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Purpose: The geometric patterns of ventricular remodeling are determined using indexed left ventricular mass (LVM), end-diastolic volume (LVEDV) and concentricity, most often measured using the mass-to-volume ratio (MVR). The aims of this study were to validate lean body mass (LBM)-based allometric coefficients for scaling and to determine an index of concentricity that is independent of both volume and LBM. Methods: Participants from the UK Biobank who underwent both CMR and dual-energy X-ray absorptiometry (DXA) during 2014–2015 were considered (n = 5064). We excluded participants aged ≥ 70 years or those with cardiometabolic risk factors. We determined allometric coefficients for scaling using linear regression of the logarithmically transformed ventricular remodeling parameters. We further defined a multiplicative allometric relationship for LV concentricity (LVC) adjusting for both LVEDV and LBM. Results: A total of 1638 individuals (1057 female) were included. In subjects with lower body fat percentage (< 25% in males, < 35% in females, n = 644), the LBM allometric coefficients for scaling LVM and LVEDV were 0.85 ± 0.06 and 0.85 ± 0.03 respectively (R2 = 0.61 and 0.57, P < 0.001), with no evidence of sex–allometry interaction. While the MVR was independent of LBM, it demonstrated a negative association with LVEDV in (females: r = − 0.44, P < 0.001; males: − 0.38, P < 0.001). In contrast, LVC was independent of both LVEDV and LBM [LVC = LVM/(LVEDV0.40 × LBM0.50)] leading to increased overlap between LV hypertrophy and higher concentricity. Conclusions: We validated allometric coefficients for LBM-based scaling for CMR indexed parameters relevant for classifying geometric patterns of ventricular remodeling. [ABSTRACT FROM AUTHOR]

Background: We implemented a blood flow restriction resistance training (BFR-RT) intervention during an 8-week rehabilitation programme in anterior cruciate ligament reconstruction (ACLR) patients within a National Health Service setting. Objective: To compare the effectiveness of BFR-RT and standard-care traditional heavy-load resistance training (HL-RT) at improving skeletal muscle hypertrophy and strength, physical function, pain and effusion in ACLR patients following surgery. Methods: 28 patients scheduled for unilateral ACLR surgery with hamstring autograft were recruited for this parallel-group, two-arm, single-assessor blinded, randomised clinical trial following appropriate power analysis. Following surgery, a criteria-driven approach to rehabilitation was utilised and participants were block randomised to either HL-RT at 70% repetition maximum (1RM) (n = 14) or BFR-RT (n = 14) at 30% 1RM. Participants completed 8 weeks of biweekly unilateral leg press training on both limbs, totalling 16 sessions, alongside standard hospital rehabilitation. Resistance exercise protocols were designed consistent with standard recommended protocols for each type of exercise. Scaled maximal isotonic strength (10RM), muscle morphology of the vastus lateralis of the injured limb, self-reported function, Y-balance test performance and knee joint pain, effusion and range of motion (ROM) were assessed at pre-surgery, post-surgery, mid-training and post-training. Knee joint laxity and scaled maximal isokinetic knee extension and flexion strength at 60°/s, 150°/s and 300°/s were measured at pre-surgery and post-training. Results: Four participants were lost, with 24 participants completing the study (12 per group). There were no adverse events or differences between groups for any baseline anthropometric variable or pre- to post-surgery change in any outcome measure. Scaled 10RM strength significantly increased in the injured limb (104 ± 30% and 106 ± 43%) and non-injured limb (33 ± 13% and 39 ± 17%) with BFR-RT and HL-RT, respectively, with no group differences. Significant increases in knee extension and flexion peak torque were observed at all speeds in the non-injured limb with no group differences. Significantly greater attenuation of knee extensor peak torque loss at 150°/s and 300°/s and knee flexor torque loss at all speeds was observed with BFR-RT. No group differences in knee extensor peak torque loss were found at 60°/s. Significant and comparable increases in muscle thickness (5.8 ± 0.2% and 6.7 ± 0.3%) and pennation angle (4.1 ± 0.3% and 3.4 ± 0.1%) were observed with BFR-RT and HL-RT, respectively, with no group differences. No significant changes in fascicle length were observed. Significantly greater and clinically important increases in several measures of self-reported function (50–218 ± 48% vs. 35–152 ± 56%), Y-balance performance (18–59 ± 22% vs. 18–33 ± 19%), ROM (78 ± 22% vs. 48 ± 13%) and reductions in knee joint pain (67 ± 15% vs. 39 ± 12%) and effusion (6 ± 2% vs. 2 ± 2%) were observed with BFR-RT compared to HL-RT, respectively. Conclusion: BFR-RT can improve skeletal muscle hypertrophy and strength to a similar extent to HL-RT with a greater reduction in knee joint pain and effusion, leading to greater overall improvements in physical function. Therefore, BFR-RT may be more appropriate for early rehabilitation in ACLR patient populations within the National Health Service. [ABSTRACT FROM AUTHOR]

