New Findings: What is the central question of this study?A few weeks of endurance training accelerate the oxygen uptake () on‐kinetics in humans. The main aim of the present study was to determine whether the acceleration ofon‐kinetics obtained by a short period of moderate‐intensity training can be explained by an intensification of mitochondrial biogenesis. What is the main finding and its importance?We demonstrated that 5 weeks of moderate‐intensity training accelerates theon‐kinetics during moderate‐intensity cycling in the absence of enhanced mitochondrial biogenesis or capillarization in the trained muscles. We postulate that in the early stages of training an intensification of ‘parallel activation’ of oxidative phosphorylation could account for the shortening of theon‐transient. The effects of 5 weeks of moderate‐intensity endurance training on pulmonary oxygen uptake kinetics (on‐kinetics) were studied in 15 healthy men (mean ± SD: age 22.7 ± 1.8 years, body weight 76.4 ± 8.9 kg and maximal46.0 ± 3.7 ml kg⁻¹min⁻¹). Training caused a significant acceleration (P= 0.003) ofon‐kinetics during moderate‐intensity cycling (time constant of the ‘primary’ component 30.0 ± 6.6versus22.8 ± 5.6 s before and after training, respectively) and a significant decrease (P= 0.04) in the amplitude of the primary component (837 ± 351versus801 ± 330 ml min⁻¹). No changes in myosin heavy chain distribution, muscle fibre capillarization, level of peroxisome proliferator‐activated receptor γ coactivator 1α and other markers of mitochondrial biogenesis (mitochondrial DNA copy number, cytochromecand cytochrome oxidase subunit I contents) in the vastus lateralis were found after training. A significant downregulation in the content of the sarcoplasmic reticulum ATPase 2 (SERCA2;P= 0.03) and a tendency towards a decrease in SERCA1 (P= 0.055) was found after training. The decrease in SERCA1 was positively correlated (P= 0.05) with the training‐induced decrease in the gain of theon‐kinetics (at steady state/Δpower output). In the early stage of training, the acceleration inon‐kinetics during moderate‐intensity cycling can occur without enhanced mitochondrial biogenesis or changes in muscle myosin heavy chain distribution and in muscle fibre capillarization. The training‐induced decrease of the O₂cost of cycling could be caused by the downregulation of SERCA pumps.

The uterus has a remarkable ability of cycling remodeling throughout the reproductive life of the female. Recent findings in the human and mouse indicate that adult stem/progenitor cells may play a prominent role in the maintenance of uterine endometrial and myometrial homeostasis. We aimed to characterize the prospective stem/progenitor cells in the porcine uterus and establish a new model for uterine stem cell research. In this study, we demonstrated that cells isolated from porcine uterus have capacity for in vitro differentiation into adipogenic and osteogenic lineages and express the mesenchymal stem cell (MSC) markers CD29, CD44, CD144, CD105, and CD140b as revealed by RT-PCR. Moreover, we showed that some cells isolated from the porcine uterus when cultured at low density produce large clones with an efficiency of 0.035%. Simultaneously, they were negative for hematopoietic stem cell markers such as CD34 and CD45. Low expression of nestin, which is specific for neural stem cells and various progenitor cells, was also detected. We conclude that the porcine uterus contains a small population of undifferentiated cells with MSC-like properties similar to human and mouse uteri.

The structure and properties of Co‐N, Co‐Fe‐N, and Co‐Zr‐N films, prepared by rf reactive sputtering using nitrogen and argon gases, have been studied. The resistivity and coercivity of Co‐N, Co‐Fe‐N, and Co‐Zr‐N films were determined as a function of nitrogen partial pressure. It was found that the properties of Co‐N and Co‐Fe‐N films were very similar where the properties were determined mainly by the nitride phases in these films. The resistivity of both Co‐N and Co‐Fe‐N films increased with the increase of nitrogen pressure. The coercivity of both films decreased with an initial increase of nitrogen pressure, then increased with a further increase of pressure so that there is a region of nitrogen pressures where the coercivity is at its lowest value. The low coercivity is attributed to the formation of the Co₄N phase in Co‐N films and both Co₄N and Fe₄N phases in Co‐Fe‐N films. For Co‐Zr‐N films, resistivity first decreased with an increase of nitrogen pressure, then increased with a further increase of pressure, indicating the presence of a Zr‐N phase in these films. The coercivity increased with an increase of nitrogen pressure. The Zr‐N phase was not observed in the x‐ray diffraction measurements due to the low concentration of Zr in these films.

Dynamic resistance training increases the force and speed of muscle contraction, but little is known about modifications to the contractile properties of the main physiological types of motor units (MUs) that contribute to these muscle adaptations. Although the contractile profile of MU muscle fibers is tightly coupled to myosin heavy chain (MyHC) protein expression, it is not well understood if MyHC transition is a prerequisite for modifications to the contractile characteristics of MUs. In this study, we examined MU contractile properties, the mRNA expression of MyHC, parvalbumin, and sarcoendoplasmic reticulum Ca²⁺pump isoforms, as well as the MyHC protein content after 5 wk of volitional progressive weight-lifting training in the medial gastrocnemius muscle in rats. The training had no effect on MyHC profiling or Ca²⁺-handling protein gene expression. Maximum force increased in slow (by 49%) and fast (by 21%) MUs. Within fast MUs, the maximum force increased in most fatigue-resistant and intermediate but not most fatigable MUs. Twitch contraction time was shortened in slow and fast fatigue-resistant MUs. Twitch half-relaxation was shortened in fast most fatigue-resistant and intermediate MUs. The force-frequency curve shifted rightward in fast fatigue-resistant MUs. Fast fatigable MUs fatigued less within the initial 15 s while fast fatigue-resistant units increased the ability to potentiate the force within the first minute of the standard fatigue test. In conclusion, at the early stage of resistance training, modifications to the contractile characteristics of MUs appear in the absence of MyHC transition and the upregulation of Ca²⁺-handling genes.