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.     

Effect of exercise on plasma pyruvate kinase and creatine kinase activity

Plasma pyruvate kinase (PK) and creatine kinase (CK) were measured in healthy subjects engaging in (a) mild exercise, 30 min on an exercise cycle maintaining a pulse rate of 150/min, (b) moderate exercise, squeezing a ball until exhaustion with a sphygmomanometer cuff inflated above systolic pressure around the arm (max. 2 min) and (c) severe exercise, completing a marathon race. Mild exercise resulted in no change in enzyme levels over 24 h. Moderate exercise produced a small increase in PK but no change in CK. PK activity rose from 35.3 +/- 10 U/l pre-exercise to 41.3 +/- 13 U/l 15 min post-exercise (n = 8, p less than 0.025). Severe exercise (completing a marathon race) resulted in a 3-fold increase in PK from 26 (4-87) U/l pre-race to 69 (21-156) U/l immediately post-race, and also, as expected, an increase in CK from 60 (15-164) U/l to 257 (72-1535) U/l (results are means and ranges, n = 69, p less than 0.001 for both enzymes). Runners showed parallel increases in PK and CK (p less than 0.05 by Spearman rank correlation). The mean post-race activity of CK-MB was less than 5% of total CK but 18 runners had values greater than 6% (mean 4.8, range 1-18). We conclude that PK, like CK, is increased following exercise due to liberation of muscle enzyme. However, only severe exercise is likely to lead to a substantial increase in plasma PK activity and therefore prejudice its clinical usefulness as a diagnostic test.     

Immunochemical extraction and automated measurement of plasma creatine kinase MB isoenzyme and creatine kinase MB2 isoform

Measurement of creatine kinase MB (CK-MB) and its isoforms CK-MB₂ and CK-MB₁ are now applied in the diagnosis of acute myocardial infarction (AMI). The most common approach for analysis includes RIA, IRMA, and electrophoresis, all of which may be time-consuming. This study examines determination of CK-MB and CK-MB₂ by a rapid immunochemical extraction method followed by an automated measurement for both analytes. The automated method was sensitive to 2 U/L, linear to 180 U/L, and gave excellent interassay precision (<10% CV). Interference studies indicated that bilirubin, hemolysis, and lipemia caused analytical problems as did the presence of high activities of other CK isoenzymes, notably CK-MM and CK-BB, requiring dilution of samples prior to analysis. Application of immunochemical extraction gave a reference interval of CK-MB (0–2.5 U/L) and CK-MB₂ (0.1–1.4 U/L) for blood donors (20–60 years), peak levels for ruled-out AMI patients of CK-MB (0.5–7.3 U/L) and CK-MB₂ (0.3–4.9), peak levels for ruled-in AMI patients of CK-MB (80–174 U/L) and CK-MB₂ (80–155 U/L). Coronary artery bypass patients (n = 24) and all trauma patients (n = 14) also demonstrated elevations in CK-MB and CK-MB₂, whereas only five of the trauma patients demonstrated increased CK-MB by IRMA. In patients (n = 7) having increased total CK and normal CK-MB by IRMA, the extraction assay for CK-MB and CK-MB₂ yielded increased values in all patients. This new approach to CK-MB and CK-MB₂ analysis can be performed within 30 minutes of sample receipt. J. Clin. Lab. Anal. 11:163–168, 1997. © 1997 Wiley-Liss. Inc.     

Cardiac work is related to creatine kinase energy supply in human heart failure: a cardiovascular magnetic resonance spectroscopy study

Background

It has been hypothesized that the supply of chemical energy may be insufficient to fuel normal mechanical pump function in heart failure (HF). The creatine kinase (CK) reaction serves as the heart’s primary energy reserve, and the supply of adenosine triphosphate (ATP flux) it provides is reduced in human HF. However, the relationship between the CK energy supply and the mechanical energy expended has never been quantified in the human heart. This study tests whether reduced CK energy supply is associated with reduced mechanical work in HF patients.

Methods

Cardiac mechanical work and CK flux in W/kg, and mechanical efficiency were measured noninvasively at rest using cardiac pressure-volume loops, magnetic resonance imaging and phosphorus spectroscopy in 14 healthy subjects and 27 patients with mild-to-moderate HF.

