Search

In this study, we investigated changes in creatine kinase, perceptual and neuromuscular fatigue of professional rugby league players after match-play. Twenty-three male rugby league players (10 backs, 13 forwards) had their creatine kinase, perceptual ratings of fatigue, attitude to training, muscle soreness, and flight time in a countermovement jump measured before and 1 and 2 days after (day 1 and day 2 respectively) league matches. Total playing time, offensive and defensive contacts were also recorded for each player. Creatine kinase was higher both 1 and 2 days after than before matches (P < 0.05) in forwards and backs. Similarly, perceived fatigue and muscle soreness were higher than pre-match on both days 1 and 2 (P < 0.05), but did not differ between groups (P > 0.05). Jump performance was lower on day 1 but not day 2 for both groups (P < 0.05). While total playing time was longer in backs (P < 0.05), relative frequencies for all contacts were greater in forwards (P < 0.05). Contacts for forwards were correlated with all markers of fatigue (P < 0.05), but only flight time was correlated with offensive contacts in backs (P < 0.05). Despite the mechanisms of fatigue being different between forwards and backs, our results highlight the multidimensional nature of fatigue after a rugby league match and that these markers do not differ between positions.

There has been no previous investigation of the concurrent validity and reliability of the current 5 Hz global positioning system (GPS) to assess sprinting speed or the reliability of integrated GPS-accelerometer technology. In the present study, we wished to determine: (1) the concurrent validity and reliability of a GPS and timing gates to measure sprinting speed or distance, and (2) the reliability of proper accelerations recorded via GPS-accelerometer integration. Nineteen elite youth rugby league players performed two over-ground sprints and were simultaneously assessed using GPS and timing gates. The GPS measurements systematically underestimated both distance and timing gate speed. The GPS measurements were reliable for all variables of distance and speed (coefficient of variation [CV] = 1.62% to 2.3%), particularly peak speed (95% limits of agreement [LOA] = 0.00 ± 0.8 km · h(-1); CV = 0.78%). Timing gates were more reliable (CV = 1% to 1.54%) than equivalent GPS measurements. Accelerometer measurements were least reliable (CV = 4.69% to 5.16%), particularly for the frequency of proper accelerations (95% LOA = 1.00 ± 5.43; CV = 14.12%). Timing gates and GPS were found to reliably assess speed and distance, although the validity of the GPS remains questionable. The error found in accelerometer measurements indicates the limits of this device for detecting changes in performance.

The aim of this study was to quantify the changes in locomotive rates across the duration of senior elite rugby league matches. A semi-automated image recognition system (ProZone 3, ProZone®, Leeds, England) was used to track the movements of 59 players from six teams during three competitive matches. The players were classified into one of four positional groups: props (n = 9), back row (n = 9), pivots (n = 14) or outside backs (n = 27). Players' movements were classified as low, high or very high intensity running and reported as locomotive rates (distance covered per minute played) for successive quarters of each match. Analysis of variance revealed that only the outside backs showed a significantly lower overall locomotive rate during the final quarter compared to the first (P < 0.05). However, locomotive rates for high and very high intensity running during the final quarter were significantly lower (P < 0.05) than the first quarter among outside backs, pivots and props despite no change in the rate of involvements in contact. On the basis of these findings, it is suggested that high and very high intensity running locomotive rates may be more affective methods of detecting fatigue during competitive matches than overall locomotive rate.

Previous research has advocated that plyometric training improves endurance performance. However, a consequence of such a training is the immediate and prolonged appearance of exercise-induced muscle damage (EIMD). This study examined whether a single bout of plyometric exercise, designed to elicit muscle damage, affected cycling endurance performance. Seventeen participants were randomly assigned to either a muscle damage (n = 7 men, 1 woman) or nonmuscle damage (n = 8 men, 1 woman) group. Before and at 48 hours, participants were measured for perceived muscle soreness, peak isokinetic strength, and physiological, metabolic, and perceptual responses during 5-minute submaximal cycling at ventilatory threshold (VT) and a 15-minute time trial. Perceived muscle soreness and isokinetic strength (p < 0.05) were significantly altered in the muscle damage group after EIMD. No changes in heart rate or blood lactate were evident during submaximal exercise (p > 0.05). However, VO2, V(E), and rating of perceived exertion (RPE) values were increased at VT in the muscle damage group at 48 hours after EIMD (p < 0.05). During the time trial, mean power output, distance covered, and VO2 were lower in the muscle damage group at 48 hours after EIMD (p < 0.05). However, there was no change in RPE (p > 0.05), suggesting effort perception was unchanged during time-trial performance after EIMD. In conclusion, individuals using concurrent plyometric and endurance training programs to improve endurance performance should be aware of the acute impact of muscle-damaging exercise on subsequent cycling performance.

