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Context Whether playing position influences injury in male academy soccer players (ASPs) is unclear. Objective To determine if playing position was associated with injury in ASPs. Design Descriptive epidemiology study. Setting English, Spanish, Uruguayan, and Brazilian soccer academies. Patients or Other Participants A total of 369 ASPs from the under-14 to under-23 age groups, classified as post-peak height velocity using maturity offset, and grouped as goalkeepers, lateral defenders, central defenders, lateral midfielders, central midfielders, or forwards. Main Outcome Measure(s) Injuries were recorded prospectively over 1 season. Injury prevalence proportion (IPP), days missed, and injury incidence rate (IIR, injuries/1000 training or match hours, n = 116) were analyzed according to playing position. Results No association with playing position was observed for any injury type or location regarding IPP (P ≥ .089) or days missed (P ≥ .235). The IIR was higher in central defenders than in lateral defenders for general (9.30 versus 4.18 injuries/1000 h, P = .009), soft tissue (5.14 versus 1.95 injuries/1000 h, P = .026), and ligament or tendon injuries (2.69 versus 0.56 injuries/1000 h, P = .040). The central versus lateral or forward positions were not associated with IPP (P ≥ .051) or days missed (P ≥ .083), but general IIR was greater in the central position than the lateral or forward positions (8.67 versus 6.12 injuries/1000 h, P = .047). Conclusions Academy soccer players' playing positions were not associated with IPP or days missed, but the higher general, soft tissue, and ligament or tendon IIRs in central defenders suggest that this position warrants specific attention regarding injury-prevention strategies. These novel findings highlight the importance of considering training or match exposure when investigating the influence of playing position on injury in ASPs.

Purpose We used a within-subject, cross-over study to determine the relationship between the intra-individual adaptations to four weeks’ resistance (RT) versus four weeks’ endurance (END) training, and we investigated whether three single nucleotide polymorphisms (SNPs) were associated with these adaptations. Methods Thirty untrained, healthy, young men completed a cycling test to exhaustion to determine peak oxygen uptake (V̇O2peak), and a knee extension (KE) maximum voluntary isometric contraction (MVIC) of the right leg before and after four weeks’ supervised RT (four sets of 10 repetitions at 80% single repetition maximum unilateral KE exercise, three times weekly) and four weeks’ supervised END (30 min combined continuous/interval cycling, three times weekly), separated by a three-week washout phase. Participants were genotyped for the ACTN3 rs1815739, NOS3 rs2070744 and VEGFA rs2010963 SNPs. Results The intra-individual adaptations regarding percentage changes in MVIC force and V̇O2peak following RT and END, respectively, were unrelated (r2 = 0.003; P = 0.79). However, a VEGFA genotype × training modality interaction (P = 0.007) demonstrated that VEGFA GG homozygotes increased their MVIC force after RT (+ 20.9 ± 13.2%) more than they increased their V̇O2peak after END (+ 8.4 ± 9.1%, P = 0.005), and more than VEGFA C-allele carriers increased their MVIC force after RT (+ 12.2 ± 8.1%, P = 0.04). There were no genotype × training modality interactions for the ACTN3 or NOS3 SNPs. Conclusion High/low responders to RT were not consequently high/low responders to END or vice versa. However, preferential adaptation of VEGFA rs2010963 GG homozygotes to RT over END, and their greater adaptation to RT compared to VEGFA C-allele carriers, indicate a novel genetic predisposition for superior RT adaptation.

We used a within-subject crossover design to examine the impact of exercise modality, i.e., resistance (RT) and endurance (END), on the acute impact of exercise on endothelial function. Then, we examined whether a 4-wk period of chronic exercise training altered the acute exercise-induced change in endothelial function in healthy individuals. Thirty-four healthy, young men (21 ± 2 yr) reported to our laboratory and completed assessment of endothelial function [using the brachial artery flow-mediated dilation test (FMD)] before and immediately after a single bout of RT (leg-extension) or END (cycling). Subsequently, participants completed a 4-wk period of training (12 sessions), followed by evaluation of the FMD before and after a single bout of exercise. Following a 3-wk washout, participants repeated these experiments with the different exercise modality (in a balanced crossover design). An exercise × modality interaction effect was found (

Generating high levels of muscular strength and power are important for success in sport and may have long-term implications for sporting careers in youth athletes. Importantly, maturation may confound the neuromuscular adaptations to resistance training when attempting to differentiate between training- vs. growth-induced strength and power gains; thus, potentially leading to erroneous conclusions regarding the efficacy of resistance training in youth athletes. The aim of this review was to critically appraise the literature concerning the efficacy of externally loaded free-weight resistance training on strength and power measures in youth athletes at different stages of maturity. Strength underpins power production; thus, developing strength through traditional resistance training methods can positively influence powerful sporting movements. In addition, weightlifting has the capacity to improve muscular power via explosive lower-body triple extension, which is essential for many sports. Despite the complexity of the techniques involved, it can be a safe and effective method to improve athletic qualities in young athletes, potentially more so than plyometric training. While low-load, high-velocity training can have a positive effect influence on high speed movements such as sprinting, the reduced intensity appears to be disadvantageous post peak-height velocity. Irrespective of age, well-coached progressive strength training adhering strictly to correct technique can then be periodised within a long-term athletic development program. It is important to primarily develop muscular strength, while concurrently refining the technical skill required for weightlifting. Physically mature athletes should undertake high-intensity resistance training to maximise neuromuscular adaptations, leading to positive changes in strength and power.

Due to the high-velocity collision-based nature of elite rugby league and union, the risk of sustaining a concussion is high. Occurrence of and outcomes following a concussion are probably affected by the interaction of multiple genes in a polygenic manner. This study investigated whether suspected concussion-associated polygenic profiles of elite rugby athletes differed from non-athletes and between rugby union forwards and backs. We hypothesised that a total genotype score (TGS) using eight concussion-associated polymorphisms would be higher in elite rugby athletes than non-athletes, indicating selection for protection against incurring or suffering prolonged effects of, concussion in the relatively high-risk environment of competitive rugby. In addition, multifactor dimensionality reduction was used to identify genetic interactions. Contrary to our hypothesis, TGS did not differ between elite rugby athletes and non-athletes (p ≥ 0.065), nor between rugby union forwards and backs (p = 0.668). Accordingly, the TGS could not discriminate between elite rugby athletes and non-athletes (AUC ~0.5), suggesting that, for the eight polymorphisms investigated, elite rugby athletes do not have a more ‘preferable’ concussion-associated polygenic profile than non-athletes. However, the COMT (rs4680) and MAPT (rs10445337) GC allele combination was more common in rugby athletes (31.7%; p < 0.001) and rugby union athletes (31.8%; p < 0.001) than non-athletes (24.5%). Our results thus suggest a genetic interaction between COMT (rs4680) and MAPT (rs10445337) assists rugby athletes in achieving elite status. These findings need exploration vis-à-vis sport-related concussion injury data and could have implications for the management of inter-individual differences in concussion risk.

We investigated whether 20 candidate single nucleotide polymorphisms (SNPs) were associated with in vivo exercise-induced muscle damage (EIMD), and with an in vitro skeletal muscle stem cell wound healing assay. Sixty-five young, untrained Caucasian adults performed 120 maximal eccentric knee-extensions on an isokinetic dynamometer to induce EIMD. Maximal voluntary isometric/isokinetic knee-extensor torque, knee joint range of motion, muscle soreness, serum creatine kinase activity and interleukin-6 concentration were assessed before, directly after and 48h after EIMD. Muscle stem cells were cultured from vastus lateralis biopsies from a separate cohort (n=12), and markers of repair were measured in vitro. Participants were genotyped for all 20 SNPs using real-time PCR. Seven SNPs were associated with the response to EIMD, and these were used to calculate a total genotype score (TGS), which enabled participants to be segregated into three polygenic groups: ‘preferential’ (more ‘protective’ alleles), ‘moderate’, and ‘non-preferential’. The non-preferential group was consistently weaker than the preferential group (1.93±0.81 vs. 2.73±0.59 N∙m/kg; P=9.51x10-4) and demonstrated more muscle soreness (P=0.011) and a larger decrease in knee joint range of motion (P=0.006) following EIMD. Two TTN-AS1 SNPs in linkage disequilibrium were associated with in vivo EIMD (rs3731749, P≤0.005) and accelerated muscle stem cell migration into the artificial wound in vitro (rs1001238, P≤0.006). Thus, we have identified a polygenic profile, linked with both muscle weakness and poorer recovery following EIMD. Moreover, we provide evidence for a novel TTN gene-cell-skeletal muscle mechanism that may help explain some of the inter-individual variability in the response to EIMD.

