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Copenhagen Muscle Research Center, Rigshospitalet, DK-2200 Copenhagen, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In the
present study, we have investigated the effect of carbohydrate and
protein hydrolysate ingestion on muscle glycogen resynthesis during 4 h
of recovery from intense cycle exercise. Five volunteers were studied
during recovery while they ingested, immediately after exercise, a
600-ml bolus and then every 15 min a 150-ml bolus containing 1)
1.67 g · kg body
wt
1 · l1 of
sucrose and 0.5 g · kg body
wt1 · l1 of a whey
protein hydrolysate (CHO/protein), 2) 1.67 g · kg body wt1 · l1 of
sucrose (CHO), and 3) water. CHO/protein and CHO ingestion caused an increased arterial glucose concentration compared with water
ingestion during 4 h of recovery. With CHO ingestion, glucose concentration was 1-1.5 mmol/l higher during the first hour of recovery compared with CHO/protein ingestion. Leg glucose uptake was
initially 0.7 mmol/min with water ingestion and decreased gradually
with no measurable glucose uptake observed at 3 h of recovery. Leg
glucose uptake was rather constant at 0.9 mmol/min with CHO/protein and
CHO ingestion, and insulin levels were stable at 70, 45, and 5 mU/l for
CHO/protein, CHO, and water ingestion, respectively.
Glycogen resynthesis rates were 52 ± 7, 48 ± 5, and 18 ± 6 for
the first 1.5 h of recovery and decreased to 30 ± 6, 36 ± 3, and 8 ± 6 mmol · kg dry
muscle1 · h1
between 1.5 and 4 h for CHO/protein, CHO, and water ingestion, respectively. No differences could be observed between CHO/protein and
CHO ingestion ingestion. It is concluded that coingestion of
carbohydrate and protein, compared with ingestion of carbohydrate alone, did not increase leg glucose uptake or glycogen resynthesis rate
further when carbohydrate was ingested in sufficient amounts every 15 min to induce an optimal rate of glycogen resynthesis.
plasma glucose; glucose uptake; insulin; glucagon
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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MUSCLE GLYCOGEN IS AN IMPORTANT fuel for prolonged aerobic high-intensity exercise (1, 7). Several investigations have demonstrated that fatigue increases in parallel with decreasing muscle glycogen stores. Furthermore, the initial muscle glycogen concentration has been shown to be related to aerobic endurance performance, and a high exercise intensity cannot be maintained once the muscle glycogen stores are depleted (4, 7). It is important for performance and most likely for effective training to have full muscle glycogen stores. Because muscle glycogen resynthesis is relatively slow, and it can take >24 h before complete restoration of muscle glycogen occurs, several studies have been conducted to determine ways to enhance the rate of muscle glycogen resynthesis (4, 9, 20). Zawadski and co-workers (20) observed a faster postexercise glycogen resynthesis rate and lower venous glucose concentration if proteins were coingested with carbohydrates compared with carbohydrate ingestion alone. They suggested that the higher insulin levels with coingestion of carbohydrates and protein might have been responsible for the increased postexercise muscle glycogen resynthesis and an increased glucose clearance by the muscle. However, as mentioned by the authors, the carbohydrate supplementation regime chosen in their study resulted in a moderate glycogen resynthesis rate. Therefore, this study was conducted to investigate whether postexercise carbohydrate intake supplemented with protein can enhance muscle glycogen resynthesis rate and leg glucose uptake when the latter is close to the maximal rate observed with only carbohydrate ingestion.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Five healthy trained volunteers participated in this study. Their mean
age, mass, height, and maximal oxygen uptake were 26 ± 2 yr, 74 ± 2 kg, 1.78 ± 0.03 m, and 61 ± 2 ml · kg body
mass1 · min1,
respectively. The subjects were informed about possible risks and
discomfort involved before giving their voluntary consent to
participate. The study was performed according to the Declaration of
Helsinki and was approved by the Ethical Committee of
Copenhagen-Frederiksberg.
