Role of glycogen in control of glycolysis and IMP formation in human muscle during exercise

1991 ◽  
Vol 260 (6) ◽  
pp. E859-E864 ◽  
Author(s):  
M. K. Spencer ◽  
A. Katz

The effect of prior glycogen depletion on glycolysis [flux through phosphofructokinase (PFK)] and inosine monophosphate (IMP) formation in human skeletal muscle has been investigated. Eight subjects cycled at a work load calculated to elicit 95% of maximal O2 uptake on two occasions, the first to fatigue [5.5 +/- 0.3 (SE) min] and the second at the same workload and for the same duration as the first. Before the first experiment, muscle glycogen stores were lowered by a combination of exercise and diet. Before the second experiment, muscle glycogen stores were supercompensated. In the low-glycogen (LG) state muscle glycogen decreased from 201 +/- 31 mmol glucosyl units/kg dry wt at rest to 105 +/- 28 after exercise, and in the high-glycogen (HG) state from 583 +/- 40 to 460 +/- 49. The accumulation of fructose 6-phosphate (F-6-P; activator of PFK) during exercise was markedly attenuated in the LG state (P less than 0.01), whereas lactate accumulation in muscle was similar between treatments, suggesting that muscle pH was also similar. Glycolysis (estimated from glycogenolysis minus accumulation of hexose monophosphates) was not measurably different between treatments (LG = 88 +/- 17, HG = 106 +/- 43 mmol/kg dry wt; P greater than 0.05). IMP was significantly greater in the LG state after exercise (3.63 +/- 0.85 vs. 1.97 +/- 0.44 mmol/kg dry wt; P less than 0.05). It is concluded that decreased glycogen availability does not measurably alter the rate of muscle glycolysis during intense exercise. It is hypothesized that the attenuated increase in F-6-P in the LG state, which should theoretically decrease glycolysis, is compensated for by increases in free ADP and AMP (activators of PFK) at the enzymatic site during the contraction phase. The greater increase in IMP in the LG state is consistent with this hypothesis, since ADP and AMP are also activators of AMP deaminase.

1985 ◽  
Vol 59 (5) ◽  
pp. 1350-1354 ◽  
Author(s):  
D. S. King ◽  
D. L. Costill ◽  
W. J. Fink ◽  
M. Hargreaves ◽  
R. A. Fielding

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.


1996 ◽  
Vol 81 (4) ◽  
pp. 1495-1500 ◽  
Author(s):  
Adrianus J. Van Den Bergh ◽  
Sibrand Houtman ◽  
Arend Heerschap ◽  
Nancy J. Rehrer ◽  
Hendrikus J. Van Den Boogert ◽  
...  

Van Den Bergh, Adrianus J., Sibrand Houtman, Arend Heerschap, Nancy J. Rehrer, Hendrikus J. Van Den Boogert, Berend Oeseburg, and Maria T. E. Hopman. Muscle glycogen recovery after exercise during glucose and fructose intake monitored by13C-NMR. J. Appl. Physiol. 81(4): 1495–1500, 1996.—The purpose of this study was to examine muscle glycogen recovery with glucose feeding (GF) compared with fructose feeding (FF) during the first 8 h after partial glycogen depletion by using13C-nuclear magnetic resonance (NMR) on a clinical 1.5-T NMR system. After measurement of the glycogen concentration of the vastus lateralis (VL) muscle in seven male subjects, glycogen stores of the VL were depleted by bicycle exercise. During 8 h after completion of exercise, subjects were orally given either GF or FF while the glycogen content of the VL was monitored by13C-NMR spectroscopy every second hour. The muscular glycogen concentration was expressed as a percentage of the glycogen concentration measured before exercise. The glycogen recovery rate during GF (4.2 ± 0.2%/h) was significantly higher ( P < 0.05) compared with values during FF (2.2 ± 0.3%/h). This study shows that 1) muscle glycogen levels are perceptible by 13C-NMR spectroscopy at 1.5 T and 2) the glycogen restoration rate is higher after GF compared with after FF.


1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.


1986 ◽  
Vol 61 (2) ◽  
pp. 654-659 ◽  
Author(s):  
S. F. Loy ◽  
R. K. Conlee ◽  
W. W. Winder ◽  
A. G. Nelson ◽  
D. A. Arnall ◽  
...  

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.


1994 ◽  
Vol 4 (3) ◽  
pp. 221-236 ◽  
Author(s):  
John A. Hawley ◽  
Steven C. Dennis ◽  
Timothy D. Noakes

Soccer requires field players to exercise repetitively at high intensities for the duration of a game, which can result in marked muscle glycogen depletion and hypoglycemia. A soccer match places heavy demands on endogenous muscle and liver glycogen stores and fluid reserves, which must be rapidly replenished when players complete several matches within a brief period of time. Low concentrations of muscle glycogen have been reported in soccer players before a game, and daily carbohydrate (CHO) intakes are often insufficient to replenish muscle glycogen stores, CHO supplementation during soccer matches has been found to result in muscle glycogen sparing (39%), greater second-half running distances, and more goals being scored with less conceded, when compared to consumption of water. Thus, CHO supplementation has been recommended prior to, during, and after matches. In contrast, there is currently insufficient evidence to recommend without reservation the addition of electrolytes to a beverage for ingestion by players during a game resulting in sweat losses of < 4% of body weight.


