Total Creatine Kinase Activity Research Articles

Creatine kinase activity associated with the contractile proteins of the guinea-pig carotid artery

Activity and role of creatine kinase associated with contractile proteins of vascular smooth muscle have been investigated using skinned guinea-pig carotid artery rings. Membrane solubilization was performed with the detergent Triton X-100. Creatine kinase activity, isoenzyme profile as well as mechanics were performed on the Triton skinned carotid artery rings. Total creatine kinase activity was 47.3 +/- 9.3 IU g-1 ww and electrophoresis showed BB, MB, and MM isoforms (BB-CK being the predominant isoenzyme). One hour incubation with Triton X-100, produced predominantly BB-CK remaining with the myofibrils with some MB, representing 23% of the preskinned creatine kinase activity. When relaxed carotid artery rings were exposed to pCa 9 in the presence of 250 microM ADP, 0 ATP, and 12 mM phosphocreatine, tension was not significantly different from resting tension, but changing to pCa 4.5 caused the carotid artery rings to generate 49.5 +/- 4.5% of maximal tension. When a high-tension rigor state was achieved (250 microM ADP, 0 ATP, 0 phosphocreatine, and pCa 9), the addition of 12 mM phosphocreatine effected significant relaxation. These observations implicate an endogenous form of creatine kinase, associated with the myofilaments, which is capable of producing enough ATP for submaximal tension generation and significant relaxation from rigor conditions. These results suggest co-localization of ATPase, MLCK, and creatine kinase on the contractile proteins of the carotid artery. Such an enzymic association may play a role in the energetic supply to the contractile apparatus of vascular smooth muscle.

Innervation of MyoD-converted human amniocytes and fibroblasts by fetal rodent spinal cord neurons

MyoD is one member of a gene family involved in the regulation of myogenesis. MyoD transfection induces myogenesis in a variety of non-muscle cells. Human amniocytes and fibroblasts were infected with a MyoD-retrovirus vector, to determine whether the converted cells can mature normally to form functional muscle fibers. MyoD-converted cells were co-cultured with fetal rat spinal cord. After 2–3 weeks of co-culture cross-striated, contracting muscle fibers were observed. Combined acetylcholinesterase cytochemistry and acetylcholine receptor labeling showed prominent staining at nerve-muscle contacts. Approximately half of the total creatine kinase activity was due to the muscle-specific isozyme. Innervated MyoD-converted cells might represent a new source of muscle cells for studying the molecular events leading toward the formation of functional muscle. This system also appears suitable for studying the pathogenesis of hereditary, often rare, myopathies affecting muscle-specific proteins, for which muscle tissue is frequently unavailable for in vitro analysis.

Thyroid hormones and the creatine kinase system in cardiac cells.

The paper reviews the current evidence on the role of thyroid hormones in regulating the creatine kinase energy transfer system at multiple structures in cardiac cells. 1) Thyroid hormones modulate the overall synthesis of phosphocreatine (PCr) by increasing the rate of mitochondrial oxidative phosphorylation. 2) Thyroid hormones regulate the total activity of creatine kinase and its isoenzyme distribution. In comparison with normal thyroid state (euthyroidism), hypothyroidism is characterized by decreased total creatine kinase activity owing to diminished fraction of creatine kinase. On the other hand, hyperthyroidism, while causing no change in total creatine kinase activity, leads to increased fractions of neonatal isoforms of creatine kinase, and, in case of prolonged hyperthyroidism, to decreased fraction of mitochondrial creatine kinase. The latter change is associated with partial uncoupling between mitochondrial creatine kinase and adenine nucleotide translocase reflected by decreased PCr/O ratio. 3) Hyperthyroidism leads to increased passive sarcolemmal permeability due to which the leakage of creatine along its concentration gradient occurs. As a result of (i) increased sarcolemmal permeability for creatine, (ii) uncoupling of mitochondrial PCr synthesis, and (iii) increased energy utilization rate the steady state intracellular PCr content decreases under hyperthyroidism which, in turn, increases the myocardial susceptibility to hypoxic damage. Thyroid state also modulates the protective effects of exogenous PCr on energetically depleted myocardium.

