Metabolic Response and Fatigue in Soccer

2007 ◽  
Vol 2 (2) ◽  
pp. 111-127 ◽  
Author(s):  
Jens Bangsbo ◽  
Fedon Marcello Iaia ◽  
Peter Krustrup
Keyword(s):  
Oxygen Uptake ◽  
Muscle Glycogen ◽  
Metabolic Response ◽  
Creatine Phosphate ◽  
Metabolic Changes ◽  
Soccer Players ◽  
Energy Status ◽  
Muscle Lactate ◽  
Muscle Ph ◽  
Muscle Energy

The physical demands in soccer have been studied intensively, and the aim of the present review is to provide an overview of metabolic changes during a game and their relation to the development of fatigue. Heart-rate and body-temperature measurements suggest that for elite soccer players the average oxygen uptake during a match is around 70% of maximum oxygen uptake (VO2 max). A top-class player has 150 to 250 brief intense actions during a game, indicating that the rates of creatine-phosphate (CP) utilization and glycolysis are frequently high during a game, which is supported by findings of reduced muscle CP levels and several-fold increases in blood and muscle lactate concentrations. Likewise, muscle pH is lowered and muscle inosine monophosphate (IMP) elevated during a soccer game. Fatigue appears to occur temporarily during a game, but it is not likely to be caused by elevated muscle lactate, lowered muscle pH, or change in muscle-energy status. It is unclear what causes the transient reduced ability of players to perform maximally. Muscle glycogen is reduced by 40% to 90% during a game and is probably the most important substrate for energy production, and fatigue toward the end of a game might be related to depletion of glycogen in some muscle fibers. Blood glucose and catecholamines are elevated and insulin lowered during a game. The blood free-fatty-acid levels increase progressively during a game, probably reflecting an increasing fat oxidation compensating for the lowering of muscle glycogen. Thus, elite soccer players have high aerobic requirements throughout a game and extensive anaerobic demands during periods of a match leading to major metabolic changes, which might contribute to the observed development of fatigue during and toward the end of a game.

Effects of prolonged low frequency stimulation on skeletal muscle sarcoplasmic reticulum

1995 ◽  
Vol 73 (8) ◽  
pp. 1154-1164 ◽  
Author(s):  
E. R. Chin ◽  
H. J Green ◽  
F. Grange ◽  
J. Dossett-Mercer ◽  
P. J. O'Brien
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Metabolic Response ◽  
Contractile Activity ◽  
Creatine Phosphate ◽  
Energy Status ◽  
Muscle Lactate ◽  
Muscle Energy

The role of prolonged electrical stimulation on sarcoplasmic reticulum (SR) Ca2+sequestration measured in vitro and muscle energy status in fast white and red skeletal muscle was investigated. Fatigue was induced by 90 min intermittent 10-Hz stimulation of rat gastrocnemius muscle, which led to reductions (p < 0.05) in ATP, creatine phosphate, and glycogen of 16, 55, and 49%, respectively, compared with non-stimulated muscle. Stimulation also resulted in increases (p < 0.05) in muscle lactate, creatine, Pi, total ADP, total AMP, IMP, and inosine. Calculated free ADP (ADPf) and free AMP (AMPf) were elevated 3- and 15-fold, respectively. No differences were found in the metabolic response between tissues obtained from the white (WG) and red (RG) regions of the gastrocnemius. No significant reductions in SR Ca2+ATPase activity were observed in homogenate (HOM) or a crude SR fraction (CM) from WG or RG muscle following exercise. Maximum Ca2+uptake in HOM and CM preparations was similar in control (C) and stimulated (St) muscles. However, Ca2+uptake at 400 nM free Ca2+was significantly reduced in CM from RG (0.108 ± 0.04 to 0.076 ± 0.02 μmol∙mg−1protein∙min−1in RG–C and RG–St, respectively). Collectively, these data suggest that reductions in muscle energy status are dissociated from changes in SR Ca2+ATPase activity in vitro but are related to Ca2+uptake at physiological free [Ca2+] in fractionated SR from highly oxidative muscle. Dissociation of SR Ca2+ATPase activity from Ca2+uptake may reflect differences in the mechanisms evaluated by these techniques.Key words: sarcoplasmic reticulum, contractile activity, Ca2+sequestration, energy status, red and white gastrocnemius.

