Skeletal muscle can undergo large changes of ATP turnover rate, and how this is controlled continues to attract interest. Earlier work on the control of glycolysis stressed the role of key enzymes such as phosphorylase and phosphofructokinase: for phosphorylase, the Ca 2+ -dependent conversion of phosphorylase b to the more active phosphorylase a, and the increase in inorganic phosphate (P i ) concentration consequent on phosphocreatine (PCr) splitting (Griffiths, 1981;Chasiotis, 1983;Connett, 1987); for phosphofructokinase, the role of activators such as AMP (Connett, 1987). In the control of tissue respiration, during e.g. aerobic exercise, attention has focused mainly on the role of the adenine nucleotide translocase and its ADP sensitivity (Chance et al. 1985;Meyer, 1988;Jeneson et al. 1996;Paganini et al. 1997). However, current theory stresses that large changes in flux can be achieved with rather small changes in concentrations of pathway metabolites, which implies that many, perhaps most, enzymes must be regulated by extra-pathway factors (Fell & Thomas, 1995). In the field of mitochondrial control, this objection takes the form of the argument that control dominated by the feedback effects of ADP cannot explain the range of ATP turnover rates observed in vivo -a dynamic range problem (Korzeniewski, 1998); conversely, it is argued that the key relationshipbetween oxidative ATP synthesis rate and [ADP] -exhibits cooperativity (Jeneson et al. 1996). In glycolysis, the argument concerns the degree to which flux correlates with key metabolite concentrations or with contraction events per se (Conley et al. 1997). To a large extent these arguments are about concepts. However, more data are Interrelations of ATP synthesis and proton handling in ischaemically exercising human forearm muscle studied by 31 P magnetic resonance spectroscopy 1. In ischaemic exercise ATP is supplied only by glycogenolysis and net splitting of phosphocreatine (PCr). Furthermore, 'proton balance' involves only glycolytic lactate/H + generation and net H + 'consumption' by PCr splitting. This work examines the interplay between these, metabolic regulation and the creatine kinase equilibrium.2. Nine male subjects (age 25-45 years) performed finger flexion (7 % maximal voluntary contraction at 0.67 Hz) under cuff ischaemia. 31P magnetic resonance spectra were acquired from finger flexor muscle in a 4.7 T magnet using a 5 cm surface coil.3. Initial PCr depletion rate estimates total ATP turnover rate; glycolytic ATP synthesis was obtained from this and changes in [PCr], and then used to obtain flux through 'distal' glycolysis (phosphofructokinase and beyond) to lactate; 'proximal' flux (through phosphorylase) was obtained from this and changes in [phosphomonoester]. -dependent conversion of phosphorylase b to a, and partly to the 'closed loop' increase in P i consequent on net PCr splitting.6. The 'settings' of these mechanisms have a strong influence on changes in pH and metabolite concentrations.
Background: Previous studies have shown an antiasthenic effect of citrulline/malate (CM) but the mechanism of action at the muscular level remains unknown. Objective: To investigate the effects of CM supplementation on muscle energetics. Methods: Eighteen men complaining of fatigue but with no documented disease were included in the study. A rest-exercise (finger flexions)-recovery protocol was performed twice before (D−7 and D0), three times during (D3, D8, D15), and once after (D22) 15 days of oral supplementation with 6 g/day CM. Metabolism of the flexor digitorum superficialis was analysed by
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