What Causes Cramps? Low O2 and CO2 Levels in Cells

Smiling medical doctors Clinical experience of Russian medical doctors suggests that people with normal body oxygen levels do not experience any types of cramps and spasms, including foot cramps, leg muscle cramps, stomach spasm and so forth. During hyperventilation, less O2 and CO2 is available to body cells (Brown et al, 1953).

Low levels of CO2 and O2 cause overexcitement of nerve cells and involuntary contraction of muscle fibers (Brown et al, 1953; Macefield et al, 1991; Schwartz et al, 1993; Seyal et al, 1998, Sparing et al, 2007. Therefore, overbreathing causes those effects in muscle and nerve cells that are directly responsible for cramping. Why are cramps so common in modern people and were very rare some 60-90 years ago? This graph explains the effect.

Hyperventilation prevalence graph that explains what causes cramps

We can see that modern people are hyperventilators or they have fast and deep breathing. The situation in people with diseases even worse (see links below). Breathing more than the medical norm reduces oxygen and carbon dioxide content in body cells. The next graph provides the exact mechanism of cramps.

Hyperventilation causes cramps in muscle cells

Hence, effective treatment of cramps and spasms should be based on learning such automatic breathing patterns that increase levels of CO2 and O2 in the muscles of legs, feet, and stomach. Breathing retraining involves breathing exercises (or a lot of physical exercise with nose breathing) and lifestyle changes. As we see below, with over 40 seconds for the body oxygen test, cramps are virtually impossible.

In order to prove that abnormal breathing is the cause of cramps, one can apply a simple breathing exercise How to Get Rid of Cramps in 1-2 Minutes (easy breathing exercise).

Deficiencies in minerals (calcium, magnesium, sodium and potassium) make spasms and cramps more frequent and severe. Learn methods and ways how to check and correct these nutritional deficiencies : Major Nutrients Guide for Body Oxygenation. Lack of nutrients is an additional factor that causes cramps.

How automatic breathing parameters relate to spasms and cramping

(muscle, stomach, leg cramps in bed, period or menstrual cramps, and many others)

with the permanent way to get rid of cramps and spasms

Respiratory Frequency*	Body Oxygen Test (morning result)	Chances of cramps
More than 20 breaths/min	Less than 20 s	Very possible
15-20 breaths/min	20-30 s	Possible
12-15 breaths/min	30-40 s	Very rare
12 or less breaths/min	> 40 s	Virtually impossible

* You cannot measure your respiratory frequency just by counting it (more info: Breathing Rates)

Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and Body Oxygen in Healthy, Normal and Sick People
Breathing norms Parameters, graph, and description of the normal breathing pattern
6 breathing myths 6 myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the Sick. Table 1. Western scientific evidence about prevalence of CHV (chronic hyperventilation) in patients with various chronic conditions (34 medical studies)
Normal Minute Ventilation in Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of Normal People (24 medical publications)
HV and hypoxia How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
Body oxygen test How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy Table 4. CP (body oxygen level) in healthy people (27 medical studies)
Body oxygen in sick Table 5. CP (body oxygen level) in sick people (14 medical studies)
Buteyko Table of Health Zones with clinical description of most common zones
Morning HV Morning hyperventilation effect or how and why critically ill people are most likely to die during early morning hours

References: CO2 Effects Web Pages
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 tissues
Cell Oxygen Levels and oxygen transport are controlled by alveolar CO2 and breathing
Oxygen Transport depends on breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by breathing since hypoxia leads to or intensifies chronic inflammation through over-expression of the hypoxia-inducible factor 1, while normal breathing reduces these processes
Nerve stabilization takes place due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
Brochodilation - dilation of airways (bronchi and bronchioles) by carbon dioxide, and their constriction due to hypocapnia
Blood pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions
CO2 myth "CO2 is a toxic waste gas" myth
Breathing control How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic

References
Brown EB Jr. Physiological effects of hyperventilation. Physiol Rev 1953, 33: 445–471.

Macefield G, Burke D. Paraesthesiae and tetany induced by voluntary hyperventilation. Increased excitability of human cutaneous and motor axons, Brain 1991, 114: 527–540.

Schwartz AR, Thut DC, Brower RG, Gauda EB, Roach D, Permutt S, Smith PL, Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2, J Appl Physiol. 1993 Apr; 74(4): 1597-605.

Seyal M, Mull B, Gage B. Increased excitability of the human corticospinal system with hyperventilation. Electroencephalogr Clin Neurophysiol, 1998, 109: 263–267.

Sparing R, Dafotakis M, Buelte D, Meister IG, Noth J, Excitability of human motor and visual cortex before, during, and after hyperventilation, J Appl Physiol. 2007 Jan; 102(1): 406-11.
Institute of Neuroscience and Biophysics, Department of Medicine, Research Centre Juelich, Juelich, Germany.
In humans, hyperventilation (HV) has various effects on systemic physiology and, in particular, on neuronal excitability and synaptic transmission. However, it is far from clear how the effects of HV are mediated at the cortical level. In this study we investigated the effects of HV-induced hypocapnia on primary motor (M1) and visual cortex (V1) excitability. We used 1) motor threshold (MT) and phosphene threshold (PT) and 2) stimulus-response (S-R) curves (i.e., recruitment curves) as measures of excitability. In the motor cortex, we additionally investigated 3) the intrinsic inhibitory and facilitatory neuronal circuits using a short-interval paired-pulse paradigm. Measurements were performed before, during, and after 10 min of HV (resulting in a minimum end-tidal Pco(2) of 15 Torr). HV significantly increased motor-evoked potential (MEP) amplitudes, particularly at lower transcranial magnetic stimulation (TMS) intensities. Paired-pulse stimulation indicated that HV decreases intracortical inhibition (ICI) without changing intracortical facilitation. The results suggest that low Pco(2) levels modulate, in particular, the intrinsic neuronal circuits of ICI, which are largely mediated by neurons containing gamma-aminobutyric acid. Modulation of MT probably resulted from alterations of Na(+) channel conductances. A significant decrease of PT, together with higher intensity of phosphenes at low stimulus intensities, furthermore suggested that HV acts on the excitability of M1 and V1 in a comparable fashion. This finding implies that HV also affects other brain structures besides the corticospinal motor system. The further exploration of these physiological mechanisms may contribute to the understanding of the various HV-related clinical phenomenona.

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