Biomedical subjects

A Bonen

Publications and source records attributed to A Bonen.

At least 91 records · Page 5Linked to original sources

PubMed1994

Expression of the insulin-regulatable transporter GLUT-4 in muscle is influenced by neurogenic factors.

To investigate whether the expression of GLUT-4 is influenced by neurogenic factor(s) released from the nerve to the muscle, we measured GLUT-4 at different time points after sectioning the sciatic nerve at different locations in two groups of rats. Specifically, GLUT-4 was measured at 12, 24, and 48 h after severing the sciatic nerve. In one group of animals the muscles were left either with a short nerve stump attached to the muscle, or, in another group of animals, a long nerve stump remained attached to the muscle. In both groups of animals the contralateral limb served as a control. We examined GLUT-4 in the red (RG) and white gastrocnemius (WG), since the RG is highly responsive to denervation and the WG is quite resistant to denervation [L. A. Megeney, P.D. Neufer, G. L. Dohm, M. H. Tan, C. A. Blewtt, G. C. B. Elder, and A. Bonen. Am. J. Physiol. 264 (Endocrinol. Metab. 27): E583-E593, 1993]. In the long nerve stump WG no change in GLUT-4 was observed at 12, 24, or 48 h after denervation (P > 0.05). In the short nerve stump WG, changes were not evident at 12 and 24 h (P > 0.05), but by 48 h a significant decrement (-12.7 +/- 6.7%) was observed (P < 0.05). GLUT-4 changes were only evident 48 h after denervation (-19.8 +/- 4.5%; P < 0.05) in the long nerve stump RG.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effects of exercise and glycogen depletion on glyconeogenesis in muscle.

In the present study, we investigated the hypotheses that 1) skeletal muscle glyconeogenesis will increase after exercise, 2) greater changes in glyconeogenesis will be observed after exercise in fast-twitch muscles than in slow-twitch muscles, and 3) glycogen repletion will reduce the rates of glyconeogenesis. Mouse soleus and extensor digitorum longus (EDL) glycogen depots were reduced to the same levels by treadmill exercise (60 min) or epinephrine injection (75 micrograms/100 g body wt ip). Untreated animals were used as controls. We were able to prevent glycogen repletion by incubating muscles in vitro with sorbitol (75 mM) and to increase glycogen concentrations in vitro by incubating muscles with glucose (75 mM). The experimental results showed that glyconeogenesis was increased by exercise (EDL, +51%; soleus, +82%) when glycogen levels were kept low. When glycogen depots were increased, the rate of glyconeogenesis was lowered in the exercised EDL (P < 0.05) but not in the soleus (P > 0.05). Reductions in muscle glycogen by epinephrine did not change the rate of glyconeogenesis in EDL, either when glycogen depots were kept low or were repleted (P > 0.05). In contrast, in the soleus, epinephrine-induced reductions in glycogen did stimulate glyconeogenesis (P < 0.05). Analyses in EDL showed that in nonexercised muscles glycogen concentrations were minimally effective in altering the rates of glyconeogenesis. A 30% decrement in glycogen increased glyconeogenesis by 5% in resting muscles, whereas the same decrement increased glyconeogenesis by 51% in exercised muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effects of pregnancy and chronic exercise on respiratory responses to graded exercise.

Effects of cycle ergometer conditioning (heart rate 143 +/- 2 beats/min, 25 min/session, 3 sessions/wk) during the second and third trimesters of pregnancy were studied in 18 healthy previously sedentary women. A nonexercising control group (n = 9) was also studied. Graded exercise tests were conducted for both groups at approximately 17, 27, and 37 wk of gestation and at 20 wk postpartum. Both groups exhibited augmented ventilatory responses to exercise throughout pregnancy. Significant aerobic conditioning effects observed in the exercised group between entry and third trimester of pregnancy testing included a 17% increase in oxygen pulse at peak exercise, reduction in the respiratory exchange ratio during standard submaximal exercise, and an increase in work rate at the onset of blood lactate accumulation. Onset of blood lactate accumulation did not change significantly in the control group. Respiratory exchange ratio at peak exercise was higher in postpartum tests compared with those conducted in late gestation in both groups. Peak postexercise lactate levels were also significantly lower in second and third trimesters of pregnancy testing compared with postpartum in the control group. This effect appeared to be prevented by physical conditioning in the exercised group. The study results support the hypothesis that moderate aerobic conditioning increases maximal aerobic power and the capacity for sustained submaximal exercise. Chronic exercise also appeared to help to preserve anaerobic working capacity in late gestation.

