Denne beskriver det aller meste om CK ifh muskelskade under trening. En av få faktorer som korresponderer med DOMS.
Baird et.al. 2012. Creatine-Kinase- and Exercise-Related Muscle Damage Implications for Muscle Performance and Recovery.
http://www.hindawi.com/journals/jnme/2012/960363/
However, raised levels of serum CK are still closely associated with cell damage, muscle cell disruption, or disease. These cellular disturbances can cause CK to leak from cells into blood serum [6].
Skeletal cell numbers are established before birth. These cells are designed to last a lifetime and are not subject to turnover and recycling processes that occur in many other cell types. Growth in muscle mass happens in magnitude only (hypertrophy via growth hormone and testosterone). While hypertrophy is readily reversible (atrophy), loss of muscle cell numbers as a result of damage would be progressively more serious.
Unaccustomed exercise, particularly eccentric muscle contractions, initiates mechanical muscle damage of varying degrees [8]. Metabolic muscle disturbance is thought to result in release of cellular components through a cascade of events, which begin with depletion of ATP and result in the leakage of extracellular calcium ions into intracellular space, due to both Na-K-ATPase and Ca2+-ATPase pump dysfunction. 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].
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].
Base levels of serum CK in general populations are variable 35–175 U/L [16] with ranges from 20 to 16,000 U/L, and this wide range reflects the inconsistent occurrence of subclinical disorders and minor injury, genetic factors, physical activity status, and medication [17].
In examples of rhabdomyolysis (clinically diagnosed muscle damage) CK levels have been found at 10,000–200,000 U/L and as high as 3×106 U/L [18]. Such levels clearly signal strong disturbance or disintegration of striated muscle tissue with concomitant leakage of intracellular muscle constituents into the circulation. In the absence of specific myocardial or brain infarction, physical trauma, or disease, serum CK levels greater than 5,000 U/L are generally considered to indicate serious disturbance to muscle [10].
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].
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].
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 PGE2 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.
When activities occur that deplete ATP levels, such as physical exercise, glucose depletion, or hypoxia, AMPK is activated. 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 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. It is likely that AMPK has a role in controlling CK activity, and some work has demonstrated that AMPK may regulate CK and is sensitive to the Cr : PCr ratio and that increased creatine levels stimulate AMPK activity [57].
For example eccentrically biased exercise (e.g., downhill running) will elicit greater postexercise levels of serum CK than equivalent concentrically biased exercise (e.g., uphill running) though the former is less energy metabolism demanding than the latter [41]. This highlights the integrated complexity of metabolism and mechanical damage as eccentric-biased exercise is associated with increased indices of muscle damage (i.e., DOMS) which is mainly a result of micro-damage within the myocyte [59, 60].
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.
Exercise modality can affect the appearance of CK in blood serum. Eccentric resistance training CK serum levels can peak between 72 hrs [31, 45] and 96 hrs [67] to 120 hrs [4] (see Figure 3(b)). Training status may affect this time response. Full body eccentric resistance training in resistance trained (RT) and untrained (UT) men elicited a significant (UT 𝑃=0.002, RT 𝑃=0.02) increase in CK serum levels at 24 hrs. This signified the peak response in the RT group, whilst levels in the UT group continued to rise and peaked at 72 hrs [68]. However, three sets of 50 maximal eccentric leg flexion contractions in untrained men resulted in a significant (𝑃<0.05) increase in CK serum levels at 24 hrs; levels decreased over the next 2 days followed by a nonsignificant (𝑃>0.05) increase at 96 hr [23], and 10 sets of 10 reps of 70% body mass barbell squats incorporating eccentric and concentric contractions in non-resistance-trained males and females resulted in a peak serum CK response at 24 hr after exercise. A series of plyometric jumps performed over 2–5 minutes by untrained men produced a peak CK serum response at 48 hrs [69], and 90 minutes of endurance cycle ergometer exercise at a set absolute workload (1.5 kilo ponds at 60 revolutions per minute) performed by untrained men three days consecutively caused a significant (𝑃<0.05) increase in serum CK levels 3 hours after the first exercise session and peak CK serum levels occurred immediately after the third day of exercise, 72 hrs from the initiation of exercise [6] (see Figure 3(a)). 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)).
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