247 resultados para Maximal unipotent subgroups


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Facial expression is an important channel of human social communication. Facial expression recognition (FER) aims to perceive and understand emotional states of humans based on information in the face. Building robust and high performance FER systems that can work in real-world video is still a challenging task, due to the various unpredictable facial variations and complicated exterior environmental conditions, as well as the difficulty of choosing a suitable type of feature descriptor for extracting discriminative facial information. Facial variations caused by factors such as pose, age, gender, race and occlusion, can exert profound influence on the robustness, while a suitable feature descriptor largely determines the performance. Most present attention on FER has been paid to addressing variations in pose and illumination. No approach has been reported on handling face localization errors and relatively few on overcoming facial occlusions, although the significant impact of these two variations on the performance has been proved and highlighted in many previous studies. Many texture and geometric features have been previously proposed for FER. However, few comparison studies have been conducted to explore the performance differences between different features and examine the performance improvement arisen from fusion of texture and geometry, especially on data with spontaneous emotions. The majority of existing approaches are evaluated on databases with posed or induced facial expressions collected in laboratory environments, whereas little attention has been paid on recognizing naturalistic facial expressions on real-world data. This thesis investigates techniques for building robust and high performance FER systems based on a number of established feature sets. It comprises of contributions towards three main objectives: (1) Robustness to face localization errors and facial occlusions. An approach is proposed to handle face localization errors and facial occlusions using Gabor based templates. Template extraction algorithms are designed to collect a pool of local template features and template matching is then performed to covert these templates into distances, which are robust to localization errors and occlusions. (2) Improvement of performance through feature comparison, selection and fusion. A comparative framework is presented to compare the performance between different features and different feature selection algorithms, and examine the performance improvement arising from fusion of texture and geometry. The framework is evaluated for both discrete and dimensional expression recognition on spontaneous data. (3) Evaluation of performance in the context of real-world applications. A system is selected and applied into discriminating posed versus spontaneous expressions and recognizing naturalistic facial expressions. A database is collected from real-world recordings and is used to explore feature differences between standard database images and real-world images, as well as between real-world images and real-world video frames. The performance evaluations are based on the JAFFE, CK, Feedtum, NVIE, Semaine and self-collected QUT databases. The results demonstrate high robustness of the proposed approach to the simulated localization errors and occlusions. Texture and geometry have different contributions to the performance of discrete and dimensional expression recognition, as well as posed versus spontaneous emotion discrimination. These investigations provide useful insights into enhancing robustness and achieving high performance of FER systems, and putting them into real-world applications.

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In this paper, the goal of identifying disease subgroups based on differences in observed symptom profile is considered. Commonly referred to as phenotype identification, solutions to this task often involve the application of unsupervised clustering techniques. In this paper, we investigate the application of a Dirichlet Process mixture (DPM) model for this task. This model is defined by the placement of the Dirichlet Process (DP) on the unknown components of a mixture model, allowing for the expression of uncertainty about the partitioning of observed data into homogeneous subgroups. To exemplify this approach, an application to phenotype identification in Parkinson’s disease (PD) is considered, with symptom profiles collected using the Unified Parkinson’s Disease Rating Scale (UPDRS). Clustering, Dirichlet Process mixture, Parkinson’s disease, UPDRS.

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We investigated performance and heart rate (HR) variability (HRV) over consecutive days of cycling with post-exercise cold water immersion (CWI) or passive recovery (PAS). In a crossover design, 11 cyclists completed two separate 3-day training blocks (120 min cycling per day, 66 maximal sprints, 9 min time trialling [TT]), followed by 2 days of recovery-based training. The cyclists recovered from each training session by standing in cold water (10 °C) or at room temperature (27 °C) for 5 min. Mean power for sprints, total TT work and HR were assessed during each session. Resting vagal-HRV (natural logarithm of square-root of mean squared differences of successive R-R intervals; ln rMSSD) was assessed after exercise, after the recovery intervention, during sleep and upon waking. CWI allowed better maintenance of mean sprint power (between-trial difference [90 % confidence limits] +12.4 % [5.9; 18.9]), cadence (+2.0 % [0.6; 3.5]), and mean HR during exercise (+1.6 % [0.0; 3.2]) compared with PAS. ln rMSSD immediately following CWI was higher (+144 % [92; 211]) compared with PAS. There was no difference between the trials in TT performance (-0.2 % [-3.5; 3.0]) or waking ln rMSSD (-1.2 % [-5.9; 3.4]). CWI helps to maintain sprint performance during consecutive days of training, whereas its effects on vagal-HRV vary over time and depend on prior exercise intensity.