Results

In HF, the resting CK flux (126?±?46 vs. 179?±?50 W/kg, p?< 0.002), the average (6.8?±?3.1 vs. 10.1?±?1.5 W/kg, p ?<0.001) and the peak (32?±?14 vs. 48?±?8 W/kg, p <?0.001) cardiac mechanical work-rates, as well as the cardiac mechanical efficiency (53%?±?16 vs. 79%?±?3, p <?0.001), were all reduced by a third compared to healthy subjects. In addition, cardiac CK flux correlated with the resting peak and average mechanical power (p <?0.01), and with mechanical efficiency (p?= 0.002).

Conclusion

These first noninvasive findings showing that cardiac mechanical work and efficiency in mild-to-moderate human HF decrease proportionately with CK ATP energy supply, are consistent with the energy deprivation hypothesis of HF. CK energy supply exceeds mechanical work at rest but lies within a range that may be limiting with moderate activity, and thus presents a promising target for HF treatment.

Trial registration

ClinicalTrials.gov Identifier: NCT00181259.

     

Creatine kinase B-subunit activity in human serum. I. Development of an immunoinhibition method for routine determination of S-creatine kinase B-sununit activity

The properties of an inhibiting antibody directed against the M-subunits of human creatine kinase (EC 2.7.3.2, CK) were investigated in the reaction system recommended by the Scandinavian Committee on Enzymes (S.C.E.).At 37° C the rate of immunoinhibition of human CK M-subunit dependent activity corresponded to a $\text{t}{}_{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}$ of 38 s giving a k value of ?2 per cent · s^?1 when samples were incubated in the S.K.E. CK reagent A in the presence of antibody. Under the selected conditions immunoinhibition of S-CK M-subunit activity up to 1800 U/l was 99 per cent completed within 5 minutes using undiluted samples. No inhibition of CK B-subunit activity occurred at the chosen concentration of antibody. The inhibition data were verified using human sera and electrophoretically homogeneous preparations of human CK isoenzymes BB and MM.Sample adenylate kinase (EC 2.7.4.3, AK) was found to constitute a potential source of falsely increased S-CK B activity. As reported in the accompanying paper a S-CK B value of 15 U/l was used as a discrimination value in the diagnosis of acute myocardial infarction. The S.C.E. CK method incorporates a combination of two AK inhibitors adenosine 5'-monophosphate and P¹, P⁵-diadenosine 5'-pentaphosphate. However, a frequency analysis of sample AK activities demonstrated that AK activities of more than 8 U/l will occur in about 10 per cent of the cases. Consequently, it was deemed necessary to measure the individual sample blank AK rates.The routine procedure developed thus included three separate measurements: determination of total S-CK and of S-CK B activities in the absence and presence of antibody, respectively. As the immunoinhibition was only 99 per cent complete a value corresponding to one per cent of the total S-CK activity was subtracted from the measured S-CK B activity. Likewise, the individual sample AK activity had to be measured and subtracted from the apparent S-CK B activity.The within-series precision of this S-CK B method at the levels of 10 U/l and 20 U/l corresponded to C.V. values of 10 and 5 per cent, respectively. Day-to-day precision at the level of 417 U/l corresponded to a C.V. of 4 per cent. The day-to-day precision of a control, total CK activity 625 U/l, gave a mean value of 53% ± 3% of CK B activity.     

Wheelchair marathon racing causes striated muscle distress in individuals with spinal cord injury

OBJECTIVE: To assess the effects of wheelchair marathon racing in individuals with spinal cord injury (SCI) on circulating muscle enzymes and myoglobin. SUBJECTS: Thirty-one men with SCI, including 25 wheelchair marathon athletes and 6 sedentary men. DESIGN: Serum myoglobin (Mb), creatine kinase (CK) activity, and lactate dehydrogenase (LDH) were measured in participants of the 1995 Oita International Wheelchair Marathon Race (42.195 km). Blood samples were obtained 24 hours before, immediately after, 24 hours after, and 7 days after the race. RESULTS: Marathon racing resulted in significant increases in serum Mb, total CK activity, and LDH (p<.01) after the race. The peak Mb and LDH levels occurred immediately after the race; total CK activity peaked 24 hours after the race. Evaluation of cardiac muscle enzymes showed no significant changes in two CK isoenzymes (CK-MM and CK-MB). CONCLUSIONS: Propulsion of the wheelchair in a marathon race induced muscle stress in athletes with SCI. Completion of the marathon race did not cause cardiac muscle damage, however. Elevated muscle enzyme levels likely resulted from muscle distress rather than from dehydration.     