Objectives: To investigate if maturity status was associated with injury risk in male academy soccer players. Design: Prospective cohort surveillance study. Setting: Professional soccer academies. Participants: 501 players (aged 9-23 years) from eight academies in England, Spain, Uruguay and Brazil. Main outcome measures: Players were grouped by maturity offset as pre-peak height velocity (PHV), circa-PHV, post-PHV or adult. Injury prevalence proportion (IPP) and days missed were recorded for one season per player, with training/match exposure recorded in a sub-sample (n = 166). Results: IPP for all injuries combined increased with advancing maturity, with circa-PHV (p = 0.032), post-PHV (p < 0.001) and adult (p < 0.001) higher than pre-PHV. IPP was higher in post-PHV and adult than pre-PHV for non-contact (p = 0.001 and p = 0.012), soft-tissue (both p < 0.001), non-contact soft tissue (p < 0.001 and p = 0.005), muscle (both p < 0.001), thigh (both p < 0.001), ankle (p = 0.035 and p = 0.007) and hamstring injuries (p = 0.041 and p = 0.017). Ligament/tendon IPP was greater in adult versus pre-PHV (p = 0.002). IPP for growth-related injuries was lower in post-PHV than pre-PHV (p = 0.039). Injury incidence rates (n = 166) exhibited similar patterns to IPP in the full cohort. Conclusions: Injury patterns were similar between post-PHV and adult academy players but, crucially, relatively more of these groups suffered injuries compared to pre-and circa-PHV (except growth-related injuries).

Purpose Due to its eccentric nature, downhill running (DR) training has been suggested to promote strength gains through neuromuscular adaptations. However, it is unknown whether short-term chronic DR can elicit such adaptations. Methods Twelve untrained, young, healthy adults (5 women, 7 men) took part in 4 weeks’ DR, comprising 10 sessions, with running speed equivalent to 60–65% maximal oxygen uptake ($$\dot{V}$$ V ˙ O2max, assessed at weeks 0 and 4). Isometric and isokinetic knee-extensor maximal voluntary torque (MVT), vastus lateralis (VL) muscle morphology/architecture (anatomical cross-sectional area, ACSA; physiological CSA, PCSA; volume; fascicle length, Lf; pennation angle, PA) and neuromuscular activation (VL EMG) were assessed at weeks 0, 2 and 4. Results MVT increased by 9.7–15.2% after 4 weeks (p p r = 0.86, p = 0.001). VL ACSA (+2.9 ± 2.7% and +7.1 ± 3.5%) and volume (+2.5 ± 2.5% and +6.6 ± 3.2%) increased after 2 and 4 weeks, respectively (p Lf (+2.7 ± 2.2%) increased after 4 weeks (p r = 0.67, p = 0.03) and PCSA (r = 0.71, p = 0.01) correlated with changes in concentric MVT from 2 to 4 weeks. $$\dot{V}$$ V ˙ O2max (49.4 ± 6.2 vs. 49.7 ± 6.3 mL·kg−1·min−1) did not change after 4 weeks (p = 0.73). Conclusion Just 4 weeks’ moderate-intensity DR promoted neuromuscular adaptations in young, healthy adults, typically observed after high-intensity eccentric resistance training. Neural adaptations appeared to contribute to most of the strength gains at 2 and 4 weeks, while muscle hypertrophy seemed to contribute to MVT changes from 2 to 4 weeks only.

Purpose Physical activity, particularly mechanical loading that results in high-peak force and is multi-directional in nature, increases bone mineral density (BMD). In athletes such as endurance runners, this association is more complex due to other factors such as low energy availability and menstrual dysfunction. Moreover, many studies of athletes have used small sample sizes and/or athletes of varying abilities, making it difficult to compare BMD phenotypes between studies. Method The primary aim of this study was to compare dual-energy X-ray absorptiometry (DXA) derived bone phenotypes of high-level endurance runners (58 women and 45 men) to non-athletes (60 women and 52 men). Our secondary aim was to examine the influence of menstrual irregularities and sporting activity completed during childhood on these bone phenotypes. Results Female runners had higher leg (4%) but not total body or lumbar spine BMD than female non-athletes. Male runners had lower lumbar spine (9%) but similar total and leg BMD compared to male non-athletes, suggesting that high levels of site-specific mechanical loading was advantageous for BMD in females only and a potential presence of reduced energy availability in males. Menstrual status in females and the number of sports completed in childhood in males and females had no influence on bone phenotypes within the runners. Conclusion Given the large variability in BMD in runners and non-athletes, other factors such as variation in genetic make-up alongside mechanical loading probably influence BMD across the adult lifespan.

A vegan diet is associated with reduced cardiovascular morbidity and mortality, but protein deficiencies may be detrimental to skeletal muscle structure and function. The aim of this study was to compare the vascular and skeletal muscle properties between young, healthy, recreationally active habitual vegan (VEG) and omnivorous (OMN) men. Sixteen OMN and nine VEG underwent ultrasound scans to determine brachial artery flow-mediated dilation (FMD) and carotid artery intima-media thickness (cIMT) and vastus lateralis (VL) muscle thickness and fascicle pennation angle. Knee extension maximal voluntary isometric contraction (MVIC) force was assessed on an isokinetic dynamometer, and V ˙ O 2 m a x on a cycle ergometer and online gas analysis system. A three-day food diary determined habitual dietary behaviour. Bayesian analyses of independent groups provided 'moderate' to 'very strong' evidence for lower consumption of absolute (63±21 g/d vs. 98±30 g/d; Bayes Factor (BF01)=0.140) and relative (0.86±0.29 g/kg/d vs. 1.36±0.52 g/kg/d; BF01=0.259) protein, absolute saturated fat (15.2±7.9 g vs. 30.3±11.8 g; BF01=0.089) and cholesterol (5.0±6.0 mg vs. 337.9±232.6 mg; BF01=0.019) in VEG compared to OMN, respectively. Further, there was 'anecdotal' evidence to support no differences in FMD (3.37±3.31% vs. 4.58±5.82%; BF01=2.591), cIMT (0.51±0.07mm vs. 0.49±0.04mm; BF01=2.510), VL thickness (26.1±3.7mm vs. 27.8±6.4mm; BF01=2.726), fascicle pennation angle (16.6±4.7° vs. 17.7±3.7°; BF01=2.844), MVIC (627±182 N vs. 551±102 N; BF01=1.656) or V ˙ O 2 m a x (40.8±9.8 ml/kg/min vs. 35.8±5.2 ml/kg/min; BF01=1.218) between VEG and OMN, respectively. Despite marked differences in habitual nutrient intake, healthy, young vegan and omnivorous men did not differ regarding vascular and skeletal muscle structure and function, or cardiovascular fitness.

Contains fulltext : 238798.pdf (Publisher’s version ) (Open Access) We used a within-subject, cross-over design study to compare the impact of 4-weeks' resistance (RT) versus endurance (END) training on vascular function. We subsequently explored the association of intra-individual effects of RT versus END on vascular function with a single nucleotide polymorphism (SNP) of the NOS3 gene. Thirty-five healthy males (21 ± 2 years old) were genotyped for the NOS3 rs2070744 SNP and completed both training modalities. Participants completed 12 sessions over a 4-week period, either RT (leg-extension) or END (cycling) training in a randomized, balanced cross-over design with a 3-week washout period. Participants performed peak oxygen uptake (peak VO(2) ) and leg-extension single-repetition maximum (1-RM) testing, and vascular function assessment using flow-mediated dilation (FMD) on 3 separated days pre/post-training. Peak VO(2) increased after END (p

Skeletal muscle tissue demonstrates global hypermethylation with age. However, methylome changes across the time-course of differentiation in aged human muscle derived cells, and larger coverage arrays in aged muscle tissue have not been undertaken. Using 850K DNA methylation arrays we compared the methylomes of young (27 ± 4.4 years) and aged (83 ± 4 years) human skeletal muscle and that of young/aged heterogenous muscle-derived human primary cells (HDMCs) over several time points of differentiation (0, 72 h, 7, 10 days). Aged muscle tissue was hypermethylated compared with young tissue, enriched for; pathways-in-cancer (including; focal adhesion, MAPK signaling, PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-signaling, axon-guidance and hippo-signalling. Aged cells also demonstrated a hypermethylated profile in pathways; axon-guidance, adherens-junction and calcium-signaling, particularly at later timepoints of myotube formation, corresponding with reduced morphological differentiation and reductions in MyoD/Myogenin gene expression compared with young cells. While young cells showed little alterations in DNA methylation during differentiation, aged cells demonstrated extensive and significantly altered DNA methylation, particularly at 7 days of differentiation and most notably in focal adhesion and PI3K-AKT signalling pathways. While the methylomes were vastly different between muscle tissue and HDMCs, we identified a small number of CpG sites showing a hypermethylated state with age, in both muscle tissue and cells on genes KIF15, DYRK2, FHL2, MRPS33, ABCA17P. Most notably, differential methylation analysis of chromosomal regions identified three locations containing enrichment of 6–8 CpGs in the HOX family of genes altered with age. With HOXD10, HOXD9, HOXD8, HOXA3, HOXC9, HOXB1, HOXB3, HOXC-AS2 and HOXC10 all hypermethylated in aged tissue. In aged cells the same HOX genes (and additionally HOXC-AS3) displayed the most variable methylation at 7 days of differentiation versus young cells, with HOXD8, HOXC9, HOXB1 and HOXC-AS3 hypermethylated and HOXC10 and HOXC-AS2 hypomethylated. We also determined that there was an inverse relationship between DNA methylation and gene expression for HOXB1, HOXA3 and HOXC-AS3. Finally, increased physical activity in young adults was associated with oppositely regulating HOXB1 and HOXA3 methylation compared with age. Overall, we demonstrate that a considerable number of HOX genes are differentially epigenetically regulated in aged human skeletal muscle and HDMCs and increased physical activity may help prevent age-related epigenetic changes in these HOX genes.