Release of creatine kinase and prostaglandin E2 from regenerating skeletal muscle fibers

To study the effect of regeneration on the release of creatine kinase (CK) and prostaglandin E2 from muscle, extensor digitorum longus muscles of mice were injected with 50 microliters of BaCl2 solution in saline (1.2% wt/vol). Injected muscles showed almost complete degeneration at 3 days postinjection but had regenerated to approximately the same fiber cross-sectional area as contralateral control muscles by 12 days postinjection. These muscles released reduced amounts of intracellular CK compared with contralateral control muscles in response to excessive isometric contractile activity or treatment with the calcium ionophore A-23187 (20 microM) in vitro. However, regenerating muscles contained a lower total CK activity than contralateral control muscles, which accounted for the reduced CK efflux after experimental damage. Regenerating muscles released an increased amount of prostaglandin E2 compared with control muscles after both damaging stimuli. We conclude that regenerated muscles show no reduced susceptibility to contraction-induced damage (as assessed by CK release) but show an elevated release of prostaglandin E2 in response to contractile activity or an increase in intracellular calcium.

Serum creatine kinase levels after a single intramuscular injection--dependence on injection volume.

Creatine kinase (CK) is an important marker in the diagnosis of acute myocardial infarction (AMI). There are, however, other clinical conditions other than AMI which cause elevation of total CK activities in serum including: skeletal muscle trauma; alcohol intoxication; uncontrolled diabetes mellitus; convulsions; pulmonary emboli; rhabdomyolysis; and many others. I•2 An increase in serum levels of CK has been demonstrated following administration of a wide variety of drugs. However, there is as yet no unifying hypothesis regarding the mechanism of this phenomenon. Steiness et al, have shown that certain medications such as diazepam cause an increase in serum CK activity as a result of muscle damage. The amount of CK liberated is determined both by the properties of the solution injected (active compound, vehicle, concentration, and volume) and by muscle factors such as local muscle blood flow, susceptibility of muscle to the damaging effect of the injection and local muscle binding to the medication. However, the common clinical notion regarding intramuscular (1M) injections as a frequent cause of serum CK elevations leading to an erroneous diagnosis of AMI in patients who have been given an 1M injection for non-cardiac reasons has been challenged by Konicoff et al.s We investigated serum CK elevation following a single 1M injection of medications commonly used in patients admitted to a medical ward.

Elevation of serum creatine kinase in divers with arterial gas embolization.

Arterial gas embolism due to pulmonary barotrauma and the resultant cerebral gas embolism are catastrophic complications of diving. Previous studies have only rarely noted evidence of gas embolism to noncranial sites. Among 142 persons with diving-related injuries evaluated between January 1982 and July 1991, we identified 29 who had arterial gas embolism and who underwent biochemical studies indicative of muscle injury. Of the 29 patients, 4 were excluded because cardiopulmonary resuscitation had been performed and 3 were excluded because the duration of their dives met or exceeded standard limits set for dives not requiring staged decompression. The outcome at the time of hospital discharge in the remaining 22 patients was correlated with clinical factors and the results of biochemical studies. We also studied 22 subjects after uncomplicated dives and 11 patients who had sustained blunt trauma. All the patients with diving-associated gas embolism had elevated serum creatine kinase activity (normal, < or = 175 U per liter); the values were markedly elevated (> 900 U per liter) in 14. The MB isoenzyme of creatine kinase was detected in the serum of 13 of 20 patients in whom it was measured and was > or = 4 percent of total creatine kinase activity in 6 patients. In three patients electrocardiography showed myocardial injury. Changes in serum creatine kinase activity of similar magnitude were not present in the subjects who had uncomplicated dives or in the patients with blunt trauma. Thirteen patients recovered fully, four had minor residual neurologic deficits, three were severely impaired, and two died. Logistic-regression analysis revealed a significant correlation between peak serum creatine kinase values and clinical outcome. Biochemical evidence of muscle injury is frequently found after diving-associated arterial gas embolism. The correlation between serum creatine kinase activity and outcome suggests that serum creatine kinase is a marker of the size and severity of arterial gas embolism.