Creatine kinase MB isoforms in patients with skeletal muscle injury: ramifications for early detection of acute myocardial infarction.

We measured total creatine kinase (CK), CK-MB isoenzyme, and the MB isoforms in 202 serum and plasma samples from nine groups of patients and normal individuals: 39 with acute myocardial infarction (MI), divided according to time between the onset of chest pain and blood collection (1-6 h, 7-12 h, and 13-48 h); 26 with chest pain for whom an MI was ruled out, sampled at admission; 17 undergoing bypass surgery or cardiac catheterization, sampled within 6 h after either procedure; 17 with acute skeletal muscle injury, sampled within 8 h after injury; 30 marathon runners immediately after a race; 17 runners and other athletes > 12 h after training or a race; 12 with cerebral injury or seizures, sampled at admission; 8 with closed head injury, sampled at admission; and 38 normal subjects. CK-MB (relative index) and MB isoforms (MB2/MB1) were respectively increased in 15% and 75% of MI patients 1-6 h after onset, 94% and 94% after 7-12 h, and 88% and 8% after 12 h, and in 87% and 82% of cardiac surgery patients. MB isoforms were increased in most patients with acute skeletal muscle trauma and in subjects examined after exercise, but were within normal limits in patients for whom MI was ruled out, patients with cerebral trauma, and normal individuals. The relative index of MB/total CK was normal in essentially all individuals in the last groups, including those with acute skeletal muscle trauma. We concluded that the CK-MB isoform ratio is increased in both acute skeletal muscle injury and MI. The isoform ratio is most useful for distinguishing recent from old (> 12 h) injury.     

Isoforms of creatine kinase MM and MB in acute myocardial infarction: a clinical evaluation

Serum creatine kinase (CK, EC 2.7.3.2) isoenzymes MM and MB were resolved, respectively, into three (MM1, MM2, MM3) and two (MB1, MB2) isoforms (subforms derived from the same isoenzyme) by electrophoresis and the isoform patterns were determined in multiple sequential serum samples, timed from the onset of chest pain, from 58 patients with acute myocardial infarction (AMI). During the first 3 h after the onset of chest pain, the serum isoform activity resembled the pattern seen in normal volunteers. Specimens obtained 6 h after AMI showed predominantly MM3 and MB2 (45% and 11% of the total CK activity, respectively). Between 10 and 72 h, there was a gradual shift in which MM3, MM2 and MB2 decreased, while MM1 and MB1 increased. MB2 and MB1 disappeared from the pattern for samples collected after 24-48 h, while MM1 was always the most prominent band at the end of the observation period (66%, range 41-77%, at 48 h). These data suggest that a single determination of CK isoform pattern, drawn between 6 and 48 h after AMI, may provide an effective means of predicting the time of onset of necrosis. There were no significant differences in the CK isoform patterns according to infarct location and functional status of patients.     

An improved method for the routine biochemical evaluation of patients with recurrent calcium oxalate stone disease

By means of a computerized calculation program, a simplified estimate of the ion-activity product of calcium oxalate was derived (AP(CaOx)-index), based on the 24-h urinary excretion of calcium (Ca), oxalate (Ox), magnesium (Mg), citrate (Cit) and the urine volume (V):

$\text{3.8 × Ca}{}^{0.71}\text{× Ox}\text{Mg}{}^{0.14}\text{× Cit}{}^{0.10}\text{× V}{}^{1.2}$

With urinary electrolyte values within the normal range, there was a good correlation between the AP(CaOx)-index and the more laboriously obtained ion-activity product (r = 0.997). To express the biochemical risk of CaOx stone formation a CaOx-risk index was designed, which also includes the inhibition of calcium oxalate crystal growth (I) and with all variables related to urinary creatinine (Cr):

$\text{(Ca/Cr)}{}^{0.71}\text{× (Ox/CR)}\text{(Mg/CR)}{}^{0.14}\text{× (Cit/Cr)}{}^{0.10}\text{× I}$

The mean CaOx-risk index (±SEM) in urine from 100 normal men and 156 male stone formers were 648±27 and 1019±38 respectively (p < 0.001). A risk index without inhibition index, had the corresponding values 366±14 and 527±17 (p < 0.001).     

