Arnold Koller

Oral creatine supplementation in Duchenne muscular dystrophy: A clinical and 31 P magnetic resonance spectroscopy study

Abstract The decrease in intracellular creatine concentration in Duchenne muscular dystrophy may contribute to the deterioration of intracellular energy homeostasis and may thus be one of the factors aggravating muscle weakness and degeneration. Oral creatine supplementation should have potential in alleviating the clinical symptoms. To test this hypothesis, creatine was orally administered over a period of 155 days to a 9-year-old patient with Duchenne muscular dystrophy. In accordance with previous investigations on normal subjects and trained athletes, the patient experienced improved muscle performance during creatine supplementation. Further evidence supporting this hypothesis derived from plasma creatine kinase and lactate dehydrogenase activities and repeated 31P magnetic resonance spectroscopy of the gastrocnemius muscle. These preliminary observations indicate a potential role for creatine supplementation in the symptomatic therapy of patients with muscle disease. [Neurol Res 2000; 22: 145-150]

Release of muscle proteins after downhill running in male and female subjects

The release of muscle proteins after downhill running, which mainly includes eccentric muscle action, was compared in females (F; n=9) and males (M; n=9). They performed 20 min of downhill treadmill running with 16% decline with a target heart rate of 70% of the individual VO2peak, which was determined two weeks before. Blood samples were drawn before, 6 and 24 h after exercise to measure plasma levels of skeletal troponin I (sTnI), myosin heavy chain fragments (MHC), creatine kinase (CK), and myoglobin (Mb). Baseline levels before exercise were significantly higher in males compared to females for the cytoplasmic proteins CK and Mb, but the difference for MHC and sTnI was not significant. Both groups displayed marked and significant early (6 h) increases (P<0.05) for sTnI (median: F: 8.2 μg/L; M: 22.0 μg/L), Mb (median: F: 86.8 μg/L; M: 407 μg/L), and CK (median: F: 162 U/L; M: 339 U/L). A significant (P<0.05) but delayed (24 h) increase was found for MHC (median: F: 482 μU/L; M: 651 μU/L). The absolute values for all four parameters were significantly (P<0.05) higher in males compared to females; however, no difference was found for the relative increases and the time course of all parameters between females and males. We conclude 1) that there were no significant differences in the basal concentrations of predominantly bound proteins, and 2) that there were no differences in the relative muscle protein release between females and males before and after one bout of high‐intensive eccentric exercise. The higher plasma concentrations of all measured muscle proteins in males are probably caused by the higher muscle mass compared to females.

Creatine kinase, myosin heavy chains and magnetic resonance imaging after eccentric exercise

The aim of this study was to examine the relationship between myosin heavy chain (MHC) release as a specific marker of slow-twitch muscle fibre breakdown and magnetic resonance imaging (MRI) of skeletal muscle injury after eccentric exercise. The effects of a single series of 70 high-intensity eccentric contractions of the quadriceps femoris muscle group (single leg) on plasma concentrations of creatine kinase and MHC fragments were assessed in 10 young male sport education trainees before and 1 and 4 days after exercise. To visualize muscle injury, MRI of the loaded thigh was performed before and 4 days after the eccentric exercise. All participants recorded an increase ( P ≪ 0.05) in creatine kinase after exercise. In five participants, T2 signal intensity was unchanged post-exercise compared with pre-exercise and MHC plasma concentration was normal; however, they showed an increase ( P ≪ 0.05) in creatine kinase after exercise. For the remaining five participants, there was an increase in T2 signal intensity of the loaded vastus intermedius and vastus lateralis. These changes in MRI were accompanied by an increase in MHC plasma concentration ( P ≪ 0.01) as well as an increase in creatine kinase ( P ≪ 0.01). We suggest that changes in MRI T2 signal intensity after muscle damage induced by eccentric exercise are closely related to damage to structurally bound contractile filaments of some muscle fibres. Additionally, MHC plasma release indicates that this damage affects not only fast-twitch fibres but also some slow-twitch fibres.

The therapeutic potential of oral creatine supplementation in muscle disease

The decrease in intracellular creatine concentration observed in a number of muscle diseases may deplete energy homeostasis and may, therefore, be one of the factors determining and/or aggravating muscle weakness and degeneration. Two hypotheses are put forward in the present communication to explain: (i) the mechanisms leading to the disturbances in creatine metabolism found in various muscle diseases; and (ii) the potential of oral creatine supplementation in alleviating the clinical symptoms.

Metabolic Changes Following Concentric and Eccentric Exercise in Trained and Untrained Subjects

Recently, we have demonstrated that myoglobin attains its peak value in the circulation as early as 2 hours after eccentric loading (2). A large increase in plasma creatine kinase and creatine kinase MB has also been shown after such exercise (1). There is only a slight increase in these proteins in the blood after concentric loading (1, 2).