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Fundamental breathing reflexes
are regulated by spinal cord and brainstem mechanisms. These centers regulate breathing, from
breath to breath, based on pH of the surrounding cerebrospinal and
interstitial fluids, along with the presence of PCO2, but
surprisingly not PO2. In
addition to receptor sites in the nervous system, however, there are also
receptor sites in the aorta and
the carotid arteries which are
sensitive not only to arterial CO2 and arterial pH, but also to
arterial PO2 (PaO2).
The Henderson-Hasselbach
(H-H) equation says: pH = [HCO3‾] ÷ PCO2. When
the numerator of the equation, bicarbonate concentration [HCO3‾],
is disturbed by a metabolic condition, there is normally reflexive breathing compensation, where PCO2, the
denominator of the equation, rises or falls, balancing the ratio, and thus
keeping the pH within its normal range, in the case of blood plasma, 7.35 to
7.45. For example, when bicarbonate
concentration is reduced as a result of ketoacidosis
(diabetes), overbreathing decreases PCO2 and restores plasma pH
(upward) toward normal. Overbreathing,
in this case, despite its potential negative side effects, is an adaptive
response to ketoacidosis. Click here
for acid-base
balance. Another important
example of reflexive respiratory compensation is during severe physical
exercise. During transition from
aerobic to anaerobic exercise, abnormal amounts of lactic acid begin to be
generated. Hydrogen ion production
begins to “outstrip” its utilization, and there may no longer be an adequate
bicarbonate reserve, resulting in lactic
acidosis. Fortunately, lung
capacity normally exceeds cardiovascular capacity, so that acidosis during strenuous exercise can be
compensated for through overbreathing, PaCO2 reduction. Observing PCO2 levels during
exercise, on a stationary bike or on a treadmill, gives sports and fitness
enthusiasts a rough indication of their anaerobic
threshold, the point at which cells derive energy from glucose in the
absence of adequate oxygen. Lactic
acid is generated faster than it can be utilized
and bicarbonates are not adequately restored for further buffering. Lowering CO2 levels compensates
for the loss of bicarbonates, and moves the pH, as shown in the H-H equation,
toward normal. The brainstem
chemo-regulatory management of breathing relies principally on the diaphragm
for its control. Thus, learned use of
accessory muscles during times of stress and challenge, chest breathing, may
lead to deregulation of brainstem reflex mechanisms, and possible
hypocapnia. The resulting unrecognized
symptoms of hypocapnia are likely to be attributed to “stress” rather than to
one’s response to challenge, a
learned maladaptive breathing behavior.
The effects may also be attributed directly to “prejudices” about
breathing mechanics, “chest breathing is bad,” rather than to the underlying
chemistry that truly accounts for the observed symptoms and deficits. Click here for more information about external respiration. Unfortunately,
practitioners, who do not understand breathing from a
behavioral-physiological perspective, almost invariably fail to (1) identify the
likely learned behaviors that may be significantly contributing to
deregulated acid-base chemistry, (2) demonstrate to their clients how learned
breathing behavior may be triggering symptoms and deficits, and (3) educate
their clients about how to modify breathing behavior based on simple
biological learning principles. Copyrighted by Behavioral Physiology Institute, Santa Fe, New Mexico USA |