Serum creatine kinase activity and its changes after a muscle biopsy

Summary. The significance of the absolute elevations of serum creatine kinase (CK) levels after intense exercise and injuries was studied by measuring CK activities from seven healthy active males during a 2-week period, with a muscle biopsy taken between the first and second week. Most of the subjects (three lifters and two runners) carried on their normal exercise activities, while two lifters stopped training during the 2 weeks. The weight of the biopsy, number of fibres, percentage of fibre types, and cross-sectional areas of the muscle fibres were measured. The CK levels of the nonactive subjects and runners remained consistently low during the control week, whereas those of the lifters were usually 500% greater than those of the other two groups, and fluctuated with the intensity of their workouts. A muscle biopsy, having a mean weight of 71.3 mg and containing 1800 fibres, increased the CK values by approximately 100 units litre^-1 (U1^-1) in most of the subjects. One runner injured his right hamstring muscles 2 days prior to the biopsy, and his CK values rose from 50 to 4400 U I^-1. The increases in CK after the biopsy were not related to fibre type, activity, weight of the biopsy, or number or size of fibres removed. These results indicate that:

• 1 CK values are consistently lower in normal subjects and runners than in lifters.
• 2 Weight training results in chronic elevations of CK.
• 3 Compared to a muscle biopsy, muscular injury dramatically increases CK levels.
• 4 Elevation of serum CK is observed as early as 1 h after an intense weight-lifting session.
• 5 The elevation of serum CK by 100 U 1^-1 is associated with damage to approximately 2000 fibres.

     

Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study

Objective: To ascertain if, after an episode of hypotension, unnoticed myocardial necrosis could occur in critical care patients with acute non-cardiac illness and to search for signs of cardiac necrosis. ¶Design: A prospective observational study.¶Setting: General intensive care unit (ICU) at a tertiary level hospital.¶Patients: Thirty-one patients in two groups. Group 1 included 19 patients with severe sepsis/septic shock (ACCP/SCCM Consensus Conference). Group 2 included 12 patients with hypovolemic shock.¶Interventions: Biochemical markers of myocardial necrosis (cardiac troponin I (cTnI), creatine kinase (CK), creatine kinase MB mass (CKMB) and myoglobin) were measured at 12 h (T1), 24 h (T2) and 48 h (T3) after enrollment.¶A standard 12-lead ECG was recorded upon enrollment (T0) and at T2. Anomalous Q-waves or ST segment depression or elevation was considered diagnostic for acute myocardial infarction (AMI). A hypotensive episode (arterial systolic pressure < 90 mmHg at heart rate > 100 bpm) was considered moderate if it lasted 30–60 min or severe if longer than 60 min.¶Measurements and results: At T0 none of the patients had AMI on ECG. At T2 a non-Q AMI developed in five patients. Increased levels of troponin I, myoglobin, CK and CKMB were found in 74.2 %, 96.8 %, 74.2 % and 67.7 % of the patients, respectively. Cardiac troponin I increased in 11 out of 19 septic patients and in all hypovolemic patients. There was a significant difference between the groups (p < 0.05). All biochemical markers increased in relationship to the degree of hypotension with cTnI again showing a significant difference. The longer the hypotensive episode was, the greater was the increase (moderate hypotension: median 1.16; quartiles 0.55–3.44 ng/ml, severe hypotension: median 8.53; quartiles 1.1–20.7 ng/ml; p < 0.05). Abnormal levels of cTnI were more frequent in non-survivors than in survivors (p < 0.05).¶Conclusions: Hypotension may cause cardiac damage in critically ill patients with acute non-cardiac diseases as shown by abnormal levels of cTnI. It is likely that a high number of these myocardial necroses may go unnoticed on the ECG.     

