Where is creatine kinase

When a blood sample is taken, a small bruise may form at the site. Each lab has a different range for what's normal. Your lab report should show the range that your lab uses for each test. The normal range is just a guide. Your doctor will also look at your results based on your age, health, and other factors. A value that isn't in the normal range may still be normal for you. Current as of: September 23, Gabica MD - Family Medicine. Author: Healthwise Staff. This information does not replace the advice of a doctor.

These diseases include:. The test can be used to help diagnose a heart attack, though not very often. 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.

However, females presented with a higher CK peak and a greater relative increase in serum CK levels after 50 maximal eccentric contractions of the arm flexor muscles, despite significantly lower baseline levels compared to males [ 39 ]. There was no significant increase in CK serum levels in the 18 men who performed the same protocol see Figure 3 c , however, the authors suggest this may in part be due to greater adaptation to this type of exercise in the males [ 12 ].

Rinard et al. This view is supported in a review by Clarkson and Hubal who conclude that any differences between genders are small and indicate that females may be more inclined to muscle disruption than males [ 41 ]. In postmenopausal women not taking hormone replacement treatment HRT [ 42 ] and amenorrheic women [ 15 ], raised levels of CK in response to exercise-induced muscle disruption were found, when compared with women on HRT and premenopausal women.

This effect was attributed to lower oestrogen levels. Oestrogen may be important in protecting cell membranes from damage [ 11 ] and reduced infiltration by leucocytes may lessen their damage causing function in the repair process.

Conversely, this may also delay the healing process [ 43 ]. Leucocytes may have a role in the activation of satellite cells [ 11 ] which proliferate and differentiate forming new muscle fibres [ 44 ]. Whether oestrogen can promote reduced CK efflux via reduced membrane permeability or whether actual muscle damage is reduced is not clear [ 43 ]. Progesterone has been suggested to interact with oestrogen and may antagonise the oestrogen disruption limiting properties [ 44 ].

A study by Arnett et al. This study concluded that oestrogen levels had no significant effect on CK levels after strenuous eccentric exercise [ 45 ]. However, knee ROM in subjects was not assessed.

Variations in ROM have been suggested as affecting the mechanical strain on the muscle during eccentric exertion [ 25 ]. This activity alters the force applied to sarcomeres and modifies the magnitude of disturbance [ 46 ]. Work volume in each group was not measured; therefore, variations between groups may have occurred, affecting associated muscle disruption, and high baseline CK levels in PM may be related to age variations in energetics.

Studies of serum CK response to exercise in aging human skeletal muscle have produced variable results. A review by Fell and Williams on the effect of aging on skeletal muscle in athletes suggests that aging can lead to greater exercise-induced damage and a slower repair and adaptation response [ 47 ]. Muscle mass and function gradually decline with age, and cell apoptosis may have a role in age-related sarcopenia [ 48 ].

Lower levels of plasma CK in older female subjects have been attributed to a decline in circulating neutrophils with age which may, in part, be due to reduced oestradiol levels and endogenous antioxidant status [ 45 ].

Circulating neutrophils produce oxidants such as superoxide free radicals, which increase cell damage and leakage. Therefore, an increased serum CK could be related to optimal functioning of the cell, which may decline with age, and is not simply a marker of less damage. Free radial production appears to moderate signalling for adaptation of skeletal muscle in response to exercise [ 49 ], and this response may be attenuated in older muscle, rendering it less adaptive to exercise stress.

Studies on humans have produced conflicting results in relation to aging muscle response to exercise. Individual ROM at the elbow was not significantly different between subjects; however, during the exercise the investigator assisted subjects in keeping the velocity of the movement constant. This may have affected the magnitude of muscle damage. Subjects in this study were described as habitually active. Regular physical activity has been shown to slow the process of sarcopenia and may reverse age-related muscle apoptosis [ 51 ].

Exercise may also attenuate and protect against exercise muscle disruption and subsequent damage. Therefore, the level of past and present physical activity may significantly affect muscle damage throughout the ageing process.

It would be of interest to explore the effects of habitual training in different age groups and its effect on CK serum levels. Exposure to exercise stress initiates adaptation in gene expression, cellular protective mechanisms, and remodelling, which help protect muscle during subsequent bouts of exercise [ 49 ].

The ability of aged muscle to adapt to environmental stress appears to be impaired, as are repair mechanisms, and heat shock protein HSP production is reduced in response to physiological stress in animals [ 49 , 52 ]. Exercise disturbs muscle homeostasis by depleting glycogen, lowering pH, increasing hyperthermia, and increasing ROS reactive oxygen species production as a by-product of energy metabolism.

