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MUSCLE FIBER NECROSIS IN MARATHON RUNNERS

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... However, Brehmer (1982), studying 11 elite marathon-runners (mean marathon time 2:23 h), found a greater degree of lactate acidosis with a mean value of 5.88 mMol 9 1-1 immediately after a competitive marathon. The effects of these stresses and the failure of normal homoeostatic, corrective mechanisms may produce numerous medical problems such as hypovolaemic collapse, hyperthermia and hypoglycaemia, apart from the recognised muscle and joint complications (Hagerman et al. 1983;Jansen et al. 1984;Pedoe 1984). ...
... The mechanical destruction of erythrocytes due to prolonged running reported in some studies (Bichler et al. 1972;Gilligan et al. 1943;R6cker et al. 1976) may play an important role in blood platelet activation, due to the resulting liberation of red blood cell ADP. Recently it has been reported that both the intensive training for, and the marathon run itself, may induce muscle fibre necrosis and degeneration in exceptional cases, resulting in clinical rhabdomyolysis and myoglobinuria (Hagerman et al. 1983). Based on a study of six wetrained runners, Jansen et al. (1984) concluded that about 60 g of muscle was damaged in marathon races. ...
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To see whether strenuous prolonged exertion increases blood platelet activation and thrombin activity in healthy well-trained men, 16 male amateur runners (mean age 31,8) were studied. A marathon race (mean time 2 h 44 min 30 s) caused a significant increase in plasma beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), fibrinopetide A (FPA) and factor VIII (F VIII) activity. Sixty min after exertion beta-TG and F VIII activity were still significantly elevated. FPA continued to rise, reaching peak values 60 min after the run. 22 h after finishing the race F VIII activity was still significantly elevated. The study has demonstrated the great inter-individual variability of marathon race-induced haemostatic changes. The elevation of beta-TG varied from 42% to 156%, F VIII from 112% to 625%, and in three runners FPA reached more than 900% of its pre-exercise value. In some individuals the haemostatic changes observed could be potentially unfavourable for coronary heart disease prevention.
... However, few studies address the impact of exercise in the profile of circulating miRNAs (Aoi et al., 2013; Baggish et al., 2011; Mizuno et al., 2011; Uhlemann et al., 2014 ). Endurance exercise, such as halfmarathon training/running, can cause muscle stress and damage (Hikida et al., 1983; Warhol et al., 1985). We formulated the hypothesis that a half-marathon run changes the circulating myomiR profile. ...
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Abstract Context: Circulating miRNAs are potential biomarkers that can be important molecules driving cell-to-cell communication. Objective: To investigate circulating muscle-specific miRNAs in recreational athletes. Materials and methods: Three miRNAs from whole plasma before and after a half-marathon were analyzed by qPCR. Results: MiR-1, -133a, and -206 significantly increased after the race. Discussion: Increased levels of miRNAs after exercise point to potential biomarkers and to the possibility of being functional players following endurance training. Conclusion: These miRNAs are potential biomarkers of muscle damage or adaptation to exercise.
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In brief: Indicators of muscular injury from overtraining were studied in 12 male runners during a road race held over 20 days. Dally mileage averaged 17.3 miles per day, twice their regular training distance. Most of the runners reported persistent mild-to-moderate thigh muscle soreness or stiffness. Serum creatine kinase (CK), an enzymatic marker of muscle tissue injury, was elevated on mornings after running but returned to normal values when the runners rested for two days after day 10. Thigh circumference became significantly reduced during the race, suggesting that the unaccustomed high running mileage also produced thigh muscle atrophy.
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In brief: Healthy people as well as highly trained athletes commonly experience delayed muscle soreness after severe exercise. Although many theories have been advanced, the pathophysiological basis for delayed muscle soreness is not known. The authors studied muscle biopsy samples from ten male runners immediately before and after a marathon and at one, three, five, and seven days after the marathon. Results showed muscle degeneration after training and after the marathon, and there was a significant inflammatory response throughout the week of recovery after the marathon. Therefore, the authors suggest that anyone experiencing postexercise delayed soreness is probably suffering from some degree of acute inflammation.
