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Cardiovascular and haematological adaptations to endurance training facilitate greater maximal oxygen consumption (V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$), and such adaptations may be augmented following puberty. Therefore, we compared left ventricular (LV) morphology (echocardiography), blood volume, haemoglobin (Hb) mass (CO rebreathing) and V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ in endurance‐trained and untrained boys (n = 42, age = 9.0–17.1 years, V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ = 61.6 ± 7.2 ml/kg/min, and n = 31, age = 8.0–17.7 years, V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ = 46.5 ± 6.1 ml/kg/min, respectively) and girls (n = 45, age = 8.2–17.0 years, V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ = 51.4 ± 5.7 ml/kg/min, and n = 36, age = 8.0–17.6 years, V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ = 39.8 ± 5.7 ml/kg/min, respectively). Pubertal stage was estimated via maturity offset, with participants classified as pre‐ or post‐peak height velocity (PHV). Pre‐PHV, only a larger LV end‐diastolic volume/lean body mass (EDV/LBM) for trained boys (+0.28 ml/kg LBM, P = 0.007) and a higher Hb mass/LBM for trained girls (+1.65 g/kg LBM, P = 0.007) were evident compared to untrained controls. Post‐PHV, LV mass/LBM (boys: +0.50 g/kg LBM, P = 0.0003; girls: +0.35 g/kg LBM, P = 0.003), EDV/LBM (boys: +0.35 ml/kg LBM, P < 0.0001; girls: +0.31 ml/kg LBM, P = 0.0004), blood volume/LBM (boys: +12.47 ml/kg LBM, P = 0.004; girls: +13.48 ml/kg LBM, P = 0.0002.) and Hb mass/LBM (boys: +1.29 g/kg LBM, P = 0.015; girls: +1.47 g/kg LBM, P = 0.002) were all greater in trained versus untrained groups. Pre‐PHV, EDV (R2adj = 0.224, P = 0.001) in boys, and Hb mass and interventricular septal thickness (R2adj = 0.317, P = 0.002) in girls partially accounted for the variance in V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$. Post‐PHV, stronger predictive models were evident via the inclusion of LV wall thickness and EDV in boys (R2adj = 0.608, P < 0.0001), and posterior wall thickness and Hb mass in girls (R2adj = 0.490, P < 0.0001). In conclusion, cardiovascular adaptation to exercise training is more pronounced post‐PHV, with evidence for a greater role of central components for oxygen delivery. Key points: It has long been hypothesised that cardiovascular adaptation to endurance training is augmented following puberty.We investigated whether differences in cardiac and haematological variables exist, and to what extent, between endurance‐trained versus untrained, pre‐ and post‐peak height velocity (PHV) children, and how these central factors relate to maximal oxygen consumption.Using echocardiography to quantify left ventricular (LV) morphology and carbon monoxide rebreathing to determine blood volume and haemoglobin mass, we identified that training‐related differences in LV morphology are evident in pre‐PHV children, with haematological differences also observed between pre‐PHV girls. However, the breadth and magnitude of cardiovascular remodelling was more pronounced post‐PHV.Cardiac and haematological measures provide significant predictive models for maximal oxygen consumption (V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$) in children that are much stronger post‐PHV, suggesting that other important determinants within the oxygen transport chain could account for the majority of variance in V̇O2max${\dot{V}_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ before puberty. [ABSTRACT FROM AUTHOR]

Key points: We sought to determine the isolated and combined influence of hypovolaemia and hypoxic pulmonary vasoconstriction on the decrease in left ventricular (LV) function and maximal exercise capacity observed under hypobaric hypoxia.We performed echocardiography and maximal exercise tests at sea level (344 m), and following 5–10 days at the Barcroft Laboratory (3800 m; White Mountain, California) with and without (i) plasma volume expansion to sea level values and (ii) administration of the pulmonary vasodilatator sildenafil in a double‐blinded and placebo‐controlled trial.The high altitude‐induced reduction in LV filling and ejection was abolished by plasma volume expansion but to a lesser extent by sildenafil administration; however, neither intervention had a positive effect on maximal exercise capacity.Both hypovolaemia and hypoxic pulmonary vasoconstriction play a role in the reduction of LV filling at 3800 m, but the increase in LV filling does not influence exercise capacity at this moderate altitude. We aimed to determine the isolated and combined contribution of hypovolaemia and hypoxic pulmonary vasoconstriction in limiting left ventricular (LV) function and exercise capacity under chronic hypoxaemia at high altitude. In a double‐blinded, randomised and placebo‐controlled design, 12 healthy participants underwent echocardiography at rest and during submaximal exercise before completing a maximal test to exhaustion at sea level (SL; 344 m) and after 5–10 days at 