"V E in phase 2 responds with first-order kinetics that are only slightly slower than those of ˙ V CO 2 but considerably slower than those for O 2 uptake ( ˙ V O 2 ) for a range of WR forcing functions, such as the step, impulse and sinusoid (e.g. Linnarsson, 1974; Miyamoto, 1989; Whipp & Ward, 1991 "
[Show abstract][Hide abstract] ABSTRACT: Below the lactate threshold ((thetaL)), ventilation (V(E))responds in close proportion to CO(2) output to regulate arterial partial pressure of CO(2) (PaCO2). While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic 'coupling' between and V(E) and V(CO2). Above (thetaL), PaCO2 is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When V(E) requirements are high (as in highly fit endurance athletes), V(E) can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance.
[Show abstract][Hide abstract] ABSTRACT: The stability of arterial blood gas tensions and pH during steady-state moderate exercise has suggested an important humoral element of ventilatory control in humans. However, the involvement of central and peripheral chemoreflexes in this humoral control remains controversial. This reflects, in large part, technical and interpretational limitations inherent in currently used estimators of chemoreflex "sensitivity." Evidence suggests that the central chemoreceptors (a) contribute little during moderate exercise, given the relative stability of cerebrospinal pH, (b) constrain the hyperpnea of high-intensity exercise, consequent to the respiratory compensation for the metabolic acidemia, and (c) may play a role in the respiratory compensation during chronic metabolic acidemia. In contrast, the peripheral chemoreceptors appear to (a) exert considerable influence on ventilatory kinetics in moderate exercise, but are less important in the steady state, and (b) induce much of the respiratory compensation of high-intensity exercise.
Canadian journal of applied physiology = Revue canadienne de physiologie appliquée 10/1994; 19(3):305-33. DOI:10.1139/h94-026 · 1.30 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Models of the exercise hyperpnoea have classically incorporated elements of proportional feedback (carotid and medullary chemosensory) and feedforward (central and/or peripheral neurogenic) control. However, the precise details of the control process remain unresolved, reflecting in part both technical and interpretational limitations inherent in isolating putative control mechanisms in the intact human, and also the challenges to linear control theory presented by multiple-input integration, especially with regard to the ventilatory and gas-exchange complexities encountered at work rates which engender a metabolic acidosis. While some combination of neurogenic, chemoreflex and circulatory-coupled processes are likely to contribute to the control, the system appears to evidence considerable redundancy. This, coupled with the lack of appreciable error signals in the mean levels of arterial blood gas tensions and pH over a wide range of work rates, has motivated the formulation of innovative control models that reflect not only spatial interactions but also temporal interactions (i.e. memory). The challenge is to discriminate between robust competing control models that: (a) integrate such processes within plausible physiological equivalents; and (b) account for both the dynamic and steady-state system response over a range of exercise intensities. Such models are not yet available.
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