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Control of Breathing During Exercise

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Abstract

Download Free Sample The control of breathing during exercise remains the source of considerable debate. Classical schemes of the exercise hyperpnea have incorporated elements of proportional feed-back from chemoreceptor sites (carotid body and brainstem) and feed-forward neurogenic (central command and muscle reflex) control. However, the precise details of the control process are still not fully resolved, reflecting in part technical and interpretational limitations inherent in isolating putative control mechanisms in the intact exercising human and also the challenges presented by the ventilatory and gas-exchange complexities encountered at work rates which engender a metabolic (lactic) acidosis. Although some combination of neurogenic, chemoreflex, and circulatory-coupled processes are likely to contribute to the control, intriguingly, the overall system appears to evidence considerable redundancy. This, coupled with the lack of appreciable steady-state error signals in the mean levels of arterial PCO2, PO2, 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., short-term and longer-term ‘memory’). The challenge remains to discriminate between robust control schemes that (a) integrate such processes within plausible physiological equivalents, and (b) account for both the dynamic and steady-state system response over the entire range of exercise intensities. Table of Contents: Introduction / Ventilatory Requirements / Ventilatory Responses / Ventilatory Control / Conclusions / References

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During dynamic exercise, the healthy pulmonary system faces several major challenges, including decreases in mixed venous oxygen content and increases in mixed venous carbon dioxide. As such, the ventilatory demand is increased, while the rising cardiac output means that blood will have considerably less time in the pulmonary capillaries to accomplish gas exchange. Blood gas homeostasis must be accomplished by precise regulation of alveolar ventilation via medullary neural networks and sensory reflex mechanisms. It is equally important that cardiovascular and pulmonary system responses to exercise be precisely matched to the increase in metabolic requirements, and that the substantial gas transport needs of both respiratory and locomotor muscles be considered. Our article addresses each of these topics with emphasis on the healthy, young adult exercising in normoxia. We review recent evidence concerning how exercise hyperpnea influences sympathetic vasoconstrictor outflow and the effect this might have on the ability to perform muscular work. We also review sex-based differences in lung mechanics. © 2012 American Physiological Society. Compr Physiol 2:1093-1142, 2012.
Article
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Article
Central chemoreception traditionally refers to a change in ventilation attributable to changes in CO2/H(+) detected within the brain. Interest in central chemoreception has grown substantially since the previous Handbook of Physiology published in 1986. Initially, central chemoreception was localized to areas on the ventral medullary surface, a hypothesis complemented by the recent identification of neurons with specific phenotypes near one of these areas as putative chemoreceptor cells. However, there is substantial evidence that many sites participate in central chemoreception some located at a distance from the ventral medulla. Functionally, central chemoreception, via the sensing of brain interstitial fluid H(+), serves to detect and integrate information on (i) alveolar ventilation (arterial PCO2), (ii) brain blood flow and metabolism, and (iii) acid-base balance, and, in response, can affect breathing, airway resistance, blood pressure (sympathetic tone), and arousal. In addition, central chemoreception provides a tonic "drive" (source of excitation) at the normal, baseline PCO2 level that maintains a degree of functional connectivity among brainstem respiratory neurons necessary to produce eupneic breathing. Central chemoreception responds to small variations in PCO2 to regulate normal gas exchange and to large changes in PCO2 to minimize acid-base changes. Central chemoreceptor sites vary in function with sex and with development. From an evolutionary perspective, central chemoreception grew out of the demands posed by air versus water breathing, homeothermy, sleep, optimization of the work of breathing with the "ideal" arterial PCO2, and the maintenance of the appropriate pH at 37°C for optimal protein structure and function. © 2012 American Physiological Society. Compr Physiol 2:221-254, 2012.
Article
