Belle Roels

Publications of Belle Roels

• Are oxygen uptake kinetics modified when using a respiratory snorkel?

  Authors: Joana F Reis, Gregoire P Millet, Davide Malatesta, Belle Roels, Fabio Borrani, Veronica E Vleck, Francisco B Alves

  International journal of sports physiology and performance. 09/2010; 5(3):292-300.

  The aim of this study was to compare VO2 kinetics during constant power cycle exercise measured using a conventional facemask (CM) or a respiratory snorkel (RS) designed for breath-by-breath analysisThe aim of this study was to compare VO2 kinetics during constant power cycle exercise measured using a conventional facemask (CM) or a respiratory snorkel (RS) designed for breath-by-breath analysis in swimming. VO2 kinetics parameters-obtained using CM or RS, in randomized counterbalanced order-were compared in 10 trained triathletes performing two submaximal heavy-intensity cycling square-wave transitions. These VO2 kinetics parameters (ie, time delay: td1, td2; time constant: τ1, τ2; amplitude: A1, A2, for the primary phase and slow component, respectively) were modeled using a double exponential function. In the case of the RS data, this model incorporated an individually determined snorkel delay (ISD). Only td1 (8.9 ± 3.0 vs 13.8 ± 1.8 s, P < .01) differed between CM and RS, whereas all other parameters were not different (τ1 = 24.7 ± 7.6 vs 21.1 ± 6.3 s; A1 = 39.4 ± 5.3 vs 36.8 ± 5.1 mL x min(-1) x kg(-1); td2 = 107.5 ± 87.4 vs 183.5 ± 75.9 s; A2' (relevant slow component amplitude) = 2.6 ± 2.4 vs 3.1 ± 2.6 mL x min(-1) x kg(-1) for CM and RS, respectively). Although there can be a small mixture of breaths allowed by the volume of the snorkel in the transition to exercise, this does not appear to significantly influence the results. Therefore, given the use of an ISD, the RS is a valid instrument for the determination of VO2 kinetics within submaximal exercise.

• The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes.

  Authors: David Bentley, Belle Roels, Claire Thomas, Robert Ives, Jacques Mercier, Grégoire Millet, David Cameron-Smith

  European journal of applied physiology. 04/2009;

  The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and enduranceThe purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean +/- SD; age 24.4 +/- 2.8 years, body mass 73.2 +/- 8.3 kg, VO(2max) 58 +/- 7 ml kg(-1) min(-1)) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO(2max) and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = -0.71 to -0.74; P < 0.06), but not MCT4. The average power output (P (average)) in the 2 min TT was significantly correlated with MCT4 (r = -0.74; P < 0.05) and HAD (r = -0.92; P < 0.01). The P (average) in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.

• Effect of intermittent hypoxic training on HIF gene expression in human skeletal muscle and leukocytes.

  Authors: Rémi Mounier, Vincent Pialoux, Belle Roels, Claire Thomas, Grégoire Millet, Jacques Mercier, Jean Coudert, Nicole Fellmann, Eric Clottes

  European journal of applied physiology. 11/2008;

  Intermittent hypoxic exposure with exercise training is based on the assumption that brief exposure to hypoxia is sufficient to induce beneficial muscular adaptations mediated via hypoxia-inducibleIntermittent hypoxic exposure with exercise training is based on the assumption that brief exposure to hypoxia is sufficient to induce beneficial muscular adaptations mediated via hypoxia-inducible transcription factors (HIF). We previously demonstrated (Mounier et al. Med Sci Sports Exerc 38:1410-1417, 2006) that leukocytes respond to hypoxia with a marked inter-individual variability in HIF-1alpha mRNA. This study compared the effects of 3 weeks of intermittent hypoxic training on hif gene expression in both skeletal muscle and leukocytes. Male endurance athletes (n = 19) were divided into an Intermittent Hypoxic Exposure group (IHE) and a Normoxic Training group (NT) with each group following a similar 3-week exercise training program. After training, the amount of HIF-1alpha mRNA in muscle decreased only in IHE group (-24.7%, P < 0.05) whereas it remained unchanged in leukocytes in both groups. The levels of vEGF(121) and vEGF(165) mRNA in skeletal muscle increased significantly after training only in the NT group (+82.5%, P < 0.05 for vEGF(121); +41.2%, P < 0.05 for vEGF(165)). In leukocytes, only the IHE group showed a significant change in vEGF(165) (-28.2%, P < 0.05). The significant decrease in HIF-1alpha mRNA in skeletal muscle after hypoxic training suggests that transcriptional and post-transcriptional regulations of the hif-1alpha gene are different in muscle and leukocytes.