Protocol. Each subject underwent three experimental trials separated by 1 mo. The three trials were identical except that during the recovery period the subjects ingested drinks that contained carbohydrate and a protein hydrolysate (CHO/protein), carbohydrate (CHO), or water (water). The CHO/protein and CHO trials were randomized, and the water trial was performed thereafter.
Before the experimental trials, maximal power output (Wmax) and maximal oxygen uptake were determined during a graded exercise test on a cycle ergometer (model 818, Monark) as described previously (10). The protocol of the experimental day is shown in Fig. 1. The subjects reported to the laboratory at 8:00 AM. After the sujects changed clothes and their body mass was measured, intense cycle ergometer exercise was started to decrease the muscle glycogen content. The glycogen-depletion protocol was described previously by Kuipers et al. (10). In short, after a warm-up period of 10 min at 50% of their Wmax, the subjects had to cycle in blocks of 2-min duration at an alternating workload of 90 and 50% of their respective Wmax. This was continued until they were not able to complete the 2 min at 90% Wmax. That moment was defined as the inability to maintain a pedal rate above 60 rpm. The high-intensity block was then reduced to 80% Wmax. Again the subjects had to cycle until they were unable to complete the 2 min at 80% Wmax. When the 80% Wmax could not be completed, subjects were allowed to stop. During the glycogen-depletion exercise, the subjects were cooled with standing floor fans and water was provided ad libitum.
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1 · l1 of
sucrose and 0.5 g · kg body
wt1 · l1 of a
whey protein hydrolysate (MD Foods, Arhus, Denmark) with an average
chain length of 3.7 (CHO/protein), 2) 1.67 g · kg body wt1 · l1
sucrose (CHO), and 3) water (water).
Muscle analysis. Muscle specimens of ~50-70 mg wet weight were immediately frozen in liquid nitrogen, freeze-dried, and freed from adherent blood and connective tissue. Glycogen was measured in duplicate with 2-3 mg of dry muscle tissue. For the glycogen determination, glycogen was hydrolyzed with 1 M HCl for 3 h at 100°C and then neutralized with 0.12 M Tris-2.1 M KOH saturated with KCl. The supernatant was analyzed for glucose (Roche UniKit, Paris, France) on an automatic analyzer (Cobas Fara, Roche, Basel, Switzerland).
Blood analysis.
Femoral arterial and venous blood was collected into EDTA-containing
tubes, immediately centrifuged at 4°C to obtain plasma, and stored
at 
40°C. Plasma glucose was analyzed on an automatic analyzer (Cobas Fara, Roche). Plasma insulin (Pharmacia, Uppsala, Sweden) and glucagon (Linco, St. Charles, MO) were determined with a
radioimmunoassay kit.
Calculations.
Glucose uptake across the leg was calculated as the difference in
concentration between femoral arterial and venous plasma multiplied by
the blood flow. Muscle glycogen resynthesis rate was calculated between
0 and 1.5 h (t1) and 1.5 and 4 h
(t2) of recovery from the following equation (in
which brackets denote concentration): glycogen resynthesis rate = {[glycogen](t2) [glycogen](t1)}/(t2t1).
Net glucose uptake in millimoles for the first 1.5 h and between 1.5 and 4 h of recovery was calculated from the leg glucose
uptake rates of the two consecutive time points, multiplied by the time
span, and summed for the time period of 0-1.5 and 1.5-4 h.
Glucose needed for glycogen resynthesis was estimated from the net
increase in muscle glycogen concentration multiplied by 1.4 kg of dry
weight muscle. If it is assumed that 6 kg of the ~8 kg of leg muscle
(1.4 kg dry wt) was engaged in the cycle exercise (15) and depleted to
the same extent as the vastus lateralis muscle.
