Training protocols differently affect AMPK–PGC-1α signaling pathway and redox state in trout muscle

International audienceBeneficial effects of physical exercise training are in part related to enhancement of muscle mitochondrial performance. The effects of two different trainings were investigated on transcripts and proteins of theAMPK–PGC-1α signaling pathway, the mitochondrial functioning (citrate synthase (CS), oxidative phosphorylationcomplexes, uncoupling proteins (UCP)) and the antioxidant defenses (superoxide dismutase (SOD),glutathione peroxidase (GPx), catalase) in rainbow trout red and white skeletal muscles. One group of troutsswam for 10 days at a moderate intensity (approximately 57% Ucrit or 2.0 body lengths/s, 23.5 h/day) andanother group at a high intensity (approximately 90% Ucrit or 3.2 body lengths/s, 2 h/day). In the red muscle,the increase of Cs mRNA levels was significantly correlated with the transcripts of Ampkα1, Ampkα2, Pgc-1α, theoxidative phosphorylation complexes, Ucp2α, Ucp2β, Sod1, Sod2 and Gpx1. After 10 days of training, high intensitytraining (HIT) stimulates more the transcription of genes involved in this aerobic pathway than moderateintensity training (MIT) in the skeletal muscles, and mainly in the red oxidative muscle. However, no changes inCS, cytochrome c oxidase (COX) and antioxidant defenses activities and in oxidative stress marker (isoprostaneplasmatic levels) were observed. The transcriptomic responses are fiber- and training-type dependent whenproteins were not yet expressed after 10 days of training. As in mammals, our results suggest that HIT couldpromote benefit effects in fish

Effect of personalized moderate exercise training on Wistar rats fed with a fructose enriched water

Abstract Background Metabolic Syndrom has become a public health problem. It mainly results from the increased consumption of fat and sugar. In this context, the benefits of personalized moderate exercise training were investigated on a metabolic syndrome male wistar rat model food with fructose drinking water (20–25% w/v). Different markers including body weight, metabolic measurements, blood biochemistry related to metabolic syndrome complications have been evaluated. Methods Male Wistar rats were randomly allocated to 4 groups: control (sedentary (C, n = 8) and exercise trained (Ex, n = 8)), fructose fed (sedentary (FF, n = 8) and exercise trained fructose fed rats (ExFF, n = 10)). ExFF and Ex rats were trained at moderate intensity during the last 6 weeks of the 12 weeks-long protocol of fructose enriched water. Metabolic control was determined by measuring body weight, fasting blood glucose, HOMA 2-IR, HIRI, MISI, leptin, adiponectin, triglyceridemia and hepatic dysfunction. Results After 12 weeks of fructose enriched diet, rats displayed on elevated fasting glycaemia and insulin resistance. A reduced food intake, as well as increased body weight, total calorie intake and heart weight were also observed in FF group. Concerning biochemical markers, theoretical creatinine clearance, TG levels and ASAT/ALAT ratio were also affected, without hepatic steatosis. Six weeks of 300 min/week of moderate exercise training have significantly improved overweight, fasting glycaemia, HOMA 2-IR, MISI without modify HIRI. Exercise also decreased the plasma levels of leptin, adiponectin and the ratio leptin/adiponectin. Regarding liver function and dyslipidemia, the results were less clear as the effects of exercise and fructose-enriched water interact together, and, sometimes counteract each other. Conclusion Our results indicated that positive health effects were achieved through a personalized moderate training of 300 min per week (1 h/day and 5 days/week) for 6 weeks. Therefore, regular practice of aerobic physical exercise is an essential triggering factor to attenuate MetS disorders induced by excessive fructose consumption

Physiological characteristics associated with increased resistance to decompression sickness in male and female rats.

Decompression sickness (DCS) is a complex and poorly understood systemic disease with wide inter-individual resistance variability. We selectively bred rats with a 3-fold greater resistance to DCS than standard ones. To investigate possible physiological mechanisms underlying the resistance to DCS, including sex-related differences in these mechanisms, 15 males and 15 females resistant to DCS were compared with aged-matched standard Wistar males (n=15) and females (n=15). None of these individuals had been previously exposed to hyperbaric treatment. Comparison of the allelic frequencies of SNPs showed a difference of one SNP located on the X chromosome. Compared with non-resistant rats, the neutrophil-to-lymphocyte ratio and the plasmatic activity of coagulation Factor X were significantly higher in DCS-resistant individuals regardless of their sex. The maximal relaxation elicited by sodium nitroprusside was lower in DCS-resistant individuals regardless of their sex. Males but not females resistant to DCS exhibited higher neutrophil and lymphocyte counts, higher prothrombin time whereas lower mitochondrial basal O2 consumption and citrate synthase activity. Principal Components Analysis showed that two principal components discriminate the DCS-resistant males but not females from the non-resistant ones. These components were loaded with aPTT, MLR, PT, FX, Fib, for PC1, and ARBC and ANC for PC2. In conclusion, the mechanisms which drive the resistance to DCS appear different between males and females; lower coagulation tendency and enhanced inflammatory response to decompression stress might be key for resistance in males. The involvement of these physiological adaptations in resistance to DCS must now be confirmed