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Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity.

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Introduction and Methods: This study compared changes in myokine and myogenic genes following resistance exercise (3 sets of 12 repetitions of maximal unilateral knee extension) in 20 elderly men (67.8 ± 1.0 years) and 15 elderly women (67.2 ± 1.5 years). Results: Monocyte chemotactic protein (MCP)-1, macrophage inhibitory protein (MIP)-1β, interleukin (IL)-6 and MyoD mRNA increased significantly (P < 0.05), whereas myogenin and myostatin mRNA decreased significantly after exercise in both groups. Macrophage-1 (Mac-1) and MCP-3 mRNA did not change significantly after exercise in either group. MIP-1β, Mac-1 and myostatin mRNA were significantly higher before and after exercise in men compared with women. In contrast, MCP-3 and myogenin mRNA were significantly higher before and after exercise in the women compared with the men. Conclusions: In elderly individuals, gender influences the mRNA expression of certain myokines and growth factors, both at rest and after resistance exercise. These differences may influence muscle regeneration following muscle injury

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Objectives In non-alcoholic fatty liver disease (NAFLD), hepatic steatosis is intricately linked with a number of metabolic alterations. We studied substrate utilisation in NAFLD during basal, insulin-stimulated and exercise conditions, and correlated these outcomes with disease severity. Methods 20 patients with NAFLD (mean±SD body mass index (BMI) 34.1±6.7 kg/m2) and 15 healthy controls (BMI 23.4±2.7 kg/m2) were assessed. Respiratory quotient (RQ), whole-body fat (Fatox) and carbohydrate (CHOox) oxidation rates were determined by indirect calorimetry in three conditions: basal (resting and fasted), insulin-stimulated (hyperinsulinaemic–euglycaemic clamp) and exercise (cycling at an intensity to elicit maximal Fatox). Severity of disease and steatosis were determined by liver histology, hepatic Fatox from plasma β-hydroxybutyrate concentrations, aerobic fitness expressed as , and visceral adipose tissue (VAT) measured by computed tomography. Results Within the overweight/obese NAFLD cohort, basal RQ correlated positively with steatosis (r=0.57, p=0.01) and was higher (indicating smaller contribution of Fatox to energy expenditure) in patients with NAFLD activity score (NAS) ≥5 vs <5 (p=0.008). Both results were independent of VAT, % body fat and BMI. Compared with the lean control group, patients with NAFLD had lower basal whole-body Fatox (1.2±0.3 vs 1.5±0.4 mg/kgFFM/min, p=0.024) and lower basal hepatic Fatox (ie, β-hydroxybutyrate, p=0.004). During exercise, they achieved lower maximal Fatox (2.5±1.4 vs. 5.8±3.7 mg/kgFFM/min, p=0.002) and lower (p<0.001) than controls. Fatox during exercise was not associated with disease severity (p=0.79). Conclusions Overweight/obese patients with NAFLD had reduced hepatic Fatox and reduced whole-body Fatox under basal and exercise conditions. There was an inverse relationship between ability to oxidise fat in basal conditions and histological features of NAFLD including severity of steatosis and NAS

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We investigated the effect of carbohydrate ingestion after maximal lengthening contractions of the knee extensors on circulating concentrations of myocellular proteins and cytokines, and cytokine mRNA expression in muscle. Using a cross-over design, 10 healthy males completed 5 sets of 10 lengthening (eccentric) contractions (unilateral leg press) at 120% 1 repetition-maximum. Subjects were randomized to consume a carbohydrate drink (15% weight per volume; 3 g/kg BM) for 3 h after exercise using one leg, or a placebo drink after exercise using the contralateral leg on another day. Blood samples (10 mL) were collected before exercise and after 0, 30, 60, 90, 120, 150, and 180 min of recovery. Muscle biopsies (vastus lateralis) were collected before exercise and after 3 h of recovery. Following carbohydrate ingestion, serum concentrations of glucose (30-90 min and at 150 min) and insulin (30-180 min) increased (P < 0.05) above pre-exercise values. Serum myoglobin concentration increased (similar to 250%; P < 0.05) after both trials. In contrast, serum cytokine concentrations were unchanged throughout recovery in both trials. Muscle mRNA expression for IL-8 (6.4-fold), MCP-1 (4.7-fold), and IL-6 (7.3-fold) increased substantially after carbohydrate ingestion. TNF-alpha mRNA expression did not change after either trial. Carbohydrate ingestion during early recovery from exercise-induced muscle injury may promote proinflammatory reactions within skeletal muscle.

