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.
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.
not all, clinical trials have found benefits of
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,
and postsurgery, chronic heart failure, ischaemic heart disease, stroke,
ventilator 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
- reduced medication and improved quality of life in people with chronic
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
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.
In 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.
Furthermore, 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.
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.
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