What Causes Cramps in Leg and Other Muscle Spasms?
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). An additional cause of muscle spasms is an electrical charge of the human
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. You can use a simple
breathing exercise that eliminates spasms in legs and other muscles in about 1-2 minute (see the link
Why are cramps so
common in modern people and were very rare some 60-90 years ago? This graph
explains the major reason behind cramps in
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.
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, muscle spasms
are virtually impossible.
Most contemporary people carry a large (hundreds of volts) positive
electrical charge (indicating electron deficiency) that interferes with work
of muscles that require only some fraction of a volt. Grounding is a very
effective method to normalize potential of the human body. You can learn
more about this cause of cramps on pages devoted to
How to ground yourself.
Nearly all people (who have poor diet) cannot get rid of their cramps
due to a lack of a certain unknown-yet chemical in vegetables. This
deficiency is an additional cause of
cramps. These vegetables (that contain this substance) are
usually dark (i.e., green or brown), such as broccoli, lentils (green and
brown lentils) and beans (but not from cans or jars). You can try this hatural home remedy and solution for spasms. Other foods, like
leafy greens (spinach, green or red lettuces, and so on) can help as well.
Try eating them for 1-2 days and monitor the effects.
In order to prove that abnormal breathing is the cause of spasms, one can
apply a simple
How to Get Rid of Spasms in 1-2 Minutes (easy breathing exercise).
Or you can click on the picture (on the right side) to watch the video clip "How
to Get Rid of Your Cramps in 1-2 min (Easy Breathing Exercise)".
provides instructions for this simple breathing cure that eliminates most
cramps in about 1 minute. However, some people require additional methods
described on this page.
minerals (calcium, magnesium, sodium and potassium) make
spasms in muscles 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
leads to cramps.
Right below here is a table that provides a link between breathing patterns (exact numbers) and chances of cramps. This Table is provided as your bonus content.
Brown EB Jr. Physiological effects of hyperventilation.
Physiol Rev 1953, 33: 445471.
Macefield G, Burke D. Paraesthesiae and tetany induced by
voluntary hyperventilation. Increased excitability of human cutaneous
and motor axons, Brain 1991, 114: 527540.
Schwartz AR, Thut DC, Brower RG, Gauda EB, Roach D, Permutt S, Smith
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: 263267.
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
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