A spatio-temporal and kinematic description of self-selected walking in adults with Achondroplasia.

BACKGROUND: Achondroplasia is characterised by a shorter appendicular limb to torso ratio, compared to age matched individuals of average stature (controls). Despite the well documented shorter leg length of individuals with compared to controls, there are few complete descriptions of gait kinematics reported for the population. AIM: The aim of this study was to report the spatio-temporal and kinematic characteristics of self-selected walking (SSW) in a group with Achondroplasia (N = 10) and age matched group without Achondroplasia (controls, N = 17). METHOD: Whole body 3D analysis of both groups was conducted using a 14 camera VICON system. Spatio-temporal and kinematic variables were determined through a Plug-in-Gait model. SSW was obtained from an average of three trials equating to a total of ∼120 m walking. RESULTS: The group with Achondroplasia were 23 % slower (P < 0.001), had a 29 % shorter stride length (P < 0.001) and a 13 % higher stride frequency (P < 0.001) compared to controls. There were no differences in time normalised temporal measures of left toe off (P = 0.365), right heel contact (P = 0.442) or the duration of double support (P = 0.588) between groups. A number of discrete joint kinematic differences existed between groups, resulting in the group with Achondroplasia having more 'flexed' lower limbs than controls throughout the gait cycle. CONCLUSION: Differences in absolute spatio-temporal variables between groups is likely due to the shorter leg length of the group with Achondroplasia, while their more flexed position of the lower limbs may facilitate toe-clearance during the swing phase.

A quantitative description of self-selected walking in adults with Achondroplasia using the gait profile score.

BACKGROUND: Achondroplasia is characterised by a shorter appendicular limb-to-torso ratio, compared to age matched individuals of average stature (controls). Previous work shows gait kinematics of individuals with Achondroplasia differing to controls, but no global quantification of gait has been made in adults with Achondroplasia. AIM: The aim of this study was to quantify gait differences between a group of adult males with Achondroplasia and controls during self-selected walking (SSW) using the Gait Profile Score (GPS). DESIGN: Whole body motion analysis of 10 adults with Achondroplasia (22 ± 3 yrs) who had not undergone leg lengthening and 17 adult controls (22 ± 2 yrs) was undertaken using a 14 camera VICON system (100 Hz). For each group, fifteen root mean squared Gait Variable Scores (GVS, units °) were computed from lower limb kinematic data and then summed to calculate GPS (°). RESULTS: The group with Achondroplasia had higher GVSs than controls in 10 of the 15 measures (P < 0.05) with the largest differences found in ankle plantar/dorsiflexion (P < 0.001), knee flexion/extension (P < 0.001), and hip internal/external rotation (P < 0.001). The GPS value of the group with Achondroplasia was 64% higher than controls (11.4° (2.0) v 4.1° (1.8), P < 0.001). CONCLUSION: Gait is quantitatively different in adults with Achondroplasia compared to controls. The differences in GPS between groups are due to differences in joint kinematics, which are possibly manifested by maintaining toe-clearance during swing. Gait models derived from the anatomy of individuals with Achondroplasia may improve these data.

TTN genotype is associated with fascicle length and marathon running performance.

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 whether 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=.003) in RA. In the absence of any TT homozygotes, reflective of the low T-allele frequency within Caucasian populations, it is unclear whether fascicle length for this group would have been smaller still. No differences in genotype frequency between the RA and MR groups were observed (P=.500), although within the MR group, the T-allele carriers demonstrated marathon personal best times 2 minutes 25 seconds faster than CC homozygotes (P=.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.

Oral contraceptive pill use and the susceptibility to markers of exercise-induced muscle damage.