Effect of fluid ingestion on muscle metabolism during prolonged exercise

1996 ◽  
Vol 80 (1) ◽  
pp. 363-366 ◽  
Author(s):  
M. Hargreaves ◽  
P. Dillo ◽  
D. Angus ◽  
M. Febbraio
Keyword(s):  
Oxygen Uptake ◽  
Muscle Glycogen ◽  
Prolonged Exercise ◽  
Vastus Lateralis ◽  
Muscle Metabolism ◽  
Dry Weight ◽  
Creatine Phosphate ◽  
Peak Oxygen Uptake ◽  
Muscle Lactate ◽  
Fluid Ingestion

Five trained men were studied during 2 h of cycling exercise at 67% peak oxygen uptake at 20-22 degrees C to examine the effect of fluid ingestion on muscle metabolism. On one occasion, the subjects completed this exercise without fluid ingestion (NF) while on the other they ingested a volume of distilled deionized water that prevented loss of body mass (FR). No differences in oxygen uptake during exercise were observed between the two trials. Heart rate was lower (P < 0.01) throughout exercise when fluid was ingested, and rectal temperature after 2 h of exercise was lower (38.0 +/- 0.2 and 38.6 +/- 0.2 degrees C for FR and NF, respectively; P < 0.01), as was muscle (vastus lateralis) temperature (38.5 +/- 0.4 and 39.1 +/- 0.5 degrees C for FR and NF, respectively; P < 0.05). Resting muscle ATP, creatine phosphate, creatine, glycogen, and lactate levels were similar in the two trials, as were the postexercise ATP, creatine phosphate, and creatine levels. In contrast, muscle glycogen was higher (P < 0.05) and muscle lactate was lower (P < 0.05) after 2 h of exercise in FR compared with NF. Net muscle glycogen utilization during exercise was reduced by 16% when fluid was ingested (318 +/- 46 and 380 +/- 53 mmol/kg dry weight for FR and NF, respectively; P < 0.05). These results indicate that fluid ingestion reduces muscle glycogen use during prolonged exercise, which may account, in part, for the improved performance previously observed with fluid ingestion.

Muscle metabolism during prolonged exercise in humans: influence of carbohydrate availability

1999 ◽  
Vol 87 (3) ◽  
pp. 1083-1086 ◽  
Author(s):  
G. McConell ◽  
R. J. Snow ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Oxygen Uptake ◽  
Vastus Lateralis ◽  
Time To Exhaustion ◽  
Endurance Capacity ◽  
Vastus Lateralis Muscle ◽  
Double Blind ◽  
Muscle Lactate ◽  
Carbohydrate Ingestion ◽  
Inosine Monophosphate ◽  
Muscle Energy

Eight endurance-trained men cycled to volitional exhaustion at 69 ± 1% peak oxygen uptake on two occasions to examine the effect of carbohydrate supplementation during exercise on muscle energy metabolism. Subjects ingested an 8% carbohydrate solution (CHO trial) or a sweet placebo (Con trial) in a double-blind, randomized order, with vastus lateralis muscle biopsies ( n = 7) obtained before and immediately after exercise. No differences in oxygen uptake, heart rate, or respiratory exchange ratio during exercise were observed between the trials. Exercise time to exhaustion was increased by ∼30% when carbohydrate was ingested [199 ± 21 vs. 152 ± 9 (SE) min, P < 0.05]. Plasma glucose and insulin levels during exercise were higher and plasma free fatty acids lower in the CHO trial. No differences between trials were observed in the decreases in muscle glycogen and phosphocreatine or the increases in muscle lactate due to exercise. Muscle ATP levels were not altered by exercise in either trial. There was a small but significant increase in muscle inosine monophosphate levels at the point of exhaustion in both trials, and despite the subjects in CHO trial cycling 47 min longer, their muscle inosine monophosphate level was significantly lower than in the Con trial (CHO: 0.16 ± 0.08, Con: 0.23 ± 0.09 mmol/kg dry muscle). These data suggest that carbohydrate ingestion may increase endurance capacity, at least in part, by improving muscle energy balance.

