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Background: The health benefits associated with recreational running are challenged by the occurrence of running-related injuries (RRIs). Effective preventive measures require knowledge of sport injury etiology. Psychological factors such as perfectionism, mental toughness, and passion are believed to predispose to sports injury by influencing training behaviors, motivation to run, and suppression of feelings of fatigue and pain. Yet their association with RRIs are understudied. Hypothesis: Perfectionism, mental toughness, and passion predict an increased risk of RRIs in recreational runners. Study Design: Prospective cohort study. Level of Evidence: Level 3. Methods: A total of 143 recreational runners (age 34.9 ± 13.9 years, 37% women) with a response rate of 76.5% answered an online questionnaire about their characteristics, running behaviors, and psychological variables (perfectionism, mental toughness, and running passion) as well as a sports injury survey. Then, as a primary outcome, RRIs were recorded biweekly for 6 months. The incidence of injuries was expressed as RRI per 1000 hours of running. The association between predictive factors and RRIs was estimated using logistic regression. Results: The incidence of RRIs during follow-up was 5.16 per 1000 hours of running. The knee was the location injured most often (26.4%), followed by the foot (18.9%) and lower leg (13.2%). Higher obsessive passion (OP) for running (odds ratio [OR], 1.11; 95% CI, 1.04-1.20) and perfectionistic concerns (OR, 1.22; CI,1.05-1.41) were associated with a greater risk of RRIs, as were previous injury (OR, 2.49; CI,1.10-5.70), weekly running distance (OR,1.10; CI, 1.03-1.16), and both supinated (OR, 4.51; CI, 1.11-18.30) and pronated (OR, 3.55; CI, 1.29-9.80) foot type. Following a running schedule (OR, 0.24; CI, 0.09-0.66) was associated with a lower risk of RRIs. Conclusion: History of previous RRI, pronated and supinated foot type, weekly running distance, perfectionistic concern

Hypertrophic cardiomyopathy (HCM) is characterised by asymmetric left ventricular hypertrophy, ventricular arrhythmias, and cardiomyocyte dysfunction that may cause sudden death. HCM is associated with mutations in sarcomeric proteins and is usually transmitted as an autosomal-dominant trait. The aim of this in silico study was to assess the mechanisms that underlie the altered electrophysiological activity, contractility, regulation of energy metabolism, and crossbridge cycling in HCM at the single-cell level. To investigate this, we developed a human ventricular cardiomyocyte model that incorporates electrophysiology, metabolism, and force generation. The model was validated by its ability to reproduce the experimentally observed kinetic properties of human HCM induced by (a) remodelling of several ion channels and Ca2+-handling proteins arising from altered Ca2+/calmodulin kinase II signalling pathways and (b) increased Ca2+ sensitivity of the myofilament proteins. Our simulation showed a decreased phosphocreatine-to-ATP ratio (-9%) suggesting a negative mismatch between energy expenditure and supply. Using a spatial myofilament half-sarcomere model, we also compared the fraction of detached, weakly bound, and strongly bound crossbridges in the control and HCM conditions. Our simulations showed that HCM has more crossbridges in force-producing states than in the control condition. In conclusion, our model reveals that impaired crossbridge kinetics is accompanied by a negative mismatch between the ATP supply and demand ratio. This suggests that improving this ratio may reduce the incidence of sudden death in HCM.

