaphragm fibers in patients with COPD. Interestingly, several of these presumed pathologic alterations are already present early in the course of the disease (GOLD I/II), although these patients appear not limited in their daily life activities. Treatment of diaphragm dysfunction in COPD is complex since its etiology is unclear, but recent findings indicate the ubiquitin-proteasome pathway as a prime target to attenuate diaphragm wasting in COPD.

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