Higher amounts of serum CK can indicate muscle damage due to chronic disease or acute muscle injury. For this reason, if you're scheduled to have blood drawn for a CK test to diagnose a potential muscle disorder, you should limit your exercise to normal activities before the test. Because elevated CK levels indicate muscle damage, many parents wonder why their children with Duchenne muscular dystrophy DMD had higher CK levels when they were younger and had more muscle function.
This seeming paradox occurs because muscle degeneration is more rapid at the earlier stages and, possibly, because there's more muscle bulk available to release CK into the circulation at this time. At the same time, some neuromuscular disorders, such as the congenital myopathies nemaline, central core disease and others and myasthenia gravis, may not trigger any elevation of CK levels. CK levels don't always reflect the level of functional impact on the individual. Manage your Quest subscription.
Our trained specialists are here to provide one-on-one support for every part of your journey. CK testing used to be a common test for heart attacks. But another test, called troponin , has been found to be better at detecting heart damage. You may also need this test if you had a muscle injury or stroke. CK levels may not peak until up to two days after certain injuries, so you may need to be tested a few times.
This test can help show if you have damage to your heart or other muscles. A health care professional will take a blood sample from a vein in your arm, using a small needle.
After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes. There is very little risk to having a blood test. You may have slight pain or bruising at the spot where the needle was put in, but most symptoms go away quickly.
If your results show you have a higher than normal level of CK, it may mean you have an injury or disease of the muscles, heart, or brain. To get more information, your provider may order tests to check the levels of specific CK enzymes:. Learn more about laboratory tests, reference ranges, and understanding results. In another study of over 10, adults, overweight and obese men had almost 2 times greater odds of having elevated CK [ 19 ].
Similarly, in 4, people, CK levels were higher in people with greater body mass [ 4 ]. Scientists may have found an explanation for this. They discovered that obese and overweight people have more fast-twitch type II muscle fibers and less slow-twitch type I muscle fibers. Fast-twitch muscle fibers have higher CK activity [ 4 ].
Creatine kinase will increase with muscle, heart, or brain damage — these can be caused by an underlying disease or disorder, including:. Interventions that damage tissues, such as injections into the muscles or any type of surgery, will increase CK levels [ 8 , 57 , 58 ].
Cocaine increases CK levels [ 59 , 60 , 61 ]. Finally, toxins like snake venom or carbon monoxide can increase CK levels [ 77 , 78 ]. A study with over 12, people found that higher CK was linked to lower hs-CRP , which is a measure of chronic inflammation [ 79 ]. The same association was found in another study of overweight and obese people [ 80 ]. High plasma CK, even in the normal range, may decrease the ability of our blood to clot properly.
This is especially the case after exercise when CK levels spike [ 81 ]. Elevated creatine kinase can be a sign of serious tissue damage or an underlying disease or disorder. Refrain from strenuous exercise before testing. It causes muscle damage and increases CK levels [ 10 , 11 , 12 ]. Discuss the lifestyle changes listed below with your doctor. None of these strategies should ever be done in place of what your doctor recommends or prescribes!
If your CK gets high because your muscles get damaged after exercise, there are some steps you can take to improve muscle recovery. Studies suggest that after strenuous exercise, an increase in creatine kinase muscle damage can be attenuated by consuming enough carbs, protein, and antioxidants [ 82 ].
ACE genotypes may be involved in the excitation coupling process and influence the risk for developing rhabdomyolysis and, conversely, protection against exercise-induced muscle injury.
However, this effect may be more noticeable in previously sedentary individuals performing intense exercise [ 65 ]. 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.
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