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The aim of this study was to determine if athletes with a history of hamstring strain injury display lower levels of surface EMG (sEMG) activity and median power frequency in the previously injured hamstring muscle during maximal voluntary contractions. Recreational athletes were recruited, 13 with a history of unilateral hamstring strain injury and 15 without prior injury. All athletes undertook isokinetic dynamometry testing of the knee flexors and sEMG assessment of the biceps femoris long head (BF) and medial hamstrings (MH) during concentric and eccentric contractions at ± 180 and ± 600.s-1. The knee flexors on the previously injured limb were weaker at all contraction speeds compared to the uninjured limb (+1800.s-1 p = 0.0036; +600.s-1 p = 0.0013; -600.s-1 p = 0.0007; -1800.s-1 p = 0.0007) whilst sEMG activity was only lower in the BF during eccentric contractions (-600.s-1 p = 0.0025; -1800.s-1 p = 0.0003). There were no between limb differences in MH sEMG activity or median power frequency from either BF or MH in the injured group. The uninjured group showed no between limb differences in any of the tested variables. Secondary analysis comparing the between limb difference in the injured and the uninjured groups, confirmed that previously injured hamstrings were mostly weaker (+1800.s-1 p = 0.2208; +600.s-1 p = 0.0379; -600.s-1 p = 0.0312; -1800.s-1 p = 0.0110) and that deficits in sEMG were confined to the BF during eccentric contractions (-600.s-1 p = 0.0542; -1800.s-1 p = 0.0473) Previously injured hamstrings were weaker and BF sEMG activity was lower than the contralateral uninjured hamstring. This has implications for hamstring strain injury prevention and rehabilitation which should consider altered neural function following hamstring strain injury.

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Background: Hamstring strain injuries are prevalent in sport and re-injury rates have been high for many years. Whilst much focus has centred on the impact of previous hamstring strain injury on maximal eccentric strength, high rates of torque development is also of interest, given the important role of the hamstrings during the terminal swing phase of running. The impact of prior strain injury on myoelectrical activity of the hamstrings during tasks requiring high rates of torque development has received little attention. Purpose: To determine if recreational athletes with a history of unilateral hamstring strain injury, who have returned to training and competition, will exhibit lower levels of myoelectrical activity during eccentric contraction, rate of torque development and impulse 30, 50 and 100ms after the onset of myoelectrical activity or torque development in the previously injured limb compared to the uninjured limb. Study design: Case-control study Methods: Twenty-six recreational athletes were recruited. Of these, 13 athletes had a history of unilateral hamstring strain injury (all confined to biceps femoris long head) and 13 had no history of hamstring strain injury. Following familiarisation, all athletes undertook isokinetic dynamometry testing and surface electromyography assessment of the biceps femoris long head and medial hamstrings during eccentric contractions at -60 and -1800.s-1. Results: In the injured limb of the injured group, compared to the contralateral uninjured limb rate of torque development and impulse was lower during -600.s-1 eccentric contractions at 50 (RTD, injured limb = 312.27 ± 191.78Nm.s-1 vs. uninjured limb = 518.54 ± 172.81Nm.s-1, p=0.008; IMP, injured limb = 0.73 ± 0.30 Nm.s vs. uninjured limb = 0.97 ± 0.23 Nm.s, p=0.005) and 100ms (RTD, injured limb = 280.03 ± 131.42Nm.s-1 vs. uninjured limb = 460.54.54 ± 152.94Nm.s-1,p=0.001; IMP, injured limb = 2.15 ± 0.89 Nm.s vs. uninjured limb = 3.07 ± 0.63 Nm.s, p<0.001) after the onset of contraction. Biceps femoris long head muscle activation was lower at 100ms at both contraction speeds (-600.s-1, normalised iEMG activity (x1000), injured limb = 26.25 ± 10.11 vs. uninjured limb 33.57 ± 8.29, p=0.009; -1800.s-1, normalised iEMG activity (x1000), injured limb = 31.16 ± 10.01 vs. uninjured limb 39.64 ± 8.36, p=0.009). Medial hamstring activation did not differ between limbs in the injured group. Comparisons in the uninjured group showed no significant between limbs difference for any variables. Conclusion: Previously injured hamstrings displayed lower rate of torque development and impulse during slow maximal eccentric contraction compared to the contralateral uninjured limb. Lower myoelectrical activity was confined to the biceps femoris long head. Regardless of whether these deficits are the cause of or the result of injury, these findings could have important implications for hamstring strain injury and re-injury. Particularly, given the importance of high levels of muscle activity to bring about specific muscular adaptations, lower levels of myoelectrical activity may limit the adaptive response to rehabilitation interventions and suggest greater attention be given to neural function of the knee flexors following hamstring strain injury.