PURPOSE: Firstly, to establish whether oral contraceptive pill (OCP) users are more susceptible to muscle damage compared to non-users, and secondly, to establish whether differences can be attributed to differences in patella tendon properties. METHODS: Nine female OCP users and 9 female non-users participated in the investigation. Combining dynamometry, electromyography and ultrasonography, patella tendon properties and vastus lateralis architectural properties were measured pre and during the first of 6 sets of 12 maximal voluntary eccentric knee extensions. Serum oestrogen levels were measured on the 7th day of the pill cycle and the 14th day of menstrual cycle in OCP users and non-users, respectively. Maximal voluntary isometric knee extension torque loss, creatine kinase and muscle soreness were measured 48 h pre-damage, post-damage, and 48, 96 and 168 h post-damage. RESULTS: Oestrogen levels were significantly lower in OCP users compared to non-users (209 ± 115 and 433 ± 147 pg/ml, respectively, p = 0.004). Proposed determinants of muscle damage, patella tendon stiffness and maximal eccentric torque did not differ between OCP users and non-users. The change in creatine kinase from pre to peak was significantly higher in OCP users compared to non-users (962 ± 968 and 386 ± 474 Ul, respectively, p = 0.016). There were no other differences in markers of muscle damage. CONCLUSION: Although our findings suggest that, when compared to non-users, the OCP may augment the creatine kinase response following eccentric exercise, it does not increase the susceptibility to any other markers of muscle damage.

Polymorphisms in PTK2 are associated with skeletal muscle specific force: an independent replication study.

PURPOSE: The aim of the study was to investigate two single nucleotide polymorphisms (SNP) in PTK2 for associations with human muscle strength phenotypes in healthy men. METHODS: Measurement of maximal isometric voluntary knee extension (MVCKE) torque, net MVCKE torque and vastus lateralis (VL) specific force, using established techniques, was completed on 120 Caucasian men (age = 20.6 ± 2.3 year; height = 1.79 ± 0.06 m; mass = 75.0 ± 10.0 kg; mean ± SD). All participants provided either a blood (n = 96) or buccal cell sample, from which DNA was isolated and genotyped for the PTK2 rs7843014 A/C and rs7460 A/T SNPs using real-time polymerase chain reaction. RESULTS: Genotype frequencies for both SNPs were in Hardy-Weinberg equilibrium (X 2 ≤ 1.661, P ≥ 0.436). VL specific force was 8.3% higher in rs7843014 AA homozygotes than C-allele carriers (P = 0.017) and 5.4% higher in rs7460 AA homozygotes than T-allele carriers (P = 0.029). No associations between either SNP and net MVCKE torque (P ≥ 0.094) or peak MVCKE torque (P ≥ 0.107) were observed. CONCLUSIONS: These findings identify a genetic contribution to the inter-individual variability within muscle specific force and provides the first independent replication, in a larger Caucasian cohort, of an association between these PTK2 SNPs and muscle specific force, thus extending our understanding of the influence of genetic variation on the intrinsic strength of muscle.

Fat mass and obesity associated (FTO) gene influences skeletal muscle phenotypes in non-resistance trained males and elite rugby playing position.

BACKGROUND: FTO gene variants have been associated with obesity phenotypes in sedentary and obese populations, but rarely with skeletal muscle and elite athlete phenotypes. METHODS: In 1089 participants, comprising 530 elite rugby athletes and 559 non-athletes, DNA was collected and genotyped for the FTO rs9939609 variant using real-time PCR. In a subgroup of non-resistance trained individuals (NT; n = 120), we also assessed structural and functional skeletal muscle phenotypes using dual energy x-ray absorptiometry, ultrasound and isokinetic dynamometry. In a subgroup of rugby athletes (n = 77), we assessed muscle power during a countermovement jump. RESULTS: In NT, TT genotype and T allele carriers had greater total body (4.8% and 4.1%) and total appendicular lean mass (LM; 3.0% and 2.1%) compared to AA genotype, with greater arm LM (0.8%) in T allele carriers and leg LM (2.1%) for TT, compared to AA genotype. Furthermore, the T allele was more common (94%) in selected elite rugby union athletes (back three and centre players) who are most reliant on LM rather than total body mass for success, compared to other rugby athletes (82%; P = 0.01, OR = 3.34) and controls (84%; P = 0.03, OR = 2.88). Accordingly, these athletes had greater peak power relative to body mass than other rugby athletes (14%; P = 2 x 10-6). CONCLUSION: Collectively, these results suggest that the T allele is associated with increased LM and elite athletic success. This has implications for athletic populations, as well as conditions characterised by low LM such as sarcopenia and cachexia.

