Eur J Appl Physiol (2009) 105:977–978 DOI 10.1007/s00421-008-0970-9

LETTER TO THE EDITOR

Comments on the paper ‘‘End-tidal pressure of CO2 and exercise performance in healthy subjects’’ by Bussotti M, Magrı` D, Previtali E, Farina S, Torri A, Matturri M, Agostoni P (2008) Eur J Appl Physiol 103(6):727–732 Alessandro Maria Ferrazza Æ Paolo Palange

Accepted: 15 December 2008 / Published online: 6 January 2009 Ó Springer-Verlag 2008

To the Editor We have read with great interest the study by M. Bussotti and co-workers (2008) entitled ‘‘End-tidal pressure of CO2 and exercise performance in healthy subjects’’. It was reported that, in some subjects (categorised as Groups 2 and 3), the end-tidal CO2 partial pressure (PET CO2) at the respiratory compensation point (RCP) and at peak exercise was higher than in others (Group 1); this being most marked in Group 3. The authors interpreted this finding as the result of a more efficient breathing pattern, i.e. higher tidal volume (VT) and lower
respiratory rate (RR) for the same minute ventilation V_E : We are, however, not fully convinced that this is the only plausible explanation and would therefore like to provide an alternative explanation that may be operative, alone or in combination with that suggested by the authors. We note that
the Group 3 subjects had a higher CO2 _ 2 than the Group 2 subjects both at RCP output VCO (although not statistically significant) and peak exercise (p \ 0.05), despite almost identical V_E and oxygen uptake
_ 2 values (their Table 2). We have attempted to VO interpret this finding. PETCO2 is known to be influenced by expiratory time
(TE) and the ventilatory equivalent for CO2 _ 2 : V_E =VCO 1.

The Group 3 subjects had a higher VT and a lower RR than the Group 2 subjects throughout exercise. Since the study included only healthy subjects, one can hypothesize that the ratio of inspiratory time (TI) to TE in Groups 2 and 3 was likely to be the same (Clark and

A. M. Ferrazza (&)  P. Palange Dipartimento di Medicina Clinica, Universita` di Roma ‘‘La Sapienza’’, Viale Universita` 37, 00185 Rome, Italy e-mail: [email protected]

2.

von Euler 1972). If so, the Group 3 subjects should have had a longer TE than the Group 2 subjects (?10% at RCP and ?13% at peak). However, this prolongation of TE seems to be too small for the higher PETCO2 reported (?14% at RCP and ?15% at peak). Unfortunately, the authors did not provide any on-line graphical displays to show the temporal profile of the respired PCO2, which would have allowed the behaviour of alveolar PCO2 (PACO2) and therefore arterial PCO2 (PaCO2) to be inferred. Group 3 had a higher V_E than Group 2 (again, not statistically significant: their Table 2). It should be _ 2 noted, however, that Group 2 had a higher V_E =VCO than Group 3, at both iso-workload (16.7% at 200 Watts: their Table 3) and, using the data from the authors’ Table 2, by 17.3% at RCP and by 21.6% at peak exercise. Given the following relationship: _ 2 ¼ k=fð1
VD =VT Þ  PaCO2 g V_E =VCO

ð1Þ

(where VD is physiological dead space, and k is a _ 2 observed in Group 3 constant), the lower V_E =VCO was likely due to a higher PaCO2 (which is consistent with the elevated PETCO2) and/or a lower VD/VT. One could reasonably assume that, because the subjects were healthy and had similar BMI and resting lung function indices, VD should be similar in Group 2 and Group 3. This, taken with the demonstration that the contribution of VD at high levels of VT is normally small (Hansen et al. 1984), permits us to assume that changes in VD (here possibly due to differences in breathing pattern) were not sufficient to significantly _ 2 : This affect the factor (1-VD/VT) and thus V_E =VCO _ _ suggests that the reduction in VE =VCO2 observed in Group 3 is most likely to reflect a proportional increase (*16–20%) in PaCO2.

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Eur J Appl Physiol (2009) 105:977–978

In the normal lung (i.e., assuming no ventilation-perfusion abnormality, although it has to be recognised that several authors have reported widened ventilation-perfusion dispersions at high work rates using the MIGET approach), the mean PaCO2 during exercise (i.e. averaged over an integral number of respiratory cycles) has been shown to correspond to the mean alveolar PACO2 (Wuipp et al. 1988). Thus, the higher PaCO2 could largely, if not completely, explain the higher PETCO2 observed in Group 3. A further point to note relates to the algorithm used to _ 2: calculate VCO _ 2 ¼ STP  ðFE CO2
FI CO2 Þ VCO  RR=ð1
FE CO2 þ FI CO2 =RERÞ

ð2Þ

where STP is a constant related to standard temperature and pressure, and FECO2 and FICO2 are the mixed expired and inspired CO2 fractions respectively. The authors stated that because RR appears in the numerator of Eq. 2, a higher _ 2 : They noted, RR would be associated with a higher VCO _ 2 and however, that the Group 3 subjects had a higher VCO a lower RR and concluded that ‘‘the algorithm used was not _ 2 differences’’. However, the the cause of observed VCO higher PETCO2 observed in Group 3, with little or no change in VD/VT, would suggest a higher FECO2 which, in turn, would both increase the numerator and decrease the denominator of the algorithm and thus result in a higher _ 2: VCO

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In conclusion, the higher PETCO2 observed in Group 3 in the study of Bussotti et al. (2008) is unlikely to have accurately reflected the PaCO2. We propose that the higher PaCO2 expected in Group 3 results from the lower V_E _ 2 ), regardless of breathing pattern. Our (relative to VCO analysis has, of course, limitations mostly because we utilized only the average data to calculate the expected changes in the variables of interest. On the other hand, as stated by the authors, the lack of direct measurements of PaCO2 did not allow evaluation of the variables affecting lung gas exchange efficiency.

References Bussotti M, Magrı` D, Previtali E, Farina S, Torri A, Matturri M, Agostoni P (2008) End-tidal pressure of CO2 and exercise performance in healthy subjects. Eur J Appl Physiol 103(6):727– 732. doi:10.1007/s00421-008-0773-z Clark FJ, von Euler C (1972) On regulation of depth and rate of breathing. J Physiol 222(2):267–295 Hansen JE, Sue DY, Wasserman K (1984) Predicted value for clinical exercise testing. Am Rev Respir Dis 129(2 Pt 2):S49–S55 Wuipp BJ, Lamarra N, Ward SA, Davis JA, Wasserman K (1988) Estimating arterial PCO2 from flow-weighted and time-average alveolar PCO2 during exercise. In: Swanson JD, Growdins FS, Hughson RL (eds) Respiratory control and modelling perspectives. Plenum Press, New York, pp 91–99