Serum creatine kinase MM sub-band determination by isoelectric focusing: a potential method for the monitoring of myocardial infarction

Fresh myocardium homogenates analyzed by thin-layer isoelectric focusing revealed the presence of two prominent creatine kinase (CK; EC 2.7.3.2) sub-bands, MMO (pI 7.10) and MM1 (pI 6.88), in approximately equal proportion. While these forms represented together as much as 85% of the cellular MM fraction, they accounted only for viz. 2.2 and 27.7% of the total serum MM activity when measured 8 h before the CK peak in patients with myocardial infarction. Incubation of the isolated MMO and MM1 with normal human serum demonstrated that the former turned to MM1 within 5 h at 37°C; further changes affecting MM1 gave rise to other sub-bands, MM2 (pI 6.70), MM3 (pI 6.45), and MM4 (pI 6.25). In our patient population, these three forms represented more than 75% of the serum CK-MM activity at the CK peak; hence, soon after the enzyme release, the serum MM isoenzyme mainly consists of degradation products arising from the labile MMO and MMl. Among the two cellular forms, MMO was the best related to the total enzyme activities and the most efficient for differentiating the patients with left ventricular failure from the others during the entire survey period (F = 3.8, p < 0.05). Because its presence in the blood provides evidence for a very recent CK release from the tissues, serum CK-MMO determinations might be proposed for following the extension of the lesion after a myocardial infarct.     

N-Acetyl-L-aspartic acid, N-acetyl-α-l-aspartyl-l-glutamic acid and β-citryl-l-glutamic acid in human urine

$\text{N-}\text{Acetyl-}\text{l}\text{-aspartic}$ acid (NA-Asp), $\text{N-}\text{acetyl}\text{-α-}\text{l}\text{-aspartyl-L-glutamic}$ acid (NA-Asp-Glu) and β-citryl-l-glutamic acid (β-CG), which are known to occur in the brain, have been isolated from human urine. Their identities were proved by comparing them with synthetic NA-Asp, NA-Asp-Glu and β-CG using electrophoretic and Chromatographie methods and by acid hydrolysis.A method was developed for the quantitation of NA-Asp, NA-Asp-Glu and β-CG in human urine. It consists of ion-exchange chromatography followed by gas-chromatographic analysis. The amounts of urinary excretion of NA-Asp, NA-Asp-Glu and ν-CG were 41.2 ± 10.1 (n = 27), 20.8 ± 9.6 (n = 27) and 30.2 ± 13.2 (n = 21) μmol/g creatinine in adult males, and 62.2 ±16.3 (n = 27), 24.0 ±8.2 (n = 27) and 40.5 ± 21.1 (n = 24) μmol/g creatinine in adult females, respectively.     

心肌肌钙蛋白I、肌钙蛋白T、肌酸激酶同工酶MB早期诊断 急性心肌梗死敏感性及特异性比较分析

目的 探讨心肌肌钙蛋白Ⅰ（cTnI)、 肌钙蛋白T（cTnT)、 肌酸激酶同工酶MB（CK－MB）早期诊断急性心肌梗死的临床应用价值。方法 对60例急性心肌梗死（AMI）和40例不稳定型心绞痛（UA）患者的同一血样标本检测cTnI、cTnT、CK－MB3项指标,分别进行两组间比较,并对 AMI组和UA组各指标作对比分析。结果 cTnI、cTnT早期诊断急性心肌梗死灵敏度高于CK－MB,阳性率分别为63.3%、46.7%、18.3％,P＜0.01;cTnI和cTnT无显著差别,P＞0.05;cTnI、cTnT、CK－MB特异性相当。结论 心肌肌钙蛋白I和肌钙蛋白T对于AMI的早期诊断具有较高灵敏度和较强特异性,是心肌损伤特异笥标志物,cTnI检测方便、快捷、准确,具有较好的临床价值。     

Creatine kinase isoenzyme BB in serum of healthy adults and children

The activity of the creatine kinase isoenzyme BB was determined in the serum of 26 healthy adults and 31 children. The isoenzyme BB could be proved as a normal component in the human serum. In the adults examined, an activity of $\text{0.56 ± 0.16}\text{I.U./l}\text{(}\text{x}\text{±}\text{S.D.}\text{)}$ was determined. The activity of creatine kinase isoenzyme BB in the serum does not depend on sex but is subject, however, to a strong age dependence. Only at an age of more than 18 years, isoenzyme BB activities adjust to those of adults.     