Objectives: To identify the most common injury types/locations in high-level male youth soccer players (YSP). Design: Prospective cohort surveillance study. Setting: Professional soccer club academies. Participants: Six hundred and twenty-four high-level male YSP [Under 9 (U9) to U23 year-old age groups] from academies in England, Spain, Uruguay and Brazil. Main outcome measures: Injury type, location and severity were recorded during one season. Injury severity was compared between age groups, while injury type and location were compared between nations. Results: Four hundred and forty-three training or match injuries were recorded, giving an injury rate of 0.71 per player. Non-contact injuries were most common (58.5%), with most (44.2%) resolved between 8 and 28 days. Most injuries (75.4%) occurred in the lower limbs, with muscle (29.6%) the most commonly injured tissue. U14 and U16 suffered a greater number of severe injuries relative to U12 and U19/U20/U23/Reserves. Tendon injury rate was higher in Brazil vs. Spain (p < 0.05), with low back/sacrum/pelvis injury rate highest in Spain (p < 0.05). Conclusions: The proportion of severe injuries in U14 and U16 suggests YSP injury risk is maturation-dependent. Minimal differences in type and location between high-level YSP from four different countries suggest injury rates in this population are geographically similar.

We investigated the association of multiple single nucleotide polymorphisms (SNPs) with athlete status and power/speed performance in elite male youth soccer players (ESP) and control participants (CON) at different stages of maturity. ESP (n = 535; aged 8-23 years) and CON (n = 151; aged 9-26 years) were genotyped for 10 SNPs and grouped according to years from predicted peak-height-velocity (PHV), i.e. pre- or post-PHV, to determine maturity status. Participants performed bilateral vertical countermovement jumps, bilateral horizontal-forward countermovement jumps, 20m sprints and modified 505-agility tests. Compared to CON, pre-PHV ESP demonstrated a higher ACTN3 (rs1815739) XX ('endurance') genotype frequency distribution, while post-PHV ESP revealed a higher frequency distribution of the PPARA (rs4253778) C-allele, AGT (rs699) GG genotype and NOS3 (rs2070744) T-allele ('power' genotypes/alleles). BDNF (rs6265) CC, COL5A1 (rs12722) CC and NOS3 TT homozygotes sprinted quicker than A-allele carriers, CT heterozygotes and CC homozygotes, respectively. COL2A1 (rs2070739) CC and AMPD1 (rs17602729) GG homozygotes sprinted faster than their respective minor allele carrier counterparts in CON and pre-PHV ESP, respectively. BDNF CC homozygotes jumped further than T-allele carriers, while ESP COL5A1 CC homozygotes jumped higher than TT homozygotes. To conclude, we have shown for the first time that pre- and post-PHV ESP have distinct genetic profiles, with pre-PHV ESP more suited for endurance, and post-PHV ESP for power and speed (the latter phenotypes being crucial attributes for post-PHV ESP). We have also demonstrated that power, acceleration and sprint performance were associated with five SNPs, both individually and in combination, possibly by influencing muscle size and neuromuscular activation.

We investigated whether single nucleotide polymorphisms (SNPs) within genes encoding the alpha-1 chain of type I ( COL1A1, rs2249492 ; rs1800012 ), type II ( COL2A1, rs2070739 ), and type V (COL5A1, rs12722 ) collagen were associated with the variable response to exercise-induced muscle damage (EIMD). Knee extensor muscle strength and soreness were assessed pre-, post-, and 48 h post-EIMD (120 maximal eccentric knee extensor contractions) in 65 young healthy participants, who were genotyped for the aforementioned SNPs. We found that COL1A1 (minor) T-allele carriers ( rs1800012 ) and (major) T-allele homozygotes ( rs2249492 ) were generally weaker ( P ≤ 0.019); and (minor) A-allele carriers of COL2A1 ( P = 0.002) and (major) T-allele carriers of COL5A1 ( P = 0.004) SNPs reported greater muscle soreness, all compared with their respective major ( rs1800012 ; rs2070739 ) and minor ( rs2249492 ; rs12722 ) allele homozygote counterparts. To conclude, the risk alleles of these four SNPs appear to negatively influence muscle strength and post-EIMD recovery, possibly via a dysregulated collagen network affecting the muscle’s mechanical properties.

Rugby League is a team sport requiring players to experience large impact collisions, thus requiring high amounts of muscle mass. Many players (academy and senior) strive to increase muscle mass during the pre-season, however, quantification of changes during this period have not been thoroughly investigated. We therefore assessed changes in body-composition using Dual X-Ray Absorptiometry (DXA) in eleven academy players over three successive pre-seasons and ninety-three senior players from four different European Super League clubs prior to, and at the end of, a pre-season training period. There was no meaningful change in lean mass of the academy players during any of the pre-season periods (year 1 = 72.3 ± 7.1–73.2 ± 7.2kg; ES 0.05, year 2 = 74.4 ± 6.9–75.5 ± 6.9kg; ES 0.07, year 3 = 75.9 ± 6.7–76.8 ± 6.6kg; ES 0.06) with small changes only occurring over the three-year study period (72.3–75.9kg; ES = 0.22). Senior players showed trivial changes in all characteristics during the pre-season period (total mass = 95.1–95.0kg; ES −0.01, lean mass = 74.6–75.1kg; ES 0.07, fat mass = 13.6–12.9kg; ES −0.17, body fat percentage = 14.8–14.1%; ES −0.19). These data suggest that academy players need time to develop towards profiles congruent with senior players. Moreover, once players reach senior level, body-composition changes are trivial during the pre-season and therefore teams may need to individualise training for players striving to gain muscle mass by reducing other training loads.

Grishina, EE, Zmijewski, P, Semenova, EA, Cieszczyk, P, Huminska-Lisowska, K, Michalowska-Sawczyn, M, Maculewicz, E, Crewther, B, Orysiak, J, Kostryukova, ES, Kulemin, NA, Borisov, OV, Khabibova, SA, Larin, AK, Pavlenko, AV, Lyubaeva, EV, Popov, DV, Lysenko, EA, Vepkhvadze, TF, Lednev, EM, Bondareva, EA, Erskine, RM, Generozov, EV, and Ahmetov, II. Three DNA polymorphisms previously identified as markers for handgrip strength are associated with strength in weightlifters and muscle fiber hypertrophy. J Strength Cond Res 33(10): 2602-2607, 2019-Muscle strength is a highly heritable trait. So far, 196 single nucleotide polymorphisms (SNPs) associated with handgrip strength have been identified in 3 genome-wide association studies. The aim of our study was to validate the association of 35 SNPs with strength of elite Russian weightlifters and replicate the study in Polish weightlifters. Genotyping was performed using micro-array analysis or real-time polymerase chain reaction. We found that the rs12055409 G-allele near the MLN gene (p = 0.004), the rs4626333 G-allele near the ZNF608 gene (p = 0.0338), and the rs2273555 A-allele in the GBF1 gene (p = 0.0099) were associated with greater competition results (total lifts in snatch and clean and jerk adjusted for sex and weight) in 53 elite Russian weightlifters. In the replication study of 76 sub-elite Polish weightlifters, rs4626333 GG homozygotes demonstrated greater competition results (p = 0.0155) and relative muscle mass (p = 0.046), adjusted for sex, weight, and age, compared with carriers of the A-allele. In the following studies, we tested the hypotheses that these SNPs would be associated with skeletal muscle hypertrophy and handgrip strength. We found that the number of strength-associated alleles was positively associated with fast-twitch muscle fiber cross-sectional area in the independent cohort of 20 male power athletes (p = 0.021) and with handgrip strength in 87 physically active individuals (p = 0.015). In conclusion, by replicating previous findings in 4 independent studies, we demonstrate that the rs12055409 G-, rs4626333 G-, and rs2273555 A-alleles are associated with higher levels of strength, muscle mass, and muscle fiber size.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation–contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (−308 G>A, rs1800629), IL6 (−174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage.