Twelve elite players from an English Super League club consented to participate in the present study using portable global positioning system (GPS) devices to assess position-specific demands. Distances covered at low-intensity running, moderate-intensity running, high-intensity running, very high-intensity running, and total distance were significantly (P < 0.05) lower in forwards compared with outside backs and adjustables. Metres per minute was higher in adjustables and forwards, owing to higher values for relative distance in medium-intensity running and a rise in high-intensity running from previous absolute values. Sprint distance, sprint frequency, and peak speed were higher in outside backs than both adjustables and forwards. A moderate, significant correlation (r = 0.62, P = 0.001) was apparent between session ratings of perceived exertion and summated heart rate. Results support the requirement for position-specific conditioning and provide preliminary evidence for the use of session ratings of perceived exertion as a measure of match load.

This study investigated the influences of player number and playing area size on the heart rate (HR) responses elicited by junior male rugby league players during small-sided games (SSGs). Twenty-two players from a professional club (n = 22, mean age: 14.5 +/- 1.5 years; stature: 172.5 +/- 11.4 cm; body mass: 67.8 +/- 15.1 kg; Vo2peak: 53.3 +/- 5.6 mL.kg.min; HRmax: 198 +/- 7.8 beats.min) participated in 2 repeated trials of six 4-minute conditioned SSGs over a 2-week period. The SSGs varied by playing area size-15 x 25 m, 20 x 30 m, and 25 x 35 m-and player number-4v4 and 6v6. HRs were recorded continuously in each game and expressed as overall and age-related (15-16 and 12-13 years) means and percent of maximum (%HRmax). Analysis revealed nonsignificant (p > 0.05) effects of trials and playing area size on HRs but a significant effect of player number in the 15-16 age group only (p < 0.001), with HRs being higher in the 4v4 (90.6% HRmax) than the 6v6 SSGs (86.2% HRmax). The HR responses were found to be repeatable in all SSG conditions (within +/- 1.9% HRmax), apart from the small 6v6 condition in the older players. The findings demonstrate that these SSGs generate physiological responses suitable for aerobic conditioning that, although unaffected by the size of the area used, are sensitive to the player number. Accordingly, among such players it is advisable that coaches use 4v4 SSGs to achieve an appropriate and consistent aerobic conditioning stimulus.

This study evaluated the effects of exercise-induced muscle damage (EIMD) on fixed-load cycling and 5-min time-trial performance. Seven recreational athletes performed two submaximal fixed-load exercise bouts followed by a 5-min time-trial before, 48 and 168 h following 100 counter-movement jumps. Measurements of V(O)(2) heart rate, RER and blood lactate concentration remained unchanged during the fixed-load bouts following jumping exercise. However, VE and VE/VO2 increased (P < 0.05) at 48 h. RPE values were higher at 48 h as were the ratio of RPE:HR and RPE:VO2 (P < 0.05). In the time-trial, mean VO2 peak power output, mean power output, distance covered and post exercise blood lactate were lower at 48 h (P < 0.05). RPE remained unchanged between trials. These findings indicate that the ventilatory equivalent for oxygen and perceived exertion at submaximal work rates are increased 48 h following eccentric exercise. Furthermore, EIMD increases perceived exertion and impairs performance during a 5-min all-out effort.

