Effects of 24-hour fast on cycling endurance time at two different intensities

1986 ◽  
Vol 61 (2) ◽  
pp. 654-659 ◽  
Author(s):  
S. F. Loy ◽  
R. K. Conlee ◽  
W. W. Winder ◽  
A. G. Nelson ◽  
D. A. Arnall ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Plasma Free Fatty Acid ◽  
Normal Diet ◽  
Glycogen Depletion ◽  
Endurance Time ◽  
Competitive Cyclists ◽  
Pedal Frequency ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Initial Intensity

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.

Muscle glycogen recovery after exercise during glucose and fructose intake monitored by13C-NMR

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 ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Glycogen Depletion ◽  
Glycogen Concentration ◽  
Fructose Intake ◽  
Glycogen Stores ◽  
Male Subjects ◽  
C Nmr

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.

Glucose turnover in 48-hour-fasted running rats

1987 ◽  
Vol 252 (3) ◽  
pp. R587-R593 ◽  
Author(s):  
B. Sonne ◽  
K. J. Mikines ◽  
H. Galbo
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Feedback Mechanisms ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Fasted Rats

In fed rats, hyperglycemia develops during exercise. This contrasts with the view based on studies of fasted human and dog that euglycemia is maintained in exercise and glucose production (Ra) controlled by feedback mechanisms. Forty-eight-hour-fasted rats (F) were compared to fed rats (C) and overnight food-restricted (FR) rats. [3-3H]- and [U-14C] glucose were infused and blood and tissue sampled. During running (21 m/min, 0% grade) Ra increased most in C and least in F and only in F did Ra not significantly exceed glucose disappearance. Plasma glucose increased more in C (3.3 mmol/l) than in FR (1.6 mmol/l) and only modestly (0.6 mmol/l) and transiently in F. Resting liver glycogen and exercise glycogenolysis were highest in C and similar in FR and F. Resting muscle glycogen and exercise glycogenolysis were highest in C and lowest in F. During running, lactate production and gluconeogenesis were higher in FR than in F. At least in rats, responses of production and plasma concentration of glucose to exercise depend on size of liver and muscle glycogen stores; glucose production matches increase in clearance better in fasted than in fed states. Probably glucose production is stimulated by “feedforward” mechanisms and “feedback” mechanisms are added if plasma glucose decreases.

Effect of various doses of cocaine on endurance capacity in rats

1989 ◽  
Vol 66 (1) ◽  
pp. 377-383 ◽  
Author(s):  
M. E. Bracken ◽  
D. R. Bracken ◽  
W. W. Winder ◽  
R. K. Conlee
Keyword(s):  
Blood Lactate ◽  
Muscle Glycogen ◽  
Plasma Norepinephrine ◽  
Endurance Capacity ◽  
Glycogen Depletion ◽  
Endurance Time ◽  
Fast Twitch Muscle ◽  
High Doses ◽  
Fast Twitch

To determine the effects of a variety of doses of cocaine on endurance capacity, rats were injected intraperitoneally with either 0.1, 0.5, 2.5, 12.5, or 20 mg/kg body wt 20 min before running to exhaustion at 26 m/min up a 10% grade. Animals given saline ran 116 +/- 9 (SE) min. At doses of 12.5 and 20 mg/kg, cocaine reduced endurance time significantly (34 and 74%, respectively). At rest the drug had no effect on liver or fast-twitch muscle glycogen but significantly reduced (20–40%) soleus glycogen at the two highest doses. However, at exhaustion, the quantity of glycogen depleted in the fast-twitch red and white vastus muscles was similar in all groups despite the reduced run times of the animals receiving a higher dose implying a greater rate of glycogenolysis due to cocaine. Blood lactate in the 20 mg/kg group (9.9 +/- 1.2 mM) at exhaustion was nearly twice that of the saline controls at exhaustion (5.1 +/- 0.6). Before exercise plasma norepinephrine (at doses of 2.5, 12.5 and 20 mg/kg) was higher than saline controls and remained higher (20 mg/kg groups) at exhaustion. We conclude that high doses of cocaine cause rapid muscle glycogen depletion and early fatigue. The mechanism by which cocaine causes these effects is not clear.