Cardiac troponin T and CK-MB mass release after visually successful percutaneous transluminal coronary angioplasty in stable angina pectoris

The incidence of cardiac troponin T (Tn-T) and creatine kinase (CK) isoenzyme MB mass release was studied in 23 patients with stable angina pectoris undergoing visually successful percutaneous transluminal coronary angioplasty (PTCA). Serial blood samples were drawn for measurement of serum Tn-T, CK-MB mass, total CK activity, CK-MB activity, and lactate dehydrogenase isoenzyme (LD-1). ST segment monitoring was carried out during PTCA and for the following 24 hours. None of the patients shoed electrocardiographic (ECG) evidence of myocardial infarction. However, Tn-T was elevated in three patients (0.23 to 1.32 μg/L), and in these three and an additional three patients CK-MB mass was also elevated (7.0 to 27.5 μg/L). Total CK activity and LD-1 were only elevated in one of these six patients. None had elevated CK-MB activity. ST segment depression on ECG recording was not predictive of Tn-T or CK-MB mass release. Patients with elevated Tn-T or CK-MB mass did not differ with respect to demographic data, stenosis characteristics, or in the PTCA procedure. We conclude that CK-MB mass uncovers clinically and ambulatory electrocardiographically inapparent severe myocardial ischemia/minor myocardial damage (microembolization) in 26% (6 of 23) of patients after visually successful PTCA; 13% (3 of 23) had elevated Tn-T, indicating minor myocardial damage. The application of these markers in the future could be of considerable value for determining the efficacy of coronary angioplasty and atherectomy, as well as for drug therapy in connection with such procedures.

Expression of creative kinase M and B mRNAs in treadmill trained rat skeletal muscle

Gastrocnemius muscle from treadmill trained rats was analyzed for creatine kinase (CK) isoenzyme activities by agarose electrophoresis and M and B CK mRNA levels by Northern blot analysis. Total CK activity in exercise-trained (143 (SD 15) U/g) and control (154 (SD 16) U/g) muscles did not differ. CK-MB increased 220% in exercised-trained muscle compared to controls. CK-B subunit mRNA increased 40%, while CK-M subunit mRNA decreased 42% in exercised-trained muscle compared to control. Thus, gene expression of CK isoenzymes appears to be partially controlled at the level of transcription following exercise training.

Immunoreactive creatine kinase-MB and creatine kinase isozyme concentrations during treatment of hypothyroid patients.

Using a highly sensitive enzyme immunoassay (EIA) system, we determined creatine kinase isozymes, namely creatine kinase-MB and creatine kinase-MM, in sera of patients suffering from primary hypothyroidism with concomitant signs of myocardial affections before and during treatment. After oral administration of L-thyroxine, the augmented mass concentrations of serum creatine kinase-MB and creatine kinase-MM, and the increased catalytic activity concentrations of serum total creatine kinase and creatine kinase-MB gradually decreased in inverse proportion to the increased concentrations of serum triiodothyronine (T3) and thyroxine (T4). By the 6th to 8th week after treatment, the elevated levels of serum total creatine kinase and creatine kinase-MB catalytic activity concentrations (assayed by a routine method) and serum creatine kinase-MM mass concentrations (assayed by EIA) declined to normal values, while serum T3, T4, and thyroid stimulating hormone attained normal values. Serum creatine kinase-MB mass concentrations (assayed by EIA), however, still remained at the higher level, without complete recovery from myocardial damage, as shown by electrocardiogram (ECG). These data indicate that metabolic distortion still exists in the myocardium, as revealed by the high creatine kinase-MB mass concentration, especially as assayed by EIA, even though the plasma levels of thyroid hormones had returned to normal.