Unaccustomed eccentric exercise has a profound impact on muscle structure and function. However, it is not known whether associated microvascular dysfunction disrupts the matching of O2 delivery (Qo2) to O2 utilization (Vo2). Near-infrared spectroscopy (NIRS) was used to test the hypothesis that eccentric exercise-induced muscle damage would elevate the muscle Qo2:Vo2 ratio during severe-intensity exercise while preserving the speed of the Vo2 kinetics at exercise onset. Nine physically active men completed "step" tests to severe-intensity exercise from an unloaded baseline on a cycle ergometer before (Pre) and 48 h after (Post) eccentric exercise (100 squats with a load corresponding to 70% of body mass). NIRS and breath-by-breath pulmonary Vo2 were measured continuously during the exercise tests and subsequently modeled using standard nonlinear regression techniques. There were no changes in phase II pulmonary Vo2 kinetics following the onset of exercise (time constant: Pre, 25 +/- 4 s; Post, 24 +/- 2 s; amplitude: Pre, 2.36 +/- 0.23 l/min; Post, 2.37 +/- 0.23 l/min; all P > 0.05). However, the primary (Pre, 14 +/- 3 s; Post, 19 +/- 3 s) and overall (Pre, 16 +/- 4 s; Post, 21 +/- 4 s) mean response time of the [HHb] response was significantly slower following eccentric exercise (P < 0.05). The slower [HHb] kinetics observed following eccentric exercise is consistent with an increased Qo2:Vo2 ratio during transitions to severe-intensity exercise. We propose that unchanged primary phase Vo2 kinetics are associated with an elevated Qo2:Vo2 ratio that preserves blood-myocyte O2 flux.

The purpose of this study was to determine the effects of plyometric exercise on unilateral balance performance. Nine healthy adults performed baseline measurements on the dominant limb that consisted of: a 20-s unilateral stability test on a tilt balance board, where a higher stability index represented deterioration in balance performance; isokinetic plantar flexion torque at 0.52 and 3.14 rad s(-1); muscle soreness in the calf region; and resting plantar flexion angle. Plyometric exercise consisted of 200 counter-movement jumps designed to elicit symptoms of muscle damage, after which baseline measurements were repeated at 30 min, 24, 48, and 72 h. Perceived muscle soreness of the calf region increased significantly following the plyometric exercise protocol (F(4,32) = 17.24, P < 0.01). Peak torque was significantly reduced after the plyometric exercise protocol (F(4,32) = 7.49, P < 0.05), with greater loss of force at the lower angular velocity (F(4,32) = 3.46, P < 0.05), while resting plantar flexion angle was not significantly altered compared with baseline values (P > 0.05). The stability index was significantly increased (F(4,32) = 3.10, P < 0.05) above baseline (mean 2.3, s = 0.3) at 24 h (3.3, s = 0.4), after which values recovered. These results indicate that there is a latent impairment of balance performance following a bout of plyometric exercise, which has implications for both the use of skill-based activities and for increased injury risk following high-intensity plyometric training.

Intraoperative gamma probe guidance has become widely utilized for sentinel lymph node dissection in patients with breast cancer and melanoma, using (99m)Tc sulfur colloid. However, new indications are possible and need to continue to be investigated. We report the use during a wedge liver biopsy of a new hand-held gamma probe designed for (123)I intraoperative guidance. The patient studied is a 5-year-old boy with history of stage 4 high-risk neuroblastoma. Anatomic imaging (CT, MRI), (99m)Tc bone scintigraphy and 2-deoxy-2-[F-18]fluoro-d-glucose-positron emission tomography/computed tomography (FDG-PET/CT) were negative, but the (123)I MIBG scintigraphy suggested recurrent liver disease. A decision was made to biopsy these lesions to obtain histopathological confirmation. Intraoperative gamma probe mapping of the liver identified areas with signal above the background, but these were prove to be hemosiderin deposits on histo-pathology examination.

