3,551 research outputs found

    Heart rate and lactate responses to taekwondo fight in elite women performers

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    The purpose of this study was to examine heart rate (HR) and blood lactate (LA) concentration before, during and after a competitive Tae kwon do (TKD) fight performed by elite women performers. Specifically, we were interested to see weather HR and LA responses to competitive fight were greater than to TKD or karate exercises published in scientific literature. Seven international-standard women TKD fighters participated in the study. HR was recorded continuously throughout the fight using Polar Vantage telemetric HR monitors. LA samples were taken before and 3 min after the fight and analysed using an Accusport portable lactate analyzer. At the beginning of the fight, HR significantly increased (p<0.01) from pre-fight values of 91.6±9.9 beats min-1 to 144.1±13.6 beats min-1. During the whole fight the HRmean was 186.6±2.5 beats min-1 and remained significantly elevated (p<0.01) at 3 min into recovery. HR values expressed as a percentage of HRmax averaged during the whole fight at 91.7±2.6% respectively. LA concentration significantly increased (p<0.01) 3 min after the fight and averaged 82% of LApeak values measured after the VO2max test. Results of the present study indicate that physiological demands of competitive TKD fight in women, measured by HR and LA responses, are considerably higher than the physiological demands of TKD or karate training exercises. The observed HR and LA responses suggest to us that conditioning for TKD should generally emphasise high-intensity anaerobic exercise

    Association of a homozygous GCK missense mutation with mild diabetes

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    Background: Homozygous inactivating GCK mutations have been repeatedly reported to cause severe hyperglycemia, presenting as permanent neonatal diabetes mellitus (PNDM). Conversely, only two cases of GCK homozygous mutations causing mild hyperglycemia have been so far described. We here report a novel GCK mutation (c.1116G&gt;C, p.E372D), in a family with one homozygous member showing mild hyperglycemia. Methods: GCK mutational screening was carried out by Sanger sequencing. Computational analyses to investigate pathogenicity and molecular dynamics (MD) were performed for GCK-E372D and for previously described homozygous mutations associated with mild (n&nbsp;=&nbsp;2) or severe (n&nbsp;=&nbsp;1) hyperglycemia, used as references. Results: Of four mildly hyperglycemic family-members, three were heterozygous and one, diagnosed in the adulthood, was homozygous for GCK-E372D. Two nondiabetic family members carried no mutations. Fasting glucose (p&nbsp;=&nbsp;0.016) and HbA1c (p&nbsp;=&nbsp;0.035) correlated with the number of mutated alleles (0–2). In-silico predicted pathogenicity was not correlated with the four mutations’ severity. At MD, GCK-E372D conferred protein structure flexibility intermediate between mild and severe GCK mutations. Conclusions: We present the third case of homozygous GCK mutations associated with mild hyperglycemia, rather than PNDM. Our in-silico analyses support previous evidences suggesting that protein stability plays a role in determining clinical severity of GCK mutations

    From Protecting the Heart to Improving Athletic Performance - the Benefits of Local and Remote Ischaemic Preconditioning

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    Remote Ischemic Preconditioning (RIPC) is a non-invasive cardioprotective intervention that involves brief cycles of limb ischemia and reperfusion. This is typically delivered by inflating and deflating a blood pressure cuff on one or more limb(s) for several cycles, each inflation-deflation being 3-5 min in duration. RIPC has shown potential for protecting the heart and other organs from injury due to lethal ischemia and reperfusion injury, in a variety of clinical settings. The mechanisms underlying RIPC are under intense investigation but are just beginning to be deciphered. Emerging evidence suggests that RIPC has the potential to improve exercise performance, via both local and remote mechanisms. This review discusses the clinical studies that have investigated the role of RIPC in cardioprotection as well as those studying its applicability in improving athletic performance, while examining the potential mechanisms involved

    Strigolactones affect phosphorus acquisition strategies in tomato plants

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    Strigolactones (SLs) are plant hormones that modulate morphological, physiological and biochemical changes as part of the acclimation strategies to phosphorus (P) deficiency, but an in‐depth description of their effects on tomato P‐acquisition strategies under P shortage is missing. Therefore, in this study, we investigate how SLs impact on root exudation and P uptake, in qualitative and quantitative terms over time, in wild‐type and SL‐depleted tomato plants grown with or without P. Under P shortage, SL‐depleted plants were unable to efficiently activate most mechanisms associated with the P starvation response (PSR), except for the up‐regulation of P transporters and increased activity of P‐solubilizing enzymes. The reduced SL biosynthesis had negative effects also under normal P provision, because plants over‐activated high‐affinity transporters and enzymatic activities (phytase, acidic phosphatase) to sustain elevated P uptake, at great carbon and nitrogen costs. A shift in the onset of PSR was also highlighted in these plants. We conclude that SLs are master kinetic regulators of the PSR in tomato and that their defective synthesis might lead both to suboptimal nutritional outcomes under P depletion and an unbalanced control of P uptake when P is available

    Reduced GABA(B) receptor subunit expression and paired-pulse depression in a genetic model of absence seizures

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    Neocortical networks play a major role in the genesis of generalized spike-and-wave (SW) discharges associated with absence seizures in humans and in animal models, including genetically predisposed WAG/Rij rats. Here, we tested the hypothesis that alterations in GABAB receptors contribute to neocortical hyperexcitability in these animals. By using Real-Time PCR we found that mRNA levels for most GABAB(1) subunits are diminished in epileptic WAG/Rij neocortex as compared with age-matched non-epileptic controls (NEC), whereas GABAB(2) mRNA is unchanged. Next, we investigated the cellular distribution of GABAB(1) and GABAB(2) subunits by confocal microscopy and discovered that GABAB(1) subunits fail to localize in the distal dendrites of WAG/Rij neocortical pyramidal cells. Intracellular recordings from neocortical cells in an in vitro slice preparation demonstrated reduced paired-pulse depression of pharmacologically isolated excitatory and inhibitory responses in epileptic WAG/Rij rats as compared with NECs; moreover, paired-pulse depression in NEC slices was diminished by a GABAB receptor antagonist to a greater extent than in WAG/Rij rats further suggesting GABAB receptor dysfunction. In conclusion, our data identify changes in GABAB receptor subunit expression and distribution along with decreased paired-pulse depression in epileptic WAG/Rij rat neocortex. We propose that these alterations may contribute to neocorticalhyperexcitability and thus to SW generation in absence epilepsy
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