Why creatine kinase increased

Your healthcare provider may order this test if you may have muscle damage or injury. But because levels of this protein may not peak for up to 2 days after certain injuries, you may need to have this test several times to see if your heart or other muscles have been damaged. You may also need this test if you have chest pain or weakness and your healthcare provider wants to see t if you've had a heart attack. If you are taking statin medicines and have unusual muscle cramping and pain or muscle weakness, your healthcare provider may also order a CK test.

Statin medicines are used to treat high cholesterol. They sometimes cause serious muscle injury. In very rare cases, they can even lead to a rapid, life-threatening muscle breakdown.

Your healthcare provider may order other tests to find out if you have had muscle injury or a heart attack. If you have had a heart attack, your healthcare provider may order a blood test to look for high levels of cardiac troponin. This is another protein found in your heart. This is because cardiac troponin is more sensitive and more specific.

Or the healthcare provider may order tests to see how you are recovering. Download Test. Useful For Suggests clinical disorders or settings where the test may be helpful Diagnosing and monitoring myopathies or other trauma, toxin, or drug-induced muscle injury.

Serum creatine kinase CK activity may increase in patients with acute cerebrovascular disease or neurosurgical intervention and with cerebral ischemia as well as in nearly all patients when injury, inflammation, or necrosis of skeletal or heart muscle occurs, including: -All types of muscular dystrophy particularly in progressive muscular dystrophy particularly Duchenne sex-linked muscular dystrophy. CK concentrations have been found to be relatively higher in black race populations.

Louis, Saunders Elsevier, ; 2. Crit Care Apr;9 2 3. Other studies featuring physically active subjects did not find a comparable association [ 7 ]. Intensive exercise initiates an immune response resulting in acute and delayed leukocytosis, featuring neutrophils predominantly.

This delayed proinflammatory response may in part be related to the serum CK response observed after exercise-induced muscle damage, due to leucocytes infiltrating and destabilising the cell membrane during the process of repair. This biphasic response has been noted in other studies [ 23 , 35 ] and may be related to the time line of inflammation. Exercise modality can affect the appearance of CK in blood serum. Training status may affect this time response.

Stepping exercise resulted in a CK serum increase in women at day 3, whereas, there was no significant increase in CK serum levels in men performing the same protocol see Figure 3 c. Pantoja et al. The duration of the ten-rep max for elbow flexion for each subject was recorded with a chronometer in order to standardise exercise in both land and water environments and induce the same energy-generating metabolic pathways. Subjects executed as many maximal effort contractions as possible for each set performing three sets in both environments with two-minute rest between sets; each environment session land or water was separated by four weeks.

A significant increase in serum CK was observed at 48 hours after exercise on land, and no significant change in baseline serum CK levels occurred in water. No further samples were taken after this time. The main mechanism hypothesised to have attenuated muscle damage in water was reduced eccentric contractions [ 70 ]. There are difficulties in comparing exercise intensity and work volume in land and water [ 71 , 72 ].

Standardisation of exercise between water and land is challenging due to the differing conditions in water compared to air resistance, temperature, and hydrostatic pressure. The significance of exercise modality on CK serum response appears to be related to the magnitude of eccentric contractions involved in the activity and the subsequent extent of muscle disruption.

Greater muscle cell disturbance delays the appearance of a CK serum peak compared to less disruption. This may be linked to the time course of inflammation; however, evidence in the literature supporting this theory remains unclear.

The molecular mechanisms that result in CK release from muscle after mild exercise are unclear. More clarification could provide important information for athletes concerned about muscle hypertrophy, performance, and the importance of rest periods between periods of exercise. Future studies should include an exploration of ethnic variations in CK response to exercise. In the absence of any mechanical muscle damage, it remains a question as to whether raised CK after exercise does represent a degree of actual muscle damage or some form of disruption in energy control processes or some other molecular reaction mechanism.

Since muscle tissue cannot ignore brain centred nerve stimulations causing increase in both the number of motor units recruited and the frequency of motor unit stimulation, as well as creation of longer tetanic contractions, it would seem logical that muscle would have some mechanism of moderation to delay the final sanction of fatigue for as long as possible. Although PCr resynthesis is greatly diminished during high-intensity exercise, AMPK may still be required to maintain the ratio.

