Markers Of Muscle Injury Research Articles

Differential Detection of Skeletal Troponin I Isoforms in Serum of a Patient with Rhabdomyolysis: Markers of Muscle Injury?

Unlike the extensive research devoted to the development of troponin-based diagnostic assays for myocardial disease, much less effort has been expended on the development of a counterpart for skeletal muscle disorders. The consensus that the cardiac troponins [cardiac troponin I (cTnI) and/or cTnT] should be used for diagnosis of myocardial infarction (MI), as well as for diagnosis and management of unstable angina, is based on their superior tissue specificity over such conventional markers as creatine kinase [(CK); see Refs. (1)(2)]. Although CK is the most common serum marker for skeletal muscle injury, it is not ideal for several reasons, including lack of tissue specificity, inability to reveal damage to specific skeletal fiber types (fast or slow), and inappropriately low values when glutathione concentrations are decreased because of liver or multiple-organ failure (3). Skeletal troponin I (sTnI), with its two distinct isoforms [fast (fsTnI) and slow (ssTnI)], like cTnI and cTnT, may have a similar advantage over conventional markers for detecting skeletal-muscle injury. In 1996, Rama et al. (4) described an experimental immunoenzymatic assay for sTnI using antibodies that cross-react with both sTnI and cTnI. The assumption of the investigators was that the concentrations of cTnI in patients with skeletal injury would be negligible. Others have since used this assay (5)(6)(7). For example, Onuoha et al. (7) found that serum sTnI reflects the severity and type of orthopedic and soft tissue injury. However, because this assay does not differentiate between the two isoforms of sTnI, which have a sequence homology of ∼56%, information about selective damage to particular fiber types is unavailable. Posttranslational modifications to the analyte, such as degradation, are also undetected by this assay. We applied our Western blot–direct serum analysis (WB-DSA) procedure (8), originally developed and successfully used for the detection …

Markers of Smooth Muscle Destruction Do Not Help Exclude Ectopic Pregnancy

Previous studies have suggested that an elevated creatine phosphokinase (CPK) level, a marker of smooth muscle injury, may be helpful in the diagnosis

Biarticular and monoarticular muscle activation and injury in human quadriceps muscle.

We hypothesized that activation of the quadriceps femoris muscle group during eccentric exercise is related to the increase in magnitude of several markers of muscle injury that developed during the next week. Fourteen male subjects performed six to eight sets of five to ten repetitions of single-leg eccentric-only seated knee extension exercise. Magnetic resonance (MR) images were collected before and immediately after exercise and on days 2-4 and 6 after eccentric exercise. Changes in maximal voluntary contraction (MVC), perceived soreness, muscle volume and muscle transverse relaxation of water protons (T2) were determined for the quadriceps femoris muscle group each day. Changes in muscle volume and T2 were determined every day for each muscle [vastus lateralis (VL), vastus medialis (VM), vastus intermedius (VI), rectus femoris (RF)] of the quadriceps femoris group. Post-exercise T2 was greater than pre-exercise T2 (P < 0.05) for all muscles. The acute deltaT2 (Post-Pre) was similar (P>0.05) among VL, VM, VI, and RF [5.5 (0.3) ms], suggesting that the four muscles were equally activated during eccentric exercise. In the week after eccentric exercise, subjects experienced delayed-onset muscle soreness (DOMS) and all muscles demonstrated a delayed increase in T2 above pre-exercise values (P < 0.05), suggesting that muscle injury had occurred. For the quadriceps femoris muscle group, there was no correlation between acute deltaT2 and delayed (peak T2 during days 2, 3, 4, 6 minus pre-exercise T2) deltaT2 (r=0.04, P>0.05). Similar results were obtained when VL, VM, VI and RF were examined separately. Of the four muscles in quadriceps femoris, the biarticular RF experienced greater muscle injury [delayed deltaT2= 15.2 (2.0) ms] compared to the three monoarticular vasti muscles [delayed deltaT2 = 7.7 (1.3) ms; P< 0.05]. We propose that the disproportionate muscle injury to RF resulted from an ineffective transfer of torque from the knee to hip joint during seated eccentric knee extension exercise, thus causing RF to dissipate greater energy than normal. We conclude that in humans, muscle activation is not a unique determinant of muscle injury.