scholarly journals Role of NADH/NAD+ transport activity and glycogen store on skeletal muscle energy metabolism during exercise: in silico studies

2009 ◽  
Vol 296 (1) ◽  
pp. C25-C46 ◽  
Author(s):  
Yanjun Li ◽  
Ranjan K. Dash ◽  
Jaeyeon Kim ◽  
Gerald M. Saidel ◽  
Marco E. Cabrera
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Glycogen ◽  
Redox State ◽  
Muscle Lactate ◽  
Mitochondrial Redox State ◽  
Muscle Energy ◽  
Muscle Energy Metabolism ◽  
Glycogen Stores ◽  
Muscle Glycogen Concentration

Skeletal muscle can maintain ATP concentration constant during the transition from rest to exercise, whereas metabolic reaction rates may increase substantially. Among the key regulatory factors of skeletal muscle energy metabolism during exercise, the dynamics of cytosolic and mitochondrial NADH and NAD+ have not been characterized. To quantify these regulatory factors, we have developed a physiologically based computational model of skeletal muscle energy metabolism. This model integrates transport and reaction fluxes in distinct capillary, cytosolic, and mitochondrial domains and investigates the roles of mitochondrial NADH/NAD+ transport (shuttling) activity and muscle glycogen concentration (stores) during moderate intensity exercise (60% maximal O2 consumption). The underlying hypothesis is that the cytosolic redox state (NADH/NAD+) is much more sensitive to a metabolic disturbance in contracting skeletal muscle than the mitochondrial redox state. This hypothesis was tested by simulating the dynamic metabolic responses of skeletal muscle to exercise while altering the transport rate of reducing equivalents (NADH and NAD+) between cytosol and mitochondria and muscle glycogen stores. Simulations with optimal parameter estimates showed good agreement with the available experimental data from muscle biopsies in human subjects. Compared with these simulations, a 20% increase (or ∼20% decrease) in mitochondrial NADH/NAD+ shuttling activity led to an ∼70% decrease (or ∼3-fold increase) in cytosolic redox state and an ∼35% decrease (or ∼25% increase) in muscle lactate level. Doubling (or halving) muscle glycogen concentration resulted in an ∼50% increase (or ∼35% decrease) in cytosolic redox state and an ∼30% increase (or ∼25% decrease) in muscle lactate concentration. In both cases, changes in mitochondrial redox state were minimal. In conclusion, the model simulations of exercise response are consistent with the hypothesis that mitochondrial NADH/NAD+ shuttling activity and muscle glycogen stores affect primarily the cytosolic redox state. Furthermore, muscle lactate production is regulated primarily by the cytosolic redox state.

Plasma glucose kinetics during exercise in subjects with high and low lactate thresholds

1992 ◽  
Vol 73 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
J. P. Kirwan ◽  
D. M. Bier ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Plasma Glucose ◽  
Glucose Oxidation ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
Vastus Lateralis ◽  
Cycle Ergometer ◽  
Vastus Lateralis Muscle ◽  
Respiratory Capacity ◽  
Group A