Statistical analysis. All data are means ± SE from five subjects. Statistical analysis of the data was done by using the nonparametric Wilcoxon signed-rank test to determine differences between data obtained in the three different trials for each point in time. Statistical significance was set at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Arterial glucose concentration and leg glucose uptake (Fig.
2).
The highest arterial glucose concentration was reached 20 min after the
first bolus of CHO/protein and CHO was ingested, with values of 8.7 ± 0.3 and 9.6 ± 0.2 mmol/l, respectively, after which glucose
concentration decreased gradually to ~6.3 mmol/l for both drinks. In
contrast, with water ingestion, glucose concentration was lower for the
first 20 min but returned to a stable level of ~5.2 mmol/l after 1 h
of recovery. The arterial glucose concentration was higher with
CHO/protein and CHO ingestion compared with the concentraton with water
ingestion for the entire 4 h of recovery.
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Arterial insulin and glucagon concentrations (Fig.
3).
Arterial insulin increased considerably during recovery as a result of
CHO ingestion. During the entire 4 h of recovery, insulin concentration was higher with CHO/protein ingestion (70-80 mU/l) than with CHO ingestion (40-50 mU/l), and it was only ~5 mU/l with water ingestion. Arterial glucagon decreased after ingestion of
the first bolus for all three drinks. The arterial glucagon concentration was higher during recovery with CHO/protein (90 ng/l)
compared with CHO ingestion (50 ng/l). With only water ingestion, the
glucagon concentration was between that of the CHO/protein and CHO
trial, but it failed to have a consistently significant difference from
either drink.
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Muscle glycogen content and resynthesis rate (Fig.
4).
The glycogen depletion exercise and the 26 min of incremental exercise
resulted in a muscle glycogen concentration that was the same for the
three trials (CHO/protein, 69 ± 10; CHO, 90 ± 23; water, 78 ± 11 mmol · glycosyl
units1 · kg dry
muscle1).
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1 and decreased to a
rate of 30 mmol glycosyl units · kg dry
muscle · h1 between 1.5 and 4 h of
recovery. With only water ingestion, the glycogen resynthesis rate
during the first 1.5 h was 18 mmol glycosyl units · kg dry
muscle1 · h1
and decreased to 8 mmol glycosyl units · kg dry
muscle1 · h1 thereafter.
Leg glucose uptake compared with glucose incorporated in muscle
glycogen (Fig. 5).
If we assume that 6 kg of muscle in the leg (of a total of 8 kg) is
depleted to the same extent as the vastus lateralis muscle during cycle exercise, the comparison between total leg glucose uptake and glucose needed for glycogen resynthesis can be made. In Fig.
5, the total leg glucose uptake during the 0-1.5 and 1.5-4 h
of recovery is shown together with the estimated amount of glucose needed for the glycogen synthesized (Fig. 4). During the first 1.5 h of
recovery, a nearly 100% match is found for the amount of glucose taken
up by the leg and the amount of glucose needed for the observed
increase in muscle glycogen content. Between 1.5 and 4 h of recovery it
appears that more glucose is taken up by the leg than is incorporated
into glycogen.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In this study we have investigated muscle glycogen resynthesis and leg glucose uptake during 4 h of recovery from intense cycle exercise leading to glycogen depletion. The major findings were that neither a high rate of muscle glycogen resynthesis with CHO intake nor leg glucose uptake was affected by additional protein ingestion.