Adult↗

PubMed1994

Exercise-induced menstrual cycle changes. A functional, temporary adaptation to metabolic stress.

Chronic exercise is now known to alter the menstrual cycle. Yet, we do not yet know the true incidence of menstrual cycle alterations in athletes, because good normative data do not exist and the metabolic cost of training has not been considered in many studies. Secondary amenorrhoea is not easily induced by exercise training alone but seems to require additional metabolic stressors. Induction of secondary amenorrhoea in prospective exercise studies has not occurred, although the onset of short luteal or inadequate luteal phase cycles may occur in women even when running distances are not extensive. Such menstrual cycles may cause infertility, but this is only a temporary phenomenon since pregnancy, if desired, will usually occur upon cessation of training. Exercise-related changes in the menstrual cycle can be viewed as a functionally adaptive rather than a maladaptive dysfunction. A strong case can be made that the changes in the menstrual cycle as a result of exercise are an energy conserving strategy to protect more important biological processes. This hypothesis is consistent with the theory of metabolic arrest that has been identified in lower organisms and hibernating mammals.

Adaptation, Physiological↗

PubMed1993

Lactate transport by skeletal muscle sarcolemmal vesicles.

Recent studies have indicated that lactate traversal of the sarcolemmal membrane of skeletal muscle could be a carrier mediated process. In the present study, the initial rates of L(+)-lactate flux (Jlact) were measured in highly purified rat hindlimb skeletal muscle sarcolemmal vesicles. Fluxes were determined by the vesicle uptake of L(+)-[U-14C]lactate from the extra-vesicular medium. Jlact was saturable with respect to increasing concentrations of L(+)-lactate. Regression of these data to the Michaelis-Menten equation yielded a Km of 12.5 mM. Jlact was inhibited 81% by 10 mM pyruvate and 83% by 5mM alpha-cyano 4 hydroxycinnamate (p < 0.05), but not by D-lactate, indicating the presence of a stereoselective monocarboxylate transporter in the sarcolemmal membrane. Preincubation of the vesicles with the protein modifier, N-ethylmaleimide (20mM), inhibited Jlact by 86% (p < 0.05). An inhibitor of the inorganic anion exchanger, SITS (1mM), had no effect on Jlact. However, Jlact was markedly sensitive to an inwardly directed proton gradient (p < 0.05), and the flux was more closely related to the concentration of external ionic L(+)-lactate than to the protonated (HLa) form. These studies suggest that skeletal muscle sarcolemmal membranes possess a specific transport system for L-lactate and other monocarboxylates, which has similar properties to the lactate carrier described for several other tissues.

Animals↗

PubMed1993

Endurance training increases skeletal muscle lactate transport.

Lactate accumulation in skeletal muscle is reduced after a period of endurance training. Explanations for this phenomena include the increased oxidative capacity of the muscle, a reduction in lactate production, and increased lactate clearance. Muscle membrane transport of lactate can be seen to be a fundamental aspect of such clearance, and transmembrane lactate flux may well be an important aspect of the training response in skeletal muscle. Therefore, the lactate transport capacity in skeletal muscle sarcolemmal membranes in endurance-trained and sedentary rats was investigated. Training consisted of 6 weeks of progressively increased treadmill exercise. Twenty-four hours before being killed, both the trained and sedentary animals completed a brief exercise bout. Studies of lactate transport (zero-trans) were conducted using highly purified sarcolemmal vesicles. When low concentrations of L-lactate (1 mM) were used a 59.4% increase in lactate transport was observed (P < 0.05). However, when a high concentration of lactate (50 mM) was used no change in lactate transport was found (P > 0.05). Several interpretations are possible for these observations: (1) that there is an alteration in the Km but not the Vmax of the lactate transport system in skeletal muscle membranes; and (2) that specific changes occur in selected isoforms of the lactate transport protein which may co-exist in muscle.

Animals↗

PubMed1993

Effects of muscle activity and fiber composition on glucose transport and GLUT-4.