1983 ◽  
Vol 55 (6) ◽  
pp. 1767-1771 ◽  
Author(s):  
L. Levine ◽  
W. J. Evans ◽  
B. S. Cadarette ◽  
E. C. Fisher ◽  
B. A. Bullen

Substrate utilization after fructose, glucose, or water ingestion was examined in four male and four female subjects during three treadmill runs at approximately 75% of maximal O2 uptake. Each test was preceded by three days of a carbohydrate-rich diet. The runs were 30 min long and were spaced at least 1 wk apart. Exercise began 45 min after ingestion of 300 ml of randomly assigned 75 g fructose (F), 75 g glucose (G), or control (C). Muscle glycogen depletion determined by pre- and postexercise biopsies (gastrocnemius muscle) was significantly (P less than 0.05) less during the F trial than during C or G. Venous blood samples revealed a significant increase in serum glucose (P less than 0.05) and insulin (P less than 0.01) within 45 min after the G drink, followed by a decrease (P less than 0.05) in serum glucose during the first 15 min of exercise, changes not observed in the C or F trials. Respiratory exchange ratio was higher (P less than 0.05) during the G than C or F trials for the first 5 min of exercise and lower (P less than 0.05) during the C trial compared with G or F for the last 15 min of exercise. These data suggest that fructose ingested before 30 min of submaximal exercise maintains stable blood glucose and insulin concentrations, which may lead to the observed sparing of muscle glycogen.


1997 ◽  
Vol 273 (2) ◽  
pp. E416-E424 ◽  
Author(s):  
J. Bangsbo ◽  
K. Madsen ◽  
B. Kiens ◽  
E. A. Richter

The present study examined the role of lactate and glucose as substrates for glyconeogenesis in muscle in recovery from high-intensity exercise in humans. Seven subjects performed approximately 100 min of intense intermittent one-legged knee extensor exercise on two occasions: with [high lactate (HL)] and without [control (C)] intense arm exercise between the leg exercise bouts, leading to end exercise arterial plasma lactate concentrations of 16.0 +/- 1.6 and 9.2 +/- 1.6 mmol/l, respectively (P < 0.05). At the end of exercise, muscle lactate and glycogen were similar in HL and C (20.5 +/- 1.3 vs. 17.3 +/- 2.0 mmol/kg wet wt and 48.1 +/- 11.3 vs. 56.3 +/- 8.6 mmol/kg wet wt, respectively). Muscle glycogen increased (P < 0.05) during the first 5 min of recovery only in HL, but after 90 min of recovery the muscle glycogen concentration was the same in C and HL (61.2 +/- 12.0 vs. 71.5 +/- 10.9 mmol/kg wet wt). Muscle lactate not released to the blood could maximally account for 28 (C) and 54% (HL) of the increase in muscle glycogen during 90 min of recovery or < 10% of glycogen synthesis after full recovery. The total net glucose uptake corresponded to 84 (C) and 57% (HL) of the glycogen synthesized. Apparently, muscle glyconeogenesis may occur in humans, but the role of lactate as a substrate is minor. Instead, blood glucose appears to be the most important precursor for muscle glycogen synthesis after intense exercise.


1992 ◽  
Vol 73 (4) ◽  
pp. 1644-1649 ◽  
Author(s):  
T. Binzoni ◽  
G. Ferretti ◽  
K. Schenker ◽  
P. Cerretelli

The kinetics of phosphocreatine (PC) breakdown in human plantar flexors at the onset of constant-load aerobic exercise was determined by high-resolution 31P-nuclear magnetic resonance spectroscopy (NMRS). The half time of the process (t1/2PC) was obtained by fitting curves (n = 13) from five subjects at various aerobic work loads for which muscle pH was not different from that at rest. Steady-state PC concentration ([PC]) was not < 70% of the resting value and was linearly related to the work load (w) ([PC] = -3.01 +/- 0.08 w + 1 (r = 0.48, 2P < 0.1)). The average t1/2PC was 16.2 s and was independent of work load. Because the half time of the muscle PC kinetics reflects the half time of the O2 uptake (MO2) kinetics (t1/2MO2), the latter is equal to that found earlier in the isolated perfused dog gastrocnemius. Whereas in the dog the above t1/2MO2 compares well with the homologous half time of the O2 uptake at the alveolar level, in humans such equivalence is found only at extremely low work loads, when the transient contribution by anaerobic glycolysis is negligible.


Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 828
Author(s):  
Lee M. Margolis ◽  
J Philip Karl ◽  
Marques A. Wilson ◽  
Julie L. Coleman ◽  
Claire C. Whitney ◽  
...  

This study used global metabolomics to identify metabolic factors that might contribute to muscle anabolic resistance, which develops when aerobic exercise is initiated with low muscle glycogen using global metabolomics. Eleven men completed this randomized, crossover study, completing two cycle ergometry glycogen depletion trials, followed by 24 h of isocaloric refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate 1.0 g/kg fat) glycogen. Participants then performed 80 min of cycling (64 ± 3% VO2 peak) while ingesting 146 g carbohydrate. Serum was collected before glycogen depletion under resting and fasted conditions (BASELINE), and before (PRE) and after (POST) exercise. Changes in metabolite profiles were calculated by subtracting BASELINE from PRE and POST within LOW and AD. There were greater increases (p < 0.05, Q < 0.10) in 64% of branched-chain amino acids (BCAA) metabolites and 69% of acyl-carnitine metabolites in LOW compared to AD. Urea and 3-methylhistidine had greater increases (p < 0.05, Q < 0.10) in LOW compared to AD. Changes in metabolomics profiles indicate a greater reliance on BCAA catabolism for substrate oxidation when exercise is initiated with low glycogen stores. These findings provide a mechanistic explanation for anabolic resistance associated with low muscle glycogen, and suggest that exogenous BCAA requirements to optimize muscle recovery are likely greater than current recommendations.


1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.


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