Joseph F Welch, Brighton R Cretney, Gordon S Mitchell, George M Balanos
{"title":"休息时的通气长期促进增加了对随后运动通气反应的前馈贡献。","authors":"Joseph F Welch, Brighton R Cretney, Gordon S Mitchell, George M Balanos","doi":"10.1152/japplphysiol.00737.2024","DOIUrl":null,"url":null,"abstract":"<p><p>The respiratory control system exhibits neural plasticity, adjusting future ventilatory responses based on experience. We tested the hypothesis that ventilatory long-term facilitation induced by hypercapnic acute intermittent hypoxia (AIH) at rest enhances subsequent ventilatory responses to steady-state exercise. Fourteen healthy adults (age = 27 ± 5 yr; 7 males) participated in the study. On <i>day 1</i>, pulmonary function testing was performed. On <i>days 2</i> and <i>3</i>, in a pseudorandomized counterbalanced order, participants were exposed to AIH or Sham; AIH consisted of 15, 1-min hypoxic episodes with 1.5-min room air intervals. Mild hypercapnia (end-tidal Pco<sub>2</sub> clamped ∼3 mmHg above baseline) was sustained throughout AIH and Sham and for 40 min after. Approximately 20-30 min later, participants performed continuous mild to moderate constant-load cycle exercise in room air at 30, 60, and 90 W for 5 min each. Inspired minute ventilation (V̇i) increased by 3.6 ± 1.2 L·min<sup>-1</sup> after AIH versus baseline and was significantly greater than Sham (<i>P</i> = 0.013), signifying the onset of ventilatory long-term facilitation. Although V̇i during subsequent steady-state exercise was not significantly different between AIH and Sham (<i>P</i> = 0.511), the slope of the relationship between V̇i and CO<sub>2</sub> production rate (i.e., the system gain) and the calculated feedforward exercise gain were significantly increased (<i>P</i> = 0.021 and <i>P</i> < 0.001, respectively). Consequently, end-tidal Pco<sub>2</sub> was regulated ∼1 mmHg lower across all exercise workloads after AIH versus Sham (<i>P</i> = 0.006). Thus, ventilatory plasticity induced at rest alters future ventilatory responses to mild or moderate steady-state exercise.<b>NEW & NOTEWORTHY</b> We demonstrate that by inducing ventilatory long-term facilitation (LTF) at rest, subsequent ventilatory responses to mild or moderate exercise are altered. When ventilatory LTF was induced via hypercapnic acute intermittent hypoxia, the feedforward contribution to exercise hyperpnea increased, accompanied by marginal increases in the overall system response and decreases in end-tidal Pco<sub>2</sub>. Thus, respiratory motor plasticity at rest can \"spill over\" to other physiological states, including mild or moderate steady-state exercise.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"426-438"},"PeriodicalIF":3.3000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ventilatory long-term facilitation at rest increases the feedforward contribution to subsequent exercise ventilatory responses.\",\"authors\":\"Joseph F Welch, Brighton R Cretney, Gordon S Mitchell, George M Balanos\",\"doi\":\"10.1152/japplphysiol.00737.2024\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The respiratory control system exhibits neural plasticity, adjusting future ventilatory responses based on experience. We tested the hypothesis that ventilatory long-term facilitation induced by hypercapnic acute intermittent hypoxia (AIH) at rest enhances subsequent ventilatory responses to steady-state exercise. Fourteen healthy adults (age = 27 ± 5 yr; 7 males) participated in the study. On <i>day 1</i>, pulmonary function testing was performed. On <i>days 2</i> and <i>3</i>, in a pseudorandomized counterbalanced order, participants were exposed to AIH or Sham; AIH consisted of 15, 1-min hypoxic episodes with 1.5-min room air intervals. Mild hypercapnia (end-tidal Pco<sub>2</sub> clamped ∼3 mmHg above baseline) was sustained throughout AIH and Sham and for 40 min after. Approximately 20-30 min later, participants performed continuous mild to moderate constant-load cycle exercise in room air at 30, 60, and 90 W for 5 min each. Inspired minute ventilation (V̇i) increased by 3.6 ± 1.2 L·min<sup>-1</sup> after AIH versus baseline and was significantly greater than Sham (<i>P</i> = 0.013), signifying the onset of ventilatory long-term facilitation. Although V̇i during subsequent steady-state exercise was not significantly different between AIH and Sham (<i>P</i> = 0.511), the slope of the relationship between V̇i and CO<sub>2</sub> production rate (i.e., the system gain) and the calculated feedforward exercise gain were significantly increased (<i>P</i> = 0.021 and <i>P</i> < 0.001, respectively). Consequently, end-tidal Pco<sub>2</sub> was regulated ∼1 mmHg lower across all exercise workloads after AIH versus Sham (<i>P</i> = 0.006). Thus, ventilatory plasticity induced at rest alters future ventilatory responses to mild or moderate steady-state exercise.