We examined glucose uptake and GLUT-4 in rat muscles [soleus (Sol), plantaris (PL), extensor digitorum longus (EDL), tibialis anterior, and the red and white gastrocnemius (WG)]. In the normally innervated perfused rat hindlimb muscles the proportion of oxidative fibers was highly correlated with the muscle's insulin-stimulated 3-O-methyl-D-glucose (3-MG) uptake (R2 = 0.78) and GLUT-4 content (r = 0.94). Insulin-stimulated 3-MG uptake and GLUT-4 were also highly correlated (R2 = 0.996). In 3-day denervated muscles, insulin-stimulated 3-MG uptake was reduced in all six muscles (-41 to -14.6%, P < 0.05), and GLUT-4 content was also reduced (-87.5 to -34.9%), except in the WG and EDL (P > 0.05). A very high correlation was observed between the decrements in GLUT-4 (%) and the decrements in 3-MG uptake (%; r = 0.99). The relatively greater loss in muscle activity (%) due to denervation in the Sol compared with the PL coincided with the reductions (%) in GLUT-4 and 3-MG uptake. These studies demonstrate that glucose uptake and GLUT-4 are regulated by insulin-independent means, namely the oxidative capacity of the muscle and the normal activity level of the muscle.

3-O-Methylglucose↗

PubMed1992

Epinephrine administration stimulates GLUT4 translocation but reduces glucose transport in muscle.

Epinephrine opposes glucose transport in muscle. Therefore, we investigated the effects of epinephrine administration (25 micrograms/100g body weight) on glucose transport and glucose transporters in rat muscle. Ninety minutes after epinephrine injection 3-O-methyl glucose transport was reduced (approximately 47%) in perfused muscles of the rat hindlimb. Translocation of the insulin-regulatable glucose transporter (GLUT4) in the epinephrine-injected animals was confirmed by the marked increments in the GLUT-4 in the plasma membranes and their concomitant reduction in the intracellular membranes. We speculate a) that it is epinephrine which translocated GLUT4 via a cAMP-linked pathway, and b) that the intrinsic activity reductions are caused either by the glycation of the transporter by the persistent hyperglycemia and/or by epinephrine via the phosphorylation of the GLUT4 transporter protein in muscle.

3-O-Methylglucose↗

PubMed1992

Recreational exercise does not impair menstrual cycles: a prospective study.

To determine whether recreational levels of training (jogging) will provoke short luteal phase menstrual cycles, a prospective study was conducted. Out of 132 women who initiated this study 57 completed it. These individuals were within normal range of cardiorespiratory fitness for 18-40-year-old women. After a control menstrual cycle (#1) and two additional menstrual cycles (#2 and #3) in which light calisthenics were performed, the subjects were then assigned to run less than 10 mi/wk, 10-20 mi/wk or 20-30 mi/wk for either two menstrual cycles (#4 and #5), or four menstrual cycles (#4, #5, #6, #7), followed by a detraining period lasting two menstrual cycles (i.e. #6 and #7 for the 2-month running groups; #8 and #9 for the 4-month running groups). Blood samples were obtained throughout every second menstrual cycle (i.e. cycles #1, #3, #5, #7, #9). Samples were assayed for LH, FSH and P. Body weight and body fat (%) were not altered by training (p greater than 0.05). Improvements in cardiovascular fitness did occur (p less than 0.05). No change in LH attributable to running was found in any of the 6 experimental groups (p greater than 0.05). In some of the groups quite large changes occurred in FSH (p less than 0.05), but there was no discernable pattern of onset of these changes among groups. Some increments in P were found (p less than 0.05) but again these were not consistent. Finally, in none of the six groups was an altered menstrual cycle length discernable (p greater than 0.05), nor was the luteal phase length altered (p greater than 0.05) by running. Therefore, in gynecologically mature women recreational running of up to 30 miles/week for 4 menstrual cycles has no deleterious effects upon their menstrual cycle.

Adult↗

PubMed1992

Glyconeogenic and oxidative lactate utilization in skeletal muscle.