Dual-energy X-ray absorptiometry (DXA) in single energy mode has been shown to permit the visualisation of bone and soft tissue, such as the patellar tendon through two-dimensional sagittal imaging. However, there is no validated DXA-based measurement of the Achilles tendon moment arm (dAT). The aims of this study were: 1) to compare in vivo DXA derived measurements of the dAT at rest against two previously validated methods: tendon excursion (TE) and magnetic resonance imaging (MRI) at three ankle angles (-5°, 0° and +10°). 2) analyse the intra-day reliability of the DXA method at all ankle angles and compare between methods. Twelve healthy adults (mean ± SD: 31.4 ± 9.5 years; 174.0 ± 9.5 cm; 76.2 ± 16.6 kg) participated in this study, involving test-retest DXA scans, ultrasound scans and one MRI scan. The dAT was defined as the distance from the centre of the calcaneal-tibial joint axis to the Achilles tendon (AT) muscle-tendon line of action. DXA derived dAT measures were significantly greater than MRI measurements (19.7-24.9%) and were 45.2% significantly larger than the TE method. The test-retest reliability of the DXA technique at 0° was high [CV = 1.38%; ICC = 0.96] and despite the consistently larger dAT lengths obtained using DXA, MRI and DEXA data were strongly correlated (r = 0.878, p

This study took a multi-analytical approach including group differences, correlations and unit-weighed directional z-score comparisons to identify the key mediators of bone health. A total of 190 participants (18&ndash, 80 years) were categorized by body fat%, body mass index (BMI) and fat mass index (FMI) to examine the effect of differing obesity criteria on bone characteristics. A subset of 50 healthy-eating middle-to-older aged adults (44&ndash, 80 years) was randomly selected to examine any added impact of lifestyle and inflammatory profiles. Diet was assessed using a 3-day food diary, bone mineral density (BMD) and content (BMC) by dual energy x-ray absorptiometry in the lumbar, thoracic, (upper and lower) appendicular and pelvic areas. Physical activity was assessed using the Baecke questionnaire, and endocrine profiling was assessed using multiplex luminometry. Obesity, classed via BMI, positively affected 20 out of 22 BMC- and BMD-related outcome measures, whereas FMI was associated with 14 outcome measures and adiposity only modulated nine out of 22 BMC- and BMD-related outcome measures. Whilst bivariate correlations only linked vitamin A and relative protein intake with BMD, the Z-score composite summary presented a significantly different overall dietary quality between healthy and osteopenic individuals. In addition, bivariate correlations from the subset revealed daily energy intake, sport-based physical activity and BMI positive mediators of seven out of 10 BMD sites with age and body fat% shown to be negative mediators of bone characteristics. In conclusion, whilst BMI is a good indicator of bone characteristics, high body fat% should also be the focus of osteoporosis risk with ageing. Interestingly, high BMI in conjunction with moderate to vigorous activity supplemented with an optimal diet (quality and quantity) are identified as positive modulators of bone heath.

Brazier, J, Antrobus, M, Stebbings, GK, Day, SH, Callus, P, Erskine, RM, Bennett, MA, Kilduff, LP, and Williams, AG. Anthropometric and physiological characteristics of elite male rugby athletes. J Strength Cond Res 34(6): 1790-1801, 2020-This is the first article to review the anthropometric and physiological characteristics required for elite rugby performance within both rugby union (RU) and rugby league (RL). Anthropometric characteristics such as height and body mass, and physiological characteristics such as speed and muscular strength, have previously been advocated as key discriminators of playing level within rugby. This review aimed to identify the key anthropometric and physiological properties required for elite performance in rugby, distinguishing between RU and RL, forwards and backs and competitive levels. There are differences between competitive standards such that, at the elite level, athletes are heaviest (RU forwards ∼111 kg, backs ∼93 kg; RL forwards ∼103 kg, backs ∼90 kg) with lowest % body fat (RU forwards ∼15%, backs ∼12%; RL forwards ∼14%, backs ∼11%), they have most fat-free mass and are strongest (back squat: RU forwards ∼176 kg, backs ∼157 kg; RL forwards ∼188 kg, backs ∼168 kg; bench press: RU forwards ∼131 kg, backs ∼118 kg; RL forwards ∼122 kg, backs ∼113 kg) and fastest (10 m: RU forwards ∼1.87 seconds, backs ∼1.77 seconds; 10 m: RL forwards ∼1.9 seconds, backs ∼1.83 seconds). We also have unpublished data that indicate contemporary RU athletes have less body fat and are stronger and faster than the published data suggest. Regardless, well-developed speed, agility, lower-body power, and strength characteristics are vital for elite performance, probably reflect both environmental (training, diet, etc.) and genetic factors, distinguish between competitive levels, and are therefore important determinants of elite status in rugby.

Purpose: The aims of our study were to investigate differences in tendon properties between elite and non-elite soccer players, and to establish whether tendon properties were related to power assessed during unilateral jumps in different directions. Methods: Elite (n=16; age, 18.1 ± 1.0yrs) and non-elite (n=13; age, 22.3 ± 2.7yrs) soccer players performed three repetitions of each type (unilateral vertical, unilateral horizontal-forward and unilateral medial) of countermovement jump (CMJ) on a force plate. Patellar tendon (PT) cross-sectional area (CSA), elongation, stiffness and Young’s modulus (measured at the highest common force interval) were assessed with ultrasonography and isokinetic dynamometry. Results: Elite soccer players demonstrated greater PT elongation (6.83±1.87 vs. 4.92±1.88 mm, P=0.011) and strain (11.73±3.25 vs. 8.38±3.06 %, P=0.009) than non-elite. Projectile range and peak horizontal power during unilateral horizontal-forward CMJ correlated positively with tendon elongation (r=0.657 and 0.693, P

Low bone mineral density (BMD) is established as a primary predictor of osteoporotic risk and can also have substantial implications for athlete health and injury risk in the elite sporting environment. BMD is a highly multi-factorial phenotype influenced by diet, hormonal characteristics and physical activity. The interrelationships between such factors, and a strong genetic component, suggested to be around 50-85% at various anatomical sites, determines skeletal health throughout life. Genome-wide association studies (GWAS) and case-control designs have revealed many loci associated with variation in BMD. However, a number of the candidate genes identified at these loci have no known associated biological function or have yet to be replicated in subsequent investigations. Furthermore, few investigations have considered gene-environment interactions - in particular, whether specific genes may be sensitive to mechanical loading from physical activity and the outcome of such an interaction for BMD and potential injury risk. Therefore, this review considers the importance of physical activity on BMD, genetic associations with BMD and how subsequent investigation requires consideration of the interaction between these strong determinants. Future research using well-defined independent cohorts such as elite athletes, who experience much greater mechanical stress than most, to study such phenotypes, can provide a greater understanding of these factors as well as the biological underpinnings of such a physiologically “extreme” population. Subsequently, modification of training, exercise or rehabilitation programmes based upon genetic characteristics could have substantial implications in both the sporting and public health domains once the fundamental research has been conducted successfully.

Titin provides a molecular blueprint for muscle sarcomere assembly and sarcomere length can vary according to titin isoform expression. If variations in sarcomere length influence muscle fascicle length, this may provide an advantage for running performance. Thus the aim of this study was to investigate if the titin (TTN) rs10497520 polymorphism was associated with muscle fascicle length in recreationally active men (RA; n = 137) and marathon personal best time in male marathon runners (MR; n = 141). Fascicle length of the vastus lateralis was assessed in vivo using B-mode ultrasonography at 50% of muscle length in RA. All participants provided either a whole blood, saliva or buccal cell sample, from which DNA was isolated and genotyped using real-time polymerase chain reaction. Vastus lateralis fascicle length was 10.4% longer in CC homozygotes, those carrying two copies of the C-allele, than CT heterozygotes (p = 0.003) in RA. In the absence of any TT homozygotes, reflective of the low T-allele frequency within Caucasian populations, it is unclear if fascicle length for this group would have been smaller still. No differences in genotype frequency between the RA and MR groups were observed (p = 0.500), although within the MR group the T-allele carriers demonstrated marathon personal best times 2 min 25 s faster than CC homozygotes (p = 0.020). These results suggest that the T-allele at rs10497520 in the TTN gene is associated with shorter skeletal muscle fascicle length and conveys an advantage for marathon running performance in habitually trained men. This article is protected by copyright. All rights reserved.

