Programme d'entrainement personnalisé en crénaux (PEP'C) chez le jeune asthmatique (mise au point et résultats(Doctorat : STAPS))

BESANCON-BU Médecine pharmacie (250562102) / SudocPARIS-BIUM (751062103) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

Intérêt d'une activité physique en piscine chez l'asthmatique

Revue générale. Natation et réentraînement à l'effort des sujets asthmatiques. Effets de l'immersion, asthme et exercice physique, asthme et immersion. Effets protecteurs de la natation en cas d'asthme d'effort

Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress

Physical exercise exacerbates the cytotoxic effects of statins in skeletal muscle. Mitochondrial impairments may play an important role in the development of muscular symptoms following statin treatment. Our objective was to characterize mitochondrial function and reactive oxygen species (ROS) production in skeletal muscle after exhaustive exercise in atorvastatin-treated rats. The animals were divided into four groups: resting control (CONT; n = 8) and exercise rats (CONT+EXE; n = 8) as well as resting (ATO; n = 10) and exercise (ATO+EXE; n = 8) rats that were treated with atorvastatin (10 mg·kg(-1)·day(-1) for 2 wk). Exhaustive exercise showed that the distance that was covered by treated animals was reduced (P < 0.05). Using dihydroethidium staining, we showed that the ROS level was increased by 60% in the plantaris muscle of ATO compared with CONT rats and was highly increased in ATO+EXE (226%) compared with that in CONT+EXE rats. The maximal mitochondrial respiration (V(max)) was decreased in ATO rats compared with that in CONT rats (P < 0.01). In CONT+EXE rats, V(max) significantly increased compared with those in CONT rats (P < 0.05). V(max) was significantly lower in ATO+EXE rats (-39%) compared with that in CONT+EXE rats (P < 0.001). The distance that was covered by rats significantly correlated with V(max) (r = 0.62, P < 0.01). The glycogen content was decreased in ATO, CONT+EXE, and ATO+EXE rats compared with that in CONT rats (P < 0.05). GLUT-4 mRNA expression was higher after exhaustive exercise in CONT+EXE rats compared with the other groups (P < 0.05). Our results show that exhaustive exercise exacerbated metabolic perturbations and ROS production in skeletal muscle, which may reduce the exercise capacity and promote the muscular symptoms in sedentary atorvastatin-treated animals

Different Timing of Changes in Mitochondrial Functions following Endurance Training

International audienceDAUSSIN, F. N., L. RASSENEUR, J. BOUITBIR, A-L. CHARLES, S. P. DUFOUR, B. GENY, Y. BURELLE, and R. RICHARD. Different Timing of Changes in Mitochondrial Functions following Endurance Training. Med. Sci. Sports Exerc., Vol. 44, No. 2, pp. 217-224, 2012. Purpose: The objective of this study was to investigate the time course of the endurance training-induced adaptations in two major mitochondrial functions. Methods: Forty rats were divided into four groups: a control group and three training groups-a 1-d training group, a 5-d training group, and a 10-d training group. The training protocol consisted of 30 min of running on a motorized treadmill (26 m.min(-1), 15% grade). Nuclear respiratory factor-1; transcription factor A, mitochondrial; superoxide dismutase-2; glutathione peroxidase-4; and citrate synthase (CS) messenger RNA levels were measured by qPCR. Mitochondrial respiration and H2O2 release were assessed using permeabilized fibers of white gastrocnemius in situ. Calculation of free radical leak was performed in two conditions where substrates were identical in both measurements. CS activity was assessed spectrophotometrically. Results: An early time-dependent modulation in messenger RNA levels was observed with training: nuclear respiratory factor-1 and superoxide dismutase-2 levels increased after acute exercise, transcription factor A, mitochondrial and CS levels improved after 5 d, and glutathione peroxidase-4 levels increased after 10 d. CS activity improved by 29% +/- 8% (P < 0.01) after 5 d together with a 50% +/- 7% reduction in the free radical leak (P < 0.05). Finally, 10 d of endurance training did not significantly alter mitochondrial H2O2 release but increased mitochondrial respiration rates in situ (P < 0.05). Conclusions: Our results demonstrate that mitochondrial adaptations follow a sequential program in which mitochondrial respiration and free radical leak adaptations occur according to a different timing. Collectively, these results suggest early mitochondrial qualitative adaptations in response to endurance training

Mitochondria of trained skeletal muscle are protected from deleterious effects of statins

Statins are associated with adverse skeletal muscle effects. Our objective was to determine if muscular adaptations following exercise training prevented deleterious effects of atorvastatin in glycolytic skeletal muscle.; Twenty rats were divided into 2 groups: a control group (n = 10; Cont) and a 10 days of training group (n = 10; Training). Using the permeabilized fibers technique, we explored mitochondrial function.; Exercise training increased V(max) and H(2)O(2) production without altering the free radical leak, and mRNA expression of SOD2 and Cox1 were higher in trained muscle. In the Cont group, atorvastatin exposure increased H(2)O(2) production and decreased skeletal muscle V(max). The decreased V(max) effect of atorvastatin was dose dependent. Interestingly, the half-maximal inhibitory concentration (IC(50)) was higher in the Training group. H(2)O(2) production increased in trained muscle after atorvastatin exposure.; These results suggest that improvements in mitochondrial respiratory and antioxidant capacities following endurance training protected mitochondria against statin exposure