Circulating palmitate uptake and oxidation are not altered by glycogen depletion in contracting skeletal muscle

1995 ◽  
Vol 78 (4) ◽  
pp. 1266-1272 ◽  
Author(s):  
L. P. Turcotte ◽  
P. Hespel ◽  
E. A. Richter
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Carbohydrate Metabolism ◽  
Muscle Glycogen ◽  
Glucose Utilization ◽  
Plasma Free Fatty Acid ◽  
Glycogen Depletion ◽  
Plasma Ffa ◽  
Ffa Metabolism ◽  
Palmitate Uptake

The extent to which muscle glycogen depletion affects plasma free fatty acid (FFA) metabolism in contracting skeletal muscle is not well characterized. To study this question, rats were glycogen depleted (GD) or supercompensated (SC) by swimming exercise and diet treatment 24 h before perfusion of their isolated hindquarters at rest and during electrically induced muscle contractions. After 20 min of equilibration with glucose (6 mM), palmitate (2,000 microM), and [1–14C]palmitate, palmitate uptake and oxidation were found to be similar between groups at rest and during electrical stimulation. Palmitate uptake increased by 55% during electrical stimulation and averaged 2.75 +/- 0.56 mumol.g-1.h-1. Resting palmitate oxidation averaged 0.14 +/- 0.03 mumol.g-1.h-1 and increased to 0.53 +/- 0.06 and 0.47 +/- 0.08 mumol.g-1.h-1 during electrical stimulation in GD and SC, respectively. Glucose uptake was significantly higher in GD than in SC at rest and during electrical stimulation and significantly increased in both groups during electrical stimulation to reach values of 11.8 +/- 1.2 and 7.6 +/- 1.4 mumol.g-1.h-1, respectively. Lactate release was lower in GD than in SC at rest and during electrical stimulation and was highest after 2 min of stimulation in both groups. Additional experiments at perfusate palmitate concentrations of 600–900 microM yielded similar results. These results show that, in contracting perfused skeletal muscle, muscle glycogen depletion increases glucose utilization but does not affect total plasma FFA oxidation, suggesting that regulation within pathways of carbohydrate metabolism takes precedence over regulation between pathways of lipid and carbohydrate metabolism.

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
Keyword(s):  
Muscle Glycogen ◽  
Work Load ◽  
Amp Deaminase ◽  
Glycogen Depletion ◽  
Intense Exercise ◽  
O2 Uptake ◽  
Contraction Phase ◽  
Muscle Ph ◽  
Glycogen Stores

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.

Carbohydrate, Fluids and Electrolyte Requirements of the Soccer Player: A Stewiew

1994 ◽  
Vol 4 (3) ◽  
pp. 221-236 ◽  
Author(s):  
John A. Hawley ◽  
Steven C. Dennis ◽  
Timothy D. Noakes
Keyword(s):  
Body Weight ◽  
Muscle Glycogen ◽  
Soccer Player ◽  
Liver Glycogen ◽  
Soccer Players ◽  
Insufficient Evidence ◽  
Glycogen Depletion ◽  
Low Concentrations ◽  
Glycogen Stores ◽  
Glycogen Sparing

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.

Effects of Propranolol and Epinephrine Infusion on Glycogenolysis in Dog Skeletal Muscle In Situ

1972 ◽  
Vol 50 (6) ◽  
pp. 471-475 ◽  
Author(s):  
C. K. Chapler
Keyword(s):  
Electrical Stimulation ◽  
Muscle Glycogen ◽  
Muscle Group ◽  
Epinephrine Infusion ◽  
Beta Receptors ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Prior Administration ◽  
Stimulation Of

The effect of intravenous administration of propranolol and/or epinephrine on glycogen stores in the dog gastrocnemius-plantaris muscle group was assessed at rest and following 30 min of contractions. In resting muscle, glycogen stores were not altered 60 min following propranolol (0.5 mg/kg) nor did a 10 min infusion of epinephrine (1 μg/kg/min) induce glycogenolysis. Following 30 min of contractions at 5 twitches/s, about 30% of the muscle glycogen stores were depleted. This rate of glycogenolysis was unaffected by prior administration of propranolol, suggesting that the breakdown of glycogen during electrical stimulation of the muscle group is not mediated through activation of beta receptors. When epinephrine was infused during the last 10 min of the contraction period, about 50% of the initial glycogen stores was depleted. This epinephrine-induced glycogenolysis was mediated through activation of beta receptors as it was abolished by pretreatment of the animals with propranolol. These data suggest that the relatively small breakdown of glycogen stores in the gastrocnemius-plantaris during electrical stimulation of the muscle group may reflect the lack of an increase in circulating catecholamines.

scholarly journals Serum Branched-Chain Amino Acid Metabolites Increase in Males When Aerobic Exercise Is Initiated with Low Muscle Glycogen

Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 828
Author(s):  
Lee M. Margolis ◽  
J Philip Karl ◽  
Marques A. Wilson ◽  
Julie L. Coleman ◽  
Claire C. Whitney ◽  
...  
Keyword(s):  
Aerobic Exercise ◽  
Muscle Glycogen ◽  
Mechanistic Explanation ◽  
Glycogen Depletion ◽  
Anabolic Resistance ◽  
Metabolite Profiles ◽  
Acid Metabolites ◽  
Global Metabolomics ◽  
Branched Chain ◽  
Glycogen Stores

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.