• Effects of intermittent hypoxic training on cycling performance in well-trained athletes.

  Authors: Belle Roels, David J Bentley, Olivier Coste, Jacques Mercier, Grégoire P Millet

  European journal of applied physiology. 11/2007; 101(3):359-68.

  This study aimed to investigate the effects of a short-term period of intermittent hypoxic training (IHT) on cycling performance in athletes. Nineteen participants were randomly assigned to twoThis study aimed to investigate the effects of a short-term period of intermittent hypoxic training (IHT) on cycling performance in athletes. Nineteen participants were randomly assigned to two groups: normoxic (NT, n = 9) and intermittent hypoxic training group (IHT, n = 10). A 3-week training program (5 x 1 h-1 h 30 min per week) was completed. Training sessions were performed in normoxia (approximately 30 m) or hypoxia (simulated altitude of 3,000 m) for NT and IHT group, respectively. Each subject performed before (W0) and after (W4) the training program, three cycling tests including an incremental test to exhaustion in normoxia and hypoxia for determination of maximal aerobic power (VO2max) and peak power output (PPO) as well as a 10-min cycle time trial in normoxia (TT) to measure the average power output (P(aver)). No significant difference in VO2max was observed between the two training groups before or after the training period. When measured in normoxia, the PPO significantly increased (P < 0.05) by 7.2 and 6.6% in NT and IHT groups, respectively. However, only the IHT group significantly improved (11.3%; P < 0.05) PPO when measured in hypoxia. The NT group improved (P < 0.05) P(aver) in TT by 8.1%, whereas IHT group did not show any significant difference. Intermittent training performed in hypoxia was less efficient for improving endurance performance at sea level than similar training performed in normoxia. However, IHT has the potential to assist athletes in preparation for competition at altitude.

• Effects of intermittent hypoxic training on amino and fatty acid oxidative combustion in human permeabilized muscle fibers.

  Authors: Belle Roels, Claire Thomas, David J Bentley, Jacques Mercier, Maurice Hayot, Grégoire Millet

  Journal of applied physiology (Bethesda, Md. : 1985). 01/2007; 102(1):79-86.

  The effects of concurrent hypoxic/endurance training on mitochondrial respiration in permeabilized fibers in trained athletes were investigated. Eighteen endurance athletes were divided into twoThe effects of concurrent hypoxic/endurance training on mitochondrial respiration in permeabilized fibers in trained athletes were investigated. Eighteen endurance athletes were divided into two training groups: normoxic (Nor, n = 8) and hypoxic (H, n = 10). Three weeks (W1-W3) of endurance training (5 sessions of 1 h to 1 h and 30 min per week) were completed. All training sessions were performed under normoxic [160 Torr inspired Po(2) (Pi(O(2)))] or hypoxic conditions ( approximately 100 Torr Pi(O(2)), approximately 3,000 m) for Nor and H group, respectively, at the same relative intensity. Before and after the training period, an incremental test to exhaustion in normoxia was performed, muscle biopsy samples were taken from the vastus lateralis, and mitochondrial respiration in permeabilized fibers was measured. Peak power output (PPO) increased by 7.2% and 6.6% (P < 0.05) for Nor and H, respectively, whereas maximal O(2) uptake (Vo(2 max)) remained unchanged: 58.1 +/- 0.8 vs. 61.0 +/- 1.2 ml.kg(-1).min(-1) and 58.5 +/- 0.7 vs. 58.3 +/- 0.6 ml.kg(-1).min(-1) for Nor and H, respectively, between pretraining (W0) and posttraining (W4). Maximal ADP-stimulated mitochondrial respiration significantly increased for glutamate + malate (6.27 +/- 0.37 vs. 8.51 +/- 0.33 mumol O(2).min(-1).g dry weight(-1)) and significantly decreased for palmitate + malate (3.88 +/- 0.23 vs. 2.77 +/- 0.08 mumol O(2).min(-1).g dry weight(-1)) in the H group. In contrast, no significant differences were found for the Nor group. The findings demonstrate that 1) a 3-wk training period increased the PPO at sea level without any changes in Vo(2 max), and 2) a 3-wk hypoxic exercise training seems to alter the intrinsic properties of mitochondrial function, i.e., substrate preference.