The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article. © 2012 American Physiological Society. Compr Physiol 2:141-219, 2012.
Article
This paper describes the interactions between ventilation and acid-base balance under a variety of conditions including rest, exercise, altitude, pregnancy, and various muscle, respiratory, cardiac, and renal pathologies. We introduce the physicochemical approach to assessing acid-base status and demonstrate how this approach can be used to quantify the origins of acid-base disorders using examples from the literature. The relationships between chemoreceptor and metaboreceptor control of ventilation and acid-base balance summarized here for adults, youth, and in various pathological conditions. There is a dynamic interplay between disturbances in acid-base balance, that is, exercise, that affect ventilation as well as imposed or pathological disturbances of ventilation that affect acid-base balance. Interactions between ventilation and acid-base balance are highlighted for moderate- to high-intensity exercise, altitude, induced acidosis and alkalosis, pregnancy, obesity, and some pathological conditions. In many situations, complete acid-base data are lacking, indicating a need for further research aimed at elucidating mechanistic bases for relationships between alterations in acid-base state and the ventilatory responses. © 2012 American Physiological Society. Compr Physiol 2:2203-2254, 2012.
Article
BABB, T. G. Exercise ventilatory limitation: the role of expiratory flow limitation. Exerc. Sport Sci. Rev., Vol. 41, No. 1, pp. 11-18, 2013. Ventilatory limitation to exercise remains an important unresolved clinical issue; as a result, many individuals misinterpret the effects of expiratory flow limitation as an all-or-nothing phenomenon. Expiratory flow limitation is not all or none; approaching maximal expiratory flow can have important effects not only on ventilatory capacity but also on breathing mechanics, ventilatory control, and possibly exertional dyspnea and exercise intolerance.
Article
In experiments with voluntary and electrically induced work on a normal subject and on a patient (tabes dorsalis) in whom all the ordinary kinesthetic sensations were completely extinguished, the pulmonary ventilation increased during both kinds of work in the normal way i.e. corresponding to the oxygen consumption, in spite of the fact, that the cortical innervation during the electrically induced work was substituted by the apparatus for electrical stimulation.Prom these experiments it is concluded, that the nervous impulses which increase the excitability of the respiratory centre, thus causing the rise in the ventilation during work, are not of cortical origin, but most probably must be brought about reflexly from the working muscles.The experiments with the patient suffering from tabes dorsalis show further, that the reflex impulses must be carried to the centre through nerve paths outside the posterior fascicles, which are known to be destroyed in this disease.
Article
Abstract  The cardioaccelerator and ventilatory responses to rhythmic exercise in the human are commonly viewed as being mediated predominantly via feedforward 'central command' mechanisms, with contributions from locomotor muscle afferents to the sympathetically mediated pressor response. We have assessed the relative contributions of three types of feedback afferents on the cardiorespiratory response to voluntary, rhythmic exercise by inhibiting their normal 'tonic' activity in healthy animals and humans and in chronic heart failure. Transient inhibition of the carotid chemoreceptors during moderate intensity exercise reduced muscle sympathetic nerve activity (MSNA) and increased limb vascular conductance and blood flow; and reducing the normal level of respiratory muscle work during heavier intensity exercise increased limb vascular conductance and blood flow. These cardiorespiratory effects were prevented via ganglionic blockade and were enhanced in chronic heart failure and in hypoxia. Blockade of μ opioid sensitive locomotor muscle afferents, with preservation of central motor output via intrathecal fentanyl: (a) reduced the mean arterial blood pressure (MAP), heart rate and ventilatory responses to all steady state exercise intensities; and (b) during sustained high intensity exercise, reduced O(2) transport, increased central motor output and end-exercise muscle fatigue and reduced endurance performance. We propose that these three afferent reflexes - probably acting in concert with feedforward central command - contribute significantly to preserving O(2) transport to locomotor and to respiratory muscles during exercise. Locomotor muscle afferents also appear to provide feedback concerning the metabolic state of the muscle to influence central motor output, thereby limiting peripheral fatigue development.