91 research outputs found

    Cardiac Parasympathetic Reactivation in Elite Soccer Players During Different Types of Traditional High-Intensity Training Exercise Modes and Specific Tests: Interests and Limits

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    Background: The cardiac parasympathetic reactivation is currently used in soccer with a daily or weekly monitoring. However, previous studies have not investigated how this cardiac parasympathetic reactivation is in elite soccer players along different types of traditional high-intensity training exercise and specific tests. In this context, the present study aim to analyse it and to determine the interests and limits of this type of physiological information. Objectives: The present study aims to examine how different traditional training exercise modes affect the cardiac parasympathetic reactivation function in elite soccer players. Materials and Methods: Twenty-two international soccer players participating in UEFA Champion’s League took part in this study (age: 24.3 ± 4.2 years; height: 178.1 ± 6.2 cm; body mass: 80.3 ± 5.7 kg). Players performed different training methods including: short-duration intermittent exercises (INT) in-line and with changes of direction (COD) (10 - 10 seconds, 15 - 15 seconds, 30 - 30 seconds, e.g. an alternance of 10 - 10 seconds is 10 seconds of running according to the maximal aerobic speed (MAS) and 10-sec of recovery), INT including agility and technical skills (8 - 24-seconds), small-sided-games (SSGs) with and without goalkeepers (2 vs. 2, 3 vs. 3, 4 vs. 4), and repeated sprint ability (RSA) efforts (10 × 20 m, 10 × 30 m, 15 × 20 m). Heart rate (HR) decline was recorded 3 minutes after each exercise. Results: HR declines were greater after the RSA compared to SSGs (P < 0.001) and INT (P < 0.01), especially at 1 min post-exercise. In addition, when the analysis focused on each type of exercise, greater HR declines were observed in on-field players at 1 minute when there was: inclusion of goalkeepers in SSGs (for 2 vs. 2 and 3 vs. 3, P < 0.01); increase of sprint distances or number of sprint repetitions in RSA (P < 0.01); increase of intensity (% of maximal aerobic speed), and the use of COD or inclusion of technical skills during INT, especially for the 30 - 30-seconds. Conclusions: This study revealed that cardiac parasympathetic reactivation function varied after INT, RSA and SSG, but also according to the rules manipulation. Therefore, this study provides interesting information for the training monitoring and players’ recovery profile, with the aim of facilitating a more efficient planning and manipulation of training recovery strategies according to their fitness markers

    Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training

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    Activation of the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays a critical role modulating cardiac function in both health and disease. Here, we determined the effect of chronic CaMKII inhibition during an exercise training program in healthy mice. CaMKII was inhibited by KN-93 injections. Mice were randomized to the following groups: sham sedentary, sham exercise, KN-93 sedentary, and KN-93 exercise. Cardiorespiratory function was evaluated by ergospirometry during treadmill running, echocardiography, and cardiomyocyte fractional shortening and calcium handling. The results revealed that KN-93 alone had no effect on exercise capacity or fractional shortening. In sham animals, exercise training increased maximal oxygen uptake by 8% (p < 0.05) compared to a 22% (p < 0.05) increase after exercise in KN-93 treated mice (group difference p < 0.01). In contrast, in vivo fractional shortening evaluated by echocardiography improved after exercise in sham animals only: from 25 to 32% (p < 0.02). In inactive mice, KN-93 reduced rates of diastolic cardiomyocyte re-lengthening (by 25%, p < 0.05) as well as Ca2+ transient decay (by 16%, p < 0.05), whereas no such effect was observed after exercise training. KN-93 blunted exercise training response on cardiomyocyte fractional shortening (63% sham vs. 18% KN-93; p < 0.01 and p < 0.05, respectively). These effects could not be solely explained by the Ca2+ transient amplitude, as KN-93 reduced it by 20% (p < 0.05) and response to exercise training was equal (64% sham and 47% KN-93; both p < 0.01). We concluded that chronic CaMKII inhibition increased time to 50% re-lengthening which were recovered by exercise training, but paradoxically led to a greater increase in maximal oxygen uptake compared to sham mice. Thus, the effect of chronic CaMKII inhibition is multifaceted and of a complex nature

    The Role of Canine Distemper Virus and Persistent Organic Pollutants in Mortality Patterns of Caspian Seals (Pusa caspica)

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    Persistent organic pollutants are a concern for species occupying high trophic levels since they can cause immunosuppression and impair reproduction. Mass mortalities due to canine distemper virus (CDV) occurred in Caspian seals (Pusa caspica), in spring of 1997, 2000 and 2001, but the potential role of organochlorine exposure in these epizootics remains undetermined. Here we integrate Caspian seal mortality data spanning 1971-2008, with data on age, body condition, pathology and blubber organochlorine concentration for carcases stranded between 1997 and 2002. We test the hypothesis that summed PCB and DDT concentrations contributed to CDV associated mortality during epizootics. We show that age is the primary factor explaining variation in blubber organochlorine concentrations, and that organochlorine burden, age, sex, and body condition do not account for CDV infection status (positive/negative) of animals dying in epizootics. Most animals (57%, n = 67) had PCB concentrations below proposed thresholds for toxic effects in marine mammals (17 ÎŒg/g lipid weight), and only 3 of 67 animals had predicted TEQ values exceeding levels seen to be associated with immune suppression in harbour seals (200 pg/g lipid weight). Mean organonchlorine levels were higher in CDV-negative animals indicating that organochlorines did not contribute significantly to CDV mortality in epizootics. Mortality monitoring in Azerbaijan 1971-2008 revealed bi-annual stranding peaks in late spring, following the annual moult and during autumn migrations northwards. Mortality peaks comparable to epizootic years were also recorded in the 1970s-1980s, consistent with previous undocumented CDV outbreaks. Gompertz growth curves show that Caspian seals achieve an asymptotic standard body length of 126-129 cm (n = 111). Males may continue to grow slowly throughout life. Mortality during epizootics may exceed the potential biological removal level (PBR) for the population, but the low frequency of epizootics suggest they are of secondary importance compared to anthropogenic sources of mortality such as fishing by-catch

