Variability in energy cost of running at the end of a triathlon and a marathon

International audienceThe aim of this study was to investigate the increase in energy cost of running occurring at the end of a triathlon and a marathon event and to link them to the metabolic and hormonal changes, as well as to variations in stride length. Seven subjects took part in 3 experimental situations: a 2 h 15 min triathlon (30 min swimming, 60 min cycling and 45 min running), a 2 h 15 min marathon (MR) were the fast 45 min were run at the same speed as the triathlon run (TR), and a 45 min isolated run (IR) done at triathlon speed. The results show that energy cost during MR was higher than during TR (p < 0.01) (+ 8.9 %). Similar observations were made for pulmonary ventilation (+ 7.9 %) and heart rate (+ 6.3 %). Moreover, the values were significantly greater than the values obtained during the IR. TR and MR lead to greater weight loss (p < 0.01) (2.4±0.3 kg) than IR (1 ± 0.2 kg). The triathlon and the marathon produced a large decrease in plasma volume (respectively 19.6 ± 1.4 % and 12.9 ± 1.1 %) compared to IR (2 ± 0.4 %). Plasma renin activity was higher for the triathlon and the marathon than for the IR (p < 0.01). MR produces a significantly greater increase in plasma free fatty acids (F.F.A.) than TR (p < 0.05) and IR (p < 0.01). In addition, the F.F.A. at the end of TR were significantly higher than IR (p < 0.05). At the end of the trial the mean stride lengths for TR and IR were greater (+ 15 %) (p <0.01) than for MR. This study, carried out with subjects running overground, confirms the decrease in running efficiency previously shown at the end of a laboratory triathlon, and demonstrates that this decrease is lower than that occurring during a marathon

Electron-hole asymmetry in two-terminal graphene devices

A theoretical model is proposed to describe asymmetric gate-voltage dependence of conductance and noise in two-terminal ballistic graphene devices. The model is analyzed independently within the self-consistent Hartree and Thomas-Fermi approximations. Our results justify the prominent role of metal contacts in recent experiments with suspended graphene flakes. The contact-induced electrostatic potentials in graphene demonstrate a power-law decay with the exponent varying from -1 to -0.5. Within our model we explain electron-hole asymmetry and strong Fabri-Perot oscillations of the conductance and noise at positive doping, which were observed in many experiments with submicrometer samples. Limitations of the Thomas-Fermi approximation in a vicinity of the Dirac point are discussed.Comment: 7 pages, 8 figure

Effects of Post-Exercise Protein Intake on Muscle Mass and Strength During Resistance Training: is There an Optimal Ratio Between Fast and Slow Proteins?

While effects of the two classes of proteins found in milk (i.e. soluble proteins, including whey, and casein) on muscle protein synthesis have been well investigated after a single bout of resistance exercise (RE), the combined effects of these two proteins on the muscle responses to resistance training (RT) have not yet been investigated. Therefore, the aim of this study was to examine the effects of protein supplementation varying by the ratio between milk soluble proteins (fast-digested protein) and casein (slow-digested protein) on the muscle to a 9-week RT program. In a double-blind protocol, 31 resistance-trained men, were assigned to 3 groups receiving a drink containing 20g of protein comprising either 100% of fast protein (FP(100), n=10), 50% of fast and 50% of slow proteins (FP(50), n=11) or 20% of fast protein and 80% of casein (FP(20), n=10) at the end of training bouts. Body composition (DXA), and maximal strength in dynamic and isometric were analyzed before and after RT. Moreover, blood plasma aminoacidemia kinetic after RE was measured. The results showed a higher leucine bioavailability after ingestion of FP(100) and FP(50) drinks, when compared with FP(20) (p<0.05). However, the RT-induced changes in lean body mass (p<0.01), dynamic (p<0.01), and isometric muscle strength (p<0.05) increased similarly in all experimental groups. To conclude, compared to the FP(20) group, the higher rise in plasma amino acids following the ingestion of FP(100) and FP(50) did not lead to higher muscle long-term adaptations

Collateral Health Issues Derived from the Covid-19 Pandemic.

At the end of 2019, a new coronavirus (Covid-19) outbreak occurred in Wuhan, China, and spread throughout the world despite efforts to contain the virus. At the end of January 2020, the General Director of the World Health Organization (WHO) declared a Public Health Emergency of International Concern, and by mid-May 2020, the worldwide number of known Covid-19 cases had surpassed 4.4 million including more than 300,000 deaths..

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy

Mammalian target of rapamycin (mTOR) is a key regulator of cell growth that associates with raptor and rictor to form the mTOR complex 1 (mTORC1) and mTORC2, respectively. Raptor is required for oxidative muscle integrity, whereas rictor is dispensable. In this study, we show that muscle-specific inactivation of mTOR leads to severe myopathy, resulting in premature death. mTOR-deficient muscles display metabolic changes similar to those observed in muscles lacking raptor, including impaired oxidative metabolism, altered mitochondrial regulation, and glycogen accumulation associated with protein kinase B/Akt hyperactivation. In addition, mTOR-deficient muscles exhibit increased basal glucose uptake, whereas whole body glucose homeostasis is essentially maintained. Importantly, loss of mTOR exacerbates the myopathic features in both slow oxidative and fast glycolytic muscles. Moreover, mTOR but not raptor and rictor deficiency leads to reduced muscle dystrophin content. We provide evidence that mTOR controls dystrophin transcription in a cell-autonomous, rapamycin-resistant, and kinase-independent manner. Collectively, our results demonstrate that mTOR acts mainly via mTORC1, whereas regulation of dystrophin is raptor and rictor independent

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy

mTor, acting mainly via mTORC1, controls dystrophin transcription in a raptor- and rictor-independent mechanism