• Leukocyte's Hif-1 expression and training-induced erythropoietic response in swimmers.

  Authors: Rémi Mounier, Vincent Pialoux, Anne Cayre, Laurent Schmitt, Jean-Paul Richalet, Paul Robach, Françoise Lasne, Belle Roels, Grégoire Millet, Jean Coudert, Eric Clottes, Nicole Fellmann

  Medicine and science in sports and exercise. 09/2006; 38(8):1410-7.

  PURPOSE: Altitude training is popular among athletes to augment oxygen delivery capabilities to tissues and to improve physical performance. Hypoxia inducible factor-1 (HIF-1) controls the expressionPURPOSE: Altitude training is popular among athletes to augment oxygen delivery capabilities to tissues and to improve physical performance. Hypoxia inducible factor-1 (HIF-1) controls the expression of several genes' encoding involved in physiological responses towards reduced oxygen availability, in particular by increasing serum erythropoietin (EPO). It may be involved in the individual variability for erythropoietic markers and/or sea-level performance of athletes using altitude during their training. Therefore, we investigated whether, before training, evolutions of hif-1alpha and ahif (HIF-1alpha natural antisense) transcript amounts and HIF-1alpha protein quantities in leukocytes measured during an acute hypoxia normobaric test (3 h at 3000 m at rest) could allow to predict poor and good responders for hematological markers after a "living high-training low" protocol. METHODS: Eighteen elite swimmers were divided into two groups that followed a 13-d training program: "living low-training low" (1200 m) (LL) or "living high (2500-3000 m)-training low (1200 m)" (LH). RESULTS: During the initial hypoxia test, a strong interindividual variability in the amounts of HIF-1alpha mRNA, aHIF transcript, and HIF-1alpha protein was observed in athlete leukocytes (after vs before): -82%/+396%, -100%/+229%, and -100%/+633%, respectively. After the test, serum erythropoietin concentration was increased (11.2 +/- 0.8 vs 9.8 +/- 0.8 IU.L(-1); +18%, P = 0.01). After the training protocol, total red cell volume (+7.6%, P = 0.04) and circulating hemoglobin amount (48.8 +/- 2.8 vs 45.5 +/- 3.0 mmol; i.e., +7.9%, P = 0.02) were significantly augmented in LH. CONCLUSION: We conclude that hif-1alpha gene expression quantification in leukocytes after a 3-h hypoxia test performed before training does not predict poor and good responder athletes to "living high-training low" model.

• Living high-training low: effect on erythropoiesis and aerobic performance in highly-trained swimmers.

  Authors: Paul Robach, Laurent Schmitt, Julien V Brugniaux, Belle Roels, Grégoire Millet, Philippe Hellard, Gérard Nicolet, Alain Duvallet, Jean-Pierre Fouillot, Stéphane Moutereau, Françoise Lasne, Vincent Pialoux, Niels V Olsen, Jean-Paul Richalet

  European journal of applied physiology. 04/2006; 96(4):423-33.