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Objective. The aim of this study was to determine any difference in performance following two different tapering protocols after a period of heavy training. Design. Twelve swimmers who regularly trained at a high volume and intensity were recruited and trained together for 3 weeks. They were then randomly split into two groups (N=6 per group). One group underwent a standard taper protocol, while the second followed a modified taper in which training load was gradually resumed for 1 week following a standard taper. Performance assessment following tapering consisted of 2 swims over a distance of 200 m, with a recovery period of 5 hours between swims. After resuming normal training, subjects tapered a second time, each group following the alternate protocol. Outcome measures. Total time and split times for each length, stroke rate, distance per stroke, and stroke index in a performance swim were determined as well as heart rate (HR), profile of mood state (POMS), rating of perceived exertion (RPE) and muscle pain during each taper. Results. Mean swim times for the modified and conventional tapers were 134.7±9.1 and 134.7±9.3 seconds, respectively (mean ±SD). There was also no difference in the split times between groups, although both became slower in the final three laps. Stroke rate, distance per stroke, and stroke index were also not different between protocols. There were no differences between protocols in HR, RPE or rating of muscle pain over the duration of the tapering period. However, there was a significant reduction in HR on day 5 of both tapers and a lower POMS on days 3, 4 and 5 on the standard taper protocol. At the time of the performance swim, however, there was no difference in POMS. Conclusion. There were no performance or physiological advantages from the modified tapering protocol. South African Journal of Sports Medicine Vol. 20 (2) 2008: pp. 49-54
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The aim of this study was to determine the effectiveness of a 7-day oral supplementation with branched-chain amino acids (BCAA) to prevent muscle damage during a marathon. Forty-six experienced runners were randomly divided into two groups, one with BCAA supplementation (n = 25, supplemented with 5 g day(-1) of powdered 1:0.5:0.5 leucine:isoleucine:valine, during the 7 days prior to the competition) and the other as a control group (n = 21, supplemented with an isocaloric placebo). Before the marathon race and within 3 min of finishing, leg muscle power was measured with a maximal countermovement jump and a urine sample was obtained. During the race, running pace was measured by means of a time-chip. Myoglobin concentration was determined in the urine samples as an indirect marker of muscle damage. A visual analog scale (0-10 points) was used to assess leg muscle pain during the race. In the BCAA group, the mean running pace during the marathon was similar to the control group (3.3 ± 0.4 vs. 3.3 ± 0.5 m s(-1), respectively, 0.98). The pre- to post-race reduction in muscle power was similar in both BCAA and control groups (-23.0 ± 16.1 vs. -17.3 ± 13.8 %, P = 0.13). Post-race urine myoglobin concentration was similar in both BCAA and control groups (5.4 ± 7.5 vs. 4.5 ± 8.6 μg mL(-1), P = 0.70). Finally, there were no differences between groups in the perceived muscle pain during the race (6 ± 1 vs. 5 ± 1 points, P = 0.80). A 7-day supplementation of BCAA (5 g day(-1)) did not increase the running performance during a marathon. Furthermore, BCAA supplementation was ineffective to prevent muscle power loss, muscle damage or perceived muscle pain during a marathon race.
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This article focuses on the pathophysiological mechanisms underlying delayed onset muscle soreness (DOMS) in order to enable preventive physiotherapy. We searched the Pubmed and Kinedoc databases as well as the Elsevier Masson search motor using the key words DOMS+physiotherapy, courbature, excentric, stretching and EIMD. The inclusion criterion was compatibility with the objective of this article. There was no exclusion criterion. DOMS are remarkable because of the late onset of the soreness following excentric work leading to micro-injury to connective tissues and muscles, amplified by an associated inflammatory process. While the literature is not in favor of the usefulness of curative treatment for DOMS, preventive physiotherapy is essential, allowing patients to avoid numerous more serious injuries. The elements of the proposed preventive treatment are based on validated physiotherapy principles and clinical trials enabling evidence-based interventions. Level of evidence: not applicable
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Rhabdomyolysis has sparked new interest in recent years. The causes of rhabdomyolysis include drugs and other toxic agents, infections, physical exertion, crush injury, and muscle diseases (dystrophinopathies and metabolic myopathies). Prompt identification of the pathophysiological mechanism is the key to rapid control of the acute episode and to prevention of recurrences. In this update, we discuss the pathophysiological mechanisms and nosology of rhabdomyolysis, as well as diagnostic investigations, with special emphasis on noninvasive methods.