**Background**\ud \ud Studies investigating associations between ACTN3 R577X and ACE I/D genotypes and endurance athletic status have been limited by small sample sizes from mixed sport disciplines and lack quantitative measures of performance. Aim: To examine the association between ACTN3 R577X and ACE I/D genotypes and best personal running times in a large homogeneous cohort of endurance runners.\ud \ud **Methods**\ud \ud We collected a total of 1064 personal best 1500, 3000, 5000 m and marathon running times of 698 male and female Caucasian endurance athletes from six countries (Australia, Greece, Italy, Poland, Russia and UK). Athletes were genotyped for ACTN3 R577X and ACE ID variants.\ud \ud **Results**\ud \ud There was no association between ACTN3 R577X or ACE I/D genotype and running performance at any distance in men or women. Mean (SD) marathon times (in s) were for men: ACTN3 RR 9149 (593), RX 9221 (582), XX 9129 (582) p = 0.94; ACE DD 9182 (665), ID 9214 (549), II 9155 (492) p = 0.85; for women: ACTN3 RR 10796 (818), RX 10667 (695), XX 10675 (553) p = 0.36; ACE DD 10604 (561), ID 10766 (740), II 10771 (708) p = 0.21. Furthermore, there were no associations between these variants and running time for any distance in a sub-analysis of athletes with personal records within 20% of world records.\ud \ud **Conclusions**\ud \ud Thus, consistent with most case-control studies, this multi-cohort quantitative analysis demonstrates it is unlikely that ACTN3 XX genotype provides an advantage in competitive endurance running performance. For ACE II genotype, some prior studies show an association but others do not. Our data indicate it is also unlikely that ACE II genotype provides an advantage in endurance running.

Purpose: To investigate differences in neuromuscular factors between elite and nonelite players and to establish which factors underpin direction-specific unilateral jump performance. Methods: Elite (n = 23; age, 18.1 [1.0] y; body mass index, 23.1 [1.8] kg·m−2) and nonelite (n = 20; age, 22.3 [2.7] y; body mass index, 23.8 [1.8] kg·m−2) soccer players performed 3 unilateral countermovement jumps (CMJs) on a force platform in the vertical, horizontal-forward, and medial directions. Knee extension isometric maximum voluntary contraction torque was assessed using isokinetic dynamometry. Vastus lateralis fascicle length, angle of pennation, quadriceps femoris muscle volume (Mvol), and physiological cross-sectional area (PCSA) were assessed using ultrasonography. Vastus lateralis activation was assessed using electromyography. Results: Elite soccer players presented greater knee extensor isometric maximum voluntary contraction torque (365.7 [66.6] vs 320.1 [62.6] N·m; P = .045), Mvol (2853 [508] vs 2429 [232] cm3; P = .001), and PCSA (227 [42] vs 193 [25] cm2; P = .003) than nonelite. In both cohorts, unilateral vertical and unilateral medial CMJ performance correlated with Mvol and PCSA (r ≥ .310, P ≤ .043). In elite soccer players, unilateral vertical and unilateral medial CMJ performance correlated with upward phase vastus lateralis activation and angle of pennation (r ≥ .478, P ≤ .028). Unilateral horizontal-forward CMJ peak vertical power did not correlate with any measure of muscle size or activation but correlated inversely with angle of pennation (r = −.413, P = .037). Conclusions: While larger and stronger quadriceps differentiated elite from nonelite players, relationships between neuromuscular factors and unilateral jump performance were shown to be direction-specific. These findings support a notion that improving direction-specific muscular power in soccer requires improving a distinct neuromuscular profile.

Background: Two common single nucleotide polymorphisms within the COL5A1 gene (SNPs; rs12722 C/T and rs3196378 C/A) have previously been associated with tendon and ligament pathologies. Given the high incidence of tendon and ligament injuries in elite rugby athletes, we hypothesised that both SNPs would be associated with career success. Methods: In 1105 participants (RugbyGene project), comprising 460 elite rugby union (RU), 88 elite rugby league athletes and 565 non-athlete controls, DNA was collected and genotyped for the COL5A1 rs12722 and rs3196378 variants using real-time PCR. Results: For rs12722, the injury-protective CC genotype and C allele were more common in all athletes (21% and 47%, respectively) and RU athletes (22% and 48%) than in controls (16% and 41%, P ≤ 0.01). For rs3196378, the CC genotype and C allele were overrepresented in all athletes (23% and 48%) and RU athletes (24% and 49%) compared with controls (16% and 41%, P ≤ 0.02). The CC genotype in particular was overrepresented in the back and centres (24%) compared with controls, with more than twice the odds (OR = 2.25, P = 0.006) of possessing the injury-protective CC genotype. Furthermore, when considering both SNPs simultaneously, the CC–CC SNP-SNP combination and C–C inferred allele combination were higher in all the athlete groups (≥ 18% and ≥ 43%) compared with controls (13% and 40%; P = 0.01). However, no genotype differences were identified for either SNP when RU playing positions were compared directly with each other. Conclusion: It appears that the C alleles, CC genotypes and resulting combinations of both rs12722 and rs3196378 are beneficial for rugby athletes to achieve elite status and carriage of these variants may impart an inherited resistance against soft tissue injury, despite exposure to the high-risk environment of elite rugby. These data have implications for the management of inter-individual differences in injury risk amongst elite athletes.

It is unknown whether loading of the lower limbs through additional storage of fat mass as evident in obesity would promote muscular adaptations similar to those seen with resistance exercise. It is also unclear whether ageing modulates any such adjustments. This study aimed to examine the relationships between adiposity, ageing and skeletal muscle size and architecture. A total of 100 untrained healthy women were categorised by age into young (Y) (mean ± SD: 26.7 ± 9.4 years) vs. old (O) (65.1 ± 7.2 years) and body mass index (BMI) classification (underweight, normal weight, overweight and obese). Participants were assessed for body fat using dual energy x-ray absorptiometry, and for gastrocnemius medialis (GM) muscle architecture (skeletal muscle fascicle pennation angle and length) and size [GM muscle volume and physiological cross-sectional area (PCSA)] using B-mode ultrasonography. GM fascicle pennation angle (FPA) in the obese Y females was 25% greater than underweight (P = 0.001) and 25% greater than normal weight (P = 0.001) individuals, while O females had 32 and 22% greater FPA than their underweight (P = 0.008) and normal weight (P = 0.003) counterparts. Furthermore, FPA correlated with body mass in both Y and O females (Y r = 0.303; P < 0.001; O r = 0.223; P = 0.001), yet no age-related differences in the slope or r-values were observed (P > 0.05). Both GM muscle volume (P = 0.003) and PCSA (P = 0.004) exhibited significant age × BMI interactions. In addition, muscle volume and PCSA correlated with BMI, body mass and fat mass. Interestingly, ageing reduced both the degree of association in these correlations (P < 0.05) and the slope of the regressions (P < 0.05). Our findings partly support our hypotheses in that obesity-associated changes in GM PCSA and volume differed between the young and old. The younger GM muscle adapted to the loading induced by high levels of body mass, adiposity and BMI by increasing its volume and increasing its pennation angle, ultimately enabling it to produce higher maximum torque. Such an adaptation to increased loading did not occur in the older GM muscle. Nonetheless, the older GM muscle FPA increased to a similar extent to that seen in young GM muscle, an effect which partly explains the relatively enhanced absolute maximum torque observed in obese older females.

Unaccustomed strenuous exercise can lead to muscle strength loss, inflammation and delayed-onset muscle soreness, which may be influenced by genetic variation. We investigated if a missense single nucleotide polymorphism (A>G, rs2275950 ) within the TRIM63 gene (encoding MuRF-1 and potentially affecting titin mechanical properties) was associated with the variable response to unaccustomed eccentric exercise. Sixty-five untrained, healthy participants (genotyped for rs2275950 : AA, AG, and GG) performed 120 maximal eccentric knee extensions (ECC) to induce muscle damage. Isometric and isokinetic maximal voluntary knee extension contractions (MVCs) and muscle soreness were assessed before, immediately after, and 48 h after ECC. AA homozygotes were consistently stronger [baseline isometric MVC: 3.23 ± 0.92 Nm/kg (AA) vs. 2.09 ± 0.67 Nm/kg (GG); P = 0.006] and demonstrated less muscle soreness over time ( P = 0.022) compared with GG homozygotes. This may be explained by greater titin stiffness in AA homozygotes, leading to intrinsically stronger muscle fibers that are more resistant to eccentric damaging contractions.