    Raman Gain Of Selected Tellurite Glasses For Ir Fibre Lasers Calculated From Spontaneous Scattering Spectra

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    In this paper, we present the spontaneous Raman scattering spectra and calculated Raman gain spectra of two TZN (TeO2-ZnO-Na2O) glasses and three tungsten tellurite glasses. Addition of lead(II) oxide to the TZN glass increased the amount of lower coordination [TeO3]/[TeO3+1] units (765 cm-1) in the glass, and decreased the higher coordination [TeO4] units (665 cm-1) and Te-O-Te chains (440 cm-1). Addition of WO3 to the tungsten-tellurite glasses also resulted in the same trend as with PbO, and an additional band at around 925 cm-1 was seen to increase in intensity due to [WO4+2] units. Finally, a band at around 370 cm-1 was seen in the bismuth-doped tungsten tellurite glass, due to Te-O-Bi linkages. The calculated Raman gain of these tellurite glasses were found to be 20-30 times that of fused-silica (0.89 × 10-13 m W-1). The calculated Raman gain of the PbO-doped TZN glass also showed good agreement with direct gain measurements previously made at 1064 nm. The minimum laser powers required to stimulate Raman amplification were calculated for one TZN glass and one tungsten-tellurite glass for optical fibre with a 10 ÎŒm core. The power densities required were of the order of MW cm-2 for fibre with 2-3 dB m-1 loss at 1550 nm and much lower than the surface optical damage thresholds of the glasses which are of the order of GW cm-2. © 2007 Elsevier B.V. All rights reserved

    Aerobic Interval Training Versus Continuous Moderate Exercise as a Treatment for the Metabolic Syndrome: A Pilot Study

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    Background-- Individuals with the metabolic syndrome are 3 times more likely to die of heart disease than healthy counterparts. Exercise training reduces several of the symptoms of the syndrome, but the exercise intensity that yields the maximal beneficial adaptations is in dispute. We compared moderate and high exercise intensity with regard to variables associated with cardiovascular function and prognosis in patients with the metabolic syndrome. Methods and Results-- Thirty-two metabolic syndrome patients (age, 52.3{+/-}3.7 years; maximal oxygen uptake [[V]O2max], 34 mL {middle dot} kg-1 {middle dot} min-1) were randomized to equal volumes of either moderate continuous moderate exercise (CME; 70% of highest measured heart rate [Hfmax]) or aerobic interval training (AIT; 90% of Hfmax) 3 times a week for 16 weeks or to a control group. [V]O2max increased more after AIT than CME (35% versus 16%; P&#60;0.01) and was associated with removal of more risk factors that constitute the metabolic syndrome (number of factors: AIT, 5.9 before versus 4.0 after; P&#60;0.01; CME, 5.7 before versus 5.0 after; group difference, P&#60;0.05). AIT was superior to CME in enhancing endothelial function (9% versus 5%; P&#60;0.001), insulin signaling in fat and skeletal muscle, skeletal muscle biogenesis, and excitation-contraction coupling and in reducing blood glucose and lipogenesis in adipose tissue. The 2 exercise programs were equally effective at lowering mean arterial blood pressure and reducing body weight (-2.3 and -3.6 kg in AIT and CME, respectively) and fat. Conclusions-- Exercise intensity was an important factor for improving aerobic capacity and reversing the risk factors of the metabolic syndrome. These findings may have important implications for exercise training in rehabilitation programs and future studie

    Carbon Monoxide Levels Experienced by Heavy Smokers Impair Aerobic Capacity and Cardiac Contractility and Induce Pathological Hypertrophy

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    Cigarette smoke contains hundreds of potentially toxic compounds and is an important risk factor for cardiovascular disease. However, the key components responsible for endothelial and myocardial dysfunction have not been fully identified. The objective of the present study was to determine the cardiovascular effects of long-term inhalation of carbon monoxide (CO) administrated to give concentrations in the blood similar to those observed in heavy smokers. Female rats were exposed to either CO or air (control group) (n = 12). The CO group was exposed to 200 ppm CO (100 h/wk) for 18 mo. Rats exposed to CO had 24% lower maximal oxygen uptake, longer (145 vs. 123 \u3bc m) and wider (47 vs. 25 \u3bc m) cardiomyocytes, reduced cardiomyocyte fractional shortening (12 vs. 7%), and 26% longer time to 50% re-lengthening than controls. In addition, cardiomyocytes from CO-exposed rats had 48% lower intracellular calcium (Ca2 +) amplitude, 22% longer time to Ca2 + decay, 34% lower capacity of sarcoplasmic reticulum Ca2 +-ATPase (SERCA2a), and 37% less t-tubule area compared to controls. Phosphorylation levels of phospholamban at Ser16 and Thr17 were significantly reduced in the CO group, whereas total concentration of phospholamban and SERCA2a were unchanged. Cardiac atrial natriuretic peptide, vascular endothelial growth factor, cyclic guanosine monophosphate, calcineurin, calmodulin, pERK, and pS6 increased, whereas pAkt and pCaMKII \u3b4 remained unchanged by CO. Endothelial function and systemic blood pressure were not affected by CO exposure. Long-term CO exposure reduces aerobe capacity and contractile function and leads to pathological hypertrophy. Impaired Ca2 + handling and increased growth factor signaling seem to be responsible for these pathological change
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