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Fundamental
breathing reflexes are regulated by spinal cord and brainstem mechanisms. These centres 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-Hasselbalch (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 utilisation, 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 utilised and
bicarbonates are not adequately restoured 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 unrecognised symptoms
of hypocapnia are likely to be attributed to “stress” rather than to one’s response to challenge, a learned
maladaptive breathing behaviour. 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 behavioural-physiological
perspective, almost invariably fail to (1) identify the likely learned
behaviours that may be significantly contributing to deregulated acid-base
chemistry, (2) demonstrate to their clients how learned breathing behaviour may
be triggering symptoms and deficits, and (3) educate their clients about how to
modify breathing behaviour based on simple biological learning principles.
Copyrighted by
Behavioral Physiology Institute, |