Plasma Creatine Kinase Values Research Articles

The upper values of plasma creatine kinase of professional soccer players during the Brazilian National Championship

The current schedule of the Brazilian Soccer Championship may not give players enough recovery time between games. This could increase the chances of muscle damage and impaired performance. We hypothesized that plasma creatine kinase (CK) activity could be a reliable indirect marker of muscle overload in soccer players, so we sought to identify the reference values for upper limits of CK activity during a real-life elite competition. This study analyzed changes in plasma CK activity in 128 professional soccer players at different times during the Brazilian Championship. The upper limits of the 97.5th and 90th percentiles determined for CK activity were 1.338U/L and 975U/L, respectively, markedly higher than values previously reported in the literature. We also evaluated a team monthly throughout the Championship. The upper limit of the 90th percentile, 975U/L, was taken as the decision limit. Six players showing plasma CK values higher than this were asked to decrease their training for 1 week. These players presented lower CK values afterwards. Only one player with a CK value higher than the decision limit (1800U/L 1 day before a game) played on the field and was unfortunately injured during the game. The CK activity in all the other players showed a significant decrease over the course of the Championship, and the values became more homogeneous at the end. The results presented here suggest that plasma CK upper limit values can be used as a practical alternative for early detection of muscle overload in competing soccer players.

Effects of induced lameness via carpal osteochondral fragmentation on plasma creatine kinase activity in horses

Objective To determine whether or not plasma creatine kinase (CK) values could be used as a reliable indicator for skeletal-based lameness. Design Pilot study. Animals Eight adult horses of Quarter Horse lineage. Procedure All 8 horses (4 treatment, 4 control) received arthroscopic surgery on bilateral carpal joints, with an osteochondral fragment created in 1 knee of the treatment group only. Two weeks post-operatively, horses began treadmill work. Pre-exercise and 4-hour post-exercise blood samples were obtained for plasma CK measurement from horses in both treatment and control groups. Results Horses that received a carpal chip fracture (treatment group) produced greater levels of change in plasma CK when pre- and post-exercise values were compared than did horses without osteochondral fragmentation. Although changes in CK activity were reported, none of the CK values were outside the normal range. Conclusions and clinical relevance Results of this study hoped to lend performance horse practitioners another reliable tool in diagnosing skeletal-based lameness, using elevations in the muscle enzyme CK as the marker. In addition, skeletal-based lameness and gait alteration as causes of increased muscle enzymes were ruled out. Changes in plasma CK values were greater for horses in the treatment group when pre- and post-exercise samples were compared. However, elevations in CK were too inconsistent to be considered diagnostic for correlating skeletal lameness, muscle health, and exercise.

Cardiovascular responses to early exercise in inferior wall ST acute myocardial infarction

The heart rate and blood pressure responses to standardized exercise tests were studied in a group of patients with electrocardiographic evidence of inferior wall acute myocardial infarction (AMI). The tests were done on a bicycle ergometer at 8 to 10 days and 10 to 12 weeks after AMI. At 8 to 10 days after AMI, those with ST AMI (n = 12) had a significantly reduced heart rate response to exercise compared with patients with Q-wave AMI (n = 25). This difference was not evident at 10 to 12 weeks. The systolic blood pressure response in patients with ST AMI was lower than that of Q-wave AMI patients during the first exercise test, although the difference did not attain statistical significance but was significantly lower than the responses of both groups at the second test. The patients with ST AMI had smaller amounts of myocardial damage than those with Q-wave AMI as indicated by plasma creatine kinase values (p < 0.01). These differences in the heart rate responses appeared to result from the preferential activation of nonmyelinated afferent fibers in the subepicardial region of the inferior wall of the myocardium.

Lack of protection of ischemic myocardium by verapamil in conscious dogs

To determine whether coronary dilation and decreased myocardial oxygen requirements resulting from administration of verapamil, a calcium and slow current antagonist, protect ischemic myocardium in conscious dogs, we studied 15 treated and 15 control animals after coronary occlusion. Verapamil (0.2–0.7 mg/kg/h) was given by continoous infusion for 17 h beginning 5 h after the initial plasma creatine kinase (CK) elevation after coronary occlusion. Observed infarct size and infarct size predicted before verapamil were estimated from hourly plasma CK values and infarct size was estimated also from myocardial CK depletion measured directly, 24 h after occlusion. Changes in heart rate, blood pressure, and frequency of premature ventricular complexes (recorded every 30 min) after occlusion were similar in treated and control dogs. Coronary flow after verapamil, measured with radioactively labeled microspheres, did not increase in ischemic zones but increased by 90% in normal myocardium ( p < 0.05). The differences between observed and predicted infarct size estimated from plasma CK changes in treated and controls were similar (3.0±2.2 (S.E.) and 2.0±1.4 CK-g-eq), and myocardial CK depletion was also comparable in the two groups (25 ± 2% and 23 ±2%). Thus although verapamil, administered five hours after the initial plasma CK elevation, increased coronary flow in normal myocardium, it did not augment flow in ischemic tissue or limit the extent of infarction.