Test Catalog Account. Outreach Solutions Tactics Articles Events. Utilization Management Algorithms. Test Catalog. 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. 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 ].
A small study with 14 men showed that sports massage 2 hours after exercise decrease CK levels [ 83 ]. Lose some weight if you are overweight. People with higher BMI and weight have increased creatine kinase levels [ 4 , 18 ].
The most common cause of low creatine kinase levels is muscle wasting muscle atrophy due to physical inactivity, illnesses, or old age [ 85 ]. Creatine kinase levels can be significantly reduced in autoimmune diseases, such as lupus and rheumatoid arthritis [ 86 , 87 , 88 , 89 ]. The more inflammation there is, the lower creatine kinase levels can get.
Total creatine kinase levels are reduced in the second trimester of pregnancy. However, they increase in late pregnancy [ 90 ]. Studies suggest that the more creatine kinase a person has within the normal range, the better their heart and muscles can function. Because creatine kinase is a measure of muscle mass, it is not surprising that a link was found between low creatine kinase levels and higher mortality. Critically ill people who are weaker with less muscle mass have a higher risk of dying [ 92 ].
In two studies with over 1. Lack of energy and metabolites will result in motor groups that are unable to fulfill the required workload. Thus, the control of peripheral systems is dependent on the prevailing local metabolism in a motor unit, whereas, in the central model of muscle fatigue, neuromuscular mechanisms aim to preserve overall integrity of the system by mechanisms such as motor unit derecruitment.
Golgi tendon organs GTOs monitor the tension produced by contraction to prevent excess forces by continuous feedback to the central nervous system CNS. Thus, the CNS is informed by collective feedback mechanisms that include chemical, mechanical, and cognitive cues.
The significance of each of these cues will depend on duration and power requirements of muscular activity. While GTO feedback can be overridden by cognitive processes in the CNS, to allow an athlete to increase performance, it is likely that local peripheral systems can prevent the level of excess muscle contraction that could result in failure or damage.
Unaccustomed exercise, particularly eccentric muscle contractions, initiates mechanical muscle damage of varying degrees [ 8 ]. Intracellular proteolytic enzyme activity can increase and promote muscle protein degradation and augmented cell permeability, which allows some cell contents to leak into the circulation [ 9 , 10 ]. The process of mechanical and metabolic initiated muscle disruption is not entirely understood; it is thought to consist of a complex range of events involving increased oxidative stress, inflammatory and immune responses.
Loss of cell myofibre proteins into the blood may occurs at several stages along this continuum see Figure 2. In most cases, isolated mild to moderate damage in otherwise healthy individuals does not appear to cause further problems, and many studies have demonstrated that the body is capable of clearing released muscle components back to baseline levels within 7—9 days [ 4 , 6 ] see Figures 3 a — 3 c.
Factors such as temperature extreme, alcohol abuse, or sporadic strenuous exercise, for example, ultra marathons, can result in more severe disturbance and may require medical intervention to prevent permanent renal damage, primarily due the nephrotoxic effects of myoglobin [ 9 ]. Some individuals are found to have high levels of serum CK compared to other similar individuals when exposed to the same exercise protocol including moderate exercise even when main comparability factors such as gender, age, and training status are accounted for in data analysis.
In some cases, this variability may indicate an underlying myosis, but in many other cases the cause is unknown [ 7 ]. The contribution of additional factors such as genetic disposition, environmental conditions, or disease may increase the risk of exertional rhabdomyolysis resulting in acute renal failure [ 13 ] see Table 1. Individuals who regularly participate in high-volume, intense exercise, tend to have significantly raised base levels of CK compared to sedentary and moderately exercising individuals [ 14 ].
Raised levels of serum CK were also found in regularly exercising pre-menopausal women compared to similar sedentary individuals [ 15 ]; this suggests that CK flux into the serum is a natural and normal reaction to regular exercise.
Such levels clearly signal strong disturbance or disintegration of striated muscle tissue with concomitant leakage of intracellular muscle constituents into the circulation. It has been recommended acceptable upper limits of normal CK levels be increased by 1.
However, there is no universally agreed or accepted standard. There are many possible reasons for a diagnosis of rhabdomyolysis and accompanying raised CK levels see Table 1. Raised levels of macro-CK tend to be associated with disease, though they can also be present in apparently healthy individuals [ 20 ].
There is extensive debate in the literature concerning the reliability of serum CK level as a marker of muscle damage. Serum CK determinations are normally initial measures of enzyme activity in blood at the time of sampling, and timeline profiles are mostly set and influenced by the requirements of diagnosis of MI and stroke rather than any exercise influence. The mechanism s by which CK is cleared from the blood has not been fully elucidated, and it is likely that observed serum CK levels reflect complex interactions associated with energy status and scale of muscle disturbance.
Thus, measured serum CK will reflect relative amounts of CK released, degree of enzyme activity of released CK, and the rate of clearance of CK from the serum [ 15 ].
In general terms, high serum CK in some ethnic groups may reflect a genetic condition of naturally increased levels of CK muscle tissue activity, which is not related to exercise frequency or muscle disturbance [ 21 ]. It has been proposed that higher than normal levels of tissue CK activity may augment the availability of cellular energy and improve myofibril contraction responses [ 21 ].
