Journal of Applied Physiology
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J Appl Physiol 103: 731-732, 2007; doi:10.1152/japplphysiol.00535.2007
8750-7587/07 $8.00
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LETTER TO THE EDITOR

Reply to Padilla, Hamilton, Lundgren, Mckenzie, and Mickleborough

To the Editor: We appreciate the interest of Padilla et al. (3) in our results showing the effect of a modified intermittent hypoxic training (IHT) in endurance athletes. Although the authors raise several comments, the main scientific question seems to concern the rationale to investigate the transcript level for carbonic anhydrase 3 (CA3) in the skeletal muscles of our athletes.

To clarify this issue, it is worth bearing in mind that the study was not specifically performed to identify muscular markers of hypoxia exposure. Rather, the objective was to highlight adaptations of athletes' skeletal muscle after performing specific hypoxia training sessions. We did not, therefore, primarily intend to describe the effects of chronic or acute hypoxia alone, as in the two studies cited by Padilla et al. Consequently, we explored the respective muscular transcript levels of genes involved in mitochondrial biogenesis, redox regulation, and glucose uptake to ascertain whether they could participate in the improvement of endurance performance following 6-wk IHT.

We chose to trace mRNA of CA3 because this enzyme is considered as a potential factor of mitochondrial flux improvement and because high cytosolic concentrations of CA3 have been reported in mammalian skeletal muscle type I (slow-oxidative fibers; Ref. 1). Its RNA level also showed significant plasticity with muscle atrophy and reloading (2). Although our data point out an involvement of CA3 to the hypoxia adaptation of muscle, there is certainly a need to study other carbonic anhydrase isoforms, which could play a role in the muscular adaptations following IHT.

Nevertheless, we thank Padilla et al. for their thorough review of our papers, which gives us the opportunity to explain some of their concerns and to correct one mistake that unfortunately appeared on Fig. 2 in the third part of the trilogy.


Figure 1
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  		Fig. 2.
 
1) A total of 18 volunteered subjects completed the research protocol (6-wk training program, pre- and post-training muscle biopsies of the vastus lateralis muscle and treadmill performance evaluations). As regularly reported in invasive human studies, biopsies did not always give us enough biological material to carry out the measurements of mitochondrial function and mRNAs expression, explaining why the population decline to 15 subjects in the second and third part of our work (4, 5).

2) By not specifying the interaction effect, our aim was to simplify the RESULT sections of the papers, which already report an important amount of data.

3) The range of values for Tlim in the printed Fig. 2 does not make sense as presented. We apologize for this mistake we did not notice and provide the exact, double-checked, correlations with the actual range of values.

In conclusion, CA3 is possibly not the best marker of hypoxia exposure, but we demonstrate that this isoenzyme of CA is specifically upregulated in hypoxia-trained subjects and presumably plays a role, together with other factors, in the ultimate improvement of endurance performance capacity.

FOOTNOTES


Address for reprint requests and other correspondence: J. Zoll, Institut de Physiologie, Faculté de Médecine, 4, rue Kirschleger, F-67085 Strasbourg Cedex, France (e-mail: zolljoffrey{at}yahoo.com)

REFERENCES

  1. Geers C, Gros G. Carbon dioxide transport and carbonic anhydrase in blood and muscle. Physiol Rev 80: 681–715, 2000.[Abstract/Free Full Text]
  2. Fluck M, Schmutz S, Wittwer M, Hoppeler H, Desplanches D. Transcriptional reprogramming during reloading of atrophied rat soleus muscle. Am J Physiol Regul Integr Comp Physiol 289: R4–R14, 2005.[Abstract/Free Full Text]
  3. Padilla J, Hamilton S, Lundgren E, Mckenzie J, Mickleborough T. Exercise training in normobaric hypoxia: is carbonic anyhdrase III the best marker of hypoxia? J Appl Physiol. doi:10.1152/japplphysiol.00408.2007.
  4. Ponsot E, Dufour SP, Zoll J, Doutrelau S, N'Guessan B, Geny B, Hoppeler H, Lampert E, Mettauer B, Ventura-Clapier R, Richard R. Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle. J Appl Physiol 100: 1249–1257, 2006.[Abstract/Free Full Text]
  5. Zoll J, Ponsot E, Dufour S, Doutreleau S, Ventura-Clapier R, Vogt M, Hoppeler H, Richard R, Fluck M. Exercise training in normobaric hypoxia in endurance runners. III. Muscular adjustments of selected gene transcripts. J Appl Physiol 100: 1258–1266, 2006.[Abstract/Free Full Text]

Joffrey Zoll1
Elodie Ponsot2
Stephane Dufour3
Martin Flück4,5
 1Service de Physiologie et d'Explorations Fonctionnelles, Hôpital Civil and Département de Physiologie, Faculté de Médecine, France; 2Institution of Clinical Medicine, Örebro University, Sweden; 3Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge, Middlesex, United Kingdom; 4Department of Anatomy, University of Bern, Bern, Switzerland; and 5Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Alsager, United Kingdom





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