The individual and combined effects of obesity- and ageing-induced systemic inflammation on human skeletal muscle properties.

BACKGROUND/OBJECTIVES: The purpose of this study was to determine whether circulating pro-inflammatory cytokines, elevated with increased fat mass and ageing, were associated with muscle properties in young and older people with variable adiposity. SUBJECTS/METHODS: Seventy-five young (18-49 yrs) and 67 older (50-80 yrs) healthy, untrained men and women (BMI: 17-49 kg/m2) performed isometric and isokinetic plantar flexor maximum voluntary contractions (MVCs). Volume (Vm), fascicle pennation angle (FPA), and physiological cross-sectional area (PCSA) of the gastrocnemius medialis (GM) muscle were measured using ultrasonography. Voluntary muscle activation (VA) was assessed using electrical stimulation. GM specific force was calculated as GM fascicle force/PCSA. Percentage body fat (BF%), body fat mass (BFM), and lean mass (BLM) were assessed using dual-energy X-ray absorptiometry. Serum concentration of 12 cytokines was measured using multiplex luminometry. RESULTS: Despite greater Vm, FPA, and PCSA (P<0.05), young individuals with BF% ⩾40 exhibited 37% less GM specific force compared to young BF%<40 (P<0.05). Older adults with BF% ⩾40 showed greater isokinetic MVC compared to older BF%<40 (P=0.019) but this was reversed when normalised to body mass (P<0.001). IL-6 correlated inversely with VA in young (r=-0.376; P=0.022) but not older adults (p>0.05), while IL-8 correlated with VA in older but not young adults (r⩾0.378, P⩽0.027). TNF-alpha correlated with MVC, lean mass, GM FPA and maximum force in older adults (r⩾0.458; P⩽0.048). CONCLUSIONS: The age- and adiposity-dependent relationships found here provide evidence that circulating pro-inflammatory cytokines may play different roles in muscle remodelling according to the age and adiposity of the individual.

Omega-3 Fatty Acids and Vitamin D in Immobilisation: Part A- Modulation of Appendicular Mass Content, Composition and Structure.

OBJECTIVES: Muscle size decreases in response to short-term limb immobilisation. This study set out to determine whether two potential protein-sparing modulators (eicosapentaenoic acid and vitamin D) would attenuate immobilisation-induced changes in muscle characteristics. DESIGN: The study used a randomised, double-blind, placebo-controlled design. SETTING: The study took part in a laboratory setting. PARTICIPANTS: Twenty-four male and female healthy participants, aged 23.0±5.8 years. INTERVENTION: The non-dominant arm was immobilised in a sling for a period of nine waking hours a day over two continuous weeks. Participants were randomly assigned to one of three groups: placebo (n=8, Lecithin, 2400 mg daily), omega-3 (ω-3) fatty acids (n=8, eicosapentaenoic acid (EPA); 1770 mg, and docosahexaenoic acid (DHA); 390 mg, daily) or vitamin D (n=8, 1,000 IU daily). MEASUREMENTS: Muscle and sub-cutaneous adipose thickness (B-mode ultrasonography), body composition (DXA) and arm girth (anthropometry) were measured before immobilisation, immediately on removal of the sling and two weeks after re-mobilisation. RESULTS: Muscle thickness (-5.4±4.3%), upper and lower arm girth (-1.3±0.4 and -0.8±0.8%, respectively), lean mass (-3.6±3.7%) and bone mineral content (BMC) (-2.3±1.5%) decreased significantly with limb immobilisation in the placebo group (P<0.05). Despite no significant effect of group, ω-3 and vitamin D supplementation showed trends (p>0.05) towards attenuating the decreases in muscle thickness, upper/lower arm girths and BMC observed in the placebo group. The ω-3 supplementation group demonstrated a non-significant attenuation of the decrease in DXA quantified lean mass observed in the placebo group. Sub-cutaneous adipose thickness increased in the placebo group (P<0.05). ω-3 and vitamin D both blunted this response, with ω-3 having a greater effect (P<0.05). All parameters had returned to baseline values at the re-mobilisation phase of the study. CONCLUSION: Overall, at the current doses, ω-3 and vitamin D supplementation only attenuated one of the changes associated with non-injurious limb immobilisation. These findings would necessitate further research into either a) supplementation linked to injury-induced immobilisation, or b) larger doses of these supplements to confirm/refute the physiological reserve potential of the two supplements.

