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Biochemistty of Erercise 73 liquid nitrogen and analyzed for glycogen. Glycogen breakdown was calculated as the difference between the control and the stimulated strip. Adrenaline caused a 10% reduction in glycogen content (pcO.04; n=18) from 120.3 & 4.7 mmol x kg-' d.w. in the control strips to 108.1 & 4.9 mmol x kg-' d.w. in the muscles exposed to adrenaline (mean & SEM). Electrical stimulation caused a 26% reduction in glycogen level (p < 0.001; n=18); the glycogen content was 152.4 4.9 and 112.3 2 5.5 mmol x kg-' d.w. in the control and stimulated strips, respectively. Electrical stimulation in the presence of adrenaline caused a marked reduction in glycogen level of 46 %; from 129.9 +2 4.1 to 69.5 3.6 mmol x kg-' d.w. (p < 0.001; n=19). These results show that adrenaline causes a small reduction in glycogen content in the resting slow-twitch soleus muscle in vifro. The electrical stimulation used in this study caused glycogen breakdown, and glycogenolysis was enhanced in the presence of adrenaline (p<O.Ol). In conclusion, both adrenaline and electrically induced contraction are able to stimulate glycogenolysis in the slow-twitch soleus muscle in vifro, and in combination they have a synergistic effect. was higher than simultaneous hepatic lactic acid uptake @<0.05), and glucose output decreased to basal levels, while lactate uptake rose to a plateau. Furthermore, in separate experiments an increase in lactate supply to isolated perfused livers increased lactate uptake but not glucose output. 4. Soleus muscles were incubated and electrically stimulated for 3-12 h. Intraarterial injection of incubation medium in anaesthetizedrats did not change plasma glucose concentrations. 5. Extracts were made from mixed muscle, liver and fat tissue. In response to intraarterial injection of either muscle or liver extracts a prolonged increase (pcO.05) in plasma glucose concentration was seen (for muscle extract from 5.220.08 mM to 8.3k1.5 mM). 6. In isolated perfused livers muscle extract increased glucose output dose dependently, whereas the effect of liver extract did not increase with dose. Furthermore, only muscle extract increased hepatic oxygen uptake. 7. Although not unambiguous the results indicate that contracting skeletal muscle may produce a hormone enhancing hepaticglycogenolysis according to energy needs. 113 EFFECTS O F PHYSIOLOGICAL CITRATE CONCENTRATIONS AND ENHANCED ENZYME AGGREGATION ON IN VITRO SKELETAL MUSCLE PHOSPHOFRUCTOKINASE ACTIVITY SJ Peters and LL Spriet, School of Human Biology, University of Guelph, Ontario, Canada, N1G 2W1. EVIDENCE THAT CONTRACTING RAT MUSCLE PRODUCES A HORMONE E N H A N C I N G H E P A T I C GLYCOGENOLYSIS XX Han, KJ Mikines, T Ploug and H Galbo. Department of Medical Physiology, The Panum Institute, University of Copenhagen, Blegdamsvej3, DK-2200 Copenhagen N, Denmark. 1. Establishedneuroendocrine signalsdo not sufficiently account for the exerciseinduced increase in glucose production. An attractivepossibilitywould be that contracting muscle produces a factor that directly stimulates hepatic glycogenolysis. 2. Isolated rat hindquarterswere perfused in series with isolated livers. Stimulation of the ischiadic nerve of one or both legs resulted in an increase in force which rapidly waned. In response to one legged contractions hepatic glucose production increased initially (from -0.93k0.48 (SE) to 3.320.7 pmol/min, ~ ~ 0 . 0 5The ) . peak did not differ significantly from that seen after 20 nM of epinephrine (5.121.2 pmoVmin, p>0.05). In response to two-legged contractions the increase in hepatic glucose production (to 5.42 1.3 pmoVmin) was higher (p<0.05) and lasted longer than during one-legged contractions. 3. During contractions peak glucose output 114 Classic in vitro studies identified citrate as a potent inhibitor of phosphofructokinase (PFK) activity. These experiments were generally performed with dilute enzyme and unphysiological citrate and effector concentrations. Recent work, using a crowding agent to mimic the physiological enzyme milieu, demonstrated that dilution affects PFK regulation and homologous protein-protein interactions are involved in the relief of ATP inhibition and increased substrate affinity. However, these studies have not examined the effects of a physiological range of citrate and effector concentrations on PFK activity. Therefore, the present study was designed to examine the effect of physiological concentrations of citrate (0-0.5 mM) on rabbit skeletal muscle PFK activity. In vitro activity was determined with and without the crowding agent polyethylene glycol (PEG), which enhances the aggregation state of the enzyme. Effector concentrations were chosen to