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The purpose of this study was to determine mitochondrial changes in fast muscles from interleukin-15 receptor alpha knockout (IL-15RαKO) mice. We tested the hypothesis that fast muscles from IL-15RαKO mice would have a greater mitochondrial density and altered internal structure compared to muscles from control mice. In fast muscles from IL-15RαKO mice, mitochondrial density was 48% greater with a corresponding increase in mitochondrial DNA content. Although there were no differences in the relative size of isolated mitochondria, internal complexity was lower in mitochondria from IL-15RαKO mice. These data support an increase in mitochondrial biogenesis and provide direct evidence for a greater density and altered internal structure of mitochondria in EDL muscles deficient in IL-15Rα.
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Muscle intolerance to exercise may result from different processes. Diagnosis involves confirming first the source of pain, then potential pathological myalgia. Delayed-onset muscle soreness (DOMS), commonly referred as tiredness, occurs frequently in sport. DOMS usually develops 12–48 h after intensive and/or unusual eccentric muscle action. Symptoms usually involve the quadriceps muscle group but may also affect the hamstring and triceps surae groups. The muscles are sensitive to palpation, contraction and passive stretch. Acidosis, muscle spasm and microlesions in both connective and muscle tissues may explain the symptoms. However, inflammation appears to be the most common explanation. Interestingly, there is strong evidence that the progression of the exercise-induced muscle injury proceeds no further in the absence of inflammation. Even though unpleasant, DOMS should not be considered as an indicator of muscle damage but, rather, a sign of the regenerative process, which is well known to contribute to the increased muscle mass. DOMS can be associated with decreased proprioception and range of motion, as well as maximal force and activation. DOMS disappears 2–10 days before complete functional recovery. This painless period is ripe for additional joint injuries.Similarly, if some treatments are well known to attenuate DOMS, none has been demonstrated to accelerate either structural or functional recovery. In terms of the role of the inflammatory process, these treatments might even delay overall recovery.
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Cytokines are a diverse family of intercellular signaling proteins that influence the movement, proliferation, differentiation, metabolism and membrane processes of target cells. Synthesis and release of cytokines from leukocytes in response to microbial stimuli are well known. This review, however, will present evidence that non-infectious stimuli can induce cytokine secretion from leukocytes and other cells (including muscle cells) following myocellular injury. The biological actions and potential adaptive values of these cytokines through the course of muscle necrosis and regeneration will be described.
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The effects of repeated biopsy sampling on muscle morphology was qualitatively and quantitatively assessed in strength-trained and untrained men and women. College-age men (13) and women (8) resistance trained twice a week for 8 weeks. A progressive resistance-training program was performed consisting of squats, leg presses, and leg extensions. Nontraining men (7) and women (5) served as controls. Muscle biopsy specimens and fasting bloods were obtained at the beginning and every 2 weeks and histochemical, biochemical, and ultrastructural methods were employed to assess the type and amount of damage. Except for a few scattered atrophic fibers in 2 of the 33 biopsy samples, all initial specimens were normal. In contrast, many of the subsequent biopsy samples from both untrained and resistance-trained men and women contained evidence of damage. Ultrastructural analysis confirmed that degenerative-regenerative processes were occurring in both groups. However, training subjects had a four-fold greater number of damaged fibers than nontraining subjects (8.53% vs 2.08%). In addition, only biopsy samples from training individuals contained fibers with internal disorganization (e.g., Z-line streaming, myofibrillar disruption). Calpain II levels in the biopsy samples and serum creatine kinase activity were not significantly affected supporting the light and electron microscopic observations that most of the damaged fibers were normal in appearance except for their small diameter. In summary, focal damage induced by the biopsy procedure is not completely repaired after 2 weeks and could affect the results, particularly cross-sectional area measurements. Moreover, resistance training appears to cause additional damage to the muscle and may delay repair of the biopsied region.