Glucose uptake by the skeletal muscle is facilitated mainly via the GLUT-4 transporter. Stimulation of glucose transport by insulin is mediated by translocation of GLUT-4 from the intracellular sites to the plasma membrane (11). Skeletal muscle translocation of GLUT-4 to the plasma membrane appears also to be facilitated by muscle contraction independent of insulin. It is suggested that, during the initial phase of recovery from exercise, GLUT-4 still resides in the plasma membrane because of contraction-mediated GLUT-4 translocation during the exercise bout, and thus glucose can be transported independently of insulin (6, 8). After the relatively short period of insulin independent muscle glucose uptake, glucose uptake and GLUT-4 translocation to the plasma membrane become insulin dependent. However, during recovery from exercise, there is a marked increase in the sensitivity to insulin of muscle glucose uptake and glycogen synthesis (14, 16, 18). Recently, evidence has been presented suggesting that the rate of muscle glucose uptake may control the rate of glycogen resynthesis after exercise. This proposed mechanism seems to fit nicely with our data from when the subjects ingested water. Glucose uptake was highest during the initial recovery period, and leg glucose uptake decreased with the longer time of recovery. GLUT-4 transporters that remained in the plasma membrane from the exercise bout may have caused the higher glucose uptake at the initial stage. As recovery proceeds, the muscle becomes more and more dependent on insulin to maintain GLUT-4 transporters in the plasma membrane and/or to translocate GLUT-4 to the plasma membrane. Because the insulin level in the water trial was low, the number of GLUT-4 transporters in the plasma membrane declined and, therefore, glucose uptake ceased. During the first hour of recovery, leg glucose uptake was the same for CHO/protein and CHO ingestion despite a substantially lower arterial glucose concentration with CHO/protein ingestion. This indicates that during the first 0.5 h of recovery, arterial glucose concentrations, which are considerably above basal concentrations, do not affect skeletal muscle glucose uptake. With CHO/protein and CHO ingestion, leg glucose uptake was higher during the initial 20-30 min of recovery. This might have been caused by a greater amount of plasma membrane-bound GLUT-4 as a result of the previous contraction. However, glucose uptake then decreased to a constant level despite a high insulin concentration. Furthermore, the higher insulin levels with CHO/protein compared with CHO ingestion did not increase leg glucose uptake in the CHO/protein trial and potentially did not affect insulin-mediated GLUT-4 translocation to the plasma membrane. Because for several hours after exercise the muscle may be more sensitive to insulin (5, 14, 16), a relative low insulin concentration may already have elicited the maximal glucose uptake and GLUT-4 translocation to the plasma membrane. Also, with CHO/protein and CHO ingestion, arterial glucose concentration did not have an effect on leg glucose uptake because glucose concentration declined with recovery time, but leg glucose uptake remained constant after 1 h of recovery. Muscle glycogen was measured after 1.5 and 4 h of recovery, and, therefore, we cannot say whether the glycogen resynthesis rate is declining over that time period.
During the first hour of recovery, arterial glucose concentration was significantly lower with CHO/protein ingestion compared with CHO alone. This lower glucose concentration might have been caused by a reduced glucose appearance from the gastrointestinal tract or a larger clearance by tissues other than the leg. Gastric emptying rate is suggested to depend on energy density of the ingested solution (17, 19), and because the energy density of the CHO/protein drink was higher than that of the CHO drink, gastric emptying may have been slowed down, thus slowing glucose appearance. This study clearly shows that changes in arterial or venous glucose concentrations do not give an indication of muscle glucose uptake because glucose uptake was not different with CHO/protein intake despite lower glucose concentrations.
Skeletal muscle glycogen resynthesis after exercise has been shown to
be biphasic (12, 14): there is the initial insulin-independent phase of
30-60 min with a high glycogen resynthesis rate followed by an
insulin-dependent phase with a slower glycogen resynthesis rate. When
Price and colleagues (14) studied glycogen resynthesis in
insulin-resistant subjects and controls they did not observe a
difference in glycogen resynthesis rate during the insulin-independent phase. However, during the insulin-dependent phase, glycogen
resynthesis rate was lower in the insulin-resistant subjects (13).
