[Study on mechanical factors involved in sports muscle injury].

Objective. To investigate the effect of eccentric strengthening (EC) exercise on muscular structure, plasma CK and biomechanical behavior under different mechanical loadings and to study the mechanical factors involved in sports muscle injury. Method. We developed an apparatus to do eccentric strength training with male SD rats under different mechanical loadings and to measure the biomechanical behavior. Result. No significant difference (P>0.05) of muscular structure, plasma CK and biomechanical behavior were found between high and low force groups. Conclusion. Skeletal muscle injury after cyclic EC with different mechanical loadings suggested that muscle damage is not simply a function of peak muscle force.

Muscular soreness following prolonged intermittent high-intensity shuttle running.

The aim of this study was to examine the impact of prolonged intermittent high-intensity shuttle running on soreness and markers of muscle damage. Sixteen males took part in the study, half of whom were assigned to a running group and half to a resting control group. The exercise protocol involved 90 min of intermittent shuttle running and walking (Loughborough Intermittent Shuttle Test: LIST), reflecting the activity pattern found in multiple-sprint sports such as soccer. Immediately after exercise, there was a significant increase (P < 0.05) in serum activities of creatine kinase and aspartate aminotransferase, and values remained above baseline for 48 h (P < 0.05). Median peak activities of creatine kinase and aspartate aminotransferase occurred 24 h post-exercise and were 774 and 43 U x l(-1), respectively. The intensity of general muscle soreness, and in the specific muscles investigated, was greater than baseline for 72 h after the shuttle test (P < 0.05), peaking 24-48 h post-exercise (P < 0.05). Muscle soreness was not correlated with either creatine kinase or aspartate aminotransferase activity. Soreness was most frequently reported in the hamstrings. Neither soreness nor serum enzyme activity changed in the controls over the 4 day observation period. It appears that unaccustomed performance of prolonged intermittent shuttle running produces a significant increase in both soreness and markers of muscle damage.

Differential patterns of PMN-elastase and type III procollagen peptide in knee joint effusions due to acute and chronic sports injuries.

In 38 traumatic knee joint effusions the proteolytic enzyme PMN-elastase (PMN-E) and the repair marker procollagen III aminoterminal peptide (PIIINP) were determined. According to the period between trauma and first aspiration of the effusion, the patients were divided into 3 groups. Group I (17 patients; period between trauma and first aspiration not longer than 72 hours) showed high concentrations of PMN-E (up to 5400 ng/ml) and low concentrations of PIIINP (less than 13 U/ml). Group II (11 patients; aspiration within 4 to 14 days) had mean PMN-E and PIIINP concentrations of 125.6 ng/ml and 52.1 U/ml, respectively. In group III (10 patients, aspiration after 14 days) mean PMN-E concentration was 123.8 ng/ml and mean PIIINP concentration was 63.4 U/ml. Graphic depiction of PMN-E and PIIINP levels in each individual sample as a function of time between trauma and fluid collection revealed highly increasing PMN-E levels during the first 24 posttraumatic hours, followed by rapidly decreasing levels within 72 hours post trauma, and no change after the 4th posttraumatic day. In contrast, PIIINP increased continuously up to the first posttraumatic week and stayed at high levels up to 90 days (end of the observation period). The differential patterns of PMN-E and PIIINP concentration in knee joint effusions may be useful in estimating the period between trauma and first treatment (aspiration of effusion) and should, therefore, be helpful in detecting degenerative lesions, which seem to be characterized by low PMN-E concomitantly with high PIIINP levels.

Enzymatic estimation of skeletal muscle damage by analysis of changes in serum creatine kinase.

Skeletal muscle damage size (SMDS) was assessed in 35 women and 34 men runners after a 42.2-km race using a method developed for estimation of myocardial infarct size. SMDS was computed according to the following equation: SMDS = (BW) (K) (CKr), where BW is body weight, K is a constant, and CKr is the cumulative amount of creatine kinase (CK) released over time. The method takes into account CK distribution space, fractional disappearance rate of CK, proportion of CK degraded in skeletal muscle, and proportion of CK released into the circulation. Assumptions are made regarding the relative amount of CK lost from skeletal muscle into the circulation. The SMDS in men, 808 +/- 1,229 (SD) CK g-eq was significantly (P less than 0.05) greater than in women, 160 +/- 147 (SD) CK g-eq. The ranges of SMDS (CK g-eq) were 23-5,397 in men and 7-624 in women. A significant difference (P less than 0.05) also remained after correction for body surface area; men 432 +/- 583 (SD), women 100 +/- 63 (SD) CK g-eq/m2. In men and women, no significant correlation existed between SMDS and age or marathon finish time. Although relatively theoretical, results indicate that greater skeletal muscle damage occurred in men vs. women runners after a marathon. Whether the release of CK from skeletal muscle is the result of irreversible and/or reversible injury has not yet been determined.

Muscle pathomorphology in m. quadriceps of marathon runners. Early signs of strain disease or functional adaptation?