Prolonged sedentary behaviour (SB) i.e. longer bouts, is suggested to have a range of negative health effects, independent of habitual light and medium-to-vigorous physical activity (LIPA or MVPA). Any effect on musculoskeletal size, architecture or morphology has seldom been reported in older adults. Moreover, no study has yet determined if any association would persist following adjustment for covariates. Therefore, the aim of the present study was to investigate the associations between SB, and properties of the Gastrocnemius Medialis (GM) muscle, in a cross-sectional sample of older adults using compositional data analysis. 105 healthy older adults (73±6y) wore a thigh mounted tri-axial accelerometer for seven consecutive days, and underwent ultrasound [e.g. muscle length (Lm), anatomical cross-sectional area (ACSA), muscle volume (VM), fascicle length (LF), & physiological cross-sectional area (PCSA)], body composition (e.g. DEXA) and health (e.g. medical history) assessments. In-unadjusted models, SB time was negatively associated with ACSA at 75% of Lm (R2adj = 0.085), VM (R2adj = 0.020), and PCSA (R2adj = 0.039). Standing was positively associated with pennation angle (R2adj = 0.110), which persisted following co-variate adjustment (R2adj = 0.296). In fully adjusted models, both SB & LIPA time were associated with ACSA at 75% of Lm (Both R2adj = 0.393). Standing and light activity time were also associated with LF, VM, & PCSA (R2adj 0.116-0.573). In fully adjusted models, SB pattern parameters (i.e. the manner in which sedentary behaviour is accumulated daily throughout waking hours such as the timing, duration and frequency of sedentary bouts), were associated with GM muscle properties (R2adj 0.156-0.564) including LM, LF, and VM. The pattern, rather than accumulated daily SB time, was associated with the size and architecture of the GM. Our results suggest that regardless of co-existing habitual physical activities, SB bouts should be kept short and freque

While physical performance decline rates accelerate after around the age of 70 years, longitudinal athletic performance trends in athletes older than 95 years are unknown. We hypothesized a further accelerated decline in human performance in athletes who still perform at the age of 100 years. To investigate this, longitudinal data of all athletes with results at or over the age of 100 years were collected from the “World Master Rankings” data base spanning 2006–2019 (138 results from 42 athletes; 5 women, 37 men; maximum 105 years) and compared to previously published longitudinal data from 80- to 96-year-old athletes from Sweden (1,134 results from 374 athletes). Regression statistics were used to compare performance decline rates between disciplines and age groups. On average, the individual decline rate of the centenarian group was 2.53 times as steep (100 m: 8.22x; long jump: 0.82x; shot put: 1.61x; discus throw: 1.04x; javelin throw: 0.98x) as that seen in non-centenarians. The steepest increase in decline was found in the 100-m sprint (t-test: p < 0.05, no sign. difference in the other disciplines). The pooled regression statistics of the centenarians are: 100 m: R = 0.57, p = 0.004; long jump: R = 0.90, p < 0.001; shot put: R = 0.65, p < 0.001; discus throw: R = 0.73, p < 0.001; javelin throw: R = 0.68, p < 0.001. This first longitudinal dataset of performance decline rates of athletes who still compete at 100 years and older in five athletics disciplines shows that there is no performance plateau after the age of 90, but rather a further acceleration of the performance decline.

Insulin sensitivity and metabolic flexibility decrease in response to bed rest, but the temporal and causal adaptations in human skeletal muscle metabolism are not fully defined. Here, we use an integrative approach to assess human skeletal muscle metabolism during bed rest and provide a multi-system analysis of how skeletal muscle and the circulatory system adapt to short- and long-term bed rest (German Clinical Trials: DRKS00015677). We uncover that intracellular glycogen accumulation after short-term bed rest accompanies a rapid reduction in systemic insulin sensitivity and less GLUT4 localization at the muscle cell membrane, preventing further intracellular glycogen deposition after long-term bed rest. We provide evidence of a temporal link between the accumulation of intracellular triglycerides, lipotoxic ceramides, and sphingomyelins and an altered skeletal muscle mitochondrial structure and function after long-term bed rest. An intracellular nutrient overload therefore represents a crucial determinant for rapid skeletal muscle insulin insensitivity and mitochondrial alterations after prolonged bed rest.

Fibre typing by immunohistochemistry on cryosections from human skeletal muscle biopsies is an essential tool in the diagnosis and research of muscular diseases, ageing, and responses to exercise training and disuse. Preserving a good quality in these frozen specimens can be challenging especially if they are stored for longer periods before histological processing, which is often the case in studies with a large number of test subjects and/or repeated sampling separated by multiple years. We demonstrate in this article that both, the morphology and reactivity of epitopes to myosin heavy chain isoforms and dystrophin are well preserved in up to 18-year-stored unfixed and unstained cryosections of human m. vastus lateralis (n = 241). Any variation in staining intensity between samples was unrelated to the age of the biopsy donor or the storage period of the unstained cryosections, and in all cases, the obtained images were appropriate for image analysis, such as the determination of the fibre type composition and the fibre cross-sectional area, and quantitative analysis of muscle capillarisation.