  The "living high-training low" model (LHTL), i.e., training in normoxia but sleeping/living in hypoxia, is designed to improve the athletes performance. However, LHTL efficacy still remainsThe "living high-training low" model (LHTL), i.e., training in normoxia but sleeping/living in hypoxia, is designed to improve the athletes performance. However, LHTL efficacy still remains controversial and also little is known about the duration of its potential benefit. This study tested whether LHTL enhances aerobic performance in athletes, and if any positive effect may last for up to 2 weeks after LHTL intervention. Eighteen swimmers trained for 13 days at 1,200 m while sleeping/living at 1,200 m in ambient air (control, n=9) or in hypoxic rooms (LHTL, n=9, 5 days at simulated altitude of 2,500 m followed by 8 days at simulated altitude of 3,000 m, 16 h day(-1)). Measures were done before 1-2 days (POST-1) and 2 weeks after intervention (POST-15). Aerobic performance was assessed from two swimming trials, exploring .VO(2max) and endurance performance (2,000-m time trial), respectively. Reticulocyte, serum EPO and soluble transferrin receptor responses were not altered by LHTL, whereas reticulocytes decreased in controls. In POST-1 (vs. before): red blood cell volume increased in LHTL only (+8.5%, P=0.03), .VO(2max) tended to increase more in LHTL (+8.1%, P=0.09) than in controls (+2.5%, P=0.21) without any difference between groups (P=0.42) and 2,000-m performance was unchanged with LHTL. In POST-15, both performance and hematological parameters were similar to initial levels. Our results indicate that LHTL may stimulate red cell production, without any concurrent amelioration of aerobic performance. The absence of any prolonged benefit after LHTL suggests that this LHTL model cannot be recommended for long-term purposes.

• Simvastatin induces impairment in skeletal muscle while heart is protected.

  Authors: Pascal Sirvent, Sylvain Bordenave, Marianne Vermaelen, Belle Roels, Guy Vassort, Jacques Mercier, Eric Raynaud, Alain Lacampagne

  Biochemical and biophysical research communications. 01/2006; 338(3):1426-34.

  3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are widely used to reduce plasma cholesterol concentration. However, statins are also known to induce various forms of muscular3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are widely used to reduce plasma cholesterol concentration. However, statins are also known to induce various forms of muscular toxicity. We have previously shown that acute application of simvastatin on human skeletal muscle samples induced a cascade of cellular events originating from mitochondria and resulting in a global alteration of Ca2+ homeostasis. The present study was designed to further define the origin of the mitochondria impairment and to understand the apparent lack of deleterious effect on the heart. Using fluorescence imaging analysis and oxygraphy on human and rat skinned skeletal muscle samples, we show that the simvastatin-induced mitochondria impairment results from inhibition of the complex I of respiratory chain. Similar simvastatin-induced mitochondria impairment and alteration of Ca2+ homeostasis occur in permeabilized but not in intact ventricular rat cardiomyocytes. In intact rat skeletal muscle fibers from the flexor digitorum brevis muscle, the simvastatin-induced alteration of Ca2+ homeostasis is abolished when monocarboxylate transporter (MCT4) is inhibited. The impairment of complex I by simvastatin might be the primary step of its cellular deleterious effects leading to muscle fiber death. This mechanism is seen specifically in skeletal muscles. This specificity should be in part attributed to a preferential uptake of statins by MCT4 that is not expressed in cardiomyocytes.

• VO2 responses to intermittent swimming sets at velocity associated with VO2max.

  Authors: Sebastien Libicz, Belle Roels, Gregoire P Millet

  Canadian journal of applied physiology = Revue canadienne de physiologie appliquée. 11/2005; 30(5):543-53.

