Éditeur(s) : HAL CCSD ACSM
Résumé : International audience
The aim of this study was to examine the effects of the cycle-run and run-cycle successions of the triathlon and duathlon, respectively, on respiratory muscle strength and endurance. Methods: Respiratory muscle strength was assessed by measuring maximal inspiratory (P1max) and expiratory {PEmax) pressures. Respiratory muscle endurance was assessed by measuring the time limit (Tlim). Twelve triathleles participated in a three-trial protocol. The first trial consisted of an incremental cycle test to assess the maximal oxygen uptake (VO2max) of triathletes. Trial 2 consisted of 20 min of cycling followed by 20 min of running (C-R), and trial 3 consisted of 20 min of running followed by 20 min of cycling (R-C). Trials 2 and 3 were performed at the same metabolic intensity (% VO2max). P1max and P1max were measured before and 10 min after C-R and R-C, and I min after the post-C-R and post-R-C Tlim measurements (P1max l'). Tlim was measured I d before and 30 min after C-R and R-C. Results: The results showed a significant decrease in P1max after C-R (126.7 ± 4.3 cmH2O, P < 0.05) and R-C (123.7 ± 4.9 cmH2O, P < 0.05) compared with the baseline values (130 ± 3.8 and 129.6 ± 4.3 cmH2O, respectively). P1max 1' showed a significantly greater decrease after R-C versus C-R(111.2 ± 5.5 cmH2O vs 121.2 ± 3.9 cmH2O,respectively, P < 0.001). Tlim after C-R (3.3 ± 0.3 min) decreased significantly compared with baseline values (4.19 ± 0.3min and 4.02 ± 0.3 min, respectively). However, the Tlim decrease after R-C was significantly greater than after C-R (P < 0.001). Conclusion: We concluded that respiratory muscle strength and endurance were less decreased after the cycle-run succession and that cycling induced a greater decrease in respiratory muscle endurance than running.
Medicine & Science in Sports & exercise

hal-00720796
https://hal.univ-antilles.fr/hal-00720796

Éditeur(s) : HAL CCSD Thieme Publishing
Résumé : International audience
The aim of the present study was to compare the effects of prior cycling and a successive run on respiratory muscle performance during a cycle-run succession as performed in the triathlon. We hypothesized that despite the moderate intensity of exercise and the absence of exhaustion, the crouched cycling position would induce a decrease in respiratory muscle performance that would be reversed by the successive vertical run position. Ten male triathletes (22.6 +/- 1.1 yr) performed a four-trial protocol: (1) an incremental cycle test to assess maximal oxygen uptake (VO2max), (2) 20 min of cycling (C), (3) 20 min of running (R), and (4) 20 min of cycling followed by 20 min of running (C-R). Trials 2, 3 and 4 were performed at the same metabolic intensity, i. e., 75 % of VO2max. Respiratory muscle force was assessed by measuring maximal expiratory (P(Emax)) and inspiratory (P(Imax)) pressures from the functional residual capacity (FRC) before and 10 min after C, R, and C-R. Respiratory muscle endurance was assessed one day before and 30 min after C, R, and C-R, by measuring the time limit (T(lim)), which corresponds to the length of time a respiratory load can be sustained before the process of fatigue develops sufficiently to cause task failure. The results showed a similar significant decrease in P(Imax) (132.4 +/- 4.9 versus 125.7 +/- 5.6 cm H2O, p < 0.05) and T(lim) (5.22 +/- 0.28 versus 3.68 +/- 0.32 min, p < 0.05) post-C and post-C-R (133.7 +/- 4.0 versus 126.9 +/- 5.2 cm H2O, and 5.29 +/- 0.18 versus 3.49 +/- 0.41 min, respectively, p < 0.05) compared with the pre-trial values. In contrast, P(Imax) and T(lim) were not significantly decreased post-R (131.8 +/- 6.1 cm H2O versus 129.6 +/- 6.4 cm H2O, and 4.90 +/- 0.69 versus 4.40 +/- 0.56 min, respectively, p > 0.05). We concluded that moderate intensity exercise not performed to exhaustion induced a decrease in respiratory muscle performance. Moreover, the respiratory muscle fatigue induced by prior cycling was maintained, and neither reversed nor worsened, by the successive run.
ISSN: 0172-4622

