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- W4290805000 abstract "In health, the near-eucapnic, highly efficient hyperpnea during mild-to-moderate intensity exercise is driven by three obligatory contributions, namely, feedforward central command from supra-medullary locomotor centers, feedback from limb muscle afferents, and respiratory CO2 exchange (V̇CO2). Inhibiting each of these stimuli during exercise elicits a reduction in hyperpnea even in the continuing presence of the other major stimuli. However, the relative contribution of each stimulus to the hyperpnea remains unknown as does the means by which V̇CO2 is sensed. Mediation of the hyperventilatory response to exercise in health is attributed to the multiple feedback and feedforward stimuli resulting from muscle fatigue. In patients with COPD, diaphragm EMG amplitude and its relation to ventilatory output are used to decipher mechanisms underlying the patients' abnormal ventilatory responses, dynamic lung hyperinflation and dyspnea during exercise. Key contributions to these exercise-limiting responses across the spectrum of COPD severity include high dead space ventilation, an excessive neural drive to breathe and highly fatigable limb muscles, together with mechanical constraints on ventilation. Major controversies concerning control of exercise hyperpnea are discussed along with the need for innovative research to uncover the link of metabolism to breathing in health and disease." @default.
- W4290805000 created "2022-08-12" @default.
- W4290805000 creator A5011098520 @default.
- W4290805000 creator A5037474136 @default.
- W4290805000 creator A5045798052 @default.
- W4290805000 creator A5086176683 @default.
- W4290805000 date "2022-01-01" @default.
- W4290805000 modified "2023-10-18" @default.
- W4290805000 title "The physiology and pathophysiology of exercise hyperpnea" @default.
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