  While the physiological adaptations following endurance training are relatively well understood, in swimming there is a dearth of knowledge regarding the metabolic responses to interval trainingWhile the physiological adaptations following endurance training are relatively well understood, in swimming there is a dearth of knowledge regarding the metabolic responses to interval training (IT). The hypothesis tested predicted that two different endurance swimming IT sets would induce differences in the total time the subjects swam at a high percentage of maximal oxygen consumption (VO(2)max). Ten trained triathletes underwent an incremental test to exhaustion in swimming so that the swimming velocity associated with VO(2)max (vVO(2)max) could be determined. This was followed by a maximal 400-m test and two intermittent sets at vVO(2)max: (a) 16 x 50 m with 15-s rest (IT(50)); (b) 8 x 100 m with 30-s rest (IT(100)). The times sustained above 95% VO(2)max (68.50 +/- 62.69 vs. 145.01 +/- 165.91 sec) and 95% HRmax (146.67 +/- 131.99 vs. 169.78 +/- 203.45 sec, p = 0.54) did not differ between IT(50) and IT(100)(values are mean +/- SD). In conclusion, swimming IT sets of equal time duration at vVO(2)max but of differing work-interval durations led to slightly different VO(2)and HR responses. The time spent above 95% of VO(2)max was twice as long in IT(100) as in IT (50), and a large variability between mean VO(2)and HR values was also observed.

• Effects of hypoxic interval training on cycling performance.

  Authors: Belle Roels, Grégoire P Millet, Christophe J L Marcoux, Olivier Coste, David J Bentley, Robin B Candau

  Medicine and science in sports and exercise. 01/2005; 37(1):138-46.

  PURPOSE: The aim of this study was to test the hypothesis that intermittent hypoxic interval training improves sea level cycling performance more than equivalent training in hypoxia or normoxia.PURPOSE: The aim of this study was to test the hypothesis that intermittent hypoxic interval training improves sea level cycling performance more than equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1)) were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2) of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia (Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program, consisting of two high-intensity (100 or 90% relative peak power output) interval training sessions each week. Each interval training session was performed in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions for the Nor and the IHT group, respectively. The IHIT group performed warm-up and cool-down plus recovery from each interval in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9, and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant differences between groups. Moreover, mean power output did not show any significant improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks of interval training induced an improvement in endurance performance. However, short-term exposure to hypoxia (approximately 114 min.wk(-1)) did not elicit a greater increase in performance or any hematological modifications.

• Simvastatin induces impairment in skeletal muscle while heart is protected

  Authors: Pascal Sirvent, Sylvain Bordenave, Marianne Vermaelen, Belle Roels, Guy Vassort, Jacques Mercier, Eric Raynaud, Alain Lacampagne

  Biochemical and Biophysical Research Communications.

  3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are widely used to reduce plasma cholesterol concentration. However, statins are also known to induce various forms of muscular3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are widely used to reduce plasma cholesterol concentration. However, statins are also known to induce various forms of muscular toxicity. We have previously shown that acute application of simvastatin on human skeletal muscle samples induced a cascade of cellular events originating from mitochondria and resulting in a global alteration of Ca2+ homeostasis. The present study was designed to further define the origin of the mitochondria impairment and to understand the apparent lack of deleterious effect on the heart. Using fluorescence imaging analysis and oxygraphy on human and rat skinned skeletal muscle samples, we show that the simvastatin-induced mitochondria impairment results from inhibition of the complex I of respiratory chain. Similar simvastatin-induced mitochondria impairment and alteration of Ca2+ homeostasis occur in permeabilized but not in intact ventricular rat cardiomyocytes. In intact rat skeletal muscle fibers from the flexor digitorum brevis muscle, the simvastatin-induced alteration of Ca2+ homeostasis is abolished when monocarboxylate transporter (MCT4) is inhibited. The impairment of complex I by simvastatin might be the primary step of its cellular deleterious effects leading to muscle fiber death. This mechanism is seen specifically in skeletal muscles. This specificity should be in part attributed to a preferential uptake of statins by MCT4 that is not expressed in cardiomyocytes.