Propagating mode-I fracture in amorphous materials using the continuous random network (CRN) model

We study propagating mode-I fracture in two dimensional amorphous materials using atomistic simulations. We used the continuous random network (CRN) model of an amorphous material, creating samples using a two dimensional analogue of the WWW (Wooten, Winer & Weaire) Monte-Carlo algorithm. For modeling fracture, molecular-dynamics simulations were run on the resulting samples. The results of our simulations reproduce the main experimental features. In addition to achieving a steady-state crack under a constant driving displacement (which had not yet been achieved by other atomistic models for amorphous materials), the runs show micro-branching, which increases with driving, transitioning to macro-branching for the largest drivings. Beside the qualitative visual similarity of the simulated cracks to experiment, the simulation also succeeds in explaining the experimentally observed oscillations of the crack velocity

Cosmic Strings Stabilized by Fermion Fluctuations

We provide a thorough exposition of recent results on the quantum stabilization of cosmic strings. Stabilization occurs through the coupling to a heavy fermion doublet in a reduced version of the standard model. The study combines the vacuum polarization energy of fermion zero-point fluctuations and the binding energy of occupied energy levels, which are of the same order in a semi-classical expansion. Populating these bound states assigns a charge to the string. Strings carrying fermion charge become stable if the Higgs and gauge fields are coupled to a fermion that is less than twice as heavy as the top quark. The vacuum remains stable in the model, because neutral strings are not energetically favored. These findings suggest that extraordinarily large fermion masses or unrealistic couplings are not required to bind a cosmic string in the standard model.Comment: Based on talk by HW at QFEXT 11 (Benasque, Spain), 15p, uses ws-ijmpcs.cls (incl

Arrested Cracks in Nonlinear Lattice Models of Brittle Fracture

We generalize lattice models of brittle fracture to arbitrary nonlinear force laws and study the existence of arrested semi-infinite cracks. Unlike what is seen in the discontinuous case studied to date, the range in driving displacement for which these arrested cracks exist is very small. Also, our results indicate that small changes in the vicinity of the crack tip can have an extremely large effect on arrested cracks. Finally, we briefly discuss the possible relevance of our findings to recent experiments.Comment: submitted to PRE, Rapid Communication

Steady-State Cracks in Viscoelastic Lattice Models

We study the steady-state motion of mode III cracks propagating on a lattice exhibiting viscoelastic dynamics. The introduction of a Kelvin viscosity $\eta$ allows for a direct comparison between lattice results and continuum treatments. Utilizing both numerical and analytical (Wiener-Hopf) techniques, we explore this comparison as a function of the driving displacement $\Delta$ and the number of transverse sites $N$. At any $N$, the continuum theory misses the lattice-trapping phenomenon; this is well-known, but the introduction of $\eta$ introduces some new twists. More importantly, for large $N$ even at large $\Delta$, the standard two-dimensional elastodynamics approach completely misses the $\eta$-dependent velocity selection, as this selection disappears completely in the leading order naive continuum limit of the lattice problem.Comment: 27 pages, 8 figure

Nonlinear lattice model of viscoelastic Mode III fracture

We study the effect of general nonlinear force laws in viscoelastic lattice models of fracture, focusing on the existence and stability of steady-state Mode III cracks. We show that the hysteretic behavior at small driving is very sensitive to the smoothness of the force law. At large driving, we find a Hopf bifurcation to a straight crack whose velocity is periodic in time. The frequency of the unstable bifurcating mode depends on the smoothness of the potential, but is very close to an exact period-doubling instability. Slightly above the onset of the instability, the system settles into a exactly period-doubled state, presumably connected to the aforementioned bifurcation structure. We explicitly solve for this new state and map out its velocity-driving relation

Titin genotype is associated with skeletal muscle fascicle length in recreationally active men and running performance in habitually trained marathon runners

Objectives The titin gene (TTN) encodes the largest described protein to date and, due to its size, provides a molecular blueprint for the organisation and assembly of the muscle sarcomere. Differences in sarcomere length, due to the expression of different titin isoforms, have been observed previously and may influence muscle fascicle length, which could provide an advantage for running performance. Thus, the aim of this study was to investigate if the TTN rs10497520 polymorphism was associated with muscle fascicle length in recreationally active men and marathon personal best time in elite male marathon runners, and to investigate any differences in genotype frequency between RA and MR.Methods The sample comprised 278 healthy, unrelated Caucasian men who all gave written consent to take part. Participants were categorised as either recreationally active [RA; n = 137; age = 20.7 (2.7) yr; height = 1.79 (0.06) m; mass = 75.3 (10.1) kg] or marathon runners [MR; n = 141; age = 34.9 (7.8) yr; height = 1.79 (0.07) m; mass = 66.5 (6.7) kg]. MR comprised Olympic, international and national level athletes, who had all achieved marathon personal best times under 2 hr 36 mins. Resting fascicle length of the vastus lateralis muscle was assessed in vivo using B-mode ultrasonography at 50% of muscle length in RA only. 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. Independent samples t-tests were used to determine any genotype-dependent differences in fascicle length in RA and marathon personal best time in MR. Pearson’s chi-square tests were conducted to compare genotype frequencies between RA and MR.Results Vastus lateralis fascicle length was 10.4% longer in CC homozygotes 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), however, within the MR group the T-allele carriers demonstrated marathon personal best times 2 min 25 s faster than CC homozygotes (P = 0.020).Conclusions 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

No association between tendon-related genes and performance in elite European Caucasian marathon runners.