hal-00720715
https://hal.univ-antilles.fr/hal-00720715

Éditeur(s) : HAL CCSD Public Library of Science
Résumé : International audience
BACKGROUND/AIM: Although it has been hypothesized that muscle metabolism and fatigability could be impaired in sickle cell patients, no study has addressed this issue. METHODS: We compared muscle metabolism and function (muscle microvascular oxygenation, microvascular blood flow, muscle oxygen consumption and muscle microvascular oxygenation variability, which reflects vasomotion activity, maximal muscle force and local muscle fatigability) and the hemorheological profile at rest between 16 healthy subjects (AA), 20 sickle cell-hemoglobin C disease (SC) patients and 16 sickle cell anemia (SS) patients. RESULTS: Muscle microvascular oxygenation was reduced in SS patients compared to the SC and AA groups and this reduction was not related to hemorhelogical abnormalities. No difference was observed between the three groups for oxygen consumption and vasomotion activity. Muscle microvascular blood flow was higher in SS patients compared to the AA group, and tended to be higher compared to the SC group. Multivariate analysis revealed that muscle oxygen consumption was independently associated with muscle microvascular blood flow in the two sickle cell groups (SC and SS). Finally, despite reduced muscle force in sickle cell patients, their local muscle fatigability was similar to that of the healthy subjects. CONCLUSIONS: Sickle cell patients have normal resting muscle oxygen consumption and fatigability despite hemorheological alterations and, for SS patients only, reduced muscle microvascular oxygenation and increased microvascular blood flow. Two alternative mechanisms can be proposed for SS patients: 1) the increased muscle microvascular blood flow is a way to compensate for the lower muscle microvascular oxygenation to maintain muscle oxygen consumption to normal values or 2) the reduced microvascular oxygenation coupled with a normal resting muscle oxygen consumption could indicate that there is slight hypoxia within the muscle which is not sufficient to limit mitochondrial respiration but increases muscle microvascular blood flow.
ISSN: 1932-6203

inserm-00849035
http://www.hal.inserm.fr/inserm-00849035
http://www.hal.inserm.fr/inserm-00849035/document
http://www.hal.inserm.fr/inserm-00849035/file/2013_Waltz_-_Normal_muscle_oxygen_consumption_and_fatigability_in_sickle_cell_patients.pdf
DOI : 10.1371/journal.pone.0052471

Éditeur(s) : HAL CCSD Thieme Publishing
Résumé : International audience
The aim of the present study was to compare the effects of prior cycling and a successive run on respiratory muscle performance during a cycle-run succession as performed in the triathlon. We hypothesized that despite the moderate intensity of exercise and the absence of exhaustion, the crouched cycling position would induce a decrease in respiratory muscle performance that would be reversed by the successive vertical run position. Ten male triathletes (22.6 +/- 1.1 yr) performed a four-trial protocol: (1) an incremental cycle test to assess maximal oxygen uptake (VO2max), (2) 20 min of cycling (C), (3) 20 min of running (R), and (4) 20 min of cycling followed by 20 min of running (C-R). Trials 2, 3 and 4 were performed at the same metabolic intensity, i. e., 75 % of VO2max. Respiratory muscle force was assessed by measuring maximal expiratory (P(Emax)) and inspiratory (P(Imax)) pressures from the functional residual capacity (FRC) before and 10 min after C, R, and C-R. Respiratory muscle endurance was assessed one day before and 30 min after C, R, and C-R, by measuring the time limit (T(lim)), which corresponds to the length of time a respiratory load can be sustained before the process of fatigue develops sufficiently to cause task failure. The results showed a similar significant decrease in P(Imax) (132.4 +/- 4.9 versus 125.7 +/- 5.6 cm H2O, p < 0.05) and T(lim) (5.22 +/- 0.28 versus 3.68 +/- 0.32 min, p < 0.05) post-C and post-C-R (133.7 +/- 4.0 versus 126.9 +/- 5.2 cm H2O, and 5.29 +/- 0.18 versus 3.49 +/- 0.41 min, respectively, p < 0.05) compared with the pre-trial values. In contrast, P(Imax) and T(lim) were not significantly decreased post-R (131.8 +/- 6.1 cm H2O versus 129.6 +/- 6.4 cm H2O, and 4.90 +/- 0.69 versus 4.40 +/- 0.56 min, respectively, p > 0.05). We concluded that moderate intensity exercise not performed to exhaustion induced a decrease in respiratory muscle performance. Moreover, the respiratory muscle fatigue induced by prior cycling was maintained, and neither reversed nor worsened, by the successive run.
ISSN: 0172-4622

hal-01622938
https://hal-umontpellier.archives-ouvertes.fr/hal-01622938
DOI : 10.1055/s-2003-37201
PUBMED : 12582954