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INTRODUCTION: Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is often greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. AIM: To determine if this preferential eccentric decline in strength is caused by declines in voluntary hamstring muscle activation. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±1800.s-1 and ±600.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused greater eccentric (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) than concentric knee flexor weakness (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, voluntary activation levels of the lateral hamstrings showed a significant decline (0.08%; 95% CI = 0.045 to 0.120; P<0.0001). In comparison, medial hamstring activation showed no change following intermittent running. CONCLUSION: Eccentric hamstring strength is decreased significantly following intermittent overground running. Voluntary activation deficits in the biceps femoris muscle are responsible for some portion of this weakness. The implications of this finding are significant because the biceps femoris muscle is the most frequently strained of all the hamstring muscles and because fatigue appears to play an important part in injury occurrence.

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Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Intermittent running has been shown to result in preferential reductions in eccentric hamstring strength, which increase the risk of sustaining a HSI. The eccentric specific nature of this decline in hamstring function implicates central mechanisms, as peripheral fatigue mechanisms tend to impact upon both concentric and eccentric contractions modes. However, neural function of the hamstrings, such as the median power frequency (MPF) of the surface electromyography signal has yet to be examined in the fatigued hamstring following intermittent sprint running. AIM: To determine the impact of fatigue induced by intermittent sprinting on the MPF of the medial and lateral hamstring muscles. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±180.s-1 and ±60.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused a significant reduction in eccentric knee flexor strength (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) but not concentric strength (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, MPF of the lateral hamstrings showed a significant decline eccentrically (0.86; 95% CI = 0.59 to 1.54; P=0.038) and concentrically (0.76; 95%CI = 0.66 to 0.83; P=0.039). Similar declines in MPF were also noted in the medial hamstrings eccentrically (1.54; 95% CI = 0.59 to 7.9; P=0.005) and concentrically (1.18; 95% CI = 0.44 to 6.8; P=0.040). CONCLUSION: Whilst sprint running induced fatigue led to a eccentric specific reduction in knee flexor torque, MPF was suppressed across both contraction modes. This would indicate that factors associated with the decline in MPF do not appear to explain the contraction mode-specific loss of strength after intermittent sprints. This would implicate other central mechanisms, such as declines in voluntary activation, in explaining the eccentric specific decline in strength seen following sprint running.

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Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is often greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. PURPOSE: To determine if this preferential eccentric decline in strength is caused by declines in voluntary hamstring muscle activation. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±1800.s-1 and ±600.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused greater eccentric (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) than concentric knee flexor weakness (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, voluntary activation levels of the lateral hamstrings showed a significant decline (0.08%; 95% CI = 0.045 to 0.120; P<0.0001). In comparison, medial hamstring activation showed an increased level of activation following intermittent running (0.12%; 95% CI = 0.049 to 0.030; P = 0.0102). CONCLUSION: Eccentric hamstring strength is decreased significantly following intermittent overground running. Voluntary activation deficits in the biceps femoris muscle are responsible for some portion of this weakness. The implications of this finding are significant because the biceps femoris muscle is the most frequently strained of all the hamstring muscles and because fatigue appears to play an important part in injury occurrence.

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Introduction: Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is sometimes greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. The purpose of this research was to determine whether declines in knee flexor strength following overground repeat sprints are caused by declines in voluntary activation of the hamstring muscles. Methods: Seventeen recreationally active males completed 3 sets of 6 by 20m overground sprints. Maximal isokinetic concentric and eccentric knee flexor and concentric knee extensor strength was determined at ±1800.s-1 and ±600.s-1 while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. Results: Overground repeat sprint running resulted in a significant decline in eccentric knee flexor strength (31.1 Nm; 95% CI = 21.8 to 40.3 Nm; p < 0.001). However, concentric knee flexor strength was not significantly altered (11.1 Nm; 95% CI= -2.8 to 24.9; p=0.2294). Biceps femoris voluntary activation levels displayed a significant decline eccentrically (0.067; 95% CI=0.002 to 0.063; p=0.0325). However, there was no significant decline concentrically (0.025; 95% CI=-0.018 to 0.043; p=0.4243) following sprinting. Furthermore, declines in average peak torque at -1800.s-1 could be explained by changes in hamstring activation (R2 = 0.70). Moreover, it was change in the lateral hamstring muscle activity that was related to the decrease in knee flexor torque (p = 0.0144). In comparison, medial hamstring voluntary activation showed no change for either eccentric (0.06; 95% CI = -0.033 to 0.102; p=0.298) or concentric (0.09; 95% CI = -0.03 to 0.16; p=0.298) muscle actions following repeat sprinting. Discussion: Eccentric hamstring strength is decreased significantly following overground repeat sprinting. Voluntary activation deficits in the biceps femoris muscle explain a large portion of this weakness. The implications of these findings are significant as the biceps femoris muscle is the most frequently strained of the knee flexors and fatigue is implicated in the aetiology of this injury.

