Neural and humoral factors affecting ventilatory response during exercise.
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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.Experimental Physiology 04/2007; 92(2):357-66. DOI:10.1113/expphysiol.2006.034371 · 2.87 Impact Factor
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ABSTRACT: The aim of this study was to evaluate the temporal response of the sympatheticvagal balance during progressive exercise in healthy people by time-frequency analysis (TFA) of heart rate variability (HRV) and apply the parameters extracted from this to detect the anaerobic threshold (AT). RR series extracted from 26 athletes (22.2 ± 5.5 years, 74.1 ± 7.4 kg, 1.76 ± 0.07 m) during progressive maximal exercise were resampled (5 Hz) and filtered (band-pass Butterworth 4th order). The power spectral density of the bands of high (PSDHF) and low (PSDLF) frequency were extracted from three TFA techniques. The AT obtained by HRV (ThHRV) was compared with the gold standard. The dynamics of HRV obtained by TFA techniques revealed a predominance of sympathetic over the vagal activity (PSDLF / PSDHF) throughout the exercise (rest: 3.19 ± 4.47 n.u.; exercise: 3.97 ± 3.49 n.u.). The ThHRV presented errors of 23.1 to 80.8% using conventional methods, and from dynamic measurements, 2.8 to 18.2%, resulting in no significant differences between these (166 bpm [144-175]) and the ventilatory threshold (154.3 bpm [147 to 168 bpm]). In conclusion: Short-Time Fourier Transform was the best TFA alternative, the predominance of the sympathetic over the vagal activity during exercise was confirmed by the three TFA techniques employed and the ThHRV based on dynamic measurements showed acceptable agreement with AT obtained by ventilatory measurements, so that we can recommend its use for obtaining the AT.06/2011, Degree: M.Sc.
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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.Respiration Physiology 10/2000; 122(2-3):149-66. DOI:10.1016/S0034-5687(00)00156-0