In this article we present a synthesis of recent information concerning the fate of lactate in skeletal muscle. This is important since lactate is continuously produced by skeletal muscle at rest and at all levels of exercise. Therefore, the disposal of lactate as an 'intermediary' metabolite is discussed. The two primary fates of lactate in skeletal muscle are (1) oxidation and (2) glycogen synthesis (glyconeogenesis). From recent evidence it seems relatively clear that glycogen formation in muscle is primarily dependent on glucose, although in fast twitch muscles a considerable proportion of lactate can account for muscle glycogen formation, especially immediately after exercise when circulating lactate levels are elevated. Exactly how lactate is converted to glycogen is not known yet, but an extramitochondrial pathway that is divergent from the hepatic gluconeogenic pathway seems likely. Oxidation of lactate is quantitatively the most important means of disposing of lactate, whether in exercising or nonexercising muscle. The lactate gradient between muscle and blood may be an important factor dictating whether lactate is taken up or released by muscle, independent of whether the muscle is active or not. Finally a novel role for epinephrine is considered that may be important for the mitochondrial oxidation of lactate.

Animals↗

PubMed1992

Increased glucose transport in nonexercising muscle.

Changes in blood flow and muscle glycogen in nonexercising muscle during exercise suggest that glucose transport may be increased in nonexercising muscles. Therefore, we compared 3-O-methyl-D-glucose (3-MG) transport in exercised and nonexercised perfused rat hindlimb muscles (soleus, plantaris, and red and white gastrocnemius), in the absence and presence of insulin (30 nM). Specifically, the following four treatments were used: 1) normal rest, 2) normal exercise animals (90 min running 15 m/min, 8% grade), 3) hindlimb-suspended animals at rest (90 min), and 4) hindlimb-suspended animals while exercising on the forelimbs (90 min running 15 m/min, 8% grade). In separate groups of animals, it was shown from the analyses of the electromyographic interference patterns that muscle activity was sharply reduced in hindlimb-suspended muscles both at rest and during exercise (soleus and plantaris). Glycogen decrements were also observed in nonexercising muscles during exercise (soleus, plantaris, and red gastrocnemius; P less than 0.05), although these decrements were less than in the exercised muscles (P less than 0.05). Glucose transport differed among muscles (soleus = plantaris greater than red gastrocnemius greater than white gastrocnemius), and typical increments were observed after exercise (P less than 0.05) and with insulin stimulation (P less than 0.05). An additive effect of insulin and exercise was also observed (P less than 0.05). In nonexercised muscles with no insulin in the perfusate, an increase in 3-MG transport occurred (P less than 0.05). In the presence of insulin, an increase in 3-MG transport was also observed in the nonexercised red and white gastrocnemius muscles (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Substrate and endocrine responses during exercise at selected stages of pregnancy.

To determine whether the concomitant effects of pregnancy and exercise yield substrate and endocrine patterns different from those expected during exercise alone, we compared the responses of glucose, lactate, free fatty acids, insulin, epinephrine (EP), norepinephrine (NE), human chorionic gonadotropin (HCG), human placental lactogen (HPL), estriol, and progesterone (P) in nonpregnant women (NP; n = 7) and pregnant women in the second (TR2; n = 6) and third trimester (TR3; n = 8) of pregnancy, before, during, and after 30 min of bicycle ergometer exercise at heart rates of 130-140 beats/min. In general, all substrates and hormone concentrations increased with exercise (P less than 0.05), except insulin, which decreased (P less than 0.05), and HCG, which did not change (P = 0.08). Differences in selected hormone concentrations (P, estriol, HCG, and HPL) among groups were already present at rest because of the different stages of pregnancy. Differences among groups at rest were also found in insulin and NE (P less than 0.05). Significantly different responses to exercise (i.e., group x time interactions) were as follows. NP vs. TR2:P, estriol, HCG, HPL, EP, and NE (P less than 0.05); NP vs. TR3: glucose, EP, and NE (P less than 0.05); TR2 vs. TR3: lactate, EP, and NE (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Persistence of glucose metabolism after exercise in trained and untrained soleus muscle.