These findings clearly indicate that from 1 h of recovery onward
insulin might play an important role in the regulation of muscle
glycogen resynthesis. Zawadzki and colleagues (20) reported a higher glycogen resynthesis rate during 4 h of recovery from exercise when
carbohydrates were coingested with protein compared with when
carbohydrates were ingested alone. They suggested that this was likely
due to the higher insulin level with protein coingestion, potentially
via stimulation of glycogen synthase and/or glucose uptake by the
muscle. Despite a substantial insulin difference between the
CHO/protein and CHO trials, we were not able to find a higher glycogen
resynthesis rate. There are several possible reasons to explain the
apparent difference. First, the glycogen resynthesis rate of ~41
µmol · kg dry
muscle1 · h1,
as observed by Zawadski and colleagues with CHO/protein intake, is
nearly identical to the glycogen resynthesis rate in this study, both
for CHO/protein and CHO ingestion if the average glycogen resynthesis
rate from 0 to 4 h of recovery is considered (39.8 µmol · kg dry
muscle1 · h1). This
glycogen resynthesis rate may be the maximal achievable after prolonged
dynamic exercise with sufficient and regular carbohydrate loading
despite higher insulin levels. Second, the higher insulin concentration
in the CHO/protein trial might not have been effective. Therefore, a
relative low insulin level might have elicited the maximal positive
achievable effect on glycogen resynthesis during recovery from intense
exercise. Third, although not directly linked to insulin levels, is the
much lower muscle glycogen content immediately after exercise in our
study, with an average of 79 vs. ~183 mmol/kg dry muscle (213 µmol/g protein), that could have had an effect on the time course of
the fast and slow glycogen recovery phase. It is suggested that
glycogen resynthesis rate is affected by initial concentration when
muscle glycogen content is <120 mmol/kg dry muscle (14).
If we assume that 6 kg of muscle in the leg (of a total of ~8 kg) is depleted to the same extent as the vastus lateralis muscle during cycle exercise, the comparison between total leg glucose uptake and glucose needed for glycogen resynthesis can be made. In Fig. 5 the total leg glucose uptake during the 0- to 1.5-h and the 1.5- to 4-h recovery period is shown together with the estimated amount of glucose needed for glycogen resynthesis. During the first 1.5 h of recovery, a nearly 100% match is found for the amount of glucose taken up by the leg and the amount of glucose needed for the observed increase in muscle glycogen content. Between 1.5 and 4 h of recovery, it appears that more glucose is taken up by the leg than incorporated into glycogen. These results indicate that during the initial phase of recovery, glucose is mainly used for glycogen resynthesis and potentially less for oxidation. Furthermore, during the early stages of recovery, glucose uptake might be the rate-limiting factor for glycogen resynthesis (see discussion above). On the other hand, between 1.5 and 4 h of recovery glucose uptake appears not to be rate limiting for glycogen resynthesis because more glucose is taken up than is stored in muscle glycogen. With water ingestion, glucose uptake is lower than the amount of glucose needed for glycogen resynthesis. This may have been due to the fact that the differences in both glucose arterial venous differences and muscle glycogen content are small and will increase variably. Another possibility is that <6 kg of muscle in the leg is depleted to the same extent as in the quadriceps and that we overestimate glucose needed for glycogen resynthesis.
In conclusion, coingestion of carbohydrate and protein compared with ingestion of carbohydrate alone did not increase leg glucose uptake or the glycogen resynthesis rate after intense cycle exercise. It seems that protein ingestion per se or via stimulation of insulin secretion cannot increase muscle glycogen resynthesis rate in humans when an optimal carbohydrate supplementation regime is followed during recovery from exercise.
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ACKNOWLEDGEMENTS |
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This study was supported by grants from MD Foods, the Danish Sport Research Council, Team Denmark Research Foundation, and the Danish National Research Foundation. G. van Hall was supported by a fellowship from the Danish Research Academy.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: G. van Hall, Copenhagen Muscle Research Center, Rigshospitalet Sect. 7652, 20 Tagensvej, DK-2200 Copenhagen N, Denmark (E-mail: RH01769{at}RH.DK).