Omega-3 Fatty Acids and Vitamin D in Immobilisation: Part B- Modulation of Muscle Functional, Vascular and Activation Profiles.

OBJECTIVES: This study set out to determine whether two potential protein-sparing modulators (eicosapentaenoic acid and vitamin D) would modulate the anticipated muscle functional and related blood vessels function deleterious effects of immobilisation. DESIGN: The study used a randomised, double-blind, placebo-controlled design. SETTING: The study took part in a laboratory setting. PARTICIPANTS: Twenty-four male and female healthy participants, aged 23.0±5.8 years. INTERVENTION: The non-dominant arm was immobilised in a sling for a period of nine waking hours a day over two continuous weeks. Participants were randomly assigned to one of three groups: placebo (n=8, Lecithin, 2400 mg daily), omega-3 (ω-3) fatty acids (n=8, eicosapentaenoic acid (EPA); 1770 mg, and docosahexaenoic acid (DHA); 390 mg, daily) or vitamin D (n=8, 1,000 IU daily). MEASUREMENTS: Isometric and isokinetic torque, antagonist muscle co-contraction (activation profile), muscle fatigability indices, and arterial resting blood flow were measured before, at the end of the immobilisation period, and two weeks after re-mobilisation. RESULTS: Muscle elbow flexion and extension isometric and isokinetic torque decreased significantly with limb immobilisation in the placebo group (P<0.05). Despite no significant effect of supplementation, ω-3 and vitamin D supplementation showed trends (P>0.05) towards attenuating the decreases observed in the placebo group. There was no significant change in muscle fatigue parameters or co-contraction values with immobilisation and no effect of supplementation group (P>0.05). Similarly, this immobilisation model had no impact on the assessed blood flow characteristics. All parameters had returned to baseline values at the re-mobilisation phase of the study. CONCLUSION: Overall, at the current doses, neither ω-3 nor vitamin D supplementation significantly attenuated declines in torque associated with immobilisation. It would appear that muscle function (described here in Part B) might not be as useful a marker of the effectiveness of a supplement against the impact of immobilisation compared to tissue composition changes (described in Part A).

Bone health measured using quantitative ultrasonography in adult males with muscular dystrophy.

OBJECTIVES: To compare muscle and bone health markers in adult males (aged 20-59 yrs) with and without muscular dystrophy (MD). METHODS: Participants included 11 Fascioscapulohumeral (FSH), 11 Becker's (Be), 9 limb girdle (LG), 11 Duchenne (DMD), and 14 non-dystrophic controls (CTRL). Physical activity was assessed using Bone (BPAQ) and disability specific (PASIPD) questionnaires. Bone QUS provided T- and Z scores from the Distal Radius (DR) and Mid-shaft tibia (MST). Tibialis anterior cross sectional area (TAACSA) was measured using B-mode ultrasound. Grip strength was measured in all but DMD. RESULTS: Physical activity was lower in DMD, FSH and BeMD than CTRL (P<0.05), and lower in DMD than other MDs (P<0.01). T and Z scores were lower in DMD and Be than CTRL (DR, P<0.05); and lower in DMD than CTRL, LG, and FSH (MST, P<0.01). TAACSA and grip strength was 35-59% and 50-58% smaller in MD than CTRL, respectively (P<0.01). Within MD, BPAQ correlated with bone QUS measures (r=0.42-0.38, P<0.01). PASIPD correlated with grip strength (r=0.65, P<0.01) and TAACSA (r=0.46, P<0.01). CONCLUSION: Muscle size, strength, and bone health was lower in adult males with MD compared to adult males without MD, the extent of this is partially determined by physical activity.