Muscle biopsies were obtained from m. vastus lateralis of five male marathon runners and five sprinters. The athletes performed their last competition at least 2 weeks prior to the investigation. No clinical signs of discomfort or injury were observed in the runners. The biopsy specimens from the sprinters showed an ordinary overall morphology, although fibre sizes varied considerably within and between the individuals. In contrast, in the marathon runners, structural deviations of pathologic value appeared in four out of five subjects. The fibre shapes were irregular, irrespective of fibre type, and internal architectural changes were common. An increased amount of connective tissue was found. A majority of fibres showed one or more central nuclei. A few fibres were flat and there were also evidence of fibre type grouping. The divergent picture might be an expression of repeated fibre injury with subsequent processes. If so, a peripheral, relative, arterial insufficiency is suggested as a possible aetiology. However, it cannot be ruled out that the deviations express a functional adaptation to the extreme endurance demands.

Chronic Achilles paratenonitis in athletes: a histological and histochemical study.

Pathological alterations of chronic Achilles paratenonitis were studied histologically and histochemically in tissue samples obtained operatively from 16 athletes with this complaint and from 3 control patients. The activities of 11 different enzymes--lactate, succinate, malate, glucose-6-phosphate and glutamate dehydrogenases, lipoamide dehydrogenase and glutathione reductase (NADH2- and NADPH2-diaphorases), acid and alkaline phosphatases, phosphorylase and leucylaminopeptidase--were studied. Pathological findings were located diffusely around the tendon. A slight inflammatory cell reaction was found in all cases. The fatty areolar tissue was clearly thickened and edematous, and showed fibrinous exudations, widespread fat necrosis, considerable connective tissue proliferation and adhesion formation. The blood vessels showed profound degenerative and necrotizing changes. The thin membranes of the paratenon were clearly hypertrophied. Increased enzyme activities were mainly found in the fibroblasts, inflammatory cells and vascular walls. A moderate activity of lysosomal enzymes, an increased activity of enzymes of electron transport, anaerobic glycolysis, pentose phosphate shunt and decreased activity of those of aerobic energy metabolism were found. Simultaneously an increased amount of both neutral and acid mucopolysaccharides and a locally increased amount of elastic fibres were found in the inflamed paratenon. These results indicate that marked metabolic changes occur in paratenonitis, i.e. an increased catabolism and decreased oxygenation of the inflamed areas. The morphological alterations suggest that the gliding function of the paratenon may be impaired.

Skeletal muscle injury and repair in marathon runners after competition.

Elevated serum creatine kinase MB isoenzyme (CK-MB) activity in marathon runners after competition may arise from injury to skeletal muscle, myocardium, or a combined tissue source. Normal radionuclide myocardial scintigraphy and the selective increase in skeletal muscle CK-MB reported in such runners strongly suggest a peripheral source. To understand this biochemical finding, the authors examined gastrocnemius muscles by electron microscopy from 40 male marathon runners at intervals after competition and from 12 male nonrunners. Muscle from runners showed post-race ultrastructural changes of focal fiber injury and repair: intra- and extracellular edema with endothelial injury; myofibrillar lysis, dilation and disruption of the T-tubule system, and focal mitochondrial degeneration without inflammatory infiltrate (1-3 days). The mitochondrial and myofibrillar damage showed progressive repair by 3-4 weeks. Late biopsies showed central nuclei and satellite cells characteristic of the regenerative response (8-12 weeks). Muscle from veteran runners showed intercellular collagen deposition suggestive of a fibrotic response to repetitive injury. Control tissue from nonrunners showed none of these findings. The sequential morphologic changes in runners suggest that the increase in skeletal muscle CK-MB is a marker of cellular regeneration.

Histochemical correlates of hamstring injuries.

This study reports the histochemical fiber type composition of the human hamstring muscles. Muscle specimens from necropsy specimens were obtained from seven locations in the hamstring, four locations in the quadriceps, and one location in the adductor magnus. The hamstring muscles are shown to have a relatively high proportion of Type II fibers. Type II fibers are more involved with exercise of higher intensity and force production and it is postulated that the hamstrings are capable of high intrinsic force production. The hamstrings are two-joint muscles and are, therefore, subject to increased stretch and force production extrinsically by motion at the hip and knee. It is proposed that high levels of tension in the hamstrings produced by intrinsic force production and extrinsic stretch may make them prone to injury in periods of intense muscular activity. This proposal is also relevant to other frequent athletic muscle injuries.

Scintigraphic evaluation of muscle damage following extreme exercise: concise communication.

Total body Tc-99m pyrophosphate scintigraphy was performed on 11 "ultramarathon" runners to assess the ability of nuclear medicine techniques to evaluate skeletal-muscle injury due to exercise. We found increased muscle radionuclide concentration in 90% of the runners. The pattern of muscle uptake correlated with the regions of maximum pain. The detection of exercise-induced rhabdomyolysis appeared to be best when scintigraphy was performed within 48 hr after the race, and to be almost undetectable after about a week. It was possible to differentiate muscle injury from joint and osseous abnormalities such as bone infarct or stress fracture. Although 77% of the runners had elevated serum creatine kinase MB activity, cardiac scintigraphy showed no evidence of myocardial injury.