Purpose: Evaluate the clinical safety, toxicity, immune activation/modulation, and maximal tolerated dose of hu14.18-IL2 (EMD 273063) in pediatric patients with recurrent/refractory neuroblastoma and other GD2-positive solid tumors., Experimental Design: Twenty-seven pediatric patients with recurrent/refractory neuroblastoma and one with melanoma were treated with a humanized anti-GD2 monoclonal antibody linked to human interleukin 2 (IL-2). Cohorts of patients received hu14.18-IL2, administered i.v. over 4 hours for three consecutive days, at varying doses. Patients with stable disease, partial, or complete responses were eligible to receive up to three additional courses of therapy., Results: Most of the clinical toxicities were anticipated and similar to those reported with IL-2 and anti-GD2 monoclonal antibody therapy and to those noted in the initial phase I study of hu14.18-IL2 in adults with metastatic melanoma. The maximal tolerated dose was determined to be 12 mg/m2/d, with agent-related dose-limiting toxicities of hypotension, allergic reaction, blurred vision, neutropenia, thrombocytopenia, and leukopenia. Three patients developed dose-limiting toxicity during course 1; seven patients in courses 2 to 4. Two patients required dopamine for hypotension. There were no treatment-related deaths, and all toxicity was reversible. Treatment with hu14.18-IL2 led to immune activation/modulation as evidenced by elevated serum levels of soluble IL-2 receptor alpha (sIL2Ralpha) and lymphocytosis. The median half-life of hu14.18-IL2 was 3.1 hours. There were no measurable complete or partial responses to hu14.18-IL2 in this study; however, three patients did show evidence of antitumor activity., Conclusion: Hu14.18-IL2 (EMD 273063) can be administered safely with reversible toxicities in pediatric patients at doses that induce immune activation. A phase II clinical trial of hu14.18-IL2, administered at a dose of 12 mg/m2/d x 3 days repeated every 28 days, will be done in pediatric patients with recurrent/refractory neuroblastoma.

Recent evidence suggests that the cut-off for age utilized in neuroblastoma risk groups should be increased from the 365-day cut-off currently in use. Separate cooperative group analyses were performed by German and Italian groups and two analyses by the Children's Oncology Group (North America, Australia, New Zealand, Switzerland, Netherlands). In general, the results are in agreement regarding the prognostic contribution of age. There is strong evidence to support an increase in the age cut-off to a value in the range of 15-18 months based on the results from the German analysis and two COG analyses. However, Italian results in INSS stage 4 patients show that outcome in patients 12-17 months is not better than that of older patients. Further analyses are warrented.

Exercise-induced muscle damage (EIMD) is a common occurrence following activities with a high eccentric component. Alterations to the torque-velocity relationship following EIMD would appear to have serious implications for athletic performance, particularly as they relate to impairment of maximal intensity exercise. However, this has been studied infrequently. The purpose of this study was to assess the effects of EIMD on maximal intermittent sprint performance. Ten male participants (age 22.4 +/- 3.2 years, height 178.6 +/- 5.2 cm, mass 80.6 +/- 10.7 kg) performed 10 x 6 s cycle ergometer sprints, interspersed with 24 s recovery against a load corresponding to 0.10 kp/kg and 10 x 10 m sprints from a standing start, each with 12 s active (walking) recovery. All variables were measured immediately before and at 30 min, 24, 48 and 72 h following a plyometric exercise protocol comprising of 10 x 10 maximal counter movement jumps. Repeated measures ANOVA showed significant changes over time (all P<0.05) for perceived soreness, plasma creatine kinase activity (CK), peak power output (PPO), sprint time and rate of fatigue. Soreness was significantly higher (P<0.01) than baseline values at all time intervals (3.1, 4.9, 5.5 and 3.2 at 30 min, 24, 48 and 72 h, respectively). CK was significantly elevated (P<0.05) at 24 h (239 IU/l) and 48 h (245 IU/l) compared to baseline (151 IU/l). PPO was significantly lower (P<0.05) than baseline (1,054 W) at all time intervals (888, 946, 852 and 895 W, at 30 min, 24, 48 and 72 h, respectively). The rate of fatigue over the ten cycling sprints was reduced compared to baseline, with the greatest reduction of 48% occurring at 48 h (P<0.01). This was largely attributed to the lower PPO in the initial repetitions, resulting in a lower starting point for the rate of fatigue. Values returned to normal at 72 h. Sprint times over 10 m were higher (P<0.05) at 30 min, 24 h and 48 h compared to baseline (1.96 s) with values corresponding to 2.01, 2.02 and 2.01 at 30 min, 24 h and 48 h, respectively. Values returned to baseline by 72 h. The results provide further evidence that, following a plyometric, muscle-damaging exercise protocol, the ability of the muscle to generate power is reduced for at least 3 days. This is also manifested by a small, but statistically significant reduction in very short-term (approximately 2 s) intermittent sprint running performance. These findings have implications for appropriate training strategies in multiple sprint sports.