<b>NEW & NOTEWORTHY</b> We demonstrate that by inducing ventilatory long-term facilitation (LTF) at rest, subsequent ventilatory responses to mild or moderate exercise are altered. When ventilatory LTF was induced via hypercapnic acute intermittent hypoxia, the feedforward contribution to exercise hyperpnea increased, accompanied by marginal increases in the overall system response and decreases in end-tidal Pco<sub>2</sub>. Thus, respiratory motor plasticity at rest can \\\"spill over\\\" to other physiological states, including mild or moderate steady-state exercise.</p>\",\"PeriodicalId\":15160,\"journal\":{\"name\":\"Journal of applied physiology\",\"volume\":\" \",\"pages\":\"426-438\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2025-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of applied physiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1152/japplphysiol.00737.2024\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/7 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of applied physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1152/japplphysiol.00737.2024","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/7 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
Ventilatory long-term facilitation at rest increases the feedforward contribution to subsequent exercise ventilatory responses.
The respiratory control system exhibits neural plasticity, adjusting future ventilatory responses based on experience. We tested the hypothesis that ventilatory long-term facilitation induced by hypercapnic acute intermittent hypoxia (AIH) at rest enhances subsequent ventilatory responses to steady-state exercise. Fourteen healthy adults (age = 27 ± 5 yr; 7 males) participated in the study. On day 1, pulmonary function testing was performed. On days 2 and 3, in a pseudorandomized counterbalanced order, participants were exposed to AIH or Sham; AIH consisted of 15, 1-min hypoxic episodes with 1.5-min room air intervals. Mild hypercapnia (end-tidal Pco2 clamped ∼3 mmHg above baseline) was sustained throughout AIH and Sham and for 40 min after. Approximately 20-30 min later, participants performed continuous mild to moderate constant-load cycle exercise in room air at 30, 60, and 90 W for 5 min each. Inspired minute ventilation (V̇i) increased by 3.6 ± 1.2 L·min-1 after AIH versus baseline and was significantly greater than Sham (P = 0.013), signifying the onset of ventilatory long-term facilitation. Although V̇i during subsequent steady-state exercise was not significantly different between AIH and Sham (P = 0.511), the slope of the relationship between V̇i and CO2 production rate (i.e., the system gain) and the calculated feedforward exercise gain were significantly increased (P = 0.021 and P < 0.001, respectively). Consequently, end-tidal Pco2 was regulated ∼1 mmHg lower across all exercise workloads after AIH versus Sham (P = 0.006). Thus, ventilatory plasticity induced at rest alters future ventilatory responses to mild or moderate steady-state exercise.NEW & NOTEWORTHY We demonstrate that by inducing ventilatory long-term facilitation (LTF) at rest, subsequent ventilatory responses to mild or moderate exercise are altered. When ventilatory LTF was induced via hypercapnic acute intermittent hypoxia, the feedforward contribution to exercise hyperpnea increased, accompanied by marginal increases in the overall system response and decreases in end-tidal Pco2. Thus, respiratory motor plasticity at rest can "spill over" to other physiological states, including mild or moderate steady-state exercise.
期刊介绍:
The Journal of Applied Physiology publishes the highest quality original research and reviews that examine novel adaptive and integrative physiological mechanisms in humans and animals that advance the field. The journal encourages the submission of manuscripts that examine the acute and adaptive responses of various organs, tissues, cells and/or molecular pathways to environmental, physiological and/or pathophysiological stressors. As an applied physiology journal, topics of interest are not limited to a particular organ system. The journal, therefore, considers a wide array of integrative and translational research topics examining the mechanisms involved in disease processes and mitigation strategies, as well as the promotion of health and well-being throughout the lifespan. Priority is given to manuscripts that provide mechanistic insight deemed to exert an impact on the field.