It is speculated here that the control involves expulsion of CK from the cytosol see Figure 3. If this is the case, then increased serum CK levels arising from normal physical exercise may be a consequence of normal metabolic activity rather than representative of physical damage to muscle. Such a system would not act in isolation but as part of a sophisticated process involving other regulatory functions in the muscle, and only when the full integrated system is understood will it be possible to explain the many anomalies associated with muscle action.

Unfortunately, it has not been possible from the available literature to extract more definitive evidence for this suggestion. The considerable variability across many studies makes interpretation more difficult, and it is clear that the lack of agreed guideline procedures and defined parameters for the conduct and evaluation of exercise-based experimental work in this area is a major barrier to the greater understanding of the influence of exercise on muscle and human health in general.

The establishment of an international committee on exercise-based experimental and laboratory protocols may be beneficial. Such a committee could provide leadership, clarity, and standardisation that would enable researchers to effectively answer related experimental questions. The authors have no conflicts of interests that are directly relevant to the content of this paper. Baird et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Baird , 1 Scott M. Graham, 1 Julien S. Baker, 1 and Gordon F.

Academic Editor: H. Received 21 Jun Revised 06 Sep Accepted 28 Sep Published 11 Jan Abstract The appearance of creatine kinase CK in blood has been generally considered to be an indirect marker of muscle damage, particularly for diagnosis of medical conditions such as myocardial infarction, muscular dystrophy, and cerebral diseases.

Figure 1. Phosphocreatine PCr circuit showing the rephosphorylation of creatine Cr in mitochondria using ATP derived from oxidative phosphorylation oxid phos and subsequent use of mitochondrial PCr by cytosolic creatine kinase CK to resupply ATP for muscle activity, adapted from Saks [ 5 ].

Figure 2. Theoretical model of muscle damage and repair cycle reproduced from Kendall and Eston [ 11 ]. Figure 3. PRE refers to the baseline period before exercise. Days 1—4 represent the 4-day immobilization and days 5—9 are the recovery period. Reprinted from Sayers and Clarkson [ 4 ]. Table 1. Figure 4. References U. Schlattner, M. Tokarska-Schlattner, and T. Liu, Y. Lai, Y. Wu, C. Tzeng, and S. Brancaccio, N. Maffulli, and F. Sayers and P. Totsuka, S. Nakaji, K. Suzuki, K. Sugawara, and K.

View at: Google Scholar Y. Heled, M. Bloom, T. Wu, Q. Stephens, and P. Brown, S. Day, and A. View at: Google Scholar A. Varon, and P. Fredsted, T. Clausen, and K. View at: Google Scholar P. Clarkson, A. Kearns, P. Rouzier, R. Rubin, and P. Chevion, D. Moran, Y. Thompson, S. Scordilis, and M.

Gagliano, D. Corona, G. Giuffrida et al. Prelle, L. Tancredi, M. Sciacco et al. Efstratiadis, A. Voulgaridou, D. Nikiforou, A. Kyventidis, E. Kourkouni, and G. View at: Google Scholar T. Kyriakides, C. Angelini, J. Schaefer et al. Galarraga, D. Sinclair, M. Will I need to do anything to prepare for the test?

You don't need any special preparations for a CK test. Are there any risks to the test? What do the results mean? To get more information, your provider may order tests to check the levels of specific CK enzymes: If you have higher than normal CK-MM enzymes, it may mean you have a muscle injury or disease, such as muscular dystrophy or rhabdomyolis.

If you have higher than normal CK-MB enzymes, it may mean you have an inflammation of the heart muscle or are having or recently had a heart attack. If you have higher than normal CK-BB enzymes, it may mean you have had a stroke or brain injury. Other conditions that can cause higher than normal CK levels include: Blood clots Infections Hormonal disorders, including disorders of the thyroid and adrenal glands Lengthy surgery Certain medicines Strenuous exercise If you have questions about your results, talk to your health care provider.

Is there anything else I need to know about a CK test? References Cedars-Sinai [Internet]. Los Angeles: Cedars-Sinai; c Neuromuscular Disorders; [cited June 12]; [about 2 screens]. The Nemours Foundation; c Your Muscles; [cited Jun 19]; [about 3 screens].