Breathing during exercise: demands, regulation, limitations.
Abstract: In humans alveolar ventilation (VA) is adjusted almost perfectly to the metabolic demands of mild and moderate exercise. For example, in exercise transitions and in the steady state, PaCO2 rarely deviates by more than 1 to 3 mmHg from the value at rest. This near-homeostasis contrasts to most other mammalian species; equines for example, demonstrate a progressive hypocapnia and alkalosis as exercise intensity is increased to moderate levels. In equines, the control systems seem programmed for a specific hyperventilation that contributes to maintenance of PaO2 homeostasis. Generally, during heavy exercise all species hyperventilate creating hypocapnia, increased PAO2, widened A-a O2 gradient, and PaO2 homeostasis. The origin of the metabolic ventilatory stimulus remains controversial. Evidence exists for: a) "neural" mediation, either central command or peripheral afferent in nature; and b) "humoral" mediation with an intra-thoracic metabolite receptor being a possibility. The mechanism of the species differences in hyperventilation during exercise does not appear to be due to species variation in chemoreceptor "fine tuning". Contrary to traditional thinking, recent findings suggest that the hyperventilation during heavy exercise might not be mediated by lactacidosis stimulation of chemoreceptors. The increase in VA during exercise is achieved efficiently in that airway diameter is modulated and the pattern of breathing and the recruitment of respiratory muscles are set to minimize the O2 cost of breathing. It has been postulated that mechanoreceptors in airways, lung parenchyma and the chest wall are important to efficient breathing. Their role and contribution to the exercise hyperpnea has been shown by reductions in respiratory neural output within breath when respiratory impedance is reduced via helium breathing. Hilar nerve afferents do not appear to be critical to this response. However, carotid chemoreceptors appear essential for "fine tuning" of VA when respiratory impedance is reduced. In most healthy exercising mammals, the efficiency component of the exercise stimulus does not compromise VA. There are two known major exceptions. One is the extremely fit human athlete during very high workloads when atypically there is minimal or no hyperventilation resulting in arterial hypoxemia. That indeed the high O2 cost of breathing compromises VA is indicated by hyperventilation and alleviation of hypoxemia with resistance unloading through helium breathing. A second example of a compromise of VA is that of a galloping racehorse at very high workloads.(ABSTRACT TRUNCATED AT 400 WORDS)
Publication Date: 1988-01-01 PubMed ID: 3289319DOI: 10.1007/978-1-4684-5481-9_23Google Scholar: Lookup
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- Journal Article
- Research Support
- U.S. Gov't
- Non-P.H.S.
- Research Support
- U.S. Gov't
- P.H.S.
- Review
Summary
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The research explores how human body regulates breathing during different intensity of exercises, indicating that the efficiency of the breathing system allows it to handle the increased oxygen demand and to dispose carbon dioxide sufficiently. Various factors are suggested to contribute to the increased ventilation during exercise.
Demand, Regulation, and Limitations of Breathing during Exercise
- This research delves into the nature of the human ventilatory responses to exercise, specifically the alveolar ventilation (VA) which adjusts almost perfectly to the metabolic demands of mild and moderate exercise. In contrast, many other animal species show a steady decrease in carbon dioxide levels and alkalisation in their blood as the intensity of their exercise increases.
- Humans and animals hyperventilate during heavy exercises which results in a decrease in carbon dioxide, an increase in oxygen pressure in the alveoli, a widening of the difference between alveolar and arterial oxygen, and the maintenance of arterial oxygen pressure. The cause of this increased ventilation remains debatable with evidence suggesting both the involvement of the nervous system and changes in body chemistry.
- Contrary to traditional thought, the increase in ventilation during heavy exercise may not be due to the presence of lactate, a byproduct of intense exercise, stimulating chemoreceptors. This suggests other factors, apart from chemoreceptor stimulation by lactate, that could be contributing to hyperventilation during heavy exercise.
Mechanisms and Efficiency of Breathing during Exercise
- Humans and animals manage the increased ventilation during exercise efficiently by modulating the airway diameter, changing breathing patterns, and recruiting different groups of respiratory muscles, all of which reduces the oxygen cost of breathing itself.
- Mechanoreceptors, which are sensory receptors that respond to mechanical pressure or distortion, in the airways, lung tissue and the chest wall, are suggested to be important to efficient breathing during exercise. This is indicated by reductions in the breath-by-breath breathing nerve activity (neural output) when the resistance to flow in the airways is reduced by breathing in helium instead of normal air.
- While carotid chemoreceptors, oxygen-sensitive cells in the neck, are important for fine-tuning ventilation when the respiratory impedance is reduced, hilar nerve afferents seem not to play a crucial role.
Exceptions to Efficiency of Breathing during Exercise
- However, there are exceptions to the efficiency of the ventilatory response during exercise. One instance is among highly fit human athletes, where heavy workloads may result in little to no hyperventilation, resulting in a decrease in arterial oxygen pressure. This inefficiency can be mitigated by reducing the resistance in the airways with the use of helium breathing.
- Another exception is seen in galloping racehorses that display compromised ventilation at very high workloads.
Cite This Article
APA
Forster HV, Pan LG.
(1988).
Breathing during exercise: demands, regulation, limitations.
Adv Exp Med Biol, 227, 257-276.
https://doi.org/10.1007/978-1-4684-5481-9_23 Publication
Researcher Affiliations
- Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
MeSH Terms
- Animals
- Humans
- Physical Exertion
- Respiration
Grant Funding
- HL-25739 / NHLBI NIH HHS
Citations
This article has been cited 8 times.- Deng Z, Li X, Li C, Zheng Y, Wu F, Wang Z, Liu S, Tian H, Zheng J, Peng J, Huang P, Yang H, Xiao S, Wen X, Yang C, Luo X, Peng G, Li B, Zhou Y, Ran P. Impaired exercise capacity in individuals with non-obstructive small airway dysfunction.. J Thorac Dis 2023 Feb 28;15(2):472-483.
- Schaeffer MR, Guenette JA, Jensen D. Impact of ageing and pregnancy on the minute ventilation/carbon dioxide production response to exercise.. Eur Respir Rev 2021 Sep 30;30(161).
- Collins SÉ, Phillips DB, Brotto AR, Rampuri ZH, Stickland MK. Ventilatory efficiency in athletes, asthma and obesity.. Eur Respir Rev 2021 Sep 30;30(161).
- Jeppesen TD, Madsen KL, Poulsen NS, Løkken N, Vissing J. Exercise Testing, Physical Training and Fatigue in Patients with Mitochondrial Myopathy Related to mtDNA Mutations.. J Clin Med 2021 Apr 20;10(8).
- Phillips DB, Collins SÉ, Stickland MK. Measurement and Interpretation of Exercise Ventilatory Efficiency.. Front Physiol 2020;11:659.
- Jeppesen TD. Aerobic Exercise Training in Patients With mtDNA-Related Mitochondrial Myopathy.. Front Physiol 2020;11:349.
- Weippert M, Behrens M, Mau-Moeller A, Bruhn S, Behrens K. Cycling before and after Exhaustion Differently Affects Cardiac Autonomic Control during Heart Rate Matched Exercise.. Front Physiol 2017;8:844.
- Gardner DS. Historical progression of racing performance in the Thoroughbred horse and man.. Equine Vet J 2006 Nov;38(6):581-3.
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