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.