It has traditionally been believed that resistance training can only induce muscle growth when the exercise intensity is greater than 65 % of the 1-repetition maximum (RM). However, more recently, the use of low-intensity resistance exercise with blood-flow restriction (BFR) has challenged this theory and consistently shown that hypertrophic adaptations can be induced with much lower exercise intensities (<50 % 1-RM). Despite the potent hypertrophic effects of BFR resistance training being demonstrated by numerous studies, the underlying mechanisms responsible for such effects are not well defined. Metabolic stress has been suggested to be a primary factor responsible, and this is theorised to activate numerous other mechanisms, all of which are thought to induce muscle growth via autocrine and/or paracrine actions. However, it is noteworthy that some of these mechanisms do not appear to be mediated to any great extent by metabolic stress but rather by mechanical tension (another primary factor of muscle hypertrophy). Given that the level of mechanical tension is typically low with BFR resistance exercise (<50 % 1-RM), one may question the magnitude of involvement of these mechanisms aligned to the adaptations reported with BFR resistance training. However, despite the low level of mechanical tension, it is plausible that the effects induced by the primary factors (mechanical tension and metabolic stress) are, in fact, additive, which ultimately contributes to the adaptations seen with BFR resistance training. Exercise-induced mechanical tension and metabolic stress are theorised to signal a number of mechanisms for the induction of muscle growth, including increased fast-twitch fibre recruitment, mechanotransduction, muscle damage, systemic and localised hormone production, cell swelling, and the production of reactive oxygen species and its variants, including nitric oxide and heat shock proteins. However, the relative extent to which these specific mechanisms are induced by the primary factors with BFR resistance exercise, as well as their magnitude of involvement in BFR resistance training-induced muscle hypertrophy, requires further exploration. [ABSTRACT FROM AUTHOR]

The common inheritance of approximately 20000 genes defines each of us as human. However, substantial variation exists between individual human genomes, including 'replication' of gene sequences (copy number variation, tandem repeats), or changes in individual base pairs (mutations if <1% fre- quency and single nucleotide polymorphisms if>l% frequency). A vast array of human phenotypes (e.g. muscle strength, skeletal structure, tendon elasticity, and heart and lung size) influences sports performance, each itself the result of a complex interaction between a myriad of anatomical, biochemical and physiological systems. This article discusses the role for genetic influences in influencing sporting performance and injury, offering specific exemplars where these are known. Many of these preferable genotypes are uncommon, and their combination even rarer. In theory, the chances of an individual having a perfect sporting genotype are much lower than 1 in 20 million-as the number of associated polymorphisms increase, the odds decrease correspondingly. Many recently discovered polymorphisms that may affect sports performance have been described in animal or other human based models, and have been included in this review if they may apply to athletic populations. Muscle performance is heavily influenced by basal muscle mass and its dy- namic response to training. Genetic factors account for approximately 50-80% of inter-individual variation in lean body mass, with impacts detected on both 'training-naive' muscle mass and its growth response. Several cyto- kines such as interleukin-6 and -15, cilliary neurotrophic factor and insulin- like growth factor (IGF) have myoanabolic effects. Genotype-associated differences in endocrine function, necessary for normal skeletal muscle growth and function, may also be of significance, with complex interactions existing between thyroxine, growth hormone and the downstream regulators of the anabolic pathways (such as IGF-l and IGF-2). Almost 200 poly- morphisms are known to exist in the vitamin D receptor (VDR) gene. VDR genotype is associated with differences in strength in premenopausal women. VDR expression decreases with age and VDR genotype is associated with fat- free mass and strength in elderly men and women. Muscle fibre type de- termination is complex. Whilst initial composition is likely to be strongly influenced by genetic factors, training has significant effects on fibre shifts. Polymorphisms of the peroxisome proliferator-activated receptor a (PPARa) gene and R577x polymorphism of the A CTN3 gene are both associated with specific fibre compositions. Alterations in cardiac size have been associated with both increased performance and excess cardiovascular mortality. PPARca is a ligand-activated transcription factor that regulates genes involved in fatty acid uptake and oxidation, lipid metabolism and inflammation. Psychology plays an important role in training, competition, tolerance of pain and motivation. However, the role of genetic variation in determining psychological state and responses remains poorly understood; only recently have specific genes been implicated in motivational behaviour and maintenance of exercise. Thyroid hormone receptors exist within the brain and influence both neurogenesis and behaviour. With the current state of knowledge, the field of genetic influences on sports performance remains in its infancy, despite over a decade of research. [ABSTRACT FROM AUTHOR]