THE EFFECT OF ELECTRICAL MUSCLE STIMULATION ON MARKERS OF MUSLE INJURY

The purpose of this study was to examine the acute and chronic effects of electrical muscle stimulation on markers of skeletal muscle injury following eccentric exercise. In a randomized crossover design, sedentary male subjects (n = 15) participated in both experimental and control conditions separated by at least two weeks. Muscle injury was induced by having the subjects perform 25 eccentric contractions of the elbow flexors. The experimental condition consisted of applying monophasic high voltage stimulation (MHVS) at the sensory level to the injured muscle. Stimulation treatments lasted 30 minutes and were administered at 5 min, 3 h, 6 h, 24 h, 48 h, 72 h, 96 h, and 120 h post exercise. Markers of muscle injury were measured both before and after the stimulation treatments at the aforementioned time points. Preliminary results (n = 5) show that significant changes in isometric strength, arm angles, arm volume, and muscle soreness occurred; although, no significant differences were noted between the treatments. Based on the preliminary data, MHVS does not appear to influence markers of muscle injury following eccentric exercise. A more definitive conclusion will be made after completing our testing of the remaining subjects. Supported by The NATA Research and Education Foundation

EFFECT OF ISCHEMIC PRECONDITIONING ON CONTRACTION-INDUCED SKELETAL MUSCLE INJURY

The purpose of this study was to determine the effect of ischemic-preconditioning (IP) on markers of skeletal muscle injury following eccentric exercise. Prior to performing 25 one-arm eccentric contractions, sedentary males (n = 10) completed either an IP protocol or a control condition. The IP protocol consisted of three 5 min cycles of inflating (180 mmHg) and deflating an upper arm blood pressure (BP) cuff. The control condition consisted of applying a deflated BP cuff for 30 min. The treatments were separated by at least 3 weeks and were performed on opposite arms. Measurements were made before the treatment, after treatment, 5 min, 3 h, 6 h, 24 h, 48 h, and 72 h post-exercise. Blood neutrophil concentrations were not significantly different between the treatments at any of the post-exercise time points but were elevated at 3 and 6 h post-exercise for both treatments. Statistical analysis by two-way repeated measures ANOVA revealed significant (p < 0.05) changes in isometric strength, arm angles, muscle soreness and blood creatine kinase activity; however, no significant differences were noted between the treatments. In conclusion, IP does not influence markers of skeletal muscle injury following eccentric arm exercise.

Nitric oxide myotoxicity is age related

Nitric oxide (NO) is generated under normal conditions in skeletal muscle and acts as a messenger that influences contractility, blood flow, and glucose metabolism. Excess NO generation may occur in pathological states, in particular inflammatory conditions. We demonstrate that incubation of rat extensor digitorum longus muscle with the NO donor, S-nitrosocysteine, leads to release of creatine kinase, a marker of muscle injury after a delay of 90 min. Muscle of old animals was more sensitive to the NO donor. Light microscopic analysis does not show abnormalities, with the exception of an increase in interfiber distance. Histological staining identified no pathological elevations of calcium. The study demonstrates the direct toxicity of NO to skeletal muscle, and that muscle of older animals is differentially susceptible to NO toxicity.