Éditeur(s) : HAL CCSD
Résumé : International audience
This study investigated the possibility of there being differences in respiratory muscle strength and endurance in elite and competition triathletes who have similar maximal oxygen uptakes (V_O2max) and ventilatory thresholds (Thvent). Five internationally-ranked elite, [mean (SD) age 23.8 (1.4) years] and six nationallyand regionally-ranked competition [age 21.1 (1.1) years] male triathletes performed two successive trials: first an incremental cycle test to assess V_O2max and Thvent and second 20 min of cycling followed by 20 min of running (C-R) at intensities higher than 85% V_O2max. Cardioventilatory data were collected every minute during the two trials, using an automated breath-by-breath system. Maximal expiratory and inspiratory (PImax) strength were assessed before and 10 min after C-R from the functional residual capacity. Respiratory muscle endurance was assessed 1 day before and 30 min after C-R by measuring the time limit (tlim). The results showed firstly that during C-R, the competition triathletes had significantly (P<0.05) higher minute ventilation [mean (SEM) 107.4 (3.1) compared to 99.8 (3.7) lÆmin-1], breathing frequency [44.4 (2.0) compared to 40.2 (3.4) Æmin-1] and heart rate [166 (3) compared to 159 (4) beatsÆmin-1] and secondly that after C-R, they had significantly lower PImax [127.1 (4.2) compared to 130.7 (3.0) cmH2O] and tlim [2:35 (0:29) compared to 4:12 (0:20) min] than the elite triathletes. We conclude that, despite similar V_O2max and Thvent, the competition triathletes showed less extensive adaptive mechanisms, including those in the respiratory muscles, than did the elite triathletes. This led to higher ventilation, which appeared to be the cause of the faster development of fatigue in the inspiratory muscles in this group.
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY

hal-00720562
https://hal.univ-antilles.fr/hal-00720562
https://hal.univ-antilles.fr/hal-00720562/document
https://hal.univ-antilles.fr/hal-00720562/file/BoussanaEJAP02_2_.pdf

Éditeur(s) : HAL CCSD Thieme Publishing
Résumé : International audience
To determine the effect of triathlete performance level on the cardiorespiratory responses elicited by the cycle-run succession, eight regionally and nationally-ranked (Competitive) and five internationally-ranked (Elite) male triathletes underwent four successive laboratory trials: 1) an incremental treadmill test, 2) an incremental cycle test, 3) 30 min of cycling followed by 20 min of running (C-R), and 4) a 20-min control run (R) at the same speed as the run in C-R. Before and 10 min after the third and fourth trials the triathletes underwent lung function testing: spirometry and diffusing capacity testing for carbon monoxide (DL(CO)). During the C-R trial blood samples were drawn to measure venous lactate concentration. During all trials ventilatory data were collected every minute using an automated breath-by-breath system. The results showed that 1) the oxygen uptake (VO2) of post-cycling running versus running alone was similar for both groups; 2) the ventilatory responses (VE, VE/VO2, VE/VC02 and f) of C-R running versus R were significantly higher (P < 0.005) for the Competitive group; and 3) a significant decrease (P< 0.05) in DL(CO) was also noted after the C-R trial in the Competitive group but not in the Elite group. We concluded that 1) the ventilatory responses during a run subsequent to cycling may be related to the triathlete performance level, and 2) the C-R trial induced specific alterations in pulmonary function that may be associated with respiratory muscle alteration and exercise-induced hypoxemia in the Competitive triathletes.
ISSN: 0172-4622

hal-00720719
https://hal.univ-antilles.fr/hal-00720719

Éditeur(s) : HAL CCSD American College of Sports Medicine (ACSM)
Résumé : International audience
PURPOSE AND METHODS: To determine the effects of cycling on a subsequent triathlon run, nine male triathletes underwent four successive laboratory trials: 1) an incremental treadmill test, 2) an incremental cycle test, 3) 30 min of cycling followed by 5 km of running (C-R), and 4) 30 min of running followed by 5 km of running (R-R). Before and 10 min after the third and fourth trials, the triathletes underwent pulmonary function testing including spirometry and diffusing capacity testing for carbon monoxide (DL(CO)). During the C-R and R-R trials, arterialized blood samples were obtained to measure arterial oxygen pressure (PaO2). During all trials, ventilatory data were collected every minute using an automated breath-by-breath system. RESULTS: The results showed that 1) the oxygen uptake (VO2) observed during subsequent running was similar for the C-R and R-R trials; 2) the ventilatory response (VE) during the first 8 min of subsequent running was significantly greater in the C-R than in R-R trial (P < 0.05); 3) only the C-R trial induced a significant increase (P < 0.05) in residual volume (RV), functional residual capacity (FRC), and the ratio of residual volume to total lung capacity (RV/TLC); and 4) although a significant decrease (P < 0.05) in DL(CO) was noted after C-R, no difference between the two exercise trials was found for the maximal drop in PaO2. CONCLUSIONS: We concluded that 1) the C-R trial induced specific alterations in pulmonary function that may be associated with respiratory muscle fatigue and/or exercise-induced hypoxemia, and 2) the greater VE observed during the first minute of running after cycling was due to the specificity of cycling. This reinforces the necessity for triathletes to practice multi-trial training to stimulate the physiological responses experienced during the swim-cycle and the cycle-run transitions.
ISSN: 0195-9131