In particular, higher levels of ROS after exercise can increase the oxidation of thiol sulphydryl groups on proteins, leading to increased protein damage, and may trigger release of HSF1 [ 54 ]. The instigation of an HSP response is dependent on a number of factors including the type and intensity of exercise, muscles involved, and the age and training status of the individual.

The aging process appears to change ATP pathways, alter muscle fibre type ratios, and reduce HSPs response, which are thought to offer some degree of protection against further exercise-induced muscle damage. AMPK AMP-activated protein kinase is an energy sensing enzyme that is widely dispersed in nature from single-cell organisms to humans, is central to the management of energy supply, and operates both locally and at whole organism see Figure 4.

When activated, it in turn stimulates a range of physiological and biochemical processes and pathways that increase ATP production and at the same time switch off pathways that involve ATP consumption. Recent work has shown a strong correlation between a sedentary lifestyle, inactive AMPK, and morbidity diseases such as metabolic syndrome, type 2 diabetes, and dementia [ 56 ].

The benefits of exercise in providing protection from such morbidity diseases are now firmly linked to activation of AMPK and associated biochemical and physiological processes that are stimulated. The primary activity of AMPK is to phosphorylate proteins especially enzymes and by this action regulate the activity of key enzymes that operate important reactions and pathways.

The role of CK in energy management is maintenance of PCr levels to provide an immediate energy supply in the first few seconds of physical activity. During intense exercise there is no PCr resynthesis and the reaction is likely blocked by more than one mechanism; however, although there is no need for PCr resynthesis, there is a need to maintain the ratio and AMPK could be part of the overall process.

It is clear that 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.

For example eccentrically biased exercise e. This highlights the integrated complexity of metabolism and mechanical damage as eccentric-biased exercise is associated with increased indices of muscle damage i. In addition, eccentric-biased contractions may be more mechanochemically efficient based on changes in the actin-myosin sliding length in that changes in sliding length produce different levels of tension and consequent different degrees of muscle damage [ 61 ].

It may be that as eccentric and concentric contractions have different demands and consequences on the metabolic and mechanical components of muscle action, there are alternate mechanisms of control via AMPK that produce different effects of CK levels. This would allow maximum flexibility for a wide range of exercise stressors to enable survival of the species in prehistoric environments where survival depended upon adaptable and flexible muscle action. ATP levels never deplete to critical levels; this is because the sensitivity of ATP is set very high to guarantee that they never deplete, so a slight reduction in high ATP level triggers an early protective reaction.

This might be a component function in the overall action of fatigue to limit muscle activity or it could be a system that evolved prior to or in parallel with fatigue mechanisms. The AMPK mechanism of control involves phosphorylation of CK, and it may be that phosphorylation provides a signal to facilitate removal of CK from the cytosol see Figure 4.

Such a mechanism would explain the appearance of serum CK following physical exercise as opposed to structural damage arising from muscle trauma. Following muscle damaging exercise, CK levels continue to rise in the blood for hours or days see Figures 3 a — 3 c despite significant metabolic disruptions having ceased. The capacity for compromised muscle tissue to generate force is impaired [ 27 , 31 , 62 ]; therefore, measures are required to protect and facilitate the repair of muscle tissue.

In addition, other processes which disrupt the cell membrane, for example, inflammation, continue [ 63 ], allowing CK to exit the cell over time. This extended loss of CK may be associated with protective mechanisms, and a prolonged involvement of AMPK, allowing repair and restoration of muscle function. Exercise-induced muscle disruption is known to produce insulin-like growth factor II IGF II in response to cell damage and is thought to stimulate satellite cells and hypertrophy.

An association has been found between a polymorphism in the sarcomeric protein myosin light chain kinase and changes in blood CK, Mb, and isometric strength, in individuals with specific genetic variations in alleles of IGF II who experienced increased muscle disruption as a result of maximal isotonic eccentric contractions [ 64 ]. This suggests that these genome variations may lead to alterations in calcium handling and force effects during exercise, thereby influencing muscle disruption.

This could explain the susceptibility of some individuals, who are otherwise healthy, to muscle disruption and exertional rhabdomyolysis [ 64 ] and the large intersubject variation in levels of serum CK found in many studies.

Heled et al. A genetic association was found between a specific CK-MM genotype of the Ncol polymorphism with an augmented response to exercise. Yamin et al. 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. 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.

These tests include:. Because levels of CK may rise if you have a thyroid problem, alcohol abuse, or kidney failure, your healthcare provider may also order tests to look for these diseases.

Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The normal range for general CK varies by age and gender.

Race is also known to affect CK levels. The test is done with a blood sample. A needle is used to draw blood from a vein in your arm or hand.