Creatine kinase in the dog: a review.

In the dog, creatine kinase (CK) is mostly present in the skeletal muscles, myocardium, brain and intestine. The MM isoenzyme predominates in muscles and myocardium. In plasma, reference values depend on the technique used and CK-MB accounts for about 30-45% of total CK activity. Sex has no influence on plasma CK activity, which is higher in young dogs than in adults. Plasma CK is elevated after physical exercise. After its release from the cells, CK reaches the plasma mostly via the lymphatic route and then remains in the plasma compartment. It is rapidly cleared with a half-life of about 2 hours. Muscle diseases are the main source of plasma CK elevations: inherited myopathies, malignant hyperthermia, hypothyroidism, vitamin E-selenium deficiency, prolonged decubitus, intramuscular injections, surgery, etc. Plasma CK is also increased in experimental myocardial infarction, for which the dog is an interesting model, allowing quantification of the damage by measuring the total CK activity released.

Non-invasive diagnosis of arterial patency after thrombolytic treatment and its relation to prognosis.

To validate a simple noninvasive method with serial creatine kinase measurements for diagnosis of early patency of the infarct related artery after thrombolytic treatment with streptokinase. To investigate the relation between early patency of the infarct related artery and prognosis. Patients under 76 years of age and seen within six hours of the start of prolonged chest pain and ST segment elevation were treated with streptokinase (1.5 x 10(6) U) intravenously over 30-60 minutes. Blood for measurement of total creatine kinase activity was taken at baseline and at 1, 2, 3, 4, 8, 12, 16, 20, and 24 hours after starting treatment. The rise in enzyme activity at each time from baseline was expressed as a proportion of the total rise from baseline to peak. Patients studied were in the following groups: (a) Sixty patients took part in a validation study with angiographic determination of patency of the infarct related coronary artery at 2.6 (0.3) hours (mean (SD)) after starting streptokinase. (b) A further 258 patients did not have early arteriography, but data were added to those from the 60 validation patients to find the relation between enzymatically determined early patency of the infarct related artery and 30 day mortality. (c) A further subset of 232 patients with first infarctions (including patients from groups (a) and (b) had angiocardiography at three weeks after infarction, and data were used to investigate the relation between early patency of the infarct related artery and left ventricular function. Normalised rate of rise of creatine kinase activity at three hours after starting streptokinase in relation to angiographic patency of the infarct related coronary artery at 2.5 hours; 30 day cardiac mortality; and left ventricular function at three weeks in survivors of first infarction. In the validation study, a rise in three hour creatine kinase activity of > 20% of peak occurred in 34/37 patients with initially patent infarct related coronary arteries (sensitivity 92%), and a rise to < 20% of peak occurred in 21/23 patients with initially occluded arteries (specificity 91%). In the prognostic study, 30 day mortality was 2.1% in the 191 patients with three hour creatine kinase > 20% of peak and 8.7% in the 127 patients with three hour creatine kinase < 20% of peak (p < 0.01). Angiocardiography in three week survivors of anterior infarction (n = 95) showed better left ventricular function when three hour creatine kinase was > or = 20% than when it was < 20% of peak (mean (SEM) end systolic volume 71 (5) v 96 (9) ml, p < 0.02; ejection fraction 56% (2%) v 51% (2%), NS). Non-invasive determination of early patency of the infarct related artery by the normalised rate of rise of creatine kinase activity at three hours seems to be reliable, and may be prognostically important and of value for use in clinical trials.