Costameres are mechano-sensory sites of focal adhesion in the sarcolemma that provide a structural anchor for myofibrils. Their turnover is regulated by integrin-associated focal adhesion kinase (FAK). We hypothesized that changes in content of costamere components (beta 1 integrin, FAK, meta-vinculin, gamma-vinculin) with increased and reduced loading of human anti-gravity muscle would: (i) relate to changes in muscle size and molecular parameters of muscle size regulation [p70S6K, myosin heavy chain (MHC)1 and MHCIIA]; (ii) correspond to adjustments in activity and expression of FAK, and its negative regulator, FRNK; and (iii) reflect the temporal response to reduced and increased loading. Unloading induced a progressive decline in thickness of human vastus lateralis muscle after 8 and 34 days of bedrest (−4% and −14%, respectively; n = 9), contrasting the increase in muscle thickness after 10 and 27 days of resistance training (+5% and +13%; n = 6). Changes in muscle thickness were correlated with changes in cross-sectional area of type I muscle fibers (r = 0.66) and beta 1 integrin content (r = 0.76) at the mid-point of altered loading. Changes in meta-vinculin and FAK-pY397 content were correlated (r = 0.85) and differed, together with the changes of beta 1 integrin, MHCI, MHCII and p70S6K, between the mid- and end-point of resistance training. By contrast, costamere protein level changes did not differ between time points of bedrest. The findings emphasize the role of FAK-regulated costamere turnover in the load-dependent addition and removal of myofibrils, and argue for two phases of muscle remodeling with resistance training, which do not manifest at the macroscopic level.

OBJECTIVES: We aimed to determine whether countermovement jumps (CMJs; unilateral and bilateral) performed in different directions assessed independent lower-limb power qualities, and if unilateral CMJs would better differentiate between elite and non-elite soccer players than the bilateral vertical (BV) CMJ. DESIGN: Elite (n=23; age, 18.1±1.0years) and non-elite (n=20; age, 22.3±2.7years) soccer players performed three BV, unilateral vertical (UV), unilateral horizontal-forward (UH) and unilateral medial (UM) CMJs. METHODS: Jump performance (height and projectile range), kinetic and kinematic variables from ground reaction forces, and peak activation levels of the vastus lateralis and biceps femoris (BF) muscles from surface electromyography, were compared between jumps and groups of players. RESULTS: Peak vertical power (V-power) was greater in BV (220.2±30.1W/kg) compared to UV (144.1±16.2W/kg), which was greater than UH (86.7±18.3W/kg) and UM (85.5±13.5W/kg) (all, p

AB Purpose: It is unclear whether protein supplementation augments the gains in muscle strength and size observed after resistance training (RT) because limitations to previous studies include small cohorts, imprecise measures of muscle size and strength, and no control of prior exercise or habitual protein intake. We aimed to determine whether whey protein supplementation affected RT-induced changes in elbow flexor muscle strength and size. Methods: We pair-matched 33 previously untrained, healthy young men for their habitual protein intake and strength response to 3-wk RT without nutritional supplementation (followed by 6 wk of no training) and then randomly assigned them to protein (PRO, n = 17) or placebo (PLA, n = 16) groups. Participants subsequently performed elbow flexor RT 3 d[middle dot]wk-1 for 12 wk and consumed PRO or PLA immediately before and after each training session. We assessed elbow flexor muscle strength (unilateral 1-repetition maximum and isometric maximum voluntary force) and size (total volume and maximum anatomical cross-sectional area determined with magnetic resonance imaging) before and after the 12-wk RT. Results: PRO and PLA demonstrated similar increases in muscle volume (PRO 17.0% +/- 7.1% vs PLA 14.9% +/- 4.6%, P = 0.32), anatomical cross-sectional area (PRO 16.2% +/- 7.1% vs PLA 15.6% +/- 4.4%, P = 0.80), 1-repetition maximum (PRO 41.8% +/- 21.2% vs PLA 41.4% +/- 19.9%, P = 0.97), and maximum voluntary force (PRO 12.0% +/- 9.9% vs PLA 14.5% +/- 8.3%, P = 0.43). Conclusions: In the context of this study, protein supplementation did not augment elbow flexor muscle strength and size changes that occurred after 12 wk of RT. (C)2012The American College of Sports Medicine

Obesity is associated with functional limitations in muscle performance and increased likelihood of developing a functional disability such as mobility, strength, postural and dynamic balance limitations. The consensus is that obese individuals, regardless of age, have a greater absolute maximum muscle strength compared to non-obese persons, suggesting that increased adiposity acts as a chronic overload stimulus on the antigravity muscles (e.g., quadriceps and calf), thus increasing muscle size and strength. However, when maximum muscular strength is normalised to body mass, obese individuals appear weaker. This relative weakness may be caused by reduced mobility, neural adaptations and changes in muscle morphology. Discrepancies in the literature remain for maximal strength normalised to muscle mass (muscle quality) and can potentially be explained through accounting for the measurement protocol contributing to muscle strength capacity that need to be explored in more depth such as antagonist muscle co-activation, muscle architecture, a criterion valid measurement of muscle size and an accurate measurement of physical activity levels. Current evidence demonstrating the effect of obesity on muscle quality is limited. These factors not being recorded in some of the existing literature suggest a potential underestimation of muscle force either in terms of absolute force production or relative to muscle mass; thus the true effect of obesity upon skeletal muscle size, structure and function, including any interactions with ageing effects, remains to be elucidated.

Objective: To determine when energy expenditure becomes elevated in infants with cystic fibrosis (CF). Design: Longitudinal studies of total energy expenditure (TEE) using doubly labeled water were conducted in infants identified with CF by newborn screening through the first year of life. Setting: Hospital and community based studies in Denver, Colorado, USA and Cambridge, UK. Results: Eight of the 12 infants enrolled had begun enzyme therapy but were clinically asymptomatic. Four of the 12 infants were heterozygous for the delta F508 mutation, however no difference was seen in TEE from the remaining homozygous infants. TEE was compared to control cohorts at 2, 6 and 12 months of age. There was no difference from the control groups in TEE/kg fat free mass (FFM)/day at 2 months. However, by 6 months of age TEE/kg FFM/day in infants with CF exceeded that of age-matched controls by 25% (P < 0.001). This elevation in TEE continued at 12 months of age exceeding that of controls by 30% (P < 0.05). Conclusions: These results indicate that infants with CF have increased energy needs by 6 months of age and that early diagnosis alone does not prevent the development of increased caloric requirements. These findings emphasize the need for close nutritional monitoring to prevent suboptimal growth during infancy in this population. Sponsorship: This research was supported by grant number 5 MO1 RR00069, General Clinical Research Centers Program, National Center for Research Resources, NIH.

This study aimed to delineate the contribution of adaptations in agonist, antagonist, and stabilizer muscle activation to changes in isometric and isoinertial lifting strength after short-term isoinertial resistance training (RT). Following familiarization, 45 men (23.2 ± 2.8 years) performed maximal isometric and isoinertial strength tests of the elbow flexors of their dominant arms before and after 3 weeks of isoinertial RT. During these tasks, surface electromyography (EMG) amplitude was recorded from the agonist (biceps brachii short and long heads), antagonist (triceps brachii lateral head), and stabilizer (anterior deltoid, pectoralis major) muscles and normalized to either Mmax (agonists) or to maximum EMG during relevant reference tasks (antagonist, stabilizers). After training, there was more than a twofold greater increase in training task-specific isoinertial than isometric strength (17% vs 7%). There were also task-specific adaptations in agonist EMG, with greater increases during the isoinertial than isometric strength task [analysis of variance (ANOVA), training × task, P = 0.005]. A novel finding of this study was that training increased stabilizer muscle activation during all the elbow flexion strength tasks (P 0.001), although these were not task-specific training effects. RT elicited specific neural adaptations to the training task that appeared to explain the greater increase in isoinertial than isometric strength.

This study aimed to establish the interplay between body mass, adiposity, ageing and determinants of skeletal muscle strength. One hundred and two untrained healthy women categorised by age into young (Y) (mean ± SD, 26.7 ± 9.4 years) vs. old (O) (65.1 ± 7.2 years) were assessed for body fat, lean mass, plantar flexion and dorsiflexion maximum voluntary isometric contraction (MVC) torque, muscle activation capacity and antagonist muscle co-contraction. MVC torque normalised to body mass in the obese group was 35 and 29 % lower (p

Background: The trace metal zinc has a wide range of important physiologic roles. Indirect evidence suggests that fat malabsorption is associated with malabsorption of zinc. The objective of this study was to evaluate the effect of pancreatic enzyme replacement on zinc absorption in children and adolescents with cystic fibrosis. Methods: Subjects were four boys and four girls ranging in age from 7 to 17 years of age. All were pancreatic insufficient. Stable isotope labels, 70Zn and67 Zn, were administered orally in divided doses on consecutive days with meals. Meals were identical on the first 2 study days. Subjects were randomized to have pancreatic enzyme replacement withheld on the first or second day. All fecal samples were collected quantitatively for 10 days after label administration and were analyzed individually for total zinc and isotopic enrichment using atomic absorption spectrophotometry and fast atom bombardment mass spectrometry, respectively. Fractional absorption of zinc was calculated from cumulative fecal excretion of unabsorbed label. Results: Fractional absorption while receiving enzymes was 0.50 ± 0.29 versus 0.38 ± 0.24 while not taking enzymes (p = 0.05). Conclusions: These results indicate that fractional absorption of zinc is impaired by pancreatic insufficiency in patients with cystic fibrosis, and is improved by exocrine pancreatic enzyme replacement.