3800 m. Plasma volume was normalised to SL values, and hypoxic pulmonary vasoconstriction was reversed by administration of sildenafil (50 mg) to create four unique experimental conditions that were compared with SL values: high altitude (HA), Plasma Volume Expansion (HA‐PVX), Sildenafil (HA‐SIL) and Plasma Volume Expansion with Sildenafil (HA‐PVX‐SIL). High altitude exposure reduced plasma volume by 11% (P < 0.01) and increased pulmonary artery systolic pressure (19.6 ± 4.3 vs. 26.0 ± 5.4, P < 0.001); these differences were abolished by PVX and SIL respectively. LV end‐diastolic volume (EDV) and stroke volume (SV) were decreased upon ascent to high altitude, but were comparable to sea level in the HA‐PVX trial. LV EDV and SV were also elevated in the HA‐SIL and HA‐PVX‐SIL trials compared to HA, but to a lesser extent. Neither PVX nor SIL had a significant effect on the LV EDV and SV response to exercise, or the maximal oxygen consumption or peak power output. In summary, at 3800 m both hypovolaemia and hypoxic pulmonary vasoconstriction contribute to the decrease in LV filling, but restoring LV filling does not confer an improvement in maximal exercise performance. Key points: We sought to determine the isolated and combined influence of hypovolaemia and hypoxic pulmonary vasoconstriction on the decrease in left ventricular (LV) function and maximal exercise capacity observed under hypobaric hypoxia.We performed echocardiography and maximal exercise tests at sea level (344 m), and following 5–10 days at the Barcroft Laboratory (3800 m; White Mountain, California) with and without (i) plasma volume expansion to sea level values and (ii) administration of the pulmonary vasodilatator sildenafil in a double‐blinded and placebo‐controlled trial.The high altitude‐induced reduction in LV filling and ejection was abolished by plasma volume expansion but to a lesser extent by sildenafil administration; however, neither intervention had a positive effect on maximal exercise capacity.Both hypovolaemia and hypoxic pulmonary vasoconstriction play a role in the reduction of LV filling at 3800 m, but the increase in LV filling does not influence exercise capacity at this moderate altitude. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?What is the role of heart muscle function in the increased output of remodelled, larger hearts?What is the main finding and its importance?The greater stroke volume of endurance athletes is not associated with enhanced function of the heart muscle (i.e. left ventricular twist, torsion and twist‐to‐shortening) in normal and low‐oxygen environments. These data indicate that, in the process of cardiac adaptation, left ventricular twist may play an important role that is not related to generating a larger output. Since enlarged hearts with low output can develop in disease, the present findings may influence the future interpretation of heart muscle function in patients. Despite increased stroke volume (SV), 'athlete's heart' has been proposed to have a similar left ventricular (LV) muscle function – as represented by LV twist – compared with the untrained state. However, the underpinning mechanisms and the associations between SV/cardiac output and LV twist during exercise are unknown. We hypothesised that endurance athletes would have a significantly lower twist‐to‐shortening ratio (TwSR, a parameter that relates twist to the shortening of heart muscle layers) at rest, but significantly greater LV muscle function during exercise. Eleven endurance trained male runners and 13 untrained males were tested at rest and during supine cycling exercise in normoxia and hypoxia (increased cardiac output but unaltered SV). Despite the expected cardiac remodelling in endurance athletes, LV twist, torsion, TwSR, strain and strain rate ('LV systolic mechanics') did not differ significantly between groups (P > 0.05). Structural remodelling, as per relative wall thickness, and LV twist did not correlate (r2 = 0.04, P = 0.33). In normoxia and hypoxia, exercise increased LV systolic mechanics in both groups (P < 0.001), but with different relationships to SV and cardiac output. Conversely to our hypothesis, hearts of different size had similar LV systolic mechanics, suggesting that similar twist, torsion and TwSR at rest and during exercise irrespective of cardiac output may be an important mechanism in healthy hearts. We hypothesise that the regulatory 'purpose' of LV twist may be related to the sensing of maximal cardiac myofibre stress, which may act as a biologically purposeful limiter to contraction. [ABSTRACT FROM AUTHOR]

The article provides information on a study which analyzed the impact of exercise duration and intensity compared with traditional endurance exercise on both novel and traditional markers of cardiovascular disease (CVD) in youth. Risk factors linked to the development of CVD are listed. Metabolic measurements are presented. The insulin concentrations, aerobic fitness, and C-reactive protein (CRP) levels of those in the moderate (MOD) and high intensity (HIT) exercise groups are also examined.