The purpose of this study was to test the hypothesis that the rate of plasma glucose oxidation during exercise is inversely related to muscle respiratory capacity. To this end, 14 subjects were studied: in 7 of these subjects, the blood lactate threshold (LT) occurred at a relatively high intensity [i.e., at 65 +/- 2% of peak cycle ergometer oxygen uptake (VO2 peak)], whereas in the other 7 subjects, LT occurred at a relatively low intensity (i.e., at 45 +/- 2% of VO2 peak). VO2peak did not differ between the two groups, but citrate synthase activity in the vastus lateralis muscle was 53% higher (P < 0.05) in the high LT group. A primed continuous infusion of [U-13C]glucose was used to quantify rates of glucose appearance (Ra), disappearance (Rd), and oxidation (R(ox)) during 90 min of exercise at 55% VO2peak. Although both absolute and relative rates of oxygen uptake during exercise were similar in the two groups, mean Ra and Rd were 17% lower (P < 0.001) in the high LT group, and mean R(ox) was 25% lower (21.0 +/- 2.6 vs. 27.9 +/- 2.6 mumol.min-1.kg-1; P < 0.001). The percentage of total energy derived from glucose oxidation was inversely related to muscle citrate synthase activity (r = -0.85; P < 0.01). These data support the concept that skeletal muscle respiratory capacity has a major role in determining the metabolic response to submaximal exercise.

Muscle glycogen repletion during active postexercise recovery

1987 ◽  
Vol 253 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
E. M. Peters Futre ◽  
T. D. Noakes ◽  
R. I. Raine ◽  
S. E. Terblanche
Keyword(s):  
Blood Lactate ◽  
Muscle Glycogen ◽  
High Intensity ◽  
Active Recovery ◽  
Muscle Lactate ◽  
Glycogen Resynthesis ◽  
Passive Recovery ◽  
Lactate Removal ◽  
Glycogen Repletion ◽  
Lactate Levels

High-intensity intermittent bicycle exercise was used to deplete muscle glycogen levels by 70% and elevate blood lactate levels to greater than 13.0 mmol/l. Thereafter subjects either cycled with one leg for 45 min followed by 45 min of passive recovery (partially active recovery) or rested for 90 min (passive recovery). During the first 45 min of partially active recovery 1) blood lactate (P less than 0.05) and pH levels (P less than 0.05) returned more rapidly to preexercise values than during passive recovery, 2) the rate of net glycogen resynthesis (0.28 mumol . g-1 . min-1) was the same in both legs, and 3) muscle lactate levels were significantly lower (P less than 0.05) in the passive than in the active leg. Thereafter the rate of net muscle glycogen resynthesis was unchanged (0.26 mumol . g-1 . min-1) and lactate removal could theoretically account for only 18% of the glycogen resynthesized. Overall, the rate of muscle glycogen resynthesis and muscle lactate removal was not different from that measured during passive recovery. After high-intensity exercise 1) glycogen repletion is not impeded by light exercise, and 2) blood glucose is an important substrate for glycogen resynthesis.

scholarly journals Regulation of muscle glycogenolytic flux during intense aerobic exercise after caffeine ingestion

1998 ◽  
Vol 275 (2) ◽  
pp. R596-R603 ◽  
Author(s):  
Alan Chesley ◽  
Richard A. Howlett ◽  
George J. F. Heigenhauser ◽  
Eric Hultman ◽  
Lawrence L. Spriet
Keyword(s):  
Aerobic Exercise ◽  
Muscle Glycogen ◽  
Glycogen Phosphorylase ◽  
Vastus Lateralis ◽  
Energy Status ◽  
Caffeine Ingestion ◽  
Sparing Effect ◽  
Muscle Biopsies ◽  
Glycogen Sparing ◽  
Epinephrine Concentration