Objective: To determine whether differences in tolerance and absorption of fat and nitrogen exist between a semi-elemental nutritional formula without enzyme replacement and a nonelemental formula with enzyme replacement. Study design: Sixteen patients (eight girls and eight boys) with cystic fibrosis, 4 to 20 years of age (12 ± 1.3, mean ± SEM), who were pancreatic insufficient completed two 6-day regimens of nocturnal continuous enteral feedings offered in random order. Forty-four percent of the total daily energy was consumed as enteral tube feedings, and the remaining oral dietary intake remained constant throughout the study. Seventy-two–hour fecal collections from each study period were analyzed for total fat, long-chain fatty acids (LCFAs), medium-chain fatty acids (MCFAs), and nitrogen. Results: Fat absorption was 80.2% ± 2.9% and 82.3% ± 3.1% ( p = 0.58) for the semi-elemental and nonelemental formulas, respectively. Similarly, the coefficient of absorption of LCFAs was 69.5% ± 4.5% and 79.6% ± 3.4% ( p = 0.30) for the semi-elemental and nonelemental formulas. Malabsorption of MCFAs contributed minimally to total fat malabsorption. There was no difference between formulas for MCFA or for nitrogen absorption, 83.7% ± 1.9% and 87.4% ± 1.4%, p = 0.48. All patients tolerated all feedings, and weight gained was 1.8 ± 0.3 kg with no difference in weight gain between the trials. Conclusion: A nonelemental formula, with enzyme replacement, is absorbed as well as a predigested formula in patients with CF who are pancreatic insufficient. (J Pediatr 1998;132:265-9)

Whilst skeletal muscle hypertrophy is considered an important adaptation to resistance training (RT), it has not previously been found to explain the inter-individual changes in strength after RT. This study investigated the contribution of hypertrophy to individual gains in isometric, isoinertial and explosive strength after 12 weeks of elbow flexor RT. Thirty-three previously untrained, healthy men (18–30 years) completed an initial 3-week period of elbow flexor RT (to facilitate neurological responses) followed by 6-week no training, and then 12-week elbow flexor RT. Unilateral elbow flexor muscle strength [isometric maximum voluntary force (iMVF), single repetition maximum (1-RM) and explosive force], muscle volume (V m), muscle fascicle pennation angle (θ p) and normalized agonist, antagonist and stabilizer sEMG were assessed pre and post 12-week RT. Percentage gains in V m correlated with percentage changes in iMVF (r = 0.527; P = 0.002) and 1-RM (r = 0.482; P = 0.005) but not in explosive force (r ≤ 0.243; P ≥ 0.175). Percentage changes in iMVF, 1-RM, and explosive force did not correlate with percentage changes in agonist, antagonist or stabilizer sEMG (all P > 0.05). Percentage gains in θ p inversely correlated with percentage changes in normalized explosive force at 150 ms after force onset (r = 0.362; P = 0.038). We have shown for the first time that muscle hypertrophy explains a significant proportion of the inter-individual variability in isometric and isoinertial strength gains following 12-week elbow flexor RT in healthy young men.

Accurate assessment of muscle-tendon forces in vivo requires knowledge of the muscle-tendon moment arm. Dual-energy X-ray absorptiometry (DXA) can produce 2D images suitable for visualising both tendon and bone, thereby potentially allowing the moment arm to be measured but there is currently no validated DXA method for this purpose. The aims of this study were (i) to compare in vivo measurements of the patellar tendon moment arm (dPT) assessed from 2D DXA and magnetic resonance (MR) images and (ii) to compare the reliability of the two methods. Twelve healthy adults (mean ± SD: 31.4 ± 9.5 yr; 174.0 ± 9.5 cm; 76.2 ± 16.6 kg) underwent two DXA and two MR scans of the fully extended knee at rest. The tibiofemoral contact point (TFCP) was used as the centre of joint rotation in both techniques, and the dPT was defined as the perpendicular distance from the patellar tendon axis to the TFCP. The dPT was consistently longer when assessed via DXA compared to MRI (+3.79 ± 1.25 mm or +9.78 ± 3.31%; P0.001). The test-retest reliability of the DXA [CV=2.13%; ICC=0.94; ratio limits of agreement (RLA)=1.01 (*/÷1.07)] and MR [(CV=2.27%; ICC=0.96; RLA=1.00 (*/÷1.07)] methods was very high and comparable between techniques. Moreover, the RLA between the mean DXA and MRI dPT values [1.097 (*/÷1.061)] demonstrated very strong agreement between the two methods. In conclusion, highly reproducible dPT measurements can be determined from DXA imaging with the knee fully extended at rest. This has implications for the calculation of patellar tendon forces in vivo where MR equipment is not available.

Alternative measures of muscle size, strength, and power to those used in previous studies could help resolve the controversy surrounding associations between polymorphisms of the angiotensin-I converting enzyme (ACE) and α-actinin-3 (ACTN3) genes and skeletal muscle phenotypes, and the responses to resistance training (RT). To this end, we measured quadriceps femoris muscle volume (Vm), physiological cross-sectional area (PCSA), maximum isometric force (Ft), specific force (Ft per unit PCSA), maximum isoinertial strength (1-RM), and maximum power (Wmax ; n = 40) before and after 9-week knee extension RT in 51 previously untrained young men, who were genotyped for the ACE I/D and ACTN3 R577X polymorphisms. ACTN3 R-allele carriers had greater Vm, 1-RM, and Wmax than XX homozygotes at baseline (all P 0.05), but responses to RT were independent of ACTN3 genotype (all P 0.05). Muscle phenotypes were independent of ACE genotype before (all P 0.05) and after RT (all P 0.01). However, people with the "optimal" ACE+ACTN3 genotype combination had greater baseline 1-RM and Wmax compared to those with the "suboptimal" profile (both P 0.0125). We show for the first time that the ACTN3 R577X polymorphism is associated with human Vm and (independently and in combination with the ACE I/D polymorphism) influences 1-RM and Wmax.

Background: Americans in Motion-Healthy Interventions (AIM-HI) is an initiative designed to assist family physicians with positioning fitness (physical activity, nutrition, and emotional well-being) as the treatment of choice for prevention and management of chronic disease. We investigated whether the concept of a culture of fitness would benefit office personnel and carry over to patient care. Methods: This randomized, controlled trial provided an intervention based on the AIM-HI curriculum to 12 enhanced offices with support for office activities, while 12 traditional offices received only AIM-HI tools with encouragement for use with patients. Before intervention, at 4 months, and at 14 months, we measured the practice personnel9s dietary behavior (PrimeScreen), physical activity (International Physical Activity Questionnaire), self-determined (intrinsic) motivation (Treatment Self-Regulation Questionnaire [TSRQ]), perceived ability to carry out health behaviors (Perceived Competence Scale), and readiness to improve and/or maintain health behaviors (Stages of Change). Results: From 24 practices we enrolled 470 subjects; 21 practices completed the study, and data from 341 patients were analyzed. Differential change from baseline between the enhanced and traditional offices was not evident for behavior changes. An overall decrease from baseline in self-reported total physical activity measured as metabolic equivalent–minutes for all surveyed groups occurred over the study time period (4-month β = −11.97; 14-month β = −9.01; P = .003). A statistically significant increase occurred at 4 months among participants from the enhanced practices for the TSRQ outcomes of Healthy Eating (baseline, 3.00 ± 0.12; 4 months, 3.26 ± 0.13; P = .013). Among clinicians, TSRQ Healthy Eating scores increased from 3.19 ± 0.13 at baseline to 3.52 ± 0.14 at 4 months (P = .005). However, increases in TSRQ Eating scores were not sustained by 14 months. Stages of Change scores decreased from baseline to 4 months in enhanced group offices. There was also a decrease in Stages of Change scores among staff from baseline to 14 months. Conclusions: Primary care clinicians and office staff are resistant to health behavior change. External motivation did not seem to help them change. The effect of this intervention on patient care is not yet known.

The protein tyrosine kinase-2 (PTK2) gene encodes focal adhesion kinase, a structural protein involved in lateral transmission of muscle fiber force. We investigated whether single-nucleotide polymorphisms (SNPs) of the PTK2 gene were associated with various indexes of human skeletal muscle strength and the interindividual variability in the strength responses to resistance training. We determined unilateral knee extension single repetition maximum (1-RM), maximum isometric voluntary contraction (MVC) knee joint torque, and quadriceps femoris muscle specific force (maximum force per unit physiological cross-sectional area) before and after 9 wk of knee extension resistance training in 51 untrained young men. All participants were genotyped for the PTK2 intronic rs7843014 A/C and 3′-untranslated region (UTR) rs7460 A/T SNPs. There were no genotype associations with baseline measures or posttraining changes in 1-RM or MVC. Although the training-induced increase in specific force was similar for all PTK2 genotypes, baseline specific force was higher in PTK2 rs7843014 AA and rs7460 TT homozygotes than in the respective rs7843014 C- ( P = 0.016) and rs7460 A-allele ( P = 0.009) carriers. These associations between muscle specific force and PTK2 SNPs suggest that interindividual differences exist in the way force is transmitted from the muscle fibers to the tendon. Therefore, our results demonstrate for the first time the impact of genetic variation on the intrinsic strength of human skeletal muscle.

