Lower CK Research Articles

Effect of cooling after human cardiac arrest on myocardial infarct size

The Hypothermia after Cardiac Arrest (HACA) trial assessed whether mild therapeutic hypothermia improved the rate of good neurological recovery in patients after ventricular fibrillation cardiac arrest of presumed cardiac origin. We evaluated the impact of hypothermia on myocardial injury. Re-analysis of a HACA trial subset for our department (cooling, n=55; controls, n=56). Plasma levels of CK, CKMB and ST-scores were used as a measure of infarct size. Area under the curve (AUC) for CK was 28,786U/l x 24 h (IQR 5646-44,998) in the cooling group and 20,373U/l x 24 h (IQR 8211-30,801) for controls (p=0.40), for CKMB AUC was 1691U/l x 24 h (IQR 724-3330) and 1187U/l x 24 h (IQR 490-2469), respectively (p=0.18). The ST score was -40% (IQR [-55]-[+16]) in the cooling group (n=23) and -22% (IQR [-84]-[+33]) for controls (n=24) (p=0.76). When the cooling group was stratified into early (< or =8h) and longer (>8h) time to target temperature, the early group displayed a significantly lower CK 7340U/l x 24 h (IQR 3921-33,753) vs. 38,986U/l x 24 h (IQR 23,945-57,514, p=0.007) and a lower CKMB. Cooling after successful resuscitation for ventricular fibrillation cardiac arrest did not influence infarct size. Cautious interpretation of the subgroup analysis may indicate a favourable trend for early cooling.

Black Tea Extract Reduces DOMS, Oxidative Stress, and Cortisol Responses to High-Intensity Interval Training

Muscle soreness and decreased performance often follow a bout of high-intensity exercise. By reducing these effects, an athlete can train more frequently and increase performance. PURPOSE: To examine whether a high-potency, black tea extract (BTE) alters delayed onset muscle soreness (DOMS), oxidative stress, and cortisol (CORT) responses to high-intensity anaerobic exercise. METHODS: College-age males (N=18) with 1+yrs of weight training experience completed a double-blind, placebo-controlled, crossover study. Each subject completed two testing sessions (T1 and T2), which consisted of a 30s Wingate Test plus eight 10s intervals. Blood samples were obtained before, and 0, 30 and 60 min following the sessions for analysis of CK, GSH:GSSG, and CORT. Muscle soreness was recorded at 24 and 48 h post-test using a visual analog scale. Subjects consumed the BTE or placebo (PLA) for 9 d. T1 occurred on day 7 and administration continued for 2 more days during the assessment of DOMS. Each subject underwent a 5 d washout before administering the product they did not receive in the initial supplementation phase. BTE supplementation consisted of 1,760mg BTE·d-1. Significance was set at p<.10 to protect against type II error. RESULTS: Across the 48 h post-exercise period, BTE produced significantly lower DOMS (24 h=1.1+0.3 cm; 48 h=0.9+0.3 cm) compared to PLA (24 h=2.1+0.4 cm; 48 h=1.9+0.5 cm), P<.001. A Time × Condition interaction (P=.044) emerged for the GSH:GSSG ratio, with BTE having less oxidative stress at 30 and 60 min post compared to PLA (P<.02). An interaction also emerged for CK (P=.005), with BTE having significantly lower CK by 30 min post (228+33 U·L−1 vs 333+41 U·L−1, P=.005) despite similar values immediately post-exercise (316+55 U·L−1 vs 334+49 U·L−1, P=.69). CORT secretion was altered both by Time (P<.001) and Condition (P=.09). Though both BTE and PLA had elevated CORT values post-exercise, the BTE condition had lower overall CORT, which was confirmed by AUC analysis (P=.098). CONCLUSIONS: BTE appears to enhance recovery or blunt some of the physiological responses to acute anaerobic intervals and is associated with a reduction in DOMS. This may help optimize performance during an acute bout of exercise while also speeding the recovery process in order to facilitate engaging in future training. Supported by WellGen, Inc.

Antioxidant supplementation attenuates the exercise‐induced increase in plasma CK, but not CRP, during moderate intensity endurance exercise in men

We investigated the effect of antioxidant supplementation and repeated bouts of moderate intensity endurance exercise on markers of muscle damage (creatine kinase-CK) and systemic inflammation (C-reactive protein-CRP). Following a placebo-controlled, double-blind, parallel, random design, 20 healthy, young, sedentary men performed two separate, but identical, bouts of cycling for 90 min at 65% VO2max. The first bout was after 8 days of supplementation with placebo (PL), whereas the second bout was after 8 days of supplementation with either PL (n = 10) or antioxidants (ANT, n = 10). Plasma was analyzed for CK and CRP at baseline, immediately post, 3 h post, and 24 h post exercise. Compared with baseline values, plasma CK was 2 fold higher at 3 h post exercise (P < 0.001) and 3.5 fold higher at 24 h post exercise (P < 0.001). Compared with PL, ANT had lower CK values at 3 h post (−31%, P = 0.079) and 24 h post (−34%, P < 0.001) exercise. A significant arm x exercise interaction (P = 0.004) indicated that 24 h post exercise values during the second bout of exercise were lower than during the first bout (−19%, P = 0.003). CRP at 24 h post exercise was 2.8–3.2 fold higher than all other values (P < 0.001), with no difference between the groups. We conclude that acute exercise increases plasma concentrations of both CK and CRP, and that only CK is attenuated with antioxidant supplementation. Antioxidant supplementation may reduce muscle damage in response to prolonged moderate intensity endurance exercise, but has no effect on the systemic inflammatory response. (Supported by NSERC Canada)