The current drastic escalation in obesity may be contributing to the exponential rise in drugs used for image enhancement. Drugs such as anabolic-androgenic steroids (AAS) are perceived as a viable method of achieving a perfect physique. They are also the most widely abused drugs in sport. The Internet has encouraged the abuse of expensive drugs, particularly human growth hormone (hGH), resulting in increased importation for personal use. The substantial increase in this market has opened up avenues for counterfeiting, estimated as a multi-million pound business. The acute adverse effects from contaminated vials may result in a variety of pathologies including communicable diseases. In 2007, in the UK, a series of intramuscular abscesses, requiring surgical treatment, led us to study samples obtained from the underground market. The analysis of 38 parenteral samples and 19 oral samples of tablets was performed by a World Anti-Doping Agency (WADA) accredited laboratory, in an attempt to establish the extent of available counterfeit products. Fifty-three per cent (20) of the injectable AAS esters and 21% (4) of the oral tablets were counterfeit. Culture and sensitivity revealed the presence of skin commensal organisms, which may have contributed to the development of the abscesses. Users of AAS and hGH for sport, including bodybuilding, are currently risking their health because of counterfeit and poorly controlled products. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Academics have a responsibility to ensure that their research findings are as truthful as possible. InIn every issue of a scientific journal, a large number of significance tests are reported (usually using P <0.05). Of course, most of these results will be true/correct. Unfortunately, due to the nature of sampling, researchers will occasionally make errors, often referred to as type I (probability = α) and type II (probability = β) errors. The power of a test (1-β) is the probability of correctly rejecting a false null hypothesis - that is, correctly detecting a real or true effect. Factors that are known to influence power include: (1) the level of significance (α), (2) the size of the difference or relationship in the population (the effect), (3) the sample size, and (4) unexplained error variance. As researchers, we have little control over most of these factors. The one factor that we have some influence over, however, is the ability to reduce the unexplained error variance. In the present article, we describe a range of methods that will increase the probability that a researcher has correctly identified a real effect by increasing the power of their statistical tests. Such methods will include ways of designing experiments to reduce error and uncertainty. The use of blocking and randomized block designs will reduce unexplained error, such as adopting matched or repeated-measures designs rather than using independent observations. The other method of reducing unexplained errors is to adopt more appropriate (e.g. biologically correct) models and checking the distribution assumptions associated with such models. In conclusion, researchers are responsible for maximizing the likelihood that their results are as accurate and truthful as possible. By carefully planning their experiments and adopting appropriate models, researchers are more likely to publish their findings with a greater degree of confidence, but not certainty. [ABSTRACT FROM AUTHOR]

This study assesses the prevalence of recently identified coronary heart disease (CHD) risk factors in young people of differing socioeconomic status (SES). From November 2001 through March 2002, 100 boys and 108 girls, of age 12.9 +/- 0.3 years, selected from differing SES were assessed for CHD risk factors. Measurements included fibrinogen (Fg), homocyst(e)ine (Hcy), and C-reactive protein (CRP). Fibrinogen was significantly greater among boys from a higher SES compared with those from a low SES (P < or = 0.05). Differences according to sex (P < or = 0.05) were identified for Fg and CRP. The data indicate the prevalence of recently identified CHD risk factors in this cohort of British schoolchildren. For the purpose of this article, the phrase "young people" embraces both children and adolescents., (Copyright 2005 Wiley-Liss, Inc)