Metabolic and endocrine responses to prolonged exercise in rats under β2-adrenergic blockade

1989 ◽  
Vol 67 (3) ◽  
pp. 192-196 ◽  
Author(s):  
F. Trudeau ◽  
F. Péronnet ◽  
L. Béliveau ◽  
G. Brisson
Keyword(s):  
Muscle Glycogen ◽  
Prolonged Exercise ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Exercise Bout ◽  
Plasma Free Fatty Acid ◽  
Adrenergic Blockade ◽  
Sympathoadrenal System ◽  
Glycogen Stores ◽  
Glycogen Breakdown

The respective roles of allosteric regulators and catecholamines in the control of muscle glycogen breakdown during exercise remain a matter of controversy. This study was designed to reassess the role of the sympathoadrenal system during prolonged exercise in rats. Animals were studied at rest or after treadmill exercise (28 m∙min−1; 8% slope) to exhaustion in a control situation or following administration of a specific β2-adrenergic receptor antagonist (ICI 118,551, 1 mg∙kg−1, i.v.). Running times to exhaustion were 54 and 36 min in control and treated rats, respectively. For the purpose of comparison, another group of control rats was studied after a 36-min exercise bout. The reduction in endurance in treated rats was associated with an impairment in glycogen utilization, as measured by muscle glycogen stores, in soleus muscle but not in superficial vastus lateralis or gastrocnemius lateralis muscles. Utilization of liver glycogen stores was similar in the two groups of animals, but plasma glucose (7 vs. 13 mM) and lactate (4 vs. 7 mM) levels were significantly lower in rats under β-blockade than in control rats run for 36 min. Plasma free fatty acid and glycerol concentrations were not significantly different between groups. On the other hand, plasma epinephrine concentration was significantly higher in treated rats (13 vs. 5 mM), which might reflect a compensatory increase in adrenal activity. These results suggest that glycogen breakdown during prolonged exercise is under the control of the sympathoadrenal system in predominantly slow-twitch but not in predominantly fast-twitch muscles. Epinephrine appears to play an important role in the maintenance of blood glucose level during prolonged exercise by (i) promoting muscle glycogen breakdown and thus reducing peripheral glucose utilization, and (ii) possibly increasing lactate availability for hepatic gluconeogenesis.Key words: glycogen, catecholamines, sympathoadrenal system, fiber type.

Respiratory capacity and glycogen depletion in thyroid-deficient muscle

1980 ◽  
Vol 49 (1) ◽  
pp. 102-106 ◽  
Author(s):  
K. M. Baldwin ◽  
A. M. Hooker ◽  
R. E. Herrick ◽  
L. F. Schrader
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Endurance Capacity ◽  
Glycogen Depletion ◽  
Respiratory Capacity ◽  
Rest And Exercise

This study was undertaken to determine the effects of propylthiouracil-induced thyroid deficiency on a) the capacity of muscle homogenates to oxidize [2-14C]pyruvate and [U-14C]palmitate and b) glycogen depletion during exercise in liver and in fast-oxidative-glycogenolytic (FOG), fast-glycogenolytic (FG), and slow-oxidative (SO) muscle. Relative to the rates for normal rats, oxidation with pyruvate was reduced by 53, 68, and 58%, and palmitate by 40, 50, and 48% in FOG, FG, and SO muscle, respectively (P less than 0.05). Normal rats ran longer than thyroid-deficient rats at 26.7 m/min (87 ± 8 vs. 37 ± 5 min). After 40 min of running (22 m/min), the amount of glycogen consumed in normal FOG, FG, and SO muscle and in liver amounted to only 23, 12, 66, and 52%, respectively, of that for their thyroid-deficient counterparts. Also, normal rats maintained higher plasma free fatty acid levels than thyroid-deficient rats during both rest and exercise (P less than 0.05). These findings suggest that thyroid deficiency causes a reduced potential for FFA utilization in skeletal muscle that enhances its consumption of glycogen, thereby limiting endurance capacity.

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