Received 29 December 1998; accepted in final form 9 December 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
Ahlborg, B,
Bergström J,
Ekelund LG,
and
Hultman E.
Muscle glycogen and muscle electrolytes during prolonged physical exercise.
Acta Physiol Scand
70:
129-142,
1967[Web of Science].
2.
Andersen, P,
and
Saltin B.
Maximal perfusion of skeletal muscle in man.
J Physiol (Lond)
366:
233-249,
1985
3.
Bergström, J.
Muscle electrolytes in man. Determination by neutron activation analysis on needle biopsy specimens. A study on normal subjects, kidney patients, and patiens with chronic diarrhea.
Scand J Clin Lab Invest Suppl
68:
7-110,
1962.
4.
Bergström, J,
Hermansen L,
Hultman E,
and
Saltin B.
Diet, muscle glycogen and physical performance.
Acta Physiol Scand
71:
140-150,
1967[Web of Science][Medline].
5.
Cartree, GD,
Young DA,
Sleeper MD,
Zierath J,
Wallenberg-Henriksson H,
and
Holloszy JO.
Prolonged increase in insulin-stimulated glucose transport in muscle after exercise.
Am J Physiol Endocrinol Metab
256:
E494-E499,
1989
6.
Hansen, PA,
Nolte LA,
Chen MM,
and
Holloszy JO.
Increased GLUT-4 translocation mediates enhanced insulin sensitivity of muscle transport after exercise.
J Appl Physiol
85:
1218-1222,
1998
7.
Hermansen, L,
Hultman E,
and
Saltin B.
Muscle glycogen during prolonged severe exercise.
Acta Physiol Scand
71:
129-139,
1967[Web of Science][Medline].
8.
Ivy, JL,
and
Kuo C-H.
Regulation of Glut 4 protein and glycogen synthase during muscle glycogen synthesis after exercise.
Acta Physiol Scand
162:
295-304,
1998[Web of Science][Medline].
9.
Ivy, JL,
Lee MC,
Brozinick JT,
and
Reed MJ.
Muscle glycogen storage after different amounts of carbohydrate ingestion.
J Appl Physiol
65:
2018-2033,
1988
10.
Kuipers, H,
Keizer HA,
Brouns F,
and
Saris WHM
Carbohydrate feeding and glycogen synthesis during exercise in man.
Pflügers Arch
410:
652-656,
1987[Web of Science][Medline].
11.
Lund, S,
Holman GD,
Schmitz O,
and
Pedersen O.
Glut 4 content in the plasma membrane of rat skeletal muscle: comparative studies of the subcellular fraction method and the exofacial photolabelling technique using ATB-BMPA.
FEBS Lett
330:
312-318,
1993[Web of Science][Medline].
12.
Mæhlum, S,
Høstmark AT,
and
Hermansen L.
Synthesis of muscle glycogen during recovery after prolonged severe exercise in diabetic subjects. Effect of insulin deprivation.
Scand J Clin Invest
38:
35-39,
1978[Web of Science][Medline].
13.
Price, TB,
Perseghin G,
Duleba A,
Chen W,
Chase J,
Rothman DL,
Shulman RG,
and
Shulman GI.
NMR studies of muscle glycogen synthesis in insulin-resistant offspring of parents with non-insulin-dependent diabetes mellitus immediately after glycogen-depleting exercise.
Proc Natl Acad Sci USA
93:
5329-5334,
1996
14.
Price, TB,
Rothman DL,
Taylor R,
Avison MJ,
Shulman GI,
and
Shulman RG.
Human muscle glycogen resynthesis after exercise: insulin-dependent and -independent phases.
J Appl Physiol
76:
104-111,
1994
15.
Richardson, RS,
Frank LR,
and
Haseler LJ.
Dynamic knee-extensor and cycle exercise: functional MRI of muscular activity.
Int J Sports Med
19:
182-187,
1998[Web of Science][Medline].
16.
Richter