We tested the hypothesis that increments in glucose metabolism in muscles from trained animals are caused by training adaptations in skeletal muscle and not by the residual effects of the last training session. The effects of a single bout of exercise on glucose metabolism (glycolysis and glycogenesis) were compared, against appropriate controls, in untrained (experiment 1) and trained (experiment 2) rat soleus muscles immediately (t = 0) and 3, 6, 24, 48, and 96 h after a standardized bout of exercise. [3H]Glucose incorporation into glycogen and glycolysis was measured in vitro in the absence and presence of insulin (0.1 and 10 nM). Experiment 1: A single bout of exercise provoked an increase in glycogenesis in the exercised, untrained muscles compared with the nonexercised, untrained muscles (0-96 h; P = 0.006). Glycolysis was not altered (0-96 h; P > 0.05). Experiment 2: In the exercised trained soleus, rates of glycolysis were greater than in the exercised, untrained soleus, at insulin concentrations of 0.1 nM (0-96 h; P = 0.005) and 10 nM (0-96 h; P = 0.01), but not in the absence of insulin (0-96 h; P > 0.05). No differences were observed in the rates of glycogenesis (0-96 h; P > 0.05). Therefore, acute exercise provokes increments in glycogenesis, whereas training increases glycolysis, in the presence of insulin, for some time after exercise. We speculate that insulin-dependent increments in glycolysis in trained muscles are a consequence of increased glucose transport caused by a greater pool of insulin-translocatable, intracellular glucose transporters.

Analysis of Variance↗

PubMed1991

Non-exercising muscle metabolism during exercise.

Glycogen decrements have been observed in non-exercising muscles during exercise. We therefore investigated whether the degraded glycogen was retained within the muscle in the form of glycolytic intermediates, or whether it was effluxed from the non-exercising muscles. For these studies a suspension harness was used to unload the hindlimb muscles at rest and during exercise [McDermott et al. (1987) J Appl Physiol 63:1275-1283]. Concentrations of glycogen and glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, glycerol 3-phosphate, and lactate) were measured in non-exercising and exercising muscles (soleus, plantaris, red and white gastrocnemius) during a 90-min exercise about 15 m/min, 8% grade). On-line electromyographic analysis showed that the contractile activity in the non-exercising muscles was markedly lower than in the exercising muscles. Similar decrements in muscle glycogen levels were observed in both the non-exercising and exercising muscles at the end of the 90-min, exercise bout (P less than 0.05), despite significantly different activity profiles. An increase in tissue lactate concentrations occurred in both non-exercising and exercising muscle (P less than 0.05), although only slight changes in the glycolytic intermediates occurred. The sum total of all the accumulated glycolytic intermediates and lactate (converted to glucosyl units) in the non-exercising muscles only accounted for a small fraction of the glycogen degraded (approximately 15%-28%). We conclude that the metabolism of glycogen is enhanced in non-exercising muscle, and that glycogen utilization is uncoupled from the energetic demands of the muscle. Furthermore, the glycogen mobilized in non-exercising muscle is not retained within the muscle in other metabolite pools.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1991

Substrate and hormonal responses to exercise in women using oral contraceptives.

Hormone and substrate responses to mild and heavy treadmill exercise were compared in women who used oral contraceptives (OC group; n = 7) and in normally menstruating women (control group; n = 8). Venous blood samples were obtained before exercise (-5 min), during exercise (15, 30, 45, and 60 min), and 30 min after exercise. All samples were analyzed for glucose, lactate, free fatty acids (FFA), glycerol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), human growth hormone (hGH), cortisol, insulin, estradiol (E2), and progesterone (P). Substrate patterns during exercise were not altered by the phase of the menstrual cycle or OC usage. However, in the OC group the FFA concentrations were consistently higher during mild exercise and the glucose concentrations were lower at rest and during exercise than in the control group (P less than 0.05). No differences in lactate or glycerol responses were observed between the groups (P greater than 0.05). The responses of insulin and hGH to exercise were not related to the OC use per se but rather to the steroid status, either endogenous or exogenous. Specifically, during the steroid phases (OC use phase and luteal phase) 1) insulin concentrations were not quite as markedly reduced (i.e., 12% higher when luteal phase and OC usage phase data were combined; P less than 0.05), and 2) hGH concentrations at rest and during light exercise were higher in the OC group during the OC use phase (P less than 0.05). LH patterns were not affected by exercise (P greater than 0.05), but a slight decrease was found in FSH (P less than 0.05). Increments in P and E2 were observed in the control group in both the follicular and luteal phase (P less than 0.05), but much greater increments in P occurred in the luteal phase than in the follicular phase (P less than 0.05). In contrast to the control group, no increments in P, E2, or cortisol occurred in the OC users during exercise (P greater than 0.05). Therefore the new observations in this study are that 1) insulin and growth hormone respond in a complex manner during exercise with either the phase of the menstrual cycle or the phases of OC use and disuse and 2) the steroid concentrations (P, E2, cortisol) are increased in the controls but not in the OC users during exercise. The latter point suggests that normal steroid increments are due to an increased rate of secretion rather than a decrease in the hepatic clearance of these steroids.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1991

The regulation of myosin gene transcription in skeletal muscle: effects of altered functional demand.

