Collision activity during training increases total energy expenditure measured via doubly labelled water

Purpose: Collision sports are characterised by frequent high intensity collisions that induce substantial muscle damage, potentially increasing the energetic cost of recovery. Therefore, this study investigated the energetic cost of collision-based activity for the first time across any sport. Methods: Using a randomised crossover design, six professional young male rugby league players completed two different five-day pre-season training microcycles. Players completed either a collision (COLL; 20 competitive one-on-one collisions) or non-collision (nCOLL; matched for kinematic demands, excluding collisions) training session on the first day of each microcycle, exactly seven days apart. All remaining training sessions were matched and did not involve any collision-based activity. Total energy expenditure was measured using doubly labelled water, the literature gold standard. Results: Collisions resulted in a very likely higher (4.96 ± 0.97 MJ; ES = 0.30 ±0.07; p=0.0021) total energy expenditure across the five-day COLL training microcycle (95.07 ± 16.66 MJ) compared with the nCOLL training microcycle (90.34 ± 16.97 MJ). The COLL training session also resulted in a very likely higher (200 ± 102 AU; ES = 1.43 ±0.74; p=0.007) session rating of perceived exertion and a very likely greater (-14.6 ± 3.3%; ES = -1.60 ±0.51; p=0.002) decrease in wellbeing 24h later. Conclusions: A single collision training session considerably increased total energy expenditure. This may explain the large energy expenditures of collision sport athletes, which appear to exceed kinematic training and match demands. These findings suggest fuelling professional collision-sport athletes appropriately for the "muscle damage caused” alongside the kinematic “work required”. Key words: Nutrition, Recovery, Contact, Rugb

Effect of bilberry juice on indices of muscle damage and inflammation in runners completing a half-marathon: a randomised, placebo-controlled trial.

Background: Emerging evidence indicates that fruits rich in polyphenols may attenuate exercise-induced muscle damage and associated markers of inflammation and soreness. This study was conducted to determine whether bilberry juice (BJ), which is particularly rich in polyphenols, reduces markers of muscle damage in runners completing a half marathon. Methods: A total of 21 recreationally trained runners (age 30.9 ± 10.4 y; mass 71.6 ± 11.0 kg; M=16; F=5) were recruited to a single blind, randomised, placebo-controlled, parallel study. Participants were block randomised to consume 2 x 200 ml of BJ or energy-matched control drink (PLA) for 5 d before the Sheffield Half Marathon, on race day, and for 2 days post-race. Measurements of delayed onset muscle soreness (DOMS), muscle damage (creatine kinase; CK) and inflammation (c-reactive protein ; CRP) were taken at baseline, pre-race, post-race, 24 h post-race and 48 h post-race. The effect of treatment on outcome measures was analysed using magnitude-based inferences based on data from 19 participants; 2 participants were excluded from the analyses because they did not provide samples for all time points. Results: The half marathon caused elevations in DOMS, CRP and CK. BJ had a possibly harmful effect on DOMS from pre-race to immediately post-race (11.6%, 90% CI ± 14.7%), a likely harmful effect on CRP from pre-race to 24 h post-race (mean difference ES 0.56, 90% CI ± 0.72) and a possibly harmful effect on CRP from pre-race to 48 h post-race (ES 0.12, 90% CI ± 0.69). At other time points, the differences between the BJ and PLA groups in DOMS and CRP were unclear, possibly trivial or likely trivial. Differences in the changes in CK between BJ and PLA were unclear at every time point other than from baseline to pre-race, where BJ had a possibly harmful effect on reducing muscle damage (ES 0.23, 90% CI ± 0.57). Conclusion: Despite being a rich source of antioxidant and anti-inflammatory phytochemicals, BJ evoked small to moderate increases in exercise-induced DOMS and CRP. Further larger studies are required to confirm these unexpected preliminary results

Eccentric Exercise Facilitates Mesenchymal Stem Cell Appearance in Skeletal Muscle

Eccentric, or lengthening, contractions result in injury and subsequently stimulate the activation and proliferation of satellite stem cells which are important for skeletal muscle regeneration. The discovery of alternative myogenic progenitors in skeletal muscle raises the question as to whether stem cells other than satellite cells accumulate in muscle in response to exercise and contribute to post-exercise repair and/or growth. In this study, stem cell antigen-1 (Sca-1) positive, non-hematopoetic (CD45-) cells were evaluated in wild type (WT) and α7 integrin transgenic (α7Tg) mouse muscle, which is resistant to injury yet liable to strain, 24 hr following a single bout of eccentric exercise. Sca-1+CD45− stem cells were increased 2-fold in WT muscle post-exercise. The α7 integrin regulated the presence of Sca-1+ cells, with expansion occurring in α7Tg muscle and minimal cells present in muscle lacking the α7 integrin. Sca-1+CD45− cells isolated from α7Tg muscle following exercise were characterized as mesenchymal-like stem cells (mMSCs), predominantly pericytes. In vitro multiaxial strain upregulated mMSC stem cells markers in the presence of laminin, but not gelatin, identifying a potential mechanistic basis for the accumulation of these cells in muscle following exercise. Transplantation of DiI-labeled mMSCs into WT muscle increased Pax7+ cells and facilitated formation of eMHC+DiI− fibers. This study provides the first demonstration that mMSCs rapidly appear in skeletal muscle in an α7 integrin dependent manner post-exercise, revealing an early event that may be necessary for effective repair and/or growth following exercise. The results from this study also support a role for the α7 integrin and/or mMSCs in molecular- and cellular-based therapeutic strategies that can effectively combat disuse muscle atrophy