hal-00720412
https://hal.univ-antilles.fr/hal-00720412
https://hal.univ-antilles.fr/hal-00720412/document
https://hal.univ-antilles.fr/hal-00720412/file/Article.pdf

Éditeur(s) : HAL CCSD
Résumé : International audience
Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24 h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17-26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V(E)), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio, ventilatory equivalent for oxygen (V(E)/VO2) and for carbon dioxide (V(E)/VCO2), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as VO2/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (VO2max) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P > 0.05) in VO2max [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml x kg(-1) x min(-1)], VT [2368 (SD 258) vs 2477 (SD 352) ml x min(-1)] and time courses of VO2 between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P < 0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24 h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pretriathlon time courses in HR or blood lactate concentration.
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY

hal-00720432
https://hal.univ-antilles.fr/hal-00720432
https://hal.univ-antilles.fr/hal-00720432/document
https://hal.univ-antilles.fr/hal-00720432/file/Article_2.pdf

Éditeur(s) : HAL CCSD Elsevier Masson
Résumé : International audience
Antisynthetase syndrome is an inflammatory myopathy frequently associated with pulmonary manifestations, especially interstitial lung diseases, and uncommonly pulmonary hypertension. In the context of a suggestive clinical and radiological picture, positive anti-RNA synthetase antibodies confirm the diagnosis. Anti-Jo1, anti-PL7, and anti-PL12 antibodies are the more commonly encountered. The presence of a number of extra-thoracic manifestations in association with pulmonary disease may suggest the diagnosis. These include: myalgia or muscular deficit, Raynaud's phenomenon, polyarthritis, fever, mechanics hands. Serum creatine kinase levels are usually increased. Electromyogram, muscular magnetic resonance imaging or muscle pathology are not mandatory to make the diagnosis. There is a high variability in symptoms and severity, between patients but also during the course of the disease in the same patient. The presence of an interstitial lung disease is a major prognostic factor and an indication for more intensive treatment, principally with systemic corticosteroids with or without immunosuppressive drugs. Improving respiratory physicians’ knowledge of this disease, which is often revealed by its pulmonary manifestations, should help diagnosis, therapeutic management, and possibly prognosis.
Le syndrome des antisynthétases correspond à une myopathie inflammatoire fréquemment associée à une atteinte pulmonaire, surtout parenchymateuse (pneumopathie infiltrante diffuse) et plus rarement vasculaire (hypertension pulmonaire). Devant un tableau clinique et radiologique évocateur, la présence d’anticorps anti-ARNt synthétases signe le diagnostic. Les plus fréquents de ces auto-anticorps sont les anti-Jo1, les anti-PL7 et les anti-PL12. De nombreuses manifestations cliniques extrathoraciques associées à l’atteinte pulmonaire peuvent orienter le diagnostic : myalgies ou déficit musculaire, phénomène de Raynaud, polyarthrite, fièvre et « mains de mécaniciens ». Une augmentation des créatine-phospho-kinases est quasi constante. Le recours à l’électromyogramme, à l’imagerie musculaire par résonance magnétique ou à l’histologie n’est pas systématique. Néanmoins, il existe une grande variabilité des symptômes et de leur sévérité d’un patient à l’autre ou au long de l’évolution de la maladie. L’atteinte pulmonaire est un facteur pronostic majeur et incite à traiter de manière intensive les patients, principalement par corticothérapie systémique, voire d’emblée par association corticoïdes et immunosuppresseurs. Mieux connaître cette pathologie qui est souvent de révélation pneumologique permettrait d’améliorer le diagnostic et la prise en charge thérapeutique, voire même le pronostic.
ISSN: 0761-8425

hal-01085369
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01085369
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01085369/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01085369/file/Manifestations%20pulmonaires%20du%20syndrome%20des%20antisynth%C3%A9tases_accepted.pdf
DOI : 10.1016/j.rmr.2014.07.013