This study examined the effects of caffeine (Caf) ingestion on muscle glycogen use and the regulation of muscle glycogen phosphorylase (Phos) activity during intense aerobic exercise. In two separate trials, 12 untrained males ingested either placebo (Pl) or Caf (9 mg/kg body wt) 1 h before cycling at 80% maximum O2 consumption (V˙o 2 max) for 15 min. Muscle biopsies were obtained from the vastus lateralis at 0, 3, and 15 min of exercise. In this study, glycogen “sparing” was defined as a 10% or greater reduction in muscle glycogen use during exercise after Caf ingestion compared with Pl. Muscle glycogen use decreased by 28% (Pl 255 ± 38 vs. Caf 184 ± 24 mmol/kg dry muscle) after Caf in six subjects [glycogen sparers (Sp)] but was unaffected by Caf in six other subjects [nonsparers (NSp), Pl 210 ± 35 vs. Caf 214 ± 37 mmol/kg dry muscle]. In both groups, Caf significantly increased resting free fatty acid concentration, significantly increased epinephrine concentration by twofold during exercise, and increased the Phos a mole fraction at 3 min of exercise compared with Pl, although not significantly. Caf improved the energy status of the muscle during exercise in the Sp group: muscle phosphocreatine (PCr) degradation was significantly reduced (Pl 47.9 ± 3.6 vs. Caf 40.4 ± 6.7 mmol/kg dry muscle at 3 min) and the accumulations of free ADP and free AMP (Pl 6.8 ± 1.3 vs. Caf 3.1 ± 1.4 μmol/kg dry muscle at 3 min; Pl 8.7 ± 0.8 vs. Caf 4.7 ± 1.1 μmol/kg dry muscle at 15 min) were significantly reduced. Caf had no effect on these measurements in the NSp group. It is concluded that the Caf-induced decrease in flux through Phos (glycogen-sparing effect) is mediated via an improved energy status of the muscle in the early stages of intense aerobic exercise. This may be related to an increased availability of fat and/or ability of mitochondria to oxidize fat during exercise preceded by Caf ingestion. It is presently unknown why the glycogen-sparing effect of Caf does not occur in all untrained individuals during intense aerobic exercise.

Lactate as substrate for glycogen resynthesis after exercise

1987 ◽  
Vol 62 (6) ◽  
pp. 2237-2240 ◽  
Author(s):  
R. W. Stevenson ◽  
D. R. Mitchell ◽  
G. K. Hendrick ◽  
R. Rainey ◽  
A. D. Cherrington ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Recovery Period ◽  
Control Level ◽  
Lactate Concentration ◽  
Perfusion Medium ◽  
Muscle Lactate ◽  
Arterial Lactate ◽  
Medium Flow ◽  
Flow Through ◽  
Lactate Levels

Muscle glycogen levels in the perfused rat hemicorpus preparation were reduced two-thirds by electrical stimulation plus exposure to epinephrine (10(-7) M) for 30 min. During the contraction period muscle lactate concentrations increased from a control level of 3.6 +/- 0.6 to a final value of 24.1 +/- 1.6 mumol/g muscle. To determine whether the lactate that had accumulated in muscle during contraction could be used to resynthesize glycogen, glycogen levels were determined after 1–3 h of recovery from the contraction period during which time the perfusion medium (flow-through system) contained low (1.3 mmol/l) or high (10.5 or 18 mmol/l) lactate concentrations but no glucose. With the low perfusate lactate concentration, muscle lactate levels declined to 7.2 +/- 0.8 mumol/g muscle by 3 h after the contraction period and muscle glycogen levels did not increase (1.28 +/- 0.07 at 3 h vs. 1.35 +/- 0.09 mg glucosyl U/g at end of exercise). Lactate disappearance from muscle was accounted for entirely by output into the venous effluent. With the high perfusate lactate concentrations, muscle lactate levels remained high (13.7 +/- 1.7 and 19.3 +/- 2.0 mumol/g) and glycogen levels increased by 1.11 and 0.86 mg glucosyl U/g, respectively, after 1 h of recovery from exercise. No more glycogen was synthesized when the recovery period was extended. Therefore, it appears that limited resynthesis of glycogen from lactate can occur after the contraction period but only when arterial lactate concentrations are high; otherwise the lactate that builds up in muscle during contraction will diffuse into the bloodstream.

Glucose uptake in rat soleus: effect of acute unloading and subsequent reloading

1988 ◽  
Vol 64 (4) ◽  
pp. 1428-1432 ◽  
Author(s):  
E. J. Henriksen ◽  
M. E. Tischler
Keyword(s):  
Maximum Voluntary Contraction ◽  
Lactate Concentration ◽  
Creatine Phosphate ◽  
Voluntary Contraction ◽  
Gradual Decline ◽  
Muscle Lactate ◽  
Generating Capacity ◽  
Target Force ◽  
Muscle Biopsies ◽  
Contractile Failure

Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.

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