RESPONSE

Abstract

Dear Editor-in-Chief: In their letter to the editor, Drs. Quaresima and Ferrari raised a concern about the physiological conclusions drawn on the basis of the interpretation of our data relating to muscle oxygenation measured with near-infrared spectroscopy (NIRS) (5). They pointed out some issues regarding the presentation of the muscle oxygenation data ("as inadequate"). Emphasizing the fact that since our NIRS device offers the possibility to provide tissue oxyhemoglobin (O2Hb) saturation (%) and total Hb ([tHb]) changes, we should have reported their respective values for a "correct" interpretation of muscle oxygenation changes. In response to this criticism, we would like to provide a rationale supporting our choice to report deoxyhemoglobin ([HHb]) data and not tissue O2Hb saturation (named TOI %) and [tHb]. Even though our NIRS system allows the quantification of TOI, [tHb], or even cytochrome oxidase changes, we did not see the need to report the data regarding these variables in response to short sprint cycling, as they were not relevant with the main goal of our study (i.e., the investigation of neural drive-related changes during repeated cycling sprints in order to detect possible central fatigue with a focus on time course of muscle deoxygenation). Importantly, we chose to report [HHb] changes since it can be regarded as being essentially blood-volume insensitive during exercise (2,4); thus, it was assumed to be a reliable estimator of changes in intramuscular oxygenation status and O2 extraction in the field of interrogation (3,4). Meanwhile, we also agree with the authors that muscle oxygenation changes based on the increase and decrease of [HHb] during the sprint exercise may not be fully reliable. In order to avoid any misunderstanding, we present the data of [tHb], [HHb], and TOI (Fig. 1). This figure shows that after a drop in blood volume (as relative decrease in [tHb] due to possible relative changes in intramuscular pressure) during the first sprints, [tHb] was not very stable across the sprint repetitions (although the slight observed increase over time was not significant, P = 0.14), leading to difficulty in interpreting [HHb] changes alone. A likely explanation for the latter [tHb] profile is an increased "contamination" of the NIRS signal by an increased volume of oxygenated blood in the skin, a consequence of cutaneous vasodilation for thermoregulatory purposes (1) across the sprint repetitions. Results of TOI show that our first speculations are in part verified: after a temporary steady state, a slight decrease in TOI from sprint 6 occurs (mean decrease of 3% at the last sprint). This supports that the 30-s rest interval between bouts was not sufficient during the last part of the sprint exercise for glycolitic and oxidative ATP synthesis necessary for PCr resynthesis after intense short exercise. This question deserves further study.FIGURE 1: Evolution of the NIRS variables during repeated-sprint exercise (S). Values are the means for all subjects (N = 9).Finally, we thank Quaresima and Ferrari for their comments on the limitations of the NIRS technique and their interest in our study, showing that the originality and importance of our investigation has called upon their attention. We hope that this debate has been fruitful and will lead to new questions being asked. Romain Denis Motor Efficiency Deficiency Lab Faculty of Sport Sciences Montpellier, France Centre for Sports Medicine and Human Performance Brunel University, Uxbridge UB8 3PH, United Kingdom Sébastien Racinais Motor Efficiency Deficiency Lab Faculty of Sport Sciences Montpellier, France ASPETAR, Qatar Orthopedic and Sports Medicine Hospital Exercise and Sports Science Department Doha, Qatar Stéphane Perrey Motor Efficiency Deficiency Lab Faculty of Sport Sciences Montpellier, France