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LETTERS |
1. From the data available in our previous paper (Haouzi et al. 2003), Poon deduces that the 
–cPa,CO2 (cephalic Pa,CO2) relationship obtained in our sheep reflects a chemosensitive control system gain as high as 14 l min–1 Torr–1, i.e. able to account for the entire
response to contractions on the basis of a 0.8 Torr increase (on average) in cPa,CO2. While this seems to ‘solve’ the problem of the 
response to muscle contractions, the argument is entirely specious.
Poon's use of ‘gain’ for the 
–cPa,CO2 relationship when Pa,CO2 was increased in the body while it is maintained constant in the carotid circulation is inappropriate. Computing this ratio using the ‘isolated’ head as the frame of reference does not reflect the chemosensitivity of the model during such intervention. It simply shows how much 
has increased from another source of stimulation (originating in the ‘rest of body’) despite a normal or decreased carotid Pa,CO2. The result is a necessarily infinite, or even negative, 
–cPa,CO2 slope; this should not be confused with any mysterious change in the gain of the chemosensitivity consistent with some ‘newfound plasticity’. Furthermore, the 
response to high systemic Pa,CO2 was trivially small in almost all instances in all our reports (Haouzi et al. 2003; Haouzi & Chenuel, 2005): the 
/systemic Pa,CO2 ratio ranged from 0.03 to 0.1 l min–1 Torr–1 (see the Result sections).
Several mechanisms were put forward in our discussion to account for such change in 
with high systemic Pa,CO2 including the systemic vascular effects of CO2 and the possibility of contamination of the cephalic circulation from the systemic blood. This latter proposal was thought to be highly unlikely, since no trace of technetium injected into the left ventricle was found in the cephalic region. As stated in our previous paper (Haouzi et al. 2003), Fig. 4 is the most extreme example of this type of response. We were so intrigued by this effect that we decided to show it in the paper. Using only this type of response to build a ‘theory’ is unjustified and does not give proper credence to the reality of the data. Indeed, the 
response to high body CO2 could be virtually absent despite, importantly, a normal ventilatory response to exercise (Haouzi & Chenuel, 2005).
What is therefore Poon's rationale for using the 
–cPa,CO2 ratio obtained during high systemic Pa,CO2 (which, as described above, has no physiological meaning) in the interpretation of the response to exercise? Whatever the mechanisms of the residual 
response to ‘body’ hypercapnia, systemic Pa,CO2 is going down by a few Torr during contractions. Even if we assume a small contamination (which will be difficult to explain anatomically), Pa,CO2 at the chemoreceptors should, as a result, be if anything slightly lower that the actual value measured in the carotid blood during the contractions.
Therefore may we respectfully recommend that Dr Poon reconsider the physiological implications of his computation: a model based on conventional chemosensitivity is unrealistic. In fact, we challenge Dr Poon to find any sheep or human beings with such a chemosensitive gain to experimentally elevated cPa,CO2. Until then, any of the ‘critiques’ regarding a major change in CO2 chemosensitivity are simply speculative and contradictory to the data provided here and elsewhere.
2. With respect to Dr Poon's concern regarding the possible effects of cutaneous stimulation during electrically induced muscle contractions, we can reassure him that: (a) With the level of anaesthesia we use our animals had no demonstrable cutaneous sensibility. We were unable to trigger any 
or HR changes (these were continuously recorded throughout the experiment) during nociceptive stimulation of the skin, i.e. cutting the skin or doing more extensive surgery: (b) Electrical stimulation eliciting cutaneous pain causes variations in the timing components of breathing without any effect on tidal volume and trivial change in 
(Duranti et al. 1991): (c) The 
response is only dependent on the tension applied on to the muscle and its ensuing metabolic response regardless of the magnitude of the stimulation: (d) The two pairs of large electrodes (10 cm–5 cm, Saint Cloud International Chantonnay, France) are routinely used in patients for rehabilitation.
3. In our sheep model, all the brain structures down to the cervical cord are supplied by the carotid circulation (and not the vertebral system) in which the perfusion pressure and the blood flow are maintained constant by the pump. Consequently, any speculation on putative effect of vertebral flow during the occlusions simply does not apply here (we refer Dr Poon to our Methods section).
4. Finally, Dr Poon's contention that ‘somatic–respiratory coupling mechanism may have more to do with coordination of movements than tracking metabolic rate per se’ is not supported by the temporal profile of the response to contractions of many of muscle endings. It has been consistently demonstrated that the activity of a large population of group III and IV afferent fibres develops progressively during contractions (Mense & Meyer, 1985) with a very long time constant – regardless of the mechanical effects of the contractions (Kaufman et al. 1983). Such a profile is inconsistent with Dr Poon's argument that only movement is monitored.
We are pleased to have had the opportunity to respond to the issues raised in Dr Poon's letter. The topic of the control of the exercise hyperpnoea is both important and poorly understood and we, as Dr Poon, continue to accept the challenge of its resolution.
Laboratoire de Physiologie, E.A. 3450 Faculté de Médecine de Nancy Université Henry Poincaré, France Email: p.haouzi{at}chu-nancy.fr
References
Duranti
R, Pantaleo
TP, Bellini
F, Bongianni
F
&
Scano
G (1991). Respiratory responses induced by the activation of somatic nociceptive afferents in humans. J Appl Physiol
71, 2440–2448.
Haouzi
P
&
Chenuel
B (2005). Control of arterial PCO2 by somatic afferents in sheep. J Physiol
569, 975–987.
Haouzi P, Chenuel B, Chalon B, Braun M, Bedez Y, Tousseul B, Claudon M & Gille JP (2003). Isolation of the arterial supply to the carotid and central chemoreceptors in the sheep. Exp Physiol 88, 581–594.[Abstract]
Kaufman
MP, Longhurst
JC, Rybicki
KJ, Wallach
JH
&
Mitchell
JH (1983). Effects of static muscular contraction on impulse activity of groups II and IV afferents in cats. J Appl Physiol
55, 105–112.
Mense
S
&
Meyer
H (1985). Different types of slowly conducting afferent units in cat skeletal muscle and tendon. J Physiol
363, 403–417.
Poon
C-S (1987). Ventilatory control in hypercapnia and exercise: optimization hypothesis. J Appl Physiol
62, 2447–2459.
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