Discrimination Between Myocardial and Skeletal Muscle Injury by Assessment of the Plasma Ratio of Myoglobin Over Fatty Acid–Binding Protein

Myoglobin and fatty acid-binding protein (FABP) each are useful as early biochemical markers of muscle injury. We studied whether the ratio of myoglobin over FABP in plasma can be used to distinguish myocardial from skeletal muscle injury. Myoglobin and FABP were assayed immunochemically in tissue samples of human heart and skeletal muscle and in serial plasma samples from 22 patients with acute myocardial infarction (AMI), from 9 patients undergoing aortic surgery (causing injury of skeletal muscles), and from 10 patients undergoing cardiac surgery. In human heart tissue, the myoglobin/FABP ratio was 4.5 and in skeletal muscles varied from 21 to 73. After AMI, the plasma concentrations of both proteins were elevated between approximately 1 and 15 to 20 hours after the onset of symptoms. In this period, the myoglobin/FABP ratio was constant both in subgroups of patients receiving and those not receiving thrombolytics and amounted to 5.3 +/- 1.2 (SD). In serum from aortic surgery patients, both proteins were elevated between 6 and 24 hours after surgery; the myoglobin/FABP ratio was 45 +/- 22 (SD), which is significantly different from plasma values in AMI patients (P < .001). In patients with cardiac surgery, the ratio increased from 11.3 +/- 4.7 to 32.1 +/- 13.6 (SD) during 24 hours after surgery, indicating more rapid release of protein from injured myocardium than from skeletal muscles. The ratio of the concentrations of myoglobin over FABP in plasma from patients with muscle injury reflects the ratio found in the affected tissue. Since this ratio is different between heart (4.5) and skeletal muscle (20 to 70), its assessment in plasma allows the discrimination between myocardial and skeletal muscle injury in humans.

Effect of training on skeletal muscle injury from downhill running in rats.

Experiments were conducted to test the hypothesis that injury to skeletal muscle in rats resulting from prolonged downhill running is prevented to a greater extent by prior downhill training than by either uphill or level training. Changes in plasma creatine phosphokinase (CPK) activity and glucose-6-phosphate dehydrogenase (G-6-PDase) activity in the soleus (S), vastus intermedius (VI), and medial head of triceps brachii (TM) muscles were evaluated as markers of muscle injury 48 h after 90 min of intermittent downhill running (16 m . min -1). Prior to this acute downhill run, groups of rats were trained by either downhill (-16 degrees), level (0 degrees), or uphill (+16 degrees) running (16 m . min -1) for 30 min/day. Training duration was either 5 days or 1 day. A training effect (i.e., reduced muscle injury) was indicated if muscle G-6-PDase or plasma CPK activity in a trained group following the 90-min downhill run was not different from that of nonexercised control animals and/or if it was lower than that of nontrained runners. A significant training effect was achieved in all three muscles with 5 days of either downhill or level training, but only in S after 5 days of uphill training. Elevation of plasma CPK activity was prevented by 5 days of training on all three inclines.(ABSTRACT TRUNCATED AT 250 WORDS)

EFFECT OF TRAINING ON SKELETAL MUSCLE INJURY FROM DOWNHILL RUNNING IN RATS

Experiments were conducted to test the hypothesis that injury to skeletal muscle in rats resulting from prolonged downhill running is prevented to a greater extent by prior downhill training than by either uphill or level training. Changes in plasma creatine phosphokinase (CPK) activity and glucose-6-phosphate dehydrogenase (G-6-PDase) activity in the soleus (S), vastus intermedius (VI), and medial head of triceps brachii (TM) muscles were evaluated as markers of muscle injury 48 h after 90 min of intermittent downhill running (16 m . min -1). Prior to this acute downhill run, groups of rats were trained by either downhill (-16 degrees), level (0 degrees), or uphill (+16 degrees) running (16 m . min -1) for 30 min/day. Training duration was either 5 days or 1 day. A training effect (i.e., reduced muscle injury) was indicated if muscle G-6-PDase or plasma CPK activity in a trained group following the 90-min downhill run was not different from that of nonexercised control animals and/or if it was lower than that of nontrained runners. A significant training effect was achieved in all three muscles with 5 days of either downhill or level training, but only in S after 5 days of uphill training. Elevation of plasma CPK activity was prevented by 5 days of training on all three inclines.(ABSTRACT TRUNCATED AT 250 WORDS)