To ascertain if muscle damage occurred in swimmers as a result of high-intensity training and to find if fluid and dietary manipulation could affect muscle damage, we studied 40 members of the University of Florida swimming team using creatine kinase (CK) and lactic dehydrogenase (LDH) as markers of muscle damage during a 6-month period of intensive training. During this time, training intensity, fluid intake during exercise and dietary supplementation were all modified one by one to examine their individual effects. During a control period of 4 weeks, all swimmers drank water before and during (120 min) workouts. CK in men at the end of this period averaged 315, SD 122 (normal less than 170 IU.l-1). Half of the swimmers were then given 500 ml of a glucose-electrolyte solution (GES) (Na 21 mmol.l-1, Cl 13 mmol.l-1, K 2.5 mmol.l-1, PO4 5 mmol.l-1 and glucose 6%) before workouts and twice at intervals during the workout, while half continued to drink the same volume of water. One week after division into fluid groups, the workout intensity was increased by about 10%. Another week later CK had increased to 500, SD 180 IU.l-1 in swimmers drinking water, but fell to 280, SD 105 IU.l-1 in those drinking GES (P less than 0.05). The second phase of the study began after a 4-week control period during which all athletes drank water before and during workouts. The swimmers were divided into four matched groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Twenty-four women completed a 20-week heavy-resistance weight training program for the lower extremity. Workouts were twice a week and consisted of warm-up exercises followed by three sets each of full squats, vertical leg presses, leg extensions, and leg curls. All exercises were performed to failure using 6-8 RM (repetition maximum). Weight training caused a significant increase in maximal isotonic strength (1 RM) for each exercise. After training, there was a decrease in body fat percentage (p less than 0.05), and an increase in lean body mass (p less than 0.05) with no overall change in thigh girth. Biopsies were obtained before and after training from the superficial portion of the vastus lateralis muscle. Sections were prepared for histological and histochemical examination. Six fiber types (I, IC, IIC, IIA, IIAB, and IIB) were distinguished following routine myofibrillar adenosine triphosphatase histochemistry. Areas were determined for fiber types I, IIA, and IIAB + IIB. The heavy-resistance training resulted in significant hypertrophy of all three groups: I (15%), IIA (45%), and IIAB + IIB (57%). These data are similar to those in men and suggest considerable hypertrophy of all major fiber types is also possible in women if exercise intensity and duration are sufficient. In addition, the training resulted in a significant decrease in the percentage of IIB with a concomitant increase in IIA fibers, suggesting that strength training may lead to fiber conversions.
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The effects of 30 min running with stepwise increasing intensity (exhaustive, energy demand approx. 50----100% of VO2max), 60 s supramaximal running (anaerobic, greater than or equal to 125% of VO2max) and 40-60 min low-intensity running (aerobic, 40-60% of VO2max) on serum concentration of muscle-derived proteins were studied in 5 male and 5 female elite orienteerers. S-Carbonic anhydrase III (S-CA III) was used as a marker of protein leakage from type I (slow oxidative) muscle fibres and S-myoglobin (S-Mb) as a non-selective (type I + II) muscular marker. The fractional increase in S-CA III (delta S-Ca III) was 0.37 +/- 0.09 (mean +/- SEM, p less than 0.001), 0.10 +/- 0.05 (N. S.) and 0.46 +/- 0.09 (p less than 0.001) 1 h after exhaustive, anaerobic and aerobic exercise, respectively. The corresponding values for delta S-Mb were 1.45 +/- 0.36 (p less than 0.001), 0.39 +/- 0.13 (p less than 0.01) and 0.67 +/- 0.18 (p less than 0.001). The value for the delta S-CA III/delta S-Mb ratio was 0.68 +/- 0.03 after the aerobic exercise, but only 0.25-0.26 (p vs. aerobic exercise less than 0.001) after the two high-intensity forms of exercise. Since type I fibres of skeletal muscle are known to be responsible for power production during low-intensity exercise, whereas fibres of both type I and type II are active at higher intensities, the delta S-CA III/delta S-Mb ratio may depend on the recruitment profile of type I vs. type I + II fibres.