Background Previous research suggests that an ageing-associated remodelling and loss of motor units due to motor neuron death contributes significantly to muscle weakness in old age. In histological sections, motor unit remodelling is reflected by increased fibre type grouping. While regular exercise may not attenuate the loss of motor units during ageing, it has been suggested to facilitate reinnervation resulting in larger motor units, and a higher number and larger fibre type groups in histological sections of muscles from aged individuals. Methods In a 10-year follow-up study, we assessed changes in the prevalence and size of fibre type groups in the vastus lateralis muscle from 34 male masters sprinters (40–85 years at start). Results Over the 10 years, there was an ageing-related reduction in performance in the 60-m sprint (P < 0.001) without significant changes in fibre type composition and fibre cross-sectional area. Neither the number of fibre type groups, defined as a fibre surrounded exclusively by fibres of the same type, nor the group size changed significantly in the 10-year period. Conclusions These histological data show that there is limited to no significant fibre type grouping over a 10-year period in masters athletes who continued sprint run training. This observation challenges the paradigm that ageing, at least in systematically trained sprinters, is associated with motor unit remodelling.

Sedentary behaviour (SB) and physical activity (PA) have been shown to be independent modulators of healthy ageing. We thus investigated the impact of activity monitor placement on the accuracy of detecting SB and PA in older adults, as well as a novel random forest algorithm trained on data from older persons. Four monitor types (ActiGraph wGT3X-BT, ActivPAL3c VT, GENEActiv Original, and DynaPort MM+) were simultaneously worn on five anatomical sites during ten different activities by a sample of twenty older adults (70.0 (12.0) years; 10 women). The results indicated that collecting metabolic equivalent (MET) data for 60 s provided the most representative results, minimising variability. In addition, thigh-worn monitors, including ActivPAL, Random Forest, and Sedentary Sphere—Thigh, exhibited superior performance in classifying SB, with balanced accuracies ≥ 94.2%. Other monitors, such as ActiGraph, DynaPort MM+, and GENEActiv Sedentary Sphere—Wrist, demonstrated lower performance. ActivPAL and GENEActiv Random Forest outperformed other monitors in participant-specific balanced accuracies for SB classification. Only thigh-worn monitors achieved acceptable overall balanced accuracies (≥80.0%) for SB, standing, and medium-to-vigorous PA classifications. In conclusion, it is advisable to position accelerometers on the thigh, collect MET data for ≥60 s, and ideally utilise population-specific trained algorithms.

Aims: Active cigarette smoking is a major risk factor for chronic obstructive pulmonary disease that remains elevated after cessation. Skeletal muscle dysfunction has been well documented after smoking, but little is known about cardiac adaptations to cigarette smoking. The underlying cellular and molecular cardiac adaptations, independent of confounding lifestyle factors, and time course of reversibility by smoking cessation remain unclear. We hypothesized that smoking negatively affects cardiac metabolism and induces local inflammation in mice, which do not readily reverse upon 2-week smoking cessation. Methods: Mice were exposed to air or cigarette smoke for 14 weeks with or without 1- or 2-week smoke cessation. We measured cardiac mitochondrial respiration by high-resolution respirometry, cardiac mitochondrial density, abundance of mitochondrial supercomplexes by electrophoresis, and capillarization, fibrosis, and macrophage infiltration by immunohistology, and performed cardiac metabolome and lipidome analysis by mass spectrometry. Results: Mitochondrial protein, supercomplex content, and respiration (all p < 0.03) were lower after smoking, which were largely reversed within 2-week smoking cessation. Metabolome and lipidome analyses revealed alterations in mitochondrial metabolism, a shift from fatty acid to glucose metabolism, which did not revert to control upon smoking cessation. Capillary density was not different after smoking but increased after smoking cessation (p = 0.02). Macrophage infiltration and fibrosis (p < 0.04) were higher after smoking but did not revert to control upon smoking cessation. Conclusions: While cigarette-impaired smoking-induced cardiac mitochondrial function was reversed by smoking cessation, the remaining fibrosis and macrophage infiltration may contribute to the increased risk of cardiovascular events after smoking cessation.

