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. However, there is controversy in the literature concerning its validity in reflecting muscle damage as a consequence of level and intensity of physical exercise. Nonmodifiable factors, for example, ethnicity, age, and gender, can also affect enzyme tissue activity and subsequent CK serum levels. The extent of effect suggests that acceptable upper limits of normal CK levels may need to be reset to recognise the impact of these factors. There is a need for standardisation of protocols and stronger guidelines which would facilitate greater scientific integrity.
The purpose of this paper is to examine current evidence and opinion relating to the release of CK from skeletal muscle in response to physical activity and examine if elevated concentrations are a health concern.
It has been reported previously that the upper body musculature is continually active during high intensity cycle ergometry. The aim of this study was to examine the effects of prior upper body exercise on subsequent Wingate (WAnT) performance. Eleven recreationally active males (20.8 ± 2.2 yrs; 77.7 ± 12.0 kg; 1.79 ± 0.04 m) completed two trials in a randomised order. In one trial participants completed 2 × 30 s WAnT tests (WAnT1 and WAnT2) with a 6 min recovery period; in the other trial, this protocol was preceded with 4 sets of biceps curls to induce localised arm fatigue. Prior upper body exercise was found to have a statistically significant detrimental effect on peak power output (PPO) during WAnT1 (P < 0.05) but no effect was observed for mean power output (MPO) (P > 0.05). Handgrip (HG) strength was also found to be significantly lower following the upper body exercise. These results demonstrate that the upper body is meaningfully involved in the generation of leg power during intense cycling.
Rationale:Following prolonged endurance events such as marathons, elevated levels of cardiospecific biomarkers are commonly reported. Although transiently raised levels are generally not considered to indicate clinical myocardial damage, comprehension of this phenomenon remains incomplete. The popularity of high-intensity interval training highlights a paucity of research measuring cardiac biomarker response to this type of exercise. This a posteriori case report discusses the elevation of cardiac troponins (cTn) associated with short interval, high-intensity exercise.Patient concerns:In this case report, an apparently healthy 29-year-old recreationally active female presented clinically raised cardiac troponin I (cTnI) levels (>0.04 ng/mL), after performing high-intensity cycle ergometer sprints. As creatine kinase (CK) is expressed by multiple organs (e.g., skeletal muscle, brain, and myocardium), cTnI assays were performed to determine any changes in total serum CK levels not originating from skeletal muscle damage.Diagnosis:A posteriori the individual's daily energy expenditure indicated chronically low-energy availability. Psychometric testing suggested that the individual scored positive for disordered eating, highly for fatigue levels, and low in mental health components.Outcomes:The current case report provides novel evidence of elevated cTnI occurring as a result of performing short duration, high intensity, cycle ergometer exercise in an individual with self-reported chronically depleted energy balance. A schematic to identify potentially “at risk” individuals is presented.Lessons:Considering this as a case report, results cannot be generalized; however, the main findings suggest that individuals who habitually restrict their calorie intake below their bodies’ daily energy requirements, may have elevated biomarkers of exercise induced myocardial stress from performing high-intensity exercise.
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