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The vastus lateralis muscles of eleven male elite sprinters (17-28 years) were investigated in order to examine the impact of high tension anaerobic muscular work on muscle fibre fine structure. In an attempt to reproduce the training regimen six subjects ran 20 repetitions of 25 s on a treadmill with 2 min 35 s in between, at a speed corresponding to 86% of their personal best 200 m time. PAS-stained sections of biopsies taken approximately 2 h after training generally indicated glycogen depletion in type 1 and type 2B fibres. At the light microscopic level, no signs of inflammation or fibre rupture were observed. However, at the ultrastructural level, frequent abnormalities of the contractile material and the cytoplasmic organelles were detected. Z-band streaming, autophagic vacuoles and abnormal mitochondria were the most conspicuous observations. Control specimens from sprinters who did not perform the acute exercise routine also displayed structural deviations, although to a lesser degree. It is hypothesized that during sprint training the leg musculature is put under great mechanical and metabolic stress which causes the degenerative response reported here.
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Soleus, extensor digitorum longus and tibialis anterior muscles of mice voluntarily running in wheels for periods of 5 to 120 days were studied in spaced serial and serial cross-sections. Shortly after the onset of running and during the next 2 weeks, degeneration, necrosis, phagocytosis and regeneration of muscle fibers, satellite cell proliferation and cellular infiltration were found in soleus muscles of mice from all strains investigated (CBA/J, NMRI, C57bl, NIH, SWS and Balb/c). Tibialis anterior but not extensor digitorum longus muscles were also damaged. Predominantly high-oxidative fibers were affected (both slow-oxidative and fast oxidative glycolytic in soleus, fast-oxidative glycolytic in tibialis anterior). Denervated soleus muscles that had been passively stretched during running were not damaged. Evidence was found that, during the early period of running, split fibers form by myogenesis within (regeneration) or outside (satellite cell proliferation) necrotic muscle fiber segments. Split fibers persisted in solei of long-term (2 to 3 months) exercised CBA/J but not NMRI mice. In 6 out of 20 solei of CBA/J runners exercised for 2 months or longer, fiber-type grouping was observed in the areas where extensive damage usually occurred in the early periods. The results show that different muscles are damaged and repaired to varying degrees and that marked interstrain and inter-individual differences are present. It appears that acute muscle injury occurring upon onset of voluntary running is a usual event in the adaptation of muscles to altered use.
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The purpose of this study was to determine the effects of short-term, 2,500-Hz carrier-wave frequency electrical stimulation on the ultrastructure of fast-twitch rat skeletal muscles. Thirteen Sprague-Dawley male rats were divided into three groups: daily treatment (Group 1), every-other-day treatment (Group 2), and control (Group 3). The medial quadriceps femoris and hamstring (semitendinosus and semimembranosus) muscles of the right thigh were treated with short-term electrical stimulation. After treatment, the animals were sacrificed, and their treated and sham quadriceps femoris and hamstring muscles were removed, fixed by immersion, and processed for electron microscopy. Morphometric measurements were made on electron micrographs using a Videoplan computer system, and the results were analyzed statistically. The results revealed that mitochondria, triads, and glycogen content of the fast-twitch muscles changed to resemble those of slow-twitch muscles. In view of these results, clinicians should consider the possibility that similar changes also might occur in human subjects under clinical conditions.
Total creatine kinase (CK) and CK MB activities were determined in gastrocnemius muscle and serum obtained from 14 female marathon runners. The level of CK MB in muscle increased significantly (p less than 0.05) after chronic exercise training from 5.3% to 10.5% of the total CK activity, but not after acute exercise (post-marathon 8.9%). No significant differences in total CK activities were detected. However, the total CK activity in the muscles were significantly (p less than 0.05) less than those previously reported from the muscle of men runners (1800 U/g, 3000 U/g respectively). No significant correlation existed between fiber type and muscle CK MB activity. Additionally, trace amounts of mitochondrial CK and CK BB were present in muscle homogenates. A significant correlation was observed in the increase in mean serum total CK (597 UL-1) and CK MB (23 UL-1) activities 24 h after the race (r = 0.97, p less than 0.05). These results suggest that gastrocnemius muscle in women adapts to training with increased CK MB activities and imply that skeletal muscle is the major source of elevated serum CK MB activities in women marathon runners.