Exercise-induced muscle damage is a well documented phenomenon particularly resulting from eccentric exercise. When eccentric exercise is unaccustomed or is performed with an increased intensity or duration, the symptoms associated with muscle damage are a common outcome and are particularly associated with participation in athletic activity. Muscle damage results in an immediate and prolonged reduction in muscle function, most notably a reduction in force-generating capacity, which has been quantified in human studies through isometric and dynamic isokinetic testing modalities. Investigations of the torque-angular velocity relationship have failed to reveal a consistent pattern of change, with inconsistent reports of functional change being dependent on the muscle action and/or angular velocity of movement. The consequences of damage on dynamic, multi-joint, sport-specific movements would appear more pertinent with regard to athletic performance, but this aspect of muscle function has been studied less often. Reductions in the ability to generate power output during single-joint movements as well as during cycling and vertical jump movements have been documented. In addition, muscle damage has been observed to increase the physiological demand of endurance exercise and to increase thermal strain during exercise in the heat. The aims of this review are to summarise the functional decrements associated with exercise-induced muscle damage, relate these decrements to theoretical views regarding underlying mechanisms (i.e. sarcomere disruption, impaired excitation-contraction coupling, preferential fibre type damage, and impaired muscle metabolism), and finally to discuss the potential impact of muscle damage on athletic performance.

Few techniques can identify interactions between proteins and individual water molecules when the protein is in solution. The present work has sought to bridge the gap between the molecular level studies and the search for a physical property of the solution (bathing the proteins) that would regulate the protein hydration level. The properties of the solution were varied by adding nondenaturing solutes and solvents to the protein solutions and then studying their effect on the intrinsic fluorescence of apomyoglobin. The resolution of the tryptophan emission into the two component spectra corresponding to tryptophans W7 (accessible to the solvent) and W14 (buried in the protein matrix) has allowed us to probe two specific parts of the protein. Whereas W14 is not affected when the medium is altered, the analysis of W7 fluorescence has shown that cosolvent diffusion plays a dominant role in the mobility of water molecules near the protein surface.

The composite fluorescence emission from the two tryptophans (W7 and W14) of horse heart apomyoglobin was explored by fluorescence quenching experiments. The fluorescence of the W7 residue is the only one involved in the quenching by iodide or trichloroethanol (TCE) titration. The fluorescence contribution of W7 is 49% of the total apomyoglobin emission, and its spectrum is red-shifted compared to the W14 emission. The fluorescence decay of Trp residues gives an average fluorescence lifetime of 2.06 ns for W14 and 2.84 ns for W7. The static fluorescence quenching by TCE was used to monitor the individual motions of the two tryptophans in apomyoglobin. The short correlation time of W7 (rho = 3 ns) explains why this residue can experience various environments without having to assume the existence of several protein conformations occurring during its lifetime emission.

