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Training of Inspiratory Muscles for Immunity, Body Oxygen, and VO2max

Training of inspiratory muscles for Sports Performance,
Asthma, COPD, Cystic Fibrosis and Other Conditions

Nearly all clinical published research in the area of inspiratory muscle training is based on myths and oversimplifications. The common assumptions that are hidden in these studies are:
- if you develop stronger respiratory muscles, you will get more oxygen in body cells, both at rest and during exercise, since you will be able to breathe more air
- deep breathing or breathing more air, during exercise and at rest, provides more oxygen for cells and is good for health
- the breathing pattern does not influence immunity and 100s of chemical and metabolic reactions including those that take place in the same respiratory muscles.

There is a strong impression that these scientists and researchers are unaware that hyperventilation (breathing more than the medical norm) reduces oxygen delivery to tissues of all vital organs disturbing, undermining, perverting, and destroying hundreds of vital processes in the human body.

Breathing rates in healthy, normal people vs diseases

Similar oversimplifications and myths are common in nutrition:
- eating foods with cholesterol increases your blood cholesterol
- eating fats make you fat
even though dozens of recent clinical studies proved that these are all wrong ideas.

In all these cases of myths, an obsession with physical or mechanical analogy (more causes more) does not provide any good service for better health.

Rowers sports performance for inspiratory muscle trainingMost, but not all, clinical trials have found benefits of inspiratory muscle training on sports performance in rowers (Volianitis et al, 2001; Klusiewicz et al, 2008; Riganas et al, 2008), cyclists (Romer et al, 2002a; Romer et al, 2002b), and swimmers (Kilding et al, 2010; Wells et al, 2005; Mickleborough et al, 2008).

Clinical trials also tested the effects of inspiratory muscle training on asthma, COPD, bronchiectasis, cystic fibrosis, diabetes, pre- and postsurgery, chronic heart failure, ischaemic heart disease, stroke, Large diaphragmatic breathing reduces brain oxygenventilator weaning, and neuromuscular diseases (some references with conclusions are provided below).

Most of these studies have demonstrated the following benefits:
- reduction in dyspnea (a sensation of breathlessness) during exercise in athletes and at rest or during very light exercise in patients
- increase in the force of inspiratory muscles during intensive exercise training for athletes
- increased endurance in patients with improvements in some lung function parameters
- reduced medication and improved quality of life in people with chronic diseases.

Athlete swimming while training muscles with strong inspirationsMost of these studies have used the following respiratory trainers or devices: UltraBreathe, Powerlung, Powerbreathe, and Expand-A-Lung.

The claimed goal of respiratory and inspiratory muscle training is to improve oxygen transport. But none of these studies explained the real causes of health improvements since these causes lie in a different realm. Let us consider problems with oxygen transport for sick people with dyspnea (shortness of breath) at rest.

Dyspnea and oxygen transport

Man with dyspnea or chest pain due to weak inspiration musclesDyspnea in patients, and in some degree in competing or training athletes, is virtually always accompanied by inefficient oxygen transport and resultant tissue hypoxia. While inspiratory muscle training is focused on mechanical effects, we are going to focus on cellular effects related to the mechanism of oxygen transport.

People with heart disease, asthma, diabetes, COPD and many other conditions, have greatly elevated minute ventilation at rest: about 2-3 times more than the medical norm. (The norm is 6 L/min for a 70-kg man.) This has been known to clinical physicians for decades and proven by dozens of studies. What are the effects?

Chronic hyperventilation, and here we have even more impressive supporting evidence, causes systemic cell hypoxia. The mechanism of inefficient O2 transport and resultant tissue hypoxia depends on the presence of lung problems (ventilation-perfusion mismatch). For patients with normal lungs (e.g., most people with heart disease and diabetes), alveolar hyperventilation leads to arterial hypocapnia (lack of CO2 in the arterial blood). Since CO2 is a potent vasodilator, hypocapnia leads to constriction of arteries and arterioles causing reduced perfusion and increased systemic resistance to blood flow.

Young MDs smilingIn addition, a lack of CO2 in tissues suppresses the Bohr effect causing reduced release of oxygen in cells. These two effects significantly reduce systemic oxygen delivery (Laffey & Kavanagh, 2002; Nunn, 1987). There are, however, some differences in the reduction of oxygen delivery to various muscle tissues. Lowered oxygenation of the heart muscle due to hypocapnic hyperventilation is well documented (Fox et al, 1979; Karlsson et al, 1994; Okazaki et al, 1991; Okazaki et al, 1992; Wexels et al, 1985). Similarly, a large reduction in partial O2 pressure takes place in the smooth muscles of the colon (Guzman et al, 1999), with a more moderate decrease in striated and skeletal muscles (Gustafsson et al, 1993; Thorborg et al, 1998; Okazaki et al, 1989). Tissue hypoxia results in anaerobic cellular respiration at rest and elevated blood lactic acid levels (common for all these health conditions). These effects sharpen the sensation of fatigue in the respiratory muscles (experienced as shortness of breath) at rest in patients and during exercise in athletes.

CO2 modelFurthermore, since carbon dioxide is a strong dilator of airways (see links to studies below), hypocapnic bronchoconstriction increases airway resistance. In addition, cell hypoxia causes generation of free radicals, suppression of the immune system, and favors chronic inflammation. Therefore, frequent infections, airway inflammation and extra mucus production can drastically worsen the symptom of dyspnea.

Hence, dyspnea is caused by factors that all originate in chronic hyperventilation at rest.

breathlessness mechanism and weak respiratory muscle causes

Effects of hyperventilation on oxygen transport during exercise

During physical exercise, if alveolar CO2 levels drop (overbreathing in relation to CO2 production), the main effects on oxygen transport are the same: less oxygen is delivered to tissues due to hypocapnic vasoconstriction and the suppressed Bohr effect.


Training inspiratory muscles can be an independent purpose for breathing exercises. However, this type of training (improved strength of the inspiratory muscles) does not address the mechanism of reduced oxygen transport during dyspnea (breathlessness or shortness of breath). Therefore, the main physiological potential and benefit of breathing training is improved breathing patterns, VO2max and body oxygenation test results at rest (slower and lighter breathing with reduced respiratory frequency and minute ventilation rate). All these effects can be achieved with longer exhalations during inspiratory muscle training. Lifestyle corrections (see Learn here Section) will improve benefits of inspiratory muscle training as well. The best sport performance effects was so far found after application of the breathing device which name is provided right below here as your bonus content.

Tweet or Share this page to reveal the bonus content.

This YouTube Video explains how to choose effective breathing techniques for high body oxygen levels:

- This page in Spanish: Entrenamiento muscular inspiratorio (Evaluación): ¿Cómo obtener más beneficios?

For references and important extracts from abstracts, visit Inspiratory muscle training studies.

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