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 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
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