The original version of this article unfortunately contained a mistake. Affiliation details for author Tomas Venckunas were incorrectly given as Department of Life Sciences, Research Centre for Musculoskeletal Science and Sports Medicine, Manchester Metropolitan University, John Dalton Building, Chester Street, Manchester M1 5GD, UK but should have been Lithuanian Sports University, Kaunas, Lithuania.

Objective: In women, the age-related decline in skeletal muscle structure and function is accelerated post menopause, which implicates the role of decreased circulating oestrogen levels. Indeed, boosting oestrogen, by means of postmenopausal hormone replacement therapy (HRT), generally proves beneficial to skeletal muscle. The evidence regarding whether these benefits persist even after cessation of HRT is limited, nor is it clear how physical behaviour (PB) impacts on benefits. Hence, this exploratory study focused on the interplay between HRT administration/cessation, PB and in vivo skeletal muscle structure and function. Methods: Fifty healthy women (≥60 years) were included; 19 had an HRT administration history (≥9 months, with now ~8-years hiatus in treatment) and 31 no such history. On seven continuous days PB data was collected using triaxial accelerometry and analysed using compositional data analysis. Gastrocnemius medialis (GM) muscle volume, architecture and function were determined using ultrasonography, electromyography, dual x-ray absorptiometry and dynamometry. Current serum oestradiol levels were measured using ELISA. Results: Only fascicle length and duration of HRT administration were positively associated. With respect to PB levels, we found a pattern suggesting greater vitality (higher physical activity and lower sedentarism) in previous HRT users, compared to non-users, despite the two groups currently no longer exhibiting significantly different levels of circulating oestradiol. Conclusion: After an 8-year hiatus in treatment, HRT provides limited advantages in GM muscle properties. Interestingly it perhaps enhances vitality despite prolonged cessation, which in the longer term would facilitate greater physical independence, especially considering the association of SB with greater frailty.

BACKGROUND: Proliferating cancer cells shift their metabolism towards glycolysis, even in the presence of oxygen, to especially generate glycolytic intermediates as substrates for anabolic reactions. We hypothesize that a similar metabolic remodelling occurs during skeletal muscle hypertrophy. METHODS: We used mass spectrometry in hypertrophying C2C12 myotubes in vitro and plantaris mouse muscle in vivo and assessed metabolomic changes and the incorporation of the [U-13C6]glucose tracer. We performed enzyme inhibition of the key serine synthesis pathway enzyme phosphoglycerate dehydrogenase (Phgdh) for further mechanistic analysis and conducted a systematic review to align any changes in metabolomics during muscle growth with published findings. Finally, the UK Biobank was used to link the findings to population level. RESULTS: The metabolomics analysis in myotubes revealed insulin-like growth factor-1 (IGF-1)-induced altered metabolite concentrations in anabolic pathways such as pentose phosphate (ribose-5-phosphate/ribulose-5-phosphate: +40%; P = 0.01) and serine synthesis pathway (serine: -36.8%; P = 0.009). Like the hypertrophy stimulation with IGF-1 in myotubes in vitro, the concentration of the dipeptide l-carnosine was decreased by 26.6% (P = 0.001) during skeletal muscle growth in vivo. However, phosphorylated sugar (glucose-6-phosphate, fructose-6-phosphate or glucose-1-phosphate) decreased by 32.2% (P = 0.004) in the overloaded muscle in vivo while increasing in the IGF-1-stimulated myotubes in vitro. The systematic review revealed that 10 metabolites linked to muscle hypertrophy were directly associated with glycolysis and its interconnected anabolic pathways. We demonstrated that labelled carbon from [U-13C6]glucose is increasingly incorporated by ~13% (P = 0.001) into the non-essential amino acids in hypertrophying myotubes, which is accompanied by an increased depletion of media serine (P = 0.006). The inhibition of Phgdh suppressed muscle protein synt