The ventilatory responses to muscular exercise, including its breathing pattern and airflow profile components, provide important information for interpretation of clinical exercise testing. The appropriateness of the ventilatory response, however, depends not simply on the level of ventilation achieved for a particular WR but also on the extent to which it subserves its pulmonary gas exchange and acid-base regulatory functions. For example, alveolar and arterial blood-gas partial-pressures can only be regulated at, or close to, resting levels if alveolar ventilation (VA) increases in proportion to the rates of pulmonary gas exchange:
2 Va,stpd v y where Fa,co2 is the fractional concentration of alveolar carbon dioxide and V'a,stpd is the flow or volume per unit time, both measured under the same conditions (standard temperature and pressure dry; sTPD).
However, as the alveolar partial pressure of carbon dioxide (Pa,co2) is of more interest physiologically, and ventilatory volumes are standardly reported at body temperature and pressure saturated with water vapour (BTPS):
The 863 in this, and related equations, derives from different frames of reference for the metabolic and ventilatory measurements and reporting carbon dioxide as partial pressure, assuming a body temperature of 37 °C. similarly, for oxygen exchange:
where Pa,o2 is the alveolar and Pi,O2 is the inspired Po2.
However, neither V9A nor the alveolar gas partial pressures in equations 16 and 17 are conceptually simple or readily measurable variables in a structure as complex as the lung. This is because it is difficult to establish a single average value for either V A or alveolar gas tensions [56, 57] when there are significant regional variations in alveolar oxygen and carbon dioxide partial pressure and alveolar ventilation to perfusion ratios (V'a/Q ' ). Typically this difficulty is overcome by the practical expedient of assuming Pa,co2 to be exactly equal to Pa,CO2; this can be readily determined by appropriate blood sampling and the equivalent V9A can consequently be computed. It is important to recognise that this V A is, in fact, a figment. It is not the actual level of ventilation of the subject's alveoli but the VA that would provide an average PA,CO2 exactly equal to that of Pa,CO2. By the same token, the Pa,o2 that is computed in equation 17 is that of the "ideal" lung. This, by definition, yields no difference between the alveolar and arterial oxygen partial pressures. In reality the "real" mean Pa,o2 will be systematically higher than the "ideal" Pa,o2.
For Pa,co2 and Pa,o2 to be maintained constantly during exercise, VA must change in precise proportion to V'CO2 and V'o2, respectively, i.e. that of pulmonary gas exchange rather than tissue metabolic rates when these rates differ. However, note that V9A is common to both relationships in equation 18. Here the effect of the slight difference in inspiratory and expiratory volumes on oxygen partial pressure that occurs when R ? 1 has been neglected, as the effect is usually relatively small and does not materially affect the argument.
863 x VCO2 863 x VO
Note, however, that VA cannot meet the regulatory demands of both oxygen and carbon dioxide exchange simultaneously under conditions in which carbon dioxide exchange rate differs from that of oxygen, either as a result of differences in substrate utilisation profiles or because of transient variations in the body gas stores.
It is often stated that ventilation during muscular exercise increases in proportion to metabolic rate. This is imprecise on two accounts. First, the body expresses a metabolic rate both for its Vo2 and its V'CO2 and under conditions in which the tissue RQ changes as a result of differences in substrate utilisation, ventilation changes as a close linear function of the VCO2 rather than VO Secondly, the assertion that ventilation during muscular exercise changes as a function of metabolic carbon dioxide production is also imprecise. This is because under conditions in which the changes in body carbon dioxide storage (e.g. in muscle and venous blood during exercise transients) dissociates the metabolic production rate from the pulmonary exchange rate, ventilation closely "tracks" the rate of pulmonary V'CO2, not the rate of muscle metabolic production [58-60]. Pa,co2 is, therefore, the more closely regulated variable for moderate intensity exercise. Any resultant changes of Po2 are normally within the relatively flat region of the oxygen dissociation curve, such that the oxygen content or saturation of the arterial blood will not be affected to any great extent.
Consequently, the demands for ventilation during exercise are usually considered using pulmonary carbon dioxide exchange as the frame of reference. At any set-point level of Pa,co2, the demand for V'A increases as a linear function of V'co2; the greater the VCO2 the greater the ventilation requirement. When Pa,CO2 is regulated at a lower level (as is the case in certain subjects with lung disease or normal sea-level subjects sojourning at high altitude), then, for any given level of V'CO2, V'A must be appropriately greater. However, it is also necessary to ventilate the dead space of the lung ( Vd):
where VE is the expiratory minute ventilation, Vt is the tidal volume and Vd/Vt is the physiological dead space fraction of the breath and equals VD/VE because VD = fR x Vd and VE = fRx Vt, where fR is the breathing frequency.
The ventilatory demand of exercise should, therefore, be considered with respect to its three defining variables: 1) the rate of pulmonary carbon dioxide clearance; 2) the "setpoint" at which Pa,CO2 is regulated; and 3) the physiological dead space fraction of the breath, which represents an index of the inefficiency of pulmonary gas exchange.
This can be considered in three forms, each providing a slightly different facet of the same inter-relationships:
Importantly, the regulatory relationship is not, strictly, determined by the slope of the linear region of the plot of VE as a function of VCO2 (this should not include the hyperventilatory component at high WRs); the intercept on the VE axis plays an important contributory role. Rather, Pa,CO2 (i.e. the functional equivalent of the "ideal"
PA,CO2) is, therefore, regulated at a particular value only if the ventilatory equivalent for carbon dioxide (VE/V'co2) changes in precise proportion to the change in Vd/Vt. Or, an abnormally high ventilatory equivalent for carbon dioxide can result from Pa,CO2 being low, Vd/Vt being high or both. However, as it is difficult to estimate Pa,CO2 noninvasively in patients with lung dysfunction, one is still left with an uncertainty as to the cause of a high VE/V'co2. For example, it could be high in a patient with normal lung function who regulates Pa,CO2 at a lower level (e.g. in a hypoxic subject or one with chronic metabolic acidosis), or Pa,co2 might be normal in a subject with a large Vd/Vt. Attempts to estimate Pa,co2 either from knowing the levels of Vt and the Pet,co2  or from attempts to establish a ''mean'' Pa,co2 [62, 63], are to be discouraged in patients with lung disease (see the next section for further discussion).
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