Introduction: The LIFE (Losartan Intervention For Endpoint reduction in hypertension) study demonstrated a 13% relative risk reduction in the primary composite endpoint (myocardial infarction, stroke or death) for patients with hypertension and electrocardiographically diagnosed left ventricular hypertrophy (LVH) treated with losartan compared with atenolol. Losartan recipients also had a 25% relative risk reduction for stroke compared with atenolol recipients. Incorporating the results found in the LIFE study into an economic model, an incremental cost-effectiveness analysis was performed comparing losartan with atenolol in the treatment of 67-year old patients with hypertension and LVH.Methods: A Markov state transition model, based on published results of the LIFE trial (mean follow-up of 4.8 years), was utilised to extrapolate the outcomes observed in this trial to the patients' lifetime. Utility estimates for the associated health states were obtained from various published sources. Lifetime treatment costs were calculated adopting a societal perspective. Both costs and benefits were discounted and incremental cost-effectiveness ratios (ICERs) were estimated. One-way and probabilistic sensitivity analyses were performed.Results: The estimated ICER for losartan versus atenolol was 1337 Canadian dollars per QALY gained (1 Canadian dollar =0.75 US dollars, 2002 values). This ICER was robust to extensive sensitivity analysis, demonstrating a 95% probability that the ICER would be <20,000 Canadian dollars per QALY gained.Conclusion: From a Canadian societal perspective, losartan appears to be a cost-effective alternative to atenolol in patients with hypertension and LVH. The estimated ICERs, including the sensitivity analyses, were within the range of cost-effectiveness ratios for various currently funded interventions and drugs in developed countries. [ABSTRACT FROM AUTHOR]

The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study demonstrated the clinical benefit of losartan-based therapy in hypertensive patients with left ventricular hypertrophy (LVH), mainly due to a highly significant 25% reduction in the relative risk of stroke compared with an atenolol-based regimen, for a similar reduction in blood pressure. The aim of this economic evaluation was to estimate the cost-effectiveness of losartan compared with atenolol from a UK national health system perspective. Quality-adjusted survival and direct medical costs were modelled beyond the trial using the within-trial incidence of stroke. Survival with stroke, study medication use and quality of life by stroke status were taken directly from the LIFE trial. The LIFE data were supplemented with UK data on lifetime direct medical costs of stroke and life expectancy in individuals without stroke. No additional stroke events or use of study treatment were assumed beyond the trial. Costs and benefits were discounted using current UK Treasury rates. In the base-case analysis, the reduction in stroke-related costs (by £968) offset 86% of the increase in study medication costs (£1128) among losartan-treated patients. The incremental cost-effectiveness ratio (ICER) for losartan versus atenolol in hypertensive patients with LVH was £2130 per quality-adjusted life year (QALY) gained (\[euro]3195/QALY), and this increased to £11 352 per QALY gained (\[euro]16 450/QALY) when the costs of stroke beyond the first 5 years were excluded. Thus, the clinical benefit of losartan was achieved at a cost well within reported thresholds for cost-effectiveness.Journal of Human Hypertension (2006) 20, 51–58. doi:10.1038/sj.jhh.1001939 [ABSTRACT FROM AUTHOR]