Following a 100 km race creatine kinase (CK) creatine kinase MB (CKMB) activities were serially measured in well trained athletes and compared with enzyme activities in patients with acute myocardial infarction (AMI). The half-time of disappearance of CK (CKt 1/2) was 1.75±0.70 days in runners who trained within the 1st week after the race, and was 0.81±0.18 days in patients with AMI, P<0.005. CKt 1/2 in runners was shorter (1.17±0.28 days) when no training was performed in the first postrace week. CKt 1/2 was linearly correlated with age (P<0.01) in the runners but not in the patients. CKMBt 1/2 was 1.30 and 1.11 days in two runners and 0.56±0.10 days in patients with AMI (P<0.05). In line with histologic and enzymatic findings in skeletal muscle of long distance runners as reported by other workers, our kinetic data provide further evidence that CK and CKMB are released from muscular compartments in runners other than those in patients with AMI.
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The proportion of creatine kinase (CK; EC 2.7.3.2) isoenzyme MB activity was increased in skeletal muscle biopsies obtained from five long-distance runners, both 2 h before (mean 7.7%, SD 2.4%) and 30 min after (mean 7.2%, SD 1.2%) a marathon race, as compared with that in biopsies from five nonrunners (controls less than or equal to 1.0%). Further, mitochondrial CK and CK-BB isoenzymes were present in homogenates of the runners' skeletal muscle samples but not in those of the nonrunners. However, there were no substantial differences in the mean total CK activities per gram (wet wt.) of muscle tissue among premarathon samples, postmarathon samples, and nonrunners' samples (3148, 3365, and 3049 U/g, respectively). We conclude that the metabolically active gastrocnemius muscle of long-distance runners is qualitatively similar to the heart muscle in its CK isoenzyme composition.
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Marathon runners have an increased risk of developing joint disease. During and after a 42-km run, elevation of multiple cytokines occurs in the blood, reflecting inflammatory processes. We compared this cytokine response with serum levels of cartilage oligomeric matrix protein (COMP) and melanoma inhibitory activity (MIA), two markers for joint metabolism and/or damage. Serum from eight endurance-trained runners was collected shortly before the start of a marathon run, after 31 km, 42 km, 2 h after the end, on the first and on the second morning after the run. For comparison, serum was obtained from 35 healthy controls and 80 patients with knee joint injury, rheumatoid arthritis or osteoarthritis. Serum levels of C-reactive protein (CRP), interleukin-1beta (IL-1beta), interleukin-1 receptor antagonist (IL-1RA), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble interleukin-6 receptor (sIL-6R, gp80), soluble tumor necrosis factor receptor II (sTNFRII, p75), COMP and MIA were measured by ELISA. Compared with healthy controls, the runner's baseline serum levels of TNF-alpha, sIL-6R, COMP and MIA were significantly increased. COMP and MIA levels, higher than the upper normal limits of 5 microg/ml and 6 ng/ml respectively, were found in seven and five of eight runners. The elevated levels of COMP were similar to those found in joint injury or osteoarthritis, and the elevated levels of MIA were comparable to those reported in rheumatoid arthritis. During the run, the serum levels of IL-1RA, IL-6, TNF-alpha and COMP rose significantly, and gradually returned to baseline within 24 h. Only modest changes of CRP, sIL-6R, sTNFRII and MIA occurred during the run. Late elevations of CRP and MIA were observed after 24 and 48 h. The correlation analysis suggests associations between COMP, sIL-6R, TNF-alpha, IL-1RA on one hand and sTNFRII, and MIA and CRP on the other hand. Elevated baseline levels of COMP and MIA might reflect increased joint matrix turnover and/or damage due to prior extreme physical training. During the run, COMP was increasing possibly due to the severe physical strain on joint structures, associated with the early inflammation. After the run, MIA and CRP increased within 24 h, suggesting a correlation with later inflammatory processes. Thus, our data suggest that COMP and MIA are markers for distinct aspects of joint metabolism and/or damage in both disease and sport.
