Models of ventilatory (VE) control during exercise have classically incorporated both proportional humoral feedback (carotid and central chemoreflex) and neurogenic feedforward (central command, muscle, cardio-circulatory) control. During moderate exercise (below lactate threshold (lt)) VE manifests first-order kinetics, increasing mono-exponentially to the new steady state; the close correlation of VE with ptihnonary CO2 output (VCO2) ensuring stability of arterial PCO2 and pH (and PO2). Above lt, VE kinetics become nonlinear. and steady states are either delayed or not attained. This reflects the influence of the developing metabolic acidemia on VE (a) indirectly via body CO2 stores washout which augments VCO2 and (b) directly to effect respiratory compensation (the hypocapnia resulting from VE increasing out of proportion to VCO2 constrains the fall of pH). The carotid bodies (CBs) are widely regarded to fine-tune arterial blood-gas and acid-base regulation, events which might be expected to lead to a loss of first-order behavior, but do not. The CBs are also important in mediating the respiratory compensation above lt, which has surprisingly slow kinetics (i.e. inconsistent with the rapidity of CB responses to infused acid loads in animals). These issues are explored in the context of recent advances in both ventilatory control and CB chemotransduction.
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