Untreated patients with Hurler syndrome (MPSIH) experience progressive neurologic deterioration and early death. Allogeneic bone marrow transplantation (BMT) ameliorates or halts this course. The Storage Disease Collaborative Study Group was formed to evaluate the effectiveness and toxicity of BMT. Effectiveness was defined as engrafted survival with continuing cognitive development. Fifty-four patients deficient in leukocyte alpha-L-iduronidase enzyme activity (median age, 1.8 years; range, 0.4 to 7.9) received high-dose chemotherapy with or without irradiation and BMT from HLA-genotypically identical sibling (GIS) or HLA-haploidentical related (HIR) donors between September 16, 1983 and July 14, 1995; all children were included in this report. Thirty-nine of 54 patients (72%) engrafted following the first BMT. The probability of grade II to IV acute graft-versus-host disease (GVHD) at 100 days was 32% for GIS and 55% for HIR patients. The probability of extensive chronic GVHD was 0% for GIS and 24% for HIR patients. The actuarial probability of survival at 5 years was 64% for all patients, 75% for GIS patients, 53% for HIR patients, and 53% for patients with donor marrow engraftment. The baseline Mental Developmental Index (MDI) was examined both for children less than and greater than 24 months of age at BMT. Children transplanted before 24 months had a mean baseline MDI of 78, while those transplanted after 24 months had a mean baseline MDI of 63 (P = . 0002). Both baseline and post-BMT neuropsychologic data were available for 26 of 30 engrafted survivors. Of 14 patients transplanted before 24 months of age, nine demonstrated developmental trajectories that were normal or somewhat slower than normal. In contrast, of 12 patients transplanted after 24 months of age, only three showed developmental trajectories that were normal or somewhat slower than normal (P = .01). For children with a baseline MDI greater than 70, there was a significant correlation between the MDI at follow-up study and leukocyte alpha-L-iduronidase enzyme activity (P = .02). Children were more likely to maintain normal cognitive development if they were fully engrafted following BMT from a donor with homozygous normal leukocyte alpha-L-iduronidase enzyme activity. Children who developed acute GVHD of grade II or worse had significantly poorer cognitive outcomes (P < .009). No difference in the post-BMT MDI was observed between patients whose preparative therapies did (n = 10; radiation dose, 300 to 1,400 cGy) or did not (n = 16) include radiation. We conclude that MPSIH patients, particularly those less than 24 months of age with a baseline MDI greater than 70, can achieve a favorable long-term outcome with continuing cognitive development and prolonged survival after successful BMT from a related donor with homozygous normal enzyme activity.

The catalytic oxidation of beta-D-glucose by the enzyme glucose oxidase involves a redox change of the flavin coenzyme. The structure and the dynamics of the two extreme glucose oxidase forms were studied by using infrared absorption spectroscopy of the amide I'band, tryptophan fluorescence quenching and hydrogen isotopic exchange. The conversion of FAD to FADH2 does not change the amount of alpha-helix present in the protein outer shell, but reorganizes a fraction of random coil to beta-sheet structure. The dynamics of the protein interior vary with the redox states of the flavin without affecting the motions of the structural elements near the protein surface. From the structure of glucose oxidase given by X-ray crystallography, these results suggest that the dynamics of the interface between the two monomers are involved in the catalytic mechanism.

A number of different biological properties have been ascribed to the hormone-like protein interleukin 2 (IL-2). However, the most salient feature of this lymphokine is its ability to sustain the long-term proliferation of T-cells from humans and mice. Reported herein are the results of studies demonstrating the isolation of growth factor-independent cell lines from the long-term IL-2-dependent murine T-cell line CTLL-2 that is used frequently as the source of target cells in IL-2 bioassays. Sustained log-phase growth of these T-cells in vitro has been achieved using Petri dishes of polymethylpentene; growth could not be sustained in similar dishes of glass, untreated polystyrene, polystyrene that had been treated for cell culture, or polycarbonate. The IL-2-independent line grew as a T-cell lymphoma when injected i.p. into pristane-treated, but not untreated, syngeneic C57BL/6 mice. In contrast, cells from the IL-2 parental line CTLL-2 did not grow in vivo. Characterization of the IL-2-independent lines propagated in vitro (denoted as line CEC) or in vivo (denoted as line CEP) demonstrated that they retained their dependency for 2-mercaptoethanol and expressed phenotypic profiles of their parental line CTLL-2 (Thy 1.2+, Lyt-1-; Lyt-2-). Isolation of an IL-2-independent T-cell lymphoma from a CTLL-2 line obtained from another investigator using a protocol that has proven reproducible under carefully controlled laboratory conditions and defined phenotypic traits of the syngeneic T-cell isolates provided evidence that the tumors were not a cross-culture contaminant arising as a result of a laboratory accident. Moreover, karyotypic analysis using a quinacrine:Hoechst banding technique revealed similar marker chromosomes in the IL-2-dependent and -independent lines. IL-2-independent lines have also been established from the IL-2-dependent murine T-cell line CT-6. Accordingly, the results of these studies suggest that, during prolonged cultivation that has included exposure to crude IL-2 preparations known to contain phorbol ester, possibly viruses, and other contaminants, the IL-2-dependent lines have developed subpopulations that are thought to have undergone malignant transformation of unknown etiology to generate IL-2-independent murine T-cell lymphomas that can be passaged repetitively either in vitro or in vivo.