Tendons adapt to load under normal physiological conditions, however, under extreme loading conditions, such as those experienced by elite endurance athletes, incomplete adaptation may occur and cause injury. The prevalence of tendinopathies in elite endurance athletes is approximately 50%, thus variability exists in an athlete's tolerance to extreme loading. A number of intrinsic and extrinsic factors contribute to modulating injury risk, some of which are modifiable and others, such as genetic variants, are non-modifiable. It was hypothesized that elite marathon runners would possess a genotype associated with enhanced tendon function, and thus protective against tendinopathy. Here, we compared the genotype frequencies of six genetic variants (COL1A1 rs1800012, VEGFA rs699947, TIMP2 rs4789932, MMP3 rs591058, MMP3 rs650108, MMP3 rs679620), previously associated with tendinopathy, in elite (men <2 h 30 min, n = 109, women <3 h 00 min, n = 99) and sub-elite (men 2 h 30 min-2 h 45 min, n = 189; women 3 h 00 min-3 h 15 min, n = 71) marathon runners with those of a non-athletic control group (n = 564). Genotype associations with marathon personal best time in the athlete group were also investigated. All participants provided either a whole blood, saliva or buccal cell sample, from which DNA was isolated, and genotyped for all six variants using real-time PCR. Genotype frequency differed between athletes and controls for TIMP2 rs4789932 (TT = 17%, CT = 51%, CC = 32% vs. TT = 22%, CT = 42%, CC = 36%, respectively; χ2 = 8.135, P = 0.017) only. However, there was no clear difference in allele frequencies between groups for TIMP2 rs4789932. MMP3 rs650108 genotype frequency differed between female elite and sub-elite athletes (χ2 = 11.913, P = 0.003) only and, as hypothesized, it was the “risk” A-allele that was ~10% less frequent in the elite, than sub-elite athletes. Following combination of all genotype data into a total genotype score, no differences in score between athletes and controls were observed (t = 2.93, P = 0.769). Similarly, no associations between total genotype score and marathon personal best time in male and female runners were observed (r ≤ 0.066, P ≥ 0.394). The results suggest elite marathon runners do not possess a genotype protective against tendinopathy, at least for the tendon-related genetic variants we investigated

The interactions of physical activity, exercise and genetics and their associations with bone mineral density: implications for injury risk in elite athletes

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, determine skeletal health throughout life. Genome-wide association studies 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 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 on genetic characteristics could have substantial implications in both the sporting and public health domains once the fundamental research has been conducted successfully

Genetic Polymorphisms Related to VO2max Adaptation Are Associated With Elite Rugby Union Status and Competitive Marathon Performance

PURPOSE: Genetic polymorphisms have been associated with the adaptation to training in maximal oxygen uptake (V˙O2max). However, the genotype distribution of selected polymorphisms in athletic cohorts is unknown, with their influence on performance characteristics also undetermined. This study investigated whether the genotype distributions of 3 polymorphisms previously associated with V˙O2max training adaptation are associated with elite athlete status and performance characteristics in runners and rugby athletes, competitors for whom aerobic metabolism is important. METHODS: Genomic DNA was collected from 732 men including 165 long-distance runners, 212 elite rugby union athletes, and 355 nonathletes. Genotype and allele frequencies of PRDM1 rs10499043 C/T, GRIN3A rs1535628 G/A, and KCNH8 rs4973706 T/C were compared between athletes and nonathletes. Personal-best marathon times in runners, as well as in-game performance variables and playing position, of rugby athletes were analyzed according to genotype. RESULTS: Runners with PRDM1 T alleles recorded marathon times ∼3 minutes faster than CC homozygotes (02:27:55 [00:07:32] h vs 02:31:03 [00:08:24] h, P = .023). Rugby athletes had 1.57 times greater odds of possessing the KCNH8 TT genotype than nonathletes (65.5% vs 54.7%, χ2 = 6.494, P = .013). No other associations were identified. CONCLUSIONS: This study is the first to demonstrate that polymorphisms previously associated with V˙O2max training adaptations in nonathletes are also associated with marathon performance (PRDM1) and elite rugby union status (KCNH8). The genotypes and alleles previously associated with superior endurance-training adaptation appear to be advantageous in long-distance running and achieving elite status in rugby union