International audienceOne outcome of contemporary climate trends is that the involvement of hypoxia and heat tolerance in determining individual fitness will increase in many fish populations. Large fish are believed to be more tolerant to hypoxia than small fish (Nilsson and Östlund-Nilsson, 2008) whereas thermal sensitivity is thought to decrease with body size (Clark et al., 2008). To better understand the bases of inter-individual variation in environmental adaptation performance, the current study examined hypoxia and heat tolerance in a fast growing (FGS; 288.3 ±14.4 g, 26.04±0.49 cm) and a slow growing (SGS; 119.95±6.41 g; 20.98±0.41 cm) strain of 1-year old rainbow trout (Oncorhynchus mykiss). This examination was conducted using two standardized challenge tests aimed at assessing individual incipient lethal oxygen saturation and incipient upper lethal temperature. Results to these tests were then cross-correlated with swim tests during which individual basal and active metabolic rate values were also measured. Measurements of permeabilized ventricular myofibers oxygen consumption were also conducted, as well as various organ-to-body-mass ratios. Experimental data showed that FGS was more hypoxia tolerant than SGS (13.4 to 16.7% air sat versus 14.7 to 18.9% air sat respectively). On the other hand, FGS was found less tolerant to heat than SGS (24.7-27.6 °C versus 28.5 to 29.7 °C respectively). Adding to the body size effect, another source of inter-individual variation in environmental tolerance was found. Residual analysis highlighted that whereas none of the individual morphometric and energetic traits correlated with hypoxia tolerance, permeabilized ventricular myofibers maximal oxygen consumption correlated well with individual tolerance to heat

We hypothesize that the part of Vmax devoted to proton leakage was decreased in trained rats, consequently improving ATP synthesis. The data suggest that, after training, there is more efficient use of electrons in respiratory chain energy production, rather than a greater ROS scavenging capacity.

Objective: This study investigated gender-dependent differences of mitochondrial function and sensitivity to in vitro ROS exposure in rat skeletal muscle at rest and after exercise training. Methods: Wistar rats underwent running training for 6 weeks. In vitro measurements of hydroxyl radical production, oxygen consumption (under basal and maximal respiration conditions) and ATP production were made on permeabilized fibers. Mitochondrial function was examined after exposure and non-exposure to an in vitro generator system of reactive oxygen species (ROS). Antioxidant enzyme activities and malondialdehyde (MDA) content were also determined. Results: Compared with sedentary males, females showed a greater resistance of mitochondrial function (oxygen consumption and ATP production) to ROS exposure, and lower MDA content and antioxidant enzyme activities. The training protocol had more beneficial effects in males than females with regard to ROS production and oxidative stress. In contrast to male rats, the susceptibility of mitochondrial function to ROS exposure in trained females was unchanged. Discussion: Exercise training improves mitochondrial function oxidative capacities in both male and female rats, but is more pronounced in males as a result of different mechanisms. The resistance of mitochondrial function to in vitro oxidative stress exposure and the antioxidant responses are gender-and training-dependent, and may be related to the protective effects of estrogen.

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The current results demonstrate that postconditioning hypothermia was associated with increased survival duration during experimental sepsis. Whether the observed benefits on survival duration are due to potential impacts on energy metabolism or to an anti-inflammatory effect of hypothermia requires further investigation.

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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.