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BACKGROUND AND AIMS: Motor unit (MU) force is regulated by neural and muscular mechanisms. Recently, effects of carnosine on skeletal muscle contractility have been broadly studied. We found that increased muscle carnosine content by beta-alanine supplementation improved MU contractility. Several studies showed that histidine-free diet decreases carnosine content and causes weight loss, anaemia or hypoproteinaemia but its effect on muscle contractility is unknown. Here we studied MU contractile properties in histidine-deprived rats with reduced muscle carnosine content. METHODS: Ten 6 mo male Wistar rats were randomly assigned to experimental (HFD) or control (CON) group fed histidine-free or standard diet for 14 days, respectively. In order to maintain the same level of body mass loss food intake was controlled and balanced between both groups. Body mass decreased by 11.7 and 10.6% in HFD and CON groups, respectively. RESULTS: In HFD group carnosine levels were lower than in CON group in white and red portion of MG muscle by 26% and 34%, respectively. Histidine deprivation did not result in lower muscle mass or muscle-to-body mass ratio. In electrophysiological experiments contractions of MUs in medial gastrocnemius (MG) muscle were evoked by electrical stimulation of ventral root filaments. MUs were classified into fast fatigable (FF), fast resistant (FR) and slow (S). Maximum tetanic force (TetF) and force profile during the two separate fatigue tests were analysed. The TetF did not differ between groups either in fast or slow MUs. During the first fatigue test in FR MU force was initially higher but from 40 to 120 s it was lower in HFD animals. Unexpectedly, in the second fatigue test the force of FR and S MU was better maintained in HFD than CON rats. CONCLUSIONS: The results indicate that short-term histidine deprivation and the carnosine decrease do not attenuate force of MUs. Moreover, compensatory mechanisms may be involved in the regulation of MU force in this condition. Support: grant 2013/09/B/NZ7/02554.
EN
Beta-alanine (BA) supplementation increases muscle carnosine concentration resulting in better muscle performance. In vitro experiments on isolated muscles and single muscle fibers indicated that carnosine improved excitation-contraction coupling and slowed fatigue. We investigated effects of BA supplementation on muscle carnosine levels and in vivo motor units (MUs) contractile properties in rat medial gastrocnemius muscle (MG). Ten male Wistar rats were randomly assigned to control (n=5) or BA (supplemented with 1% BA in the drinking water for 10 weeks; n=5) groups. Contractions of 258 MUs were evoked by electrical stimulation of ventral root filaments. MUs were classified into fast fatigable (FF), fast resistant (FR) and slow (S) according to the standard criteria. Twitch force (TwF), maximum tetanic force (TetF) and force profile during the fatigue test were analyzed. BA supplementation enhanced carnosine levels in white and red portion of MG muscle by 94% and 56%, respectively. After BA supplementation TwF in FF and TetF in FR MUs increased, and force was better maintained from 20th to 130th s of the applied fatigue test in FR MUs. In conclusion, BA supplementation primarily improves contractile performance of FR MUs.
EN
INTRODUCTION: Carnosine (beta-alanyl-L-histidine) is predominantly present in skeletal muscle but also in other excitable tissues. It was suggested that muscle carnosine concentration can decrease with ageing. There is growing evidence that supplementation of carnosine can be effective for the treatment of age related disorders as well as neurological disorders e.g. Alzheimer’s disease or Parkinson’s disease. AIM(S): Here we investigate the effects of orally supplemented carnosine in aged rats on motor units (MUs) contractile properties. METHOD(S): 42 male Wistar rats aged 15 months were randomly assigned to three groups: control (CON; n=15), treated with carnosine for 8 months (CAR8M; n=15) or treated with lated and fixed. In one set of experiments the brains were frozen and cut with the use of cryotome. Then, slices were used either for Nissl staining to visualise anatomical structure, or in situ hybridisation for gene expression analysis. In another set of experiments, fixed brains were dissected into two hemispheres, after which a small DiI crystal was inserted into the thalamus. After incubation, the hemispheres were cut with a vibratome and DiI-stained axons were visualised under fluorescent microscope. RESULTS: We show here, that TCF7L2‑deficent mice displayed major changes in the anatomy of the thalamus and habenulae, as well as partial malformations of the striatum. Furthermore, Tcf7l2-/- mice most often completely failed to produce thalamocortical axons; if some were visible, they did not reach their cortical targets. CONCLUSIONS: The study demonstrated a critical involvement of TCF7L2 in thalamic nucleogenesis and establishment of thalamocortical axons. FINANCIAL SUPPORT: Work supported by NCN grants 2011/03/B/NZ3/04480 and 2015/19/B/NZ3/02949.
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