Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol 105: 391, 2008; doi:10.1152/japplphysiol.90637.2008
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LETTER TO THE EDITOR

Reply to Dr. Poon

TO THE EDITOR: Thank you for the opportunity to respond to the letter from Dr. Poon (7) regarding our manuscript (10). Our purpose was to translate work establishing short-term modulation (STM) of the exercise ventilatory response in an animal model (goats) to healthy humans using similar protocols. Contrary to Dr. Poon's assertion, the nomenclature of "short-term modulation" has been used consistently since 1993 in reference to the augmented exercise ventilatory response with increased respiratory dead space (DS) in goats (1, 2, 5, 8). We believe our study differs from previous human studies concerning DS effects on the exercise ventilatory response in several important respects (6, 9). Our study focused on STM using a standardized protocol developed in goat studies, whereas earlier studies focused on small vs. large DS volumes (9) or differences in response to DS vs. inhaled CO2 (6). Our sample size was greater than the other two studies combined and was sufficient to make robust statistical inferences concerning changes in the exercise ventilatory response with DS; further, our subject group was homogeneous, thus ruling out confounding effects of age (6) or sex (9), and standardized protocols for work rate and DS volume were used in all subjects. Although our observations agree in part with those of Dr. Poon (6), in the study by Ward and Whipp (9), the effects of DS varied between subjects. Hence we cannot agree with Dr. Poon's assertion that the "classic potentiation of the VE-VCO2 relationship" has been long established in humans (7).

Changes in end-tidal PCO2 (PETCO2) from rest to exercise were measured only to confirm that changes in CO2 chemoreceptor feedback from rest to exercise could not account for STM; in this context, changes in PETCO2, arterial PCO2 (PaCO2), or alveolar PCO2 (PACO2) are relevant vs. their absolute values. Indeed, our findings are in general agreement with PaCO2 (6) and PACO2 responses (9) reported previously. As highlighted by Dr. Poon (7), we should have pointed out that estimates of PaCO2 from PETCO2 using the Jones method have not been validated with increased external DS (a major reason we did not present these estimates). We consider it unlikely that use of changes in PETCO2 misrepresented relative PaCO2 regulation from rest to exercise.

We respectfully disagree with Dr. Poon's contention that spinal mechanisms of STM (2, 5) "cannot explain" the range of conditions cited. Although human STM has not been demonstrated to result from the same spinal, serotonergic mechanism causing STM in goats (5), it is reasonable to postulate similar neural mechanisms pending direct experimental tests of this hypothesis. Indeed, spinal mechanisms leading to STM suggest a general neural mechanism of optimization whereby the exercise ventilatory response is linked to resting ventilatory drive as postulated in 1984 (4). Spinal, serotonin-dependent neural mechanisms exhibit considerable plasticity and metaplasticity (3) and may very well adapt ventilatory responses in individuals as they age or develop cardiorespiratory disease (2, 5); these are interesting areas for future investigation. The optimization model of Dr. Poon may describe these phenomena accurately, but modeling cannot replace careful experimentation to determine fundamental neural mechanisms.

FOOTNOTES


Address for reprint requests and other correspondence: H. E. Wood, Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Dallas, TX 75231 (e-mail: helenwood{at}texashealth.org)

REFERENCES

  1. Bach KB, Lutcavage ME, Mitchell GS. Serotonin is necessary for short-term modulation of the exercise ventilatory response. Respir Physiol 91: 57–70, 1993.[CrossRef][Web of Science][Medline]
  2. Mitchell GS, Babb TG. Layers of exercise hyperpnea: modulation and plasticity. Respir Physiol Neurobiol 151: 251–266, 2006.[CrossRef][Web of Science][Medline]
  3. Mitchell GS, Johnson SM. Neuroplasticity in respiratory motor control. J Appl Physiol 94: 358–374, 2003.[Abstract/Free Full Text]
  4. Mitchell GS, Smith CA, Dempsey JA. Changes in the VI-VCO2 relationship during exercise in goats: role of carotid bodies. J Appl Physiol 57: 1894–1900, 1984.[Abstract/Free Full Text]
  5. Mitchell GS, Turner DL, Henderson DR, Foley KT. Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats. Respir Physiol Neurobiol 161: 230–238, 2008.[CrossRef][Web of Science][Medline]
  6. Poon CS. Potentiation of exercise ventilatory response by airway CO2 and dead space loading. J Appl Physiol 73: 591–595, 1992.[Abstract/Free Full Text]
  7. Poon CS. The classic potentiation of exercise ventilatory response by increased dead space in humans is more than short-term modulation. J Appl Physiol. doi:10.1152/japplphysiol.90543.2008.[Free Full Text]
  8. Turner DL, Bach KB, Martin PA, Olsen EB, Brownfield M, Foley KT, Mitchell GS. Modulation of ventilatory control during exercise. Respir Physiol 110: 277–285, 1997.[CrossRef][Web of Science][Medline]
  9. Ward SA, Whipp BJ. Ventilatory control during exercise with increased external dead space. J Appl Physiol 48: 225–231, 1980.[Abstract/Free Full Text]
  10. Wood HE, Mitchell GS, Babb TG. Short-term modulation of the exercise ventilatory response in young men. J Appl Physiol 104: 244–252, 2008.[Abstract/Free Full Text]

Helen E. Wood1
Gordon S. Mitchell2
Tony G. Babb1
 1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas and University of Texas Southwestern Medical Center-Dallas, Dallas, Texas; and 2Department of Comparative Bioscience, University of Wisconsin-Madison, Madison, Wisconsin





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