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

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

Adherence of hip and knee arthroplasty studies to RSA standardization guidelines

Peer reviewe

Mechanisms and mediators of the skeletal muscle repeated bout effect

Skeletal muscle adapts to exercise-induced damage by orchestrating several but still poorly understood mechanisms that endow protection from subsequent damage. Known widely as the repeated bout effect, we propose that neural adaptations, alterations to muscle mechanical properties, structural remodeling of the extracellular matrix, and biochemical signaling work in concert to coordinate the protective adaptation

Skeletal muscle inflammation following repeated bouts of lengthening contractions in humans

Skeletal muscle responds to exercise-induced damage by orchestrating an adaptive process that protects the muscle from damage by subsequent bouts of exercise, a phenomenon called the repeated bout effect (RBE). The mechanisms underlying the RBE are not understood. We hypothesized that an attenuated inflammation response following a repeated bout of lengthening contractions (LC) would be coincidental with a RBE, suggesting a potential relationship. Fourteen men (n=7) and women (n=7) completed 2 bouts of lengthening contractions (LC) separated by 28 days. Muscle biopsies were taken before the first bout (B1) from the non-exercised leg, and from the exercised leg 2- and 27-d post-B1 and 2-d following the second bout (B2). A 29-plex cytokine array identified alterations in inflammatory cytokines. Immunohistochemistry quantified inflammatory cell infiltration and major histocompatibility complex class 1 (MHC-1). Muscle soreness was attenuated in the days following B2 relative to B1, indicating a RBE. Intramuscular monocyte chemoattractant protein (MCP1) and interferon gamma-induced protein 10 (IP10) increased following B2 relative to the pre-exercise sample (7 pg/ml to 52 pg/ml, and 11 pg/ml to 36 pg/ml, respectively p<0.05). Interleukin 4 (IL4) decreased (26 pg/ml to 13 pg/ml, p<0.05) following B2 relative to the pre-exercise sample. Infiltration of CD68+ macrophages and CD8+ T-cells were evident following B2, but not B1. Moreover, CD8+ T-cells were observed infiltrating apparently necrotic muscle fibers. No changes in MHC-1 were found. We conclude that inflammation is not attenuated following a repeated bout of LC and that CD8+ T-cells may play a role in muscle adaptation following LC. Moreover, it appears that the muscle or the immune system becomes sensitized to an initial bout of damaging exercise such that inflammatory cell infiltration into the muscle is enhanced upon a repeated bout of damaging exercise

Use of admission serum neutrophil gelatinase-associated lipocalin (NGAL) concentrations as a marker of sepsis and outcome in neonatal foals.

BackgroundEquine neonatal sepsis can be challenging to diagnose and prognosticate. Neutrophil gelatinase-associated lipocalin (NGAL), a new marker of renal damage and inflammation, can potentially be helpful.ObjectivesTo evaluate NGAL in neonatal foals with sepsis, and assess its relation to outcome.AnimalsFoals ≤ 14 days, with admission blood analysis and stored serum.MethodsNGAL was measured on stored serum from 91 foals. Foals were scored for sepsis and survival and categorized according to sepsis status (septic, sick non-septic, healthy, and uncertain sepsis status) and outcome groups (survivors and non-survivors). The septic foals were further sub-categorized according to severity (normal sepsis, severe sepsis and septic shock). A Kruskal-Wallis test was used to compare serum NGAL concentrations in survivors and non-survivors, in the sepsis status groups, and in the sepsis severity groups. Optimal cut-off values for serum NGAL concentrations to diagnose sepsis and outcome were determined with receiver operating characteristic (ROC) curves. NGAL was compared to creatinine and SAA.ResultsMedian serum NGAL concentrations were significantly higher in septic than non-septic foals. However, serum NGAL concentrations did not differ between sepsis severity subgroups. Serum NGAL concentrations were significantly lower in survivors than in non-survivors. Optimal cut-off values of serum NGAL concentrations were 455 μg/L (sensitivity 71.4%, specificity 100%) and 1104 μg/L (sensitivity 39.3%, specificity 95.2%) for predicting sepsis and non-survival, respectively. NGAL correlated to SAA, but not to creatinine. NGAL performed similarly to SAA to diagnose sepsis.ConclusionSerum NGAL concentrations may be useful for diagnosing sepsis and predicting outcome