Objective We have previously shown in an acute inpatient setting that dietary substitution of 77.5% of fat kcal as medium chain triglycerides (MCT) increased insulin-mediated glucose metabolism in patients with non-insulin-dependent diabetes mellitus (NIDDM), and that this effect appeared to be mediated by increases in insulin-mediated glucose disposal. The purpose of this study was to test the application of dietary substitution of medium chain triglycerides as an adjunctive tool in ambulatory therapy of NIDDM. Methods Five subjects with NIDDM underwent a baseline 6 hour insulin/glucose euglycemic clamp study, with simultaneous 3H-glucose infusion for calculation of glucose disposal rate and hepatic glucose output. Subjects were then randomized to begin one of two 30-day experimental diets, with long chain (LCT) or medium chain triglycerides (MCT), and subsequent crossover to the other diet. A 6 hour euglycemic clamp was repeated after each diet phase. Results Diet records and urinary organic acid excretion indicated a high level of dietary compliance by the study participants. Postprandial blood glucose excursions were less after one month on the diet with MCT than after the LCT diet (p = 0.004). However, fasting serum glucose, serum fructosamine (a measure of glycemia), fasting insulin, hepatic glucose output, and insulin-mediated glucose metabolism were not improved by the dietary substitution of MCT. Conclusion These data indicate that supplementation of a tolerable amount of MCT in a conventional diabetic exchange diet has little impact on glycemic control in subjects with NIDDM in an ambulatory setting.

It is not known why in vivo muscle specific tension increases following resistance training in humans but changes in muscle fibre-type composition, increased single-fibre specific tension or lateral force transmission might provide explanations. Lateral force transmission would increase specific tension but decrease contraction velocity, thus not affecting maximal power per unit muscle volume. In vivo muscle specific tension, power output and muscle volume were determined in the quadriceps femoris of 42 young men, while myosin heavy chain (MyHC) isoform composition, single-fibre (SF) specific tension, SF maximal shortening velocity (V(max)) and SF peak power (W(max)) of the vastus lateralis were established in a subsample (n = 17) before and after high-intensity leg-extension resistance training (3 sessions week(-1) for 9 weeks). Following training, in vivo muscle specific tension increased by 17% but the power output/muscle volume ratio remained unaltered. Furthermore, there was no relationship between the training-induced decrease in MyHC IIX and the change in specific tension in vivo. In addition, SF specific tension, V(max) and W(max) were unchanged following training. In conclusion, a change in fibre-type composition does not explain the increased in vivo specific tension, nor does it seem likely that increased myofilament packing occurred with resistance training. However, an unchanged in vivo power per unit muscle volume is in accordance with the notion of enhanced lateral force transmission after strength training.

Aim: The present study investigated whether in vivo human quadriceps femoris (QF) muscle specific tension changed following strength training by systematically determining QF maximal force and physiological cross-sectional area (PCSA). Methods: Seventeen untrained men (20 +/- 2 yrs) performed high-intensity leg-extension training 3 times a week for 9 weeks. Maximum tendon force (F(t)) was calculated from maximum voluntary contraction (MVC) torque, corrected for agonist and antagonist muscle activation, and moment arm length (d(PT)) before and after training. QF PCSA was calculated as the sum of the four component muscle volumes, each divided by its fascicle length. Dividing F(t) by the sum of the component muscle PCSAs, each multiplied by the cosine of the respective fascicle pennation angle, provided QF specific tension. Results: MVC torque and QF activation increased by 31% (P < 0.01) and 3% (P < 0.05), respectively, but there was no change in antagonist co-activation or d(PT). Subsequently, F(t) increased by 27% (P < 0.01). QF volume increased by 6% but fascicle length did not change in any of the component muscles, leading to a 6% increase in QF PCSA (P < 0.05). Fascicle pennation angle increased by 5% (P < 0.01) but only in the vastus lateralis muscle. Consequently, QF specific tension increased by 20% (P < 0.01). Conclusion: An increase in human muscle specific tension appears to be a real consequence of resistance training rather than being an artefact of measuring errors but the underlying cause of this phenomenon remains to be determined.

Considerable variation exists between people in the muscle response to resistance training, but there are numerous ways muscle might adapt to overload that might explain this variable response. Therefore, the aim of this study was to quantify the range of responses concerning the training-induced change in maximum voluntary contraction (MVC) knee joint torque, quadriceps femoris (QF) maximum muscle force (F), physiological cross-sectional area (PCSA) and specific tension (F/PCSA). It was hypothesized that the variable change in QF specific tension between individuals would be less than that of MVC. Fifty-three untrained young men performed progressive leg-extension training three times a week for 9 weeks. F was determined from MVC torque, voluntary muscle activation level, antagonist muscle co-activation and patellar tendon moment arm. QF specific tension was established by dividing F by QF PCSA, which was calculated from the ratio of QF muscle volume to muscle fascicle length. MVC torque increased by 26 ± 11% (P < 0.0001; range −1 to 52%), while F increased by 22 ± 11% (P < 0.0001; range −1 to 44%). PCSA increased by 6 ± 4% (P < 0.001; range −3 to 18%) and specific tension increased by 17 ± 11% (P < 0.0001; range −5 to 39%). In conclusion, training-induced changes in F and PCSA varied substantially between individuals, giving rise to greater inter-individual variability in the specific tension response compared to that of MVC. Furthermore, it appears that the change in specific tension is responsible for the variable change in MVC.

It is not known to what extent the inter-individual variation in human muscle strength is explicable by differences in specific tension. To investigate this, a comprehensive approach was used to determine in vivo specific tension of the quadriceps femoris (QF) muscle (Method 1). Since this is a protracted technique, a simpler procedure was also developed to accurately estimate QF specific tension (Method 2). Method 1 comprised calculating patellar tendon force (F (t)) in 27 young, untrained males, by correcting maximum voluntary contraction (MVC) for antagonist co-activation, voluntary activation and moment arm length. For each component muscle, the physiological cross-sectional area (PCSA) was calculated as volume divided by fascicle length during MVC. Dividing F (t) by the sum of the four PCSAs (each multiplied by the cosine of its pennation angle during MVC) provided QF specific tension. Method 2 was a simplification of Method 1, where QF specific tension was estimated from a single anatomical CSA and vastus lateralis muscle geometry. Using Method 1, the variability in MVC (18%) and specific tension (16%) was similar. Specific tension from Method 1 (30 +/- 5 N cm(-2)) was similar to and correlated with that of Method 2 (29 +/- 5 N cm(-2); R (2) = 0.67; P < 0.05). In conclusion, most of the inter-individual variability in MVC torque remains largely unexplained. Furthermore, a simple method of estimating QF specific tension provided similar values to the comprehensive approach, thereby enabling accurate estimations of QF specific tension where time and resources are limited.

To obtain a better understanding of the adaptations of human tendon to chronic overloading, we examined the relationships between these adaptations and the changes in muscle structure and function. Fifteen healthy male subjects (20 ± 2 yr) underwent 9 wk of knee extension resistance training. Patellar tendon stiffness and modulus were assessed with ultrasonography, and cross-sectional area (CSA) was determined along the entire length of the tendon by using magnetic resonance imaging. In the quadriceps muscles, architecture and volume measurements were combined to obtain physiological CSA (PCSA), and maximal isometric force was recorded. Following training, muscle force and PCSA increased by 31% ( P < 0.0001) and 7% ( P < 0.01), respectively. Tendon CSA increased regionally at 20–30%, 60%, and 90–100% of tendon length (5–6%; P < 0.05), and tendon stiffness and modulus increased by 24% ( P < 0.001) and 20% ( P < 0.01), respectively. Although none of the tendon adaptations were related to strength gains, we observed a positive correlation between the increase in quadriceps PCSA and the increases in tendon stiffness ( r = 0.68; P < 0.01) and modulus ( r = 0.75; P < 0.01). Unexpectedly, the increase in muscle PCSA was inversely related to the distal and the mean increases in tendon CSA (in both cases, r = −0.64; P < 0.05). These data suggest that, following short-term resistance training, changes in tendon mechanical and material properties are more closely related to the overall loading history and that tendon hypertrophy is driven by other mechanisms than those eliciting tendon stiffening.