Differential diagnosis of patients with abnormal serum creatine kinase isoenzymes

For the diagnosis of myocardial injury, particularly AMI, CK-MB has become the gold standard. Changing CK-MB activities in serially collected blood from patients with suggestive signs and symptoms of AMI is almost pathognomonic for infarction. Nevertheless, an increased CK-MB cannot be equated with AMI owing to the many other types of inflammatory, traumatic, and miscellaneous forms of injury to the heart and the trace activities of CK-MB in skeletal muscle. Other enzyme tests for AMI are less efficient. In order of decreasing efficiency, the tests are CK-MB, CK, LD1 greater than LD2 or LD1/LD2 greater than 0.76, AST and LD; the latter two tests are not cost effective and add little or nothing when results for CK-MB, CK, and LD isoenzymes are available. The value of the isoforms of CK-MM and CK-MB remains to be established. Early evidence suggests that they could be helpful in the diagnosis of AMI; however, owing to the greater technical difficulties in performing these tests, their use is necessarily more restricted. Enzyme testing on admission and then every 12 hours for 2 days is sufficient and effective in making the initial diagnosis. In patients presenting early after an attack, CK and CK-MB are often normal. Decisions on AMI cannot be made on blood tests collected in the emergency department. Clot-lysing agents like streptokinase, urokinase, and tPA have changed the therapy of AMI dramatically. Enzyme tests clearly separate patients with and without successful therapeutic or spontaneous reperfusion. With successful reperfusion, the uniform finding has been a "washout" phenomenon with significantly earlier peaking times for CK and CK-MB. The isoforms of CK and myoglobin give the earliest peaks after successful reperfusion. With faster turnaround times for these tests, they may become important tools in patient management.     

Low serum creatine kinase activity is associated with worse outcome in critically ill patients

Purpose

To investigate the prognostic significance of low serum creatine kinase (CK) activity in intensive care unit patients.

Materials and methods

The study population consisted of 1899 patients, divided in a “normal” (CK > 20 U/L) and “low” CK group (CK ≤ 20 U/L). The latter group was divided into 2 subgroups by duration of CK activity decrease. Measurement of routine clinical chemistry parameters, calculation of critical care severity scores, and registration of length of stay and mortality rates were performed.

Results

The proportion of patients showing a low serum CK activity for at least 1 day was 15.5%. In this group, 24.5% had a prolonged CK activity decrease for at least 5 days. Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were lower in the normal than in the low CK group (P < .0001) and higher in the prolonged CK activity decrease group in comparison with the short-term CK activity decrease group (P < .0001, P = .001). A low serum CK activity was an independent predictor of mortality. Kaplan-Meier analysis showed an overall survival in the low CK group of 243 ± 152 vs 291 ± 139 days in the normal CK group (P < .0001).

Conclusions

Low serum CK activities are associated with a higher severity of illness and higher mortality rates.     

Individual responses in biomarkers of health after marathon and half-marathon running: is age a factor in troponin changes?

Although strenuous physical activity is known to cause notable perturbations in blood chemistries, only few studies exist observing exercise-induced simultaneous changes in biomarkers of health status. We compared markers of muscle, cardiovascular, renal, hepatic and inflammatory status at baseline and at 3-h and at 48-h postrace in recreational runners who successfully completed either a marathon (mean age 27?±?13 years, finishing time 199?±?8?min, n?=?4) or half-marathon (mean age 38?±?13 years, finishing time 131?±?6?min, n?=?6) race. Significant postrace changes occurred in myoglobin (p?p?p?p?p?p?p?p?p?p?p?p?p?p?p?相似文献   

Target-flow Inspiratory Muscle Training Improves Running Performance in Recreational Runners: A Randomized Controlled Trial

Inspiratory muscle training (IMT) has been shown to possibly improve exercise performance, but reports on IMT and running performance are rare. The objective of the present study was to examine the effect of target-flow IMT on running performance in recreational runners. Sixteen healthy recreational runners (five females) were recruited for the present study. They were randomly allocated into either an experimental or control group. Participants in the experimental group underwent a 6-week target-flow IMT programme, while those in the control group underwent a 6-week shoulder circumduction exercise programme. Running performance during a 1,500-m time trial run was assessed before and after the intervention period. After the intervention period, only the experimental group demonstrated an increase in inspiratory muscle strength (by 16.15 ± 7.44 cmH₂O; p < 0.05) and reduced completion time in the 1,500-m time trial (by 9.63 ± 5.42 seconds; p < 0.05). Exertion sensation was reduced by 1.63 ± 0.74 points (p < 0.05). No changes were observed in maximal aerobic capacity and pulmonary function in either group after the intervention period. A 6-week target-flow IMT programme enhanced running performance in recreational runners.