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Background: Hamstring strain injuries (HSIs) are prevalent in sport and re-injury rates have been high for many years. Whilst much focus has centred on the impact of previous hamstring strain injury on maximal eccentric strength, high rates of torque development is also of interest, given the important role of the hamstrings during the terminal swing phase of gait. The impact of prior strain injury on neuromuscular function of the hamstrings during tasks requiring high rates of torque development has received little attention. The purpose of this study is to determine if recreational athletes with a history of unilateral hamstring strain injury, who have returned to training and competition, will exhibit lower levels of eccentric muscle activation, rate of torque development and impulse 30, 50 and 100ms after the onset of electromyographical or torque development in the previously injured limb compared to the uninjured limb. Methods: Twenty-six recreational athletes were recruited. Of these, 13 athletes had a history of unilateral hamstring strain injury (all confined to biceps femoris long head) and 13 had no history of hamstring strain injury. Following familiarisation, all athletes undertook isokinetic dynamometry testing and surface electromyography assessment of the biceps femoris long head and medial hamstrings during eccentric contractions at -60 and -1800.s-1. Results: In the injured limb of the injured group, compared to the contralateral uninjured limb rate of torque development and impulse was lower during -600.s-1 eccentric contractions at 50 (RTD, p=0.008; IMP, p=0.005) and 100ms (RTD, p=0.001; IMP p<0.001) after the onset of contraction. There was also a non-significant trend for rate of torque development during -1800.s-1 to be lower 100ms after onset of contraction (p=0.064). Biceps femoris long head muscle activation was lower at 100ms at both contraction speeds (-600.s-1, p=0.009; -1800.s-1, p=0.009). Medial hamstring activation did not differ between limbs in the injured group. Comparisons in the uninjured group showed no significant between limbs difference for any variables. Conclusion: Previously injured hamstrings displayed lower rate of torque development and impulse during eccentric contraction. Lower muscle activation was confined to the biceps femoris long head. Regardless of whether these deficits are the cause of or the result of injury, these findings have important implications for hamstring strain injury and re-injury and suggest greater attention be given to neural function of the knee flexors.

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Purpose: To assess the effects of pre-cooling volume on neuromuscular function and performance in free-paced intermittent-sprint exercise in the heat. Methods: Ten male, teamsport athletes completed four randomized trials involving an 85-min free-paced intermittentsprint exercise protocol in 33°C±33% relative humidity. Pre-cooling sessions included whole body (WB), head+hand (HH), head (H) and no cooling (CONT), applied for 20-min pre-exercise and 5-min mid exercise. Maximal voluntary contractions (MVC) were assessed pre- and postintervention and mid- and post-exercise. Exercise performance was assessed with sprint times, % decline and distances covered during free-paced bouts. Measures of core(Tc) and skin (Tsk) temperatures, heart rate, perceptual exertion and thermal stress were monitored throughout. Venous and capillary blood was analyzed for metabolite, muscle damage and inflammatory markers. Results: WB pre-cooling facilitated the maintenance of sprint times during the exercise protocol with reduced % decline (P=0.04). Mean and total hard running distances increased with pre cooling 12% compared to CONT (P<0.05), specifically, WB was 6-7% greater than HH (P=0.02) and H (P=0.001) respectively. No change was evident in mean voluntary or evoked force pre- to post-exercise with WB and HH cooling (P>0.05). WB and HH cooling reduced Tc by 0.1-0.3°C compared to other conditions (P<0.05). WB Tsk was suppressed for the entire session(P=0.001). HR responses following WB cooling were reduced(P=0.05; d=1.07) compared to CONT conditions during exercise. Conclusion: A relationship between pre-cooling volume and exercise performance seems apparent, as larger surface area coverage augmented subsequent free-paced exercise capacity, in conjunction with greater suppression of physiological load. Maintenance of MVC with pre-cooling, despite increased work output suggests the role of centrally-mediated mechanisms in exercise pacing regulation and subsequent performance.