Perturbations in the activity patterns of skeletal muscle have been used to probe adaptive mechanisms that occur when the function of a muscle is altered. A plethora of information is available concerning the phenotypic changes that occur in the skeletal muscle myosin patterns when the load placed on a muscle is changed. More recently, technological advances in molecular biology have facilitated investigations concerning how these changes at the protein level are mediated via transcription of the genome. The focus of this review will be the recent evidence concerning the regulation of transcription of the myosin isogenes in skeletal muscle. In addition, putative regulatory factors are discussed which may link an alteration in function to altered transcription of the genome.

Adaptation, Physiological↗

PubMed1990

A model for nonexercising hindlimb muscles in exercising animals.

Nonexercising muscles appear to be metabolically active during exercise. Animal models for this purpose have not been established. However, we have been able to teach animals to run on their forelimbs while their hindlimbs are suspended above the treadmill with no visible limb movement. To document that indeed this mode of exercise does not provoke additional muscle activity, we have compared the levels of neural activation of the soleus and plantaris muscles using a computer analysis of the electromyographic interference pattern, recorded from bipolar fine wire electrodes implanted across each muscle. Via computer analyses of the electromyographic interference patterns the frequencies and amplitudes of motor unit action potentials were obtained. The data were sampled during 20 s of every minute of observation. Comparisons were made in four conditions: (i) resting on the treadmill while bearing weight on the hindlimbs (normal rest), (ii) running on the treadmill (15 m/min, 8% grade) on all four limbs (normal exercise), (iii) resting while the hindlimbs were suspended in a harness above the treadmill (suspended rest), and (iv) exercising with the forelimbs (15 m/min, 8% grade) while the hindlimbs were suspended above the treadmill (suspended exercise). All four experimental conditions were carried out for 90 min each and were performed by each animal. The results clearly show that muscle activities (frequencies and amplitudes), when the hindlimbs are suspended above the treadmill, at rest or during exercise, are lower than the activities in these same muscles when the animals are at rest, supporting only their body weight. Activities in the same muscles during exercise were from 300 to 2000% greater than during hindlimb suspension.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1990

Glycogenesis and glyconeogenesis in skeletal muscle: effects of pH and hormones.

We examined the effects of selected hormones and pH on the rates of glyconeogenesis (L-[U-14C]-lactate----glycogen) and glycogenesis (D-[U-14C]glucose----glycogen) in mouse fast-twitch (FT) and slow-twitch muscles incubated in vitro (37 degrees C). Glyconeogenesis and glycogenesis increased linearly with increasing concentrations of lactate (5-20 mM) and glucose (2.5-10 mM), respectively, in both muscles. Glyconeogenesis was approximately three- to fourfold greater in the extensor digitorum longus (EDL) than in the soleus, whereas basal glycogenesis was twofold greater in the soleus muscle than in the EDL. Lactate accounted for up to 5% of the glycogen formed in the soleus and up to 32% in the EDL relative to the rates of glycogenesis (i.e., 5 mM glucose + 10 nM insulin) in each muscle. Corticosterone (10(-12)-10(-6) M) failed to alter glyconeogenesis, whereas this hormone reduced glycogenesis. Insulin (10 nM) markedly stimulated glycogenesis but failed to stimulate glyconeogenesis. The rates of both glycogenesis and glyconeogenesis were pH sensitive, with optimal rates at pH 6.5-7.0 in both muscles. Glyconeogenesis increased by 49% in the soleus and by 39% EDL at pH 6.5 compared with pH 7.4. Glycogenesis increased in the soleus (SOL) and EDL in the absence (SOL: +22%; EDL: +52%) and presence of insulin (SOL: +22%; EDL: +51%) at pH 6.5 when compared with pH 7.4. In additional experiments with the perfused rat hindquarter, rates of glyconeogenesis were shown to be highly correlated with proportion of FT muscle fibers in a muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