Muscle Damage following Maximal Eccentric Knee Extensions in Males and Females.

AIM: To investigate whether there is a sex difference in exercise induced muscle damage. MATERIALS AND METHOD: Vastus Lateralis and patella tendon properties were measured in males and females using ultrasonography. During maximal voluntary eccentric knee extensions (12 reps x 6 sets), Vastus Lateralis fascicle lengthening and maximal voluntary eccentric knee extensions torque were recorded every 10° of knee joint angle (20-90°). Isometric torque, Creatine Kinase and muscle soreness were measured pre, post, 48, 96 and 168 hours post damage as markers of exercise induced muscle damage. RESULTS: Patella tendon stiffness and Vastus Lateralis fascicle lengthening were significantly higher in males compared to females (p<0.05). There was no sex difference in isometric torque loss and muscle soreness post exercise induced muscle damage (p>0.05). Creatine Kinase levels post exercise induced muscle damage were higher in males compared to females (p<0.05), and remained higher when maximal voluntary eccentric knee extension torque, relative to estimated quadriceps anatomical cross sectional area, was taken as a covariate (p<0.05). CONCLUSION: Based on isometric torque loss, there is no sex difference in exercise induced muscle damage. The higher Creatine Kinase in males could not be explained by differences in maximal voluntary eccentric knee extension torque, Vastus Lateralis fascicle lengthening and patella tendon stiffness. Further research is required to understand the significant sex differences in Creatine Kinase levels following exercise induced muscle damage.

The impact of obesity on skeletal muscle strength and structure through adolescence to old age.

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.

Gastrocnemius medialis muscle architecture and physiological cross sectional area in adult males with Duchenne muscular dystrophy.

OBJECTIVES: To describe muscle size and architecture of the gastrocnemius medialis (GM) muscle in eleven adult males with Duchenne Muscular Dystrophy (DMD, age 24.5±5.4 years), and a control group of eleven males without DMD (CTRL, age 22.1±0.9 years). METHODS: GM anatomical cross sectional area (ACSA), volume (VOL), physiological cross sectional area (PCSA), fascicle length (Lf) and pennation angle (θ) were assessed using B-Mode Ultrasonography. GM ACSA was measured at 25, 50 and 75% of muscle length (Lm), from which VOL was calculated. At 50% of Lm, sagittal plane images were analysed to determine GM Lf and θ. GM PCSA was calculated as: VOL/Lf. The ratio of Lf and Lm was also calculated. RESULTS: GM ACSA at 50% Lm, VOL and PCSA were smaller in DMD males compared to CTRL males by 36, 47 and 43%, respectively (P<0.01). There were no differences in Lf and θ. GM Lm was 29% shorter in DMD compared to CTRL. Lf/Lm was 29% longer in DMD (P<0.01). CONCLUSIONS: Unlike previous data in children with DMD, our results show significant atrophy in adult males with DMD, and no change in Lf or θ. The shorter Lm may have implications for joint flexibility.

The impact of obesity on skeletal muscle architecture in untrained young vs. old women.

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.

Combined effects of body composition and ageing on joint torque, muscle activation and co-contraction in sedentary women.

