Effect of creatine supplementation on creatine and glycogen content in rat skeletal muscle.
ABSTRACT The effects of high dose creatine feeding (5 g kg(-1) BW day(-1), 5 days) on creatine content, glucose transport, and glycogen accumulation in white gastrocnemius, red gastrocnemius and soleus muscles of the rat was investigated. Isolated rat hindquarters of creatine fed and control rats were perfused with a standard medium containing either insulin alone (0, 100 or 20 000 microU mL(-1)) or in combination with creatine (2 or 10 mmol L(-1)). Furthermore, plasma insulin concentration was measured in normal rats during creatine feeding, as well as in anaesthetized rats during intravenous creatine infusion. Five days of creatine feeding increased (P < 0.05) total creatine content in soleus (+ 20%) but not in red gastrocnemius (+15%, n.s.) and white gastrocnemius (+ 10%, n.s.). In parallel, glycogen content was markedly elevated (P < 0.05) in soleus (+ 40%), less (P < 0.05) in red gastrocnemius (+ 15%), and not in white gastrocnemius (+ 10%, n.s.). Glucose transport rate, muscle GLUT-4 content, glycogen synthase activity in perfused muscles and glycogen synthesis rate were not significantly altered by creatine feeding in either muscle type. Furthermore, high dose creatine feeding raised (P < 0.05) plasma creatine concentration fivefold but did not alter circulating insulin level. It is concluded that short-term high dose creatine feeding enhances creatine disposal and glycogen storage in rat skeletal muscle. However, the creatine and glycogen response to creatine supplementation is markedly greater in oxidative than in glycolytic muscles.
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ABSTRACT: INTRODUCTION: Fluorescence recovery after photobleaching (FRAP) is a confocal microscopy- based technique widely used for in vivo quantification of intracellular molecular movements and interactions. FRAP is very useful for elucidating several fundamental but complicated cellular activities, such as cell membrane diffusion and protein binding. AIM: The aim of this study was to investigate whether it is possible to develop stochastic simulation strategies for interpretation of FRAP kinetics. METHODS: A simulation algorithm based on a stochastic simulation of the time evolution of coupled reaction-diffusion biochemical systems was developed for investigating and interpreting FRAP experiments in terms of diffusion and binding. The proposed algorithm was compared with standard deterministic methods that are currently being used for analysis of FRAP curves. RESULTS AND DISCUSSION: Predictions of recovery times of FRAP curves and sum of residuals revealed a good agreement (Table I), at the level of both timescale and intensity, between the proposed model and the standard deterministic methods. The stochastic simulation algorithm presents a firmer physical basis that its deterministic counterparts and might be used to successfully model probabilistic events in the cell, deciphering information in FRAP experiments that cannot be computed using deterministic models.
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ABSTRACT: The use and effects of selected performance-enhancing drugs and nutritional supplements are reviewed. Recent sports medicine studies are mostly double blind and placebo controlled but contain relatively small sample sizes. Their data appear reliable and are reported in reputable journals. Definitions and methods used in sports medicine are provided to enhance the understanding of this literature. The use of performance-enhancing substances is probably under-reported. Anabolic-androgenic steroids are reportedly used in 0% to 1% of women, 0.5% to 3% of high school girls, 1% to 5% of men, 1% to 12% of high school boys, and up to 67% of some groups of elite athletes. The use of combinations of performance-enhancing substances is common. Carbohydrate loading, adequate protein intake, creatine, blood doping, and erythropoietin (epoetin alfa) appear to enhance performance. Anabolic-androgenic steroids enhance performance, but health risks limit their use. Growth hormones and β2-selective adrenergic agonists may enhance performance, but additional studies are needed. Androstenedione, caffeine, amphetamines, and nonprescription sympathomimetics do not appear to enhance performance. Performance-enhancing drugs have shown some benefit in diseased patients with malnutrition and/or decreases in physical ability. Pharmacists and other health care providers have opportunities to improve the understanding, use, and monitoring of performance-enhancing substances.Journal of Pharmacy Practice 02/2003; 16:22-36.
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ABSTRACT: To investigate the effects of dietary creatine supplementation alone and in combination with exercise on basal cardiac function, susceptibility to ischaemia/reperfusion injury and mitochondrial oxidative function. There has been an increase in the use of creatine supplementation among sports enthusiasts, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but not in the myocardium. Male Wistar rats were swim-trained for 8 weeks, 5 days per week. Hearts were excised and either freeze-clamped for biochemical analysis or perfused on the isolated heart perfusion system to assess function and ischaemia/reperfusion tolerance. Mechanical function was documented in working heart and retrograde mode. The left coronary artery was ligated and infarct size determined. Mitochondrial oxidative capacity was quantified. Aortic output recovery of hearts from the sedentary controls (CSed) was significantly higher than those from creatine-supplemented sedentary (CrSed), creatine-supplemented exercised (CrEx) as well as control exercised (CEx) groups. Ischaemic contracture of hearts from CrEx was significantly higher than that of CSed. There were no differences in infarct size and mitochondrial oxygen consumption. This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise-trained animals, by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation.Acta Physiologica 06/2012; 206(1):6-19. · 4.25 Impact Factor