Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise

Dr, Brown; Hv, Forster; Lg, Pan; Ag, Brice; Cl, Murphy; Tf, Lowry; Sm, Gutting; Funahashi, Akio; Hoffman, Mark D.; Powers, S. K.

doi:10.1152/jappl.1990.68.6.2312

Cited by 24 publications

(22 citation statements)

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“…However, other studies have shown that spinal cord trans-section does not abolish the hyperpnea of electrically induced muscle contraction in anesthetized animals (112,524,566). These experimental findings in animals are consistent with data on electrically induced contractions in humans with spinal cord injury (77,79) or in spinal cord-intact humans with epidural anesthesia to block peripheral afferents (160).…”

Section: Exercising Limbssupporting

confidence: 77%

Ventilation and Respiratory Mechanics

Sheel

Romer

2012

Comprehensive Physiology

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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.

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Section: Exercising Limbssupporting

confidence: 77%

Ventilation and Respiratory Mechanics

Sheel

Romer

2012

Comprehensive Physiology

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“…An isocapnic hyperpnea is elicited during electrically induced contractions in paraplegic humans (3,19,55,57) These data appear inconsistent with mediation of the hyperpnea by spinal afferents, and since in spinal cord intact humans, theV E response to electrically induced and voluntary contractions does not differ, it would appear that a humoral mechanism mediates the hyperpnea. A major limitation of these studies is that the 50% to 100% increase in metabolic rate is within the physiologic variation that occurs at rest.…”

Section: Responses To Electrically Induced Muscle Contractionmentioning

confidence: 97%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

193

203

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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“…This phase I response is observed during not only during voluntary and passive movement, but also during an electrically induced muscle contraction (Adams et al 1984;Brice et al 1988;Brown et al 1990;Miyamura l994). Nevertheless, many investigators have pursued the mechanisms of this phase I response, and their opinions as to its nature are still a matter of dispute.…”

Section: Introductionmentioning

confidence: 96%

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

Miyamura

Ishida

Hashimoto

et al. 1997

European Journal of Applied Physiology

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The present study was performed to examine whether or not the ventilatory response at the onset of voluntary exercise and passive movement in endurance runners is the same as in untrained subjects. Twelve long-distance runners belonging to the varsity athletic club and 13 untrained subjects of our university participated as subjects in this study. Maximum oxygen uptake was significantly higher in the endurance runner group [mean (SD) 70.8 (4.7) ml.kg-1.min-1] than in the untrained group [49.8 (6.3) ml.kg-1.min-1]. Cardiorespiratory responses during voluntary exercise and passive movement of alternate flexion-extension of the right and left legs for about 15 s at a frequency of about 60 rpm, were determined by means of breath-by-breath techniques. Minute inspiratory ventilation (VI), tidal volume (VT), respiratory frequency (fb), cardiac output (Qc), stroke volume (SV) and heart rate (HR) increased significantly immediately at the onset of voluntary exercise and passive movement. The incremental rate for VI was greater than that for Qc. Average values and standard deviations of changes in VI were calculated as the difference between the mean of the first and second breath and the mean of five breaths preceding the exercise or movement. The rates obtained in voluntary exercise and passive movement in the endurance runner group [2.34 (0.82) and 1.72 (0.71 l.min-1), respectively] were significantly (P < 0.05) lower than those in the untrained group [4.16 (2.66) and 2.71 (1.56 l.min-1), respectively]. Also changes in VT and HR were significantly lower in the endurance group than in the untrained group with regard to both voluntary exercise and passive movement. The results suggest that the magnitude of cardiorespiratory responses at the onset of voluntary exercise and passive movement in humans is influenced by chronic endurance training for long periods.

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Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise

Cited by 24 publications

References 0 publications

Ventilation and Respiratory Mechanics

Ventilation and Respiratory Mechanics

Control of Breathing During Exercise

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

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