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 < 0.05) in Y and 34 and 31 % lower (p < 0.05) in O, compared with underweight and normal weight individuals, respectively. Y with ≥40 % body fat had significantly lower activation than Y with <40 % body fat (88.3 vs. 94.4 %, p < 0.05), but O did not exhibit this effect. Co-contraction was affected by ageing (16.1 % in O vs. 13.8 % in Y, p < 0.05) but not body composition. There were significant associations between markers of body composition, age, strength and activation capacity, with the strongest correlation between muscle strength and total body mass (r (2) = 0.508 in Y, p < 0.001, vs. r (2) = 0.204 in O, p < 0.01). Furthermore, the age-related loss in plantar flexion (PF) MVC torque was exacerbated in obese compared to underweight, normal weight and overweight individuals (-0.96 vs. -0.54, -0.57 and -0.57 % per year, p < 0.05). The negative impact of adiposity on muscle performance is associated with not only muscular but also neural factors. Overall, the effects of ageing and obesity on this system are somewhat cumulative.

Gender differences in fascicular lengthening during eccentric contractions: the role of the patella tendon stiffness.

AIM: Elastic tendons have been suggested to attenuate fascicle lengthening during eccentric contractions; however, there is no in vivo evidence to support this hypothesis. Therefore, the aim of this study was to determine whether patella tendon stiffness modulates vastus lateralis (VL) fascicle lengthening during eccentric contractions in males and females. METHOD: Vastus lateralis and patella tendon properties were measured in males and females owing to previously reported intrinsic gender differences in tendon properties. During maximal voluntary eccentric knee extensions, VL fascicle lengthening and torque were recorded at every 10° (range of motion 20-90°). RESULTS: A significant correlation between maximal patella tendon stiffness and change in fascicle length (r=0.476, P=0.023) was observed. Similarly, there was a significant correlation between maximal Young's modulus and change in fascicle length (r=0.470, P=0.049). As expected, patella tendon stiffness and Young's modulus were significantly higher in males compared with females (P<0.05). Interestingly, change in VL fascicle length during the eccentric contractions was significantly greater in males compared with females (P<0.05). Based on patella tendon moment arm measurements, VL muscle-tendon unit elongation was estimated to be significantly greater in males compared with females (5.24 and 4.84 cm respectively). CONCLUSION: The significant difference in fascicle lengthening during eccentric contractions may be partly explained by the significantly higher patella tendon moment arm, patella tendon stiffness and Young's modulus found in males compared with females. The current study provides in vivo evidence to support the hypothesis that the tendon acts as a 'mechanical buffer' during eccentric contractions.

Passive stiffness of the gastrocnemius muscle in athletes with spastic hemiplegic cerebral palsy.

The passive properties of the muscle-tendon unit are regularly assessed in individuals with cerebral palsy (CP). However, no information is available on the passive properties of adult muscle, and whether any differences exist between the paretic and control muscles. Eleven ambulant male athletes with spastic hemiplegic CP (21.2 ± 3.0 years) and controls without neurological impairment (age = 21.8 ± 2.2 years) completed two and one passive stretch session, respectively. During each session, the ankle was passively dorsiflexed until end range of motion (ROM), whilst recording passive ankle angle, torque and gastrocnemius medialis (GM) myotendinous junction (MTJ) displacement. In addition, GM cross-sectional area (CSA) and length were measured. Subsequently, in vivo stress and strain were determined to calculate elastic modulus. Passive stiffness, MTJ displacement and ROM of the paretic GM were not different from the control muscles. However, the elastic modulus of the paretic GM was two times stiffer than the control GM muscles. In conclusion, athletes with CP exhibit absolute passive muscle stiffness similar to the controls; however, the elastic modulus of the CP muscle was significantly greater. Therefore, throughout the same ROM a smaller GM CSA in CP athletes has to dissipate larger relative torque compared to the control muscles, consequently causing the muscle to elongate to the same extent as the non-paretic muscle under stretch.

