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Updated: Aug 11, 2026

Induction and Assessment of Exertional Skeletal Muscle Damage in Humans
Published on: December 11, 2016
Serum and organ creatine phosphokinase alterations in exercise
Swimming exercise in rats significantly elevates serum creatine phosphokinase (SCPK) levels, primarily due to the BB isoenzyme. Organs like the kidney, liver, and brain are suggested as the primary sources of this exercise-induced SCPK release.
Area of Science:
- Biochemistry
- Exercise Physiology
- Enzymology
Background:
- Creatine phosphokinase (CPK) is a key enzyme in cellular energy metabolism.
- Elevated serum CPK (SCPK) levels can indicate tissue damage or physiological stress.
- Understanding the source of SCPK release during exercise is crucial for interpreting its diagnostic value.
Purpose of the Study:
- To investigate the changes in SCPK activity and isoenzyme distribution in rats following strenuous swimming exercise.
- To identify the potential organs responsible for CPK release during swimming.
Main Methods:
- Rats underwent 3 hours of swimming exercise.
- Serum CPK activity and isoenzyme profiles (BB, MB, MM) were analyzed post-exercise.
- CPK isoenzyme distribution was also examined in various tissues (kidney, liver, brain, lung, heart, skeletal muscle).
Main Results:
- Swimming induced a 6-fold increase in SCPK activity, returning to baseline within 7 hours.
- The excess SCPK was predominantly the BB isoenzyme (77%).
- Kidney, liver, and brain tissues showed high proportions of BB isoenzyme, while skeletal muscle was mainly MM, and heart was a mix of MB and MM.
Conclusions:
- Skeletal muscle and heart are unlikely sources of the increased SCPK observed after swimming.
- The kidney, liver, and brain are implicated as potential sites of CPK release during swimming exercise.
- The BB isoenzyme of CPK is the primary contributor to elevated SCPK levels following prolonged swimming in rats.
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