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31P magnetic resonance spectroscopy (MRS) was used to document long lasting losses in muscle oxidative capacity after bouts of intense endurance exercise. The subject was a 34 year old highly fit female cyclist (VO2MAX = 53.3 ml/kg/min). Over a five month period, she participated in three separate intense bouts of acute unaccustomed exercise. 31P MRS measurements were performed seven weeks after the first bout and every two weeks for 14 more weeks. In all cases, 31P MRS measurements followed three days after each bout. The subject showed a decreased ability to generate ATP from oxidative phosphorylation and an increased reliance on anaerobic ATP production during the 70% and 100% maximal voluntary contractions after the exercise bouts. Increased rates of fatigue and increased indicators of exercise difficulty also accompanied these reductions in muscle oxidative capacity. Increased oxidative and anaerobic ATP production were needed to maintain the work level during a submaximal 45% maximal voluntary contraction exercise. Acute increases in intensity accompanied by a change in exercise mode can influence the ability of muscle to generate ATP. The muscles were less economical and required more ATP to generate force during the submaximal exercises. During the maximal exercises, the muscle's mitochondria showed a reduced oxidative capacity. However, these reductions in oxidative capacity at the muscle level were not associated with changes in whole body maximal oxygen uptake. Finally, these reductions in muscular oxidative capacity were accompanied by increased rates of anaerobic ATP production, fatigue, and indicators of exercise difficulty.
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Rhabdomyolysis has sparked new interest in recent years. The causes of rhabdomyolysis include drugs and other toxic agents, infections, physical exertion, crush injury, and muscle diseases (dystrophinopathies and metabolic myopathies). Prompt identification of the pathophysiological mechanism is the key to rapid control of the acute episode and to prevention of recurrences. In this update, we discuss the pathophysiological mechanisms and nosology of rhabdomyolysis, as well as diagnostic investigations, with special emphasis on noninvasive methods.
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There is concern about whether cardiac damage occurs as a result of prolonged strenuous exercise. To investigate whether competing in a triathlon is associated with cardiac damage based on a sustained increase in cardiac troponin T (cTnT), and whether such an increase correlates with echocardiographic changes cTnT and echocardiographic measurements were made in 38 participants in the 2001 Australian ironman triathlon. cTnT was measured the day before, immediately after, and the day following the race. Echocardiography was done the day before, immediately after, and two to six weeks later for measurement of ejection fraction, stroke volume, cardiac output, wall motion analysis, and global left ventricular function (LVF). No subject had detectable cTnT in the pre-race sample. Following the race, 32 subjects (86.5%) had detectable levels of cTnT (>0.01 ng/ml), with six (16.2%) having >0.10 ng/ml. The day after the race, nine subjects (23.7%) still had detectable cTnT, with two recording a level >0.10 ng/ml. Previously described echocardiographic changes of "cardiac fatigue" were observed in the whole cohort. There was a modest but significant correlation between change in ejection fraction and peak cTnT level (p = 0.02, r = 0.39). Athletes with a post-race cTnT >0.10 ng/ml had a greater decrease in global LVF (p = 0.02) and a trend toward a greater fall in ejection fraction and stroke volume than athletes with cTnT levels <0.10 ng/ml. Cardiac output fell in the group with cTnT >0.10 ng/ml (p>0.05). Participation in ironman triathlon often resulted in persistently raised cTnT levels, and the troponin rise was associated with echocardiographic evidence of abnormal left ventricular function. The clinical significance and long term sequelae of such damage remains to be determined.
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The regeneration of soleus muscle injury induced by the bupivacaine model was studied ultrastructurally and immunohistochemically. Twenty-one young (age range 3-3.5 months) male Wistar rats were subjected to a single intramuscular injection of 1 mL of 0.5% Marcaine. The muscles were examined on biopsy days 1, 2, 3, 5, 7, 14, and 21. By day 1, mononuclear inflammatory cells had invaded the necrotic sarcoplasm. Degenerative morphological findings counted mainly for the hypercontracted fibers, dilation of sarcoplasmic reticulum, plasma membrane defects, mitochondrial alterations, and myofibril discontinuities. By day 2 proliferating myoblasts were seen with variety in shape, which fused on the day 3. Myotubes with multiple central nuclei and euchromatic nucleoli were formed by day 5. Asynchronous repair events were seen with bundles of myofilaments toward the core of the fibers, in contrast to the least mature distal growth cones, which had free myoblasts in proximity and formatted pseudopods. Chronologically asynchronous regeneration stages possibly suggested successive satellite cell activation profiles or heterogeneity in satellite cell population. In parallel with the electron microscopy, in light microscope immunocytochemistry, desmin- and vimentin-positive mononuclear cells were observed within the first 3 biopsy days, but as regeneration proceeded, desmin predominated over vimentin. Merosin immunoreactivity revealed preservation of the basal lamina, which is crucial for the stability and survival of myotubes. By day 21, fibers restored the overall control architecture.
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