The effect of the oral contraceptive pill on the passive stiffness of the human gastrocnemius muscle in vivo.

The aim of this investigation was to determine the effect of sustained monophasic oral contraceptive pill (MOCP) use on the in vivo passive stiffness of the gastrocnemius medialis (GM) muscle-tendon unit. Twenty four females volunteered for this study (age range 20-25 yrs); twelve participants had been taking the combined MOCP for a minimum of 12 months, and twelve participants, who had never taken the MOCP, formed a control group. Distal displacement of the GM myotendinous junction (MTJ) was measured during passive dorsiflexion at 2 Nm increments to 20 Nm, and at end range of motion using ultrasonography. In addition, GM MTJ displacement was measured at passive torques equivalent to 5, 10 and 15% of plantarflexion maximal voluntary contraction (MVC) torque, and relative to GM length. MOCP users had significantly greater GM MTJ displacement at all passive torques (P<0.01), reaching 40% more at 20 Nm; these displacements remained significantly different when MVC and GM length were accounted for (P<0.01). Passive muscle stiffness from 0-20 Nm was 31% less in MOCP users compared to non-users (P<0.01). In conclusion, based on the in vivo assessment of GM MTJ displacement, passive muscle stiffness is less in MOCP using females, compared to non-pill users.

Disproportionate changes in skeletal muscle strength and size with resistance training and ageing.

The ability of a muscle to shorten and produce force is crucial for locomotion, posture, balance and respiration. During a contraction, myosin heads on the myosin filament propel the actin filament via ATP hydrolysis, resulting in shortening of the muscle and/or force generation. The maximal shortening velocity of a muscle fibre is largely determined by the myosin ATPase activity, while maximal force is primarily determined by the cross-sectional area. Since most muscles are pennate rather than parallel-fibred and work at different lever ratios, muscle architecture and joint-tendon anatomy has to be taken into account to obtain the force and velocity characteristics of a muscle. Additionally, the recruitment of agonistic and antagonistic muscles will contribute to the torque generated during a contraction. Finally, tendon compliance may impact on the rate of force rise and force generated if it is such that the muscle contraction proceeds in the ascending limb of the length-tension relation. Even when magnetic resonance imaging and ultrasound, combined with EMG and/or electrical stimulation, have been applied to relate changes in muscle contractile properties to alterations in muscle size and architecture during ageing and resistance training, a disproportionate change in muscle strength and size remains to be explained.

Carbon monoxide inhalation reduces skeletal muscle fatigue resistance.

AIM: To determine whether inhalation of carbon monoxide (CO), resulting in carboxyhaemoglobin (COHb) levels observed in smokers, had an effect on muscle fatigue during electrically evoked and voluntary muscle contractions. METHODS: Young non-smoking males inspired CO from a Douglas bag until their COHb level reached 6%. During the control condition the same participants inspired ambient air from a Douglas bag for 6 min. Fatigue was assessed as the decline in torque in isometric knee extensions, during 2 min of electrically evoked contractions (30 Hz, 1 s on, 1 s off) and during 2 min of maximal isometric voluntary contractions (1 s on, 1 s off). A fatigue index (FI) was calculated as the ratio of final torque : initial torque. Time to peak torque (TPT) and half relaxation time ((1/2)RT) were also determined for the electrically evoked contractions. RESULTS: The FI during both the voluntary fatigue test (control: 0.80 +/- 0.09 vs. CO: 0.70 +/- 0.08; mean +/- SD) and that of the fatigue test with electrically evoked contractions (control: 0.61 +/- 0.09 vs. CO: 0.53 +/- 0.12) was significantly lower after CO inhalation than after inhalation of ambient air (P < 0.05). There was, however, no effect of CO on the changes in TPT or (1/2)RT during the fatigue test. CONCLUSION: Carbon monoxide inhalation resulting in COHb levels found in smokers has an acute impact on the ability of the muscle to resist fatigue.