Therefore, high levels of serum CK, in the absence of muscle damage or other pathological conditions, may reflect the level of enzyme tissue activity of the individual. Serum CK levels alone may not provide a fully accurate reflection of structural damage to muscle cells [ 22 , 23 ].
Some studies have reported that serum CK levels were affected by hydration status prior to eccentric exercise and varied within subject groups of comparable male volunteers, whilst muscle biopsies revealed similar ultrastructure damage to Z-band muscle fibres.
Muscle soreness did not differ between groups [ 24 ]. Biopsies are specific only to a small area of investigation and therefore may not represent the universal extent of damage to the muscle groups exercised.
Indeed, the biopsy procedure may itself cause damage to muscle fibres. Other additional indirect indices of muscle damage such as magnetic resonance studies and assessment of delayed onset muscle soreness DOMS which include reduced muscle force post exercise, swelling, perception of pain, and reduced range of movement ROM have been utilized in many studies [ 25 , 26 ] as have other blood chemical markers of inflammation and stress [ 27 , 28 ]. These additional measures can assist in quantifying and substantiating muscle disturbance parameters.
Although sets and reps were matched in this study, work volume was not standardised. Dynamic concentric and eccentric leg extensions were performed by 21 untrained men and women [ 30 ]. Therefore, as the volume of exercise performed increased metabolic demands, as might be anticipated, indices of muscle damage were augmented.
These results suggest that the magnitude of exercise intensity has greater influence on cellular response to exercise-induced muscle damage than the duration. Another research [ 31 ] compared equal volumes of high- and low-intensity eccentric leg extensions on untrained subjects. In this study, work volume was equalised using an isokinetic dynamometer. However, high-intensity HI exercise did elicit larger declines in muscle performance and a slower recovery.
This may be due to a greater recruitment of type II muscle fibres in high-intensity eccentric exercise, which have been found to be more susceptible to disruption compared to type I [ 23 , 32 ]. Serum CK levels were higher with high intensity, but not significantly. Subjective measurement of pain and ROM measurements showed no significant difference between groups.
In this study, equal volumes of work result in similar indices of muscle disruption, but with less decrement in muscle performance, and greater recovery with low intensity compared to high intensity. There is evidence to suggest that the degree of muscle damage is greater in elbow flexion compared to knee extension [ 26 ]. However, both studies did agree in their findings concerning greater declines in muscle performance after HI compared to LI. Trained soldiers age 1 9.
There was no significant difference in the total volume of exercise among the groups. The variances observed in studies [ 29 — 31 , 33 ] may be due to disparities in study methods, and the large variation in CK response within and between studies makes a definitive conclusion on the contribution of intensity and volume of exercise on cell changes difficult. Considering the significant increase in CK levels which have been found as a result of high-intensity exercise compared to lower intensity [ 29 , 30 ], the decrements in performance experienced [ 29 , 31 ], and higher levels of PGE 2 reported [ 33 ] even when exercise volume is standardised suggests that higher-intensity exercise will cause the greater disruption of cell membranes; however, with adequate recovery, it may also elicit the greatest adaptations to exercise in the shortest time.
Seven continuous days of the same isokinetic maximal elbow flexion protocol ECC2 to ECC7 did not increase indices of muscle disturbance compared to a control group who performed only one session of the exercise protocol ECC1 [ 27 ]. There was a decline in levels over the course of the next 6 days, and both groups had insignificant CK plasma levels at day 7; there was no significant difference between groups at any time.
This was attributed to increased resistance to muscle stress or to that no further muscle disruption had occurred [ 27 ]. Total work was reduced in the ECC2 to ECC7 group at each of the six further exercise sessions compared to the first day of exercise; however, they were considered to be of the maximal intensity possible, even if at a lower absolute magnitude. Despite theories of muscle protection and reduced disruption from further consecutive eccentric disruption afforded by the initial exercise bout in this study, the loss of muscle force which resulted in reduced work load presumably would have influenced the results.
It is interesting to consider whether the initial loss of CK contributed to the loss of strength over the 6-day period or whether the loss was associated with disruption to type II fibres. A number of studies have used very high intensity or volume of exercise, or both, to ensure muscle disruption is elicited [ 34 , 35 ].
Evans et al. It has been proposed that, in fact, moderate levels of force may produce superior measurement parameters [ 35 ]. Gender difference in muscle disturbance and repair processes has frequently been reported in the literature.
Studies on female animals have demonstrated lower baseline levels of CK and an attenuated CK response to exercise [ 37 , 38 ]. 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.
If you live outside the U. Skip to main content. Search MDA. Search Donate. Blog Podcast Newsletter Magazine. CK tests are used to evaluate neuromuscular diseases in five basic ways: To confirm a suspected muscle problem before other symptoms occur To determine whether symptoms of muscle weakness are caused by a muscle or a nerve problem To differentiate between some types of disorders such as dystrophies versus congenital myopathies To detect "carriers" of neuromuscular disorders, particularly in Duchenne muscular dystrophy.
A carrier has a genetic defect, but doesn't get the full-blown disease. A carrier's child may have the full disease.
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