Less calcemic Vitamin D analogs enhance creatine kinase specific activity and modulate responsiveness to gonadal steroids in the vasculature

Vitamin D receptors are widely expressed in the cardiovascular system, in which Vitamin D and its metabolites exert a variety of biological activities such as regulation of cellular proliferation and differentiation, cell calcium transients and cell energy metabolism in vitro. The latter is mediated through the control of the brain type creatine kinase specific activity (CK), which serves to provide a readily available reservoir for ATP generation under increased work-load. In the present study we undertook to assess the role of Vitamin D on energy metabolism in the rat heart and aorta in vivo by using CK, which is a key energy metabolizing enzyme and compare Vitamin D depleted and repleted animals. Vascular tissues from female or male Vitamin D-depleted rats showed 61–80% lower CK activity in the aorta (Ao) and left ventricle of the heart (Lv) than control, Vitamin D-replete rats. Moreover, neither estradiol-17β (E 2) nor dihydrotestosterone (DHT), which increases CK specific activity in Ao and Lv of intact female or male rats, respectively, were able to stimulate CK in Vitamin D-depleted rats. Treatment of intact female rats for 2 weeks or 2 months with the less-calcemic Vitamin D analogs JKF 1624F 2-2 (JKF) or QW 1624F 2-2 (QW) ( Fig. 1), did not significantly affect CK specific activity. However, after pretreatment with these analogs, there was an up regulation of the E 2-induced CK response in Ao and Lv. In intact female rats, all Vitamin D analogs also potentiated the in vivo CK response to the SERMs raloxifene (Ral) and tamoxifen (TAM) in Ao and Lv. However the inhibitory effect of Ral or TAM on E 2-induced CK activity was lost after pretreatment with Vitamin D analogs. The non-calcemic analog CB 1093 (CB) induced a significant increase in estradiol receptor α (ERα) protein in both myocardial and aortic tissue from intact and from ovariectomized female rats. Collectively, these results indicate that Vitamin D analogs modulate cell energy homeostasis in vascular tissues through induction of CK and up regulation of the response and sensitivity of CK in vascular tissues to E 2 and to SERMs, possibly through via an increase in ERα protein in female derived organs. These results corroborate our previous in vitro studies in human vascular cells and further suggest that the Vitamin D system plays an important physiological role in maintaining normal cell energy reservoir in the vasculature.

Influence of estrogen on markers of muscle tissue damage following eccentric exercise.

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill running bout at approximately 60% VO2max. The OC completed the exercise during the mid-luteal phase (day 22.9 +/- 1.5; high estrogen) while the EU did their exercise in the mid-follicular phase (day 9.6 +/- 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed pre-exercise, immediately post-, 24, 48 and 72 h post-exercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p < 0.001), and the interaction of group x time was significantly different (p < 0.01). The OC group had lower CK at 72 h post-exercise than did the EU group. Pre-exercise estrogen levels correlated with the overall mean CK (r = -0.43, p < 0.05) and 72 h (r = -0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p < 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear but may be related to the anti-oxidant characteristics and membrane stability properties associated with estrogen and its derivatives.

Phosphoglycerate mutase, 2,3-bisphosphoglycerate phosphatase and creatine kinase activity and isoenzymes in human brain tumours

The distribution of phosphoglycerate mutase (EC 5.4.2.1, PGM), 2,3-bisphosphoglycerate phosphatase (EC 3.1.3.13, BPGP) and creatine kinase (EC 2.7.3.2, CK) activity and isoenzymes in various regions of adult human brain and in brain tumours (astrocytomas, anaplastic astrocytomas, glioblastomas and meningiomas) has been determined using electrophoresis. PGM and cytosolic CK exist in mammalian tissues as three isoenzymes that result from the homodimeric and heterodimeric combinations of two subunits [types M (muscle) and B (brain)] coded by separated genes. In addition, a dimeric form and an octameric form of mitochondrial CK exist in mammals. Type BB-PGM was the major PGM isoenzyme found in normal brain, although type MB-PGM and type MM-PGM were also detected. All brain tumours possessed lower PGM activity than normal brain, and meningiomas showed higher BPGP activity. In astrocytic tumours, the proportion of type MB- and type MM-PGM decreased, and in meningiomas these isoenzymes were not detected. Type BB-CK and mitochondrial CK were the only CK isoenzymes detected in normal brain. Astrocytomas possessed lower CK activity than anaplastic astrocytomas and glioblastomas and, in addition, tended to possess lower CK content than normal brain. No qualitative changes of the normal CK isoenzyme pattern were observed in the tumours.

Prognostic Implications of Elevated Creatine Kinase After Coronary Angioplasty-Reply

To the Editor. —Dr Kong and colleagues 1 reported that elevation of CK following elective coronary artery intervention is associated with increased late cardiac mortality. 1 Earlier reports of placebo-controlled animal studies with pretreatment with coenzyme Q 10 (CoQ 10 ) 2,3 found that the animals pretreated with CoQ 10 had less ischemia-reperfusion cardiac injury. They showed less myocardial tissue injury and lower CK and malondialdehyde release.