Serum macro creatine kinase type 2 in asphyxiated newborn infants

The presence of macro creatine kinase type 2 (MCK2) activity was noted in the serum of seven out of 32 newborn infants with perinatal asphyxia or birth trauma. MCK2 isoenzyme, when present, represented 15–35% of the total creatine kinase (CK) activity. The clinical and biochemical features of the seven MCK2-positive and 25 MCK2-negative newborns were compared. The infants with MCK2 activity were all males and clinically appeared to be more severely injured, requiring longer hospitalization. Total CK activity was similar in the two groups and CK-MB and CK-BB isoenzyme fractions were present in a similar proportion of infants in both groups. Two infants in each group had long-term neurological disorders. Although the presence of MCK2 has been noted in adult patients with end-stage metastatic solid tumors, the presence of this isoenzyme has not previously been reported in newborn infants.

Brain creatine kinase activity during ontogeny of the cichlid fish oreochromis mossambicus and the clawed toad xenopus laevis, influence of gravity?

The development of creatine kinase (CK) activity was studied in the brain of cichlid fish and clawed toads. The activity of CK in the whole brain of the fish decreases immediately after hatching (stage 6) from values of about 135 nmol substrate cleaved/mg protein/min to a value of about 105 at stage 8 (5 days post hatch at 20°C). With the exception of a significant peak (125 nmol) between stages 9 and 10 (7 and 9 days respectively, post hatch at 20°C) and a small intermediate peak at stages 12 and 13 (about 10 days post hatch at 20°C) a constant level of about 100 nmol cleaved substrate is maintained until maturity. In contrast, CK activity was determined to be 3-fold higher in the whole brain of the clawed toad. With the exception of two significant peaks at stages 47 and 49 (5 and 12 days respectively, post fertilization at 23°C) a value of about 360 nmol was found during larval development and metamorphosis, as well as in the adult brain. In investigating the possible influence of gravity on CK activity during early ontogeny of the brain both animal species were exposed to hyper-gravity (3±1 g) for 7 days. A significant decrease of total CK activity of 20% was found in the fish brain and of about 5% in the toad. Changes in total CK activity during brain development, as well as after the influence of altered gravitational forces, suggests that this enzyme is well adapted to critical phases of brain development and reacts very sensitively during this period to changes in environmental conditions.

Use of creatine kinase isoforms for diagnosis of infarct artery patency after thrombolytic therapy with streptokinase.

We investigated whether the proportion of creatine kinase (CK) MM3 to total MM isoform, measured in a single blood specimen taken at 3 hours after starting intravenous administration of streptokinase to patients with developing myocardial infarction, would give reliable information on patency or occlusion of the infarct-related coronary artery. Fifty-nine patients received streptokinase 1.5 x 10(6) U intravenously within 6 hours of onset of prolonged chest pain and ST-segment elevation. Patency of the infarct-related coronary artery was assessed by arteriography at 2.6 +/- 0.3 (SD) hours after starting streptokinase. Creatine kinase MM isoforms were measured by chromatofocusing in blood taken at 3 hours after streptokinase. A proportion of CKMM3 to total CKMM of greater than 50% was present in 34 of 34 patients (100%) with a patent, infarct-related artery at arteriography and whose peak total CK activity reached twice the upper normal limit for our laboratory (600 U/L). CKMM3/total CKMM was less than 50% in 14 of 18 patients (78%) in whom the infarct-related artery was occluded. In five of six patients with a nondiagnostic total CK rise (peak < 600 U/L), 3-hour CKMM3/total CKMM was less than 50% despite a patent artery. CKMM3 was not measurable in one patient. A proportion of CKMM3/total CKMM of greater than 50% is highly sensitive for prediction of infarct artery patency at 3 hours after administration of streptokinase. However, the test used in this way is not reliable for patients with "prevented" myocardial infarction. Also, positive tests do occur in patients with angiographically occluded arteries, possibly signifying intermittent reperfusion and occlusion.

Functional Maturation of Creatine Kinase in Rat Brain

The physiological role of the phosphocreatine (PCr)/creatine kinase (CK) system has been studied in rat brain by comparing maturational changes in in vivo CK-catalyzed reaction rate and activities of CK isoenzymes. The CK-catalyzed reaction rates, measured by 31P-nuclear magnetic resonance spectroscopy, increased 4-fold between 12 and 17 days of age. The mitochondrial CK (Mi-CK) isoenzyme, as a percentage of total CK, increased to the same extent over this relatively narrow age period. Cytosolic CK (B-CK) was active earlier and, with the total CK activity, increased steadily over a longer time course. An immunohistochemical study of cerebellum showed Mi-CK predominantly in gray matter, while the cytosolic CK was present in rather large concentrations in both gray and white matter. In the molecular layer, B-CK was most prominent in the Bergmann glial cells, while Mi-CK was more prominent in Purkinje neurons. During development a redistribution of Mi-CK from the Purkinje cell bodies to their processes was observed. These results point to regional differences in CK content and in isoenzyme-specific localizations. The increase in CK activity is temporally coincident with the maturational appearance of closely coupled decreases in brain PCr and ATP during hypoxia. These maturational changes suggest that the activity of the PCr/CK system, particularly the Mi-CK isoenzyme, is central in regulation of brain ATP.

Altering creatine kinase isoenzymes in transgenic mouse muscle by overexpression of the B subunit.

To change the levels of expression and isoenzyme distribution of creatine kinase (CK) in muscle, transgenic technology was used to express the B subunit of CK in mouse muscle. Normally, mammalian skeletal muscle contains the MM dimer of CK. The BB dimer and MB heterodimer of CK can be found in brain and heart, respectively. Heterologous genes consisting of skeletal and cardiac muscle-specific actin promoters fused to the genomic coding region of the B form of CK were used to create transgenic mice. Lines were established from the three highest expressing founders. Analysis of skeletal muscle extracts revealed that all three lines had an increase in total CK activity measured under maximal velocity conditions. The highest expressing line, 7001, had a CK activity 150% that of control muscle. Nuclear magnetic resonance saturation transfer was used to measure the in vivo rate of the CK reaction. In 7001 hindlimb muscles, the CK catalyzed reaction was 200% that of control muscle. The elevation in CK activity in transgenic muscle was accompanied by significant changes in the composition of the cytosolic isoenzyme ratio of CK. In control, 100% of CK was MM, whereas 7001 had 60 +/- 18% MM, 32 +/- 10% MB, and 8 +/- 2% BB. There were no changes in ATP, phosphocreatine, Pi, or creatine levels in transgenic muscle compared with control. Immunofluorescence of myofibrils isolated from control and transgenic muscle revealed specific association of CK to the M line. Small amounts of MB CK were detected on myofibrils from transgenic mice. Transgenic mice expressing the B subunit of CK in muscle represent a first step toward altering CK isoforms so as to elucidate the specific roles of these isoforms in energy metabolism.

Analytical and Clinical Evaluation of Creatine Kinase MB Mass Assay by IMx: Comparison with MB Isoenzyme Activity and Serum Myoglobin for Early Diagnosis of Myocardial Infarction

We analytically and clinically evaluated Abbott's IMx assay for creatine kinase (CK) isoenzyme MB (CK-MB) in serum. Over a 1-year period, the method was more specific but less precise than catalytic isoenzyme measurements by electrophoresis or immunoinhibition. Sera from different individuals without electrophoretic evidence of CK-MB but containing macro CK type 1 (n = 20), mitochondrial CK (n = 5), or CK-BB (n = 5) were scored as CK-MB negative by the IMx. Likewise, CK-MB-negative by the sera remained so after addition of purified human CK-MM (< or = 7600 U/L) or CK-BB (< or = 8100 U/L). For 39 patients admitted for suspicion of uncomplicated acute myocardial infarction (precordial pain for < or = 4 h), the diagnostic performance of the IMx CK-MB assay on admission and 4 h later was superior to that of total CK activity and compared well with that of CK-MB activity measured by electrophoresis or immunoinhibition. An admission, myoglobin showed a higher diagnostic sensitivity, specificity, and predictive value than did CK-MB and was the most informative test. Diagnostic performance on admission and 4 h later was further improved by considering positivity for myoglobin and for CK-MB by IMx and for the change in each over the first 4 h of hospitalization as criteria. Twelve hours after admission, diagnostic performance was further improved for all CK and CK-MB methods but began to decline for myoglobin.

Serum creatine kinase isoenzyme measurements in master male and female marathon runners

This study investigated exercise‐induced muscle enzyme release in master runners by assessing the activity of total serum creatine kinase (total CK) and the concentration of the isoenzyme creatine kinase MB (CK‐MB). Subjects were 12 male (54 ± 9 years) and seven female (50 ± 6 years) master marathon runners. Premarathon (24 hours before) and postmarathon serum samples were collected (24, 48, 72, and 96 hours after the race). Total CK was measured enzymatically and CK‐MB concentration was assayed utilizing a double antibody procedure. The men's and women's 24 hour (1012 U/L, 782 U/L) and 48 hour (581 U/L, 441 U/L) postrace mean total CK activities were significantly (p≤0.05) elevated above prerace values (66 U/L, 119 U/L). CK‐MB concentration 24 hours postrace was also significantly (≤0.05) elevated from prerace values (0.27 ng/ml, 0.0 ng/ml) in both males (34.4 ng/ml) and females (16.7 ng/ml). The results of this study indicate that the pattern of exercise‐induced muscle enzyme release from the stress of ...

Ratio of Creatine Kinase 2 Mass Concentration to Total Creatine Kinase Activity not Altered by Heavy Physical Exercise

Serum creatine kinase isoenzyme 2 concentrations (CK 2 mass) were measured in marathon runners during training and 1 and 2 days after a race and compared with values from 36 acute myocardial infarction (AMI) patients whose total CK and (or) CK 2 activities were similar to those of runners in the basal state. During training, runners had CK and CK 2 activities 53% and 43% above reference values, respectively, and 36% had CK 2 activity > 5% of total CK. Nine runners (26%) showed CK 2 mass values > 6 micrograms/L but < or = 10 micrograms/L; 35 of the AMI subjects, despite having CK activities similar to those of runners, had values > 10 micrograms/L. The ratio of CK 2 mass to total CK activity was significantly (P < 0.0002) different between sexes for runners. At 1 and 2 days after racing, 100% of CK and CK 2 activities and 71% and 57% of the percentages of CK 2 activity, respectively, were abnormally high; 57% and 43% of CK 2 mass values were > 10 micrograms/L, being comparable with those observed for the AMI group. Basal CK 2 mass values of the runners appeared only slightly higher than that for sedentary subjects, but after exercise half the subjects presented increased values similar to those observed for AMI subjects. The ratio of CK 2 mass to total CK activity appeared unaltered by exercise in all but one of the samples assayed, indicating its utility in evaluating CK 2 mass increases originating in skeletal muscle.

Partial correction of impaired creatine kinase activity in diabetic rat heart by physical training

The effect of physical training on total creatine kinase (CK), CK-MM, and CK-MB isoenzyme activity was studied in hearts of diabetic and control rats. Diabetes was induced with streptozotocin (50 mg/kg), and only rats with blood glucose levels between 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise training was performed on a treadmill in a progressive 10-week program. Physical training did not induce any significant changes in plasma glucose or insulin levels in diabetic rats. Total CK, CK-MM, and CK-MB activity was decreased in diabetic rat heart by 27%, 22%, and 56%, respectively. Physical training did not induce any important changes in CK activity in heart of nondiabetic rats. However, in diabetic rat heart, training increased total CK activity by 13%, CK-MM activity by 12%, and CK-MB activity by 31%. We conclude that the decrease in cardiac CK activity observed in chronic experimental diabetes mellitus can be partly alleviated by a program of physical training. This may be one of the mechanisms whereby physical conditioning improves cardiac function in experimental diabetes.