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  • Title: Control of blood-gas and acid-base status during isometric exercise in humans.
    Author: Poole DC, Ward SA, Whipp BJ.
    Journal: J Physiol; 1988 Feb; 396():365-77. PubMed ID: 3137328.
    Abstract:
    1. At a given level of pulmonary gas exchange, ventilation (VE) is appreciably higher during isometric exercise than during isotonic exercise. It is presently not clear whether the resultant hypocapnia represents a compensatory hyperventilation for an arterial metabolic acidaemia or whether it might reflect a primary respiratory alkalaemia. 2. To resolve this issue, five subjects performed isometric leg exercise designed to induce exhaustion in ca. 5 min and, on a separate occasion, ca. 8 min. VE, CO2 output (VCO2), O2 uptake (VO2) and end-tidal gas tensions (PET,CO2, PET,O2) were measured breath-by-breath during exercise and recovery; arterialized venous blood (drawn from the dorsum of the heated hand) was sampled frequently and analysed for PCO2, PO2, pH, bicarbonate and lactate. These response profiles were compared with those resulting from exhausting bouts of isotonic leg exercise (cycle ergometry) of similar duration. 3. The isotonic exercise induced a metabolic (lactic) acidaemia with partial respiratory compensation. In contrast, isometric exercise consistently resulted in a respiratory alkalaemia, with little or no increase of blood [lactate]. At the end of the isometric exercise, VE fell abruptly and then rose again after a short interval (20 s, on average). This secondary stimulation presumably reflected the acid-base consequences of the increased blood [lactate] (3-5 mM, on average) which occurred in the recovery phase. 4. We therefore conclude that a primary respiratory alkalaemia occurs during isometric exercise, and that this results from ventilatory stimulation at a time when the 'exercise' metabolites are trapped within the contracting muscles as a consequence of impeded blood flow. The initial rapid reduction of ventilation which occurred at the cessation of the isometric exercise is consistent with a washing-out of 'hyperpnoea-inducing' metabolites from the muscles. Allowing for transit to the central circulation, the reduced ventilation is subsequently supplemented by a powerful humoral drive to breathe which results in a further hyperpnoea and secondary hypocapnia. Because of its latency, we hypothesize that this secondary hypocapnia is of peripheral chemoreceptor origin. 5. The ventilatory response profile for isometric exercise, and the subsequent recovery phase, supports the contention that both the exercising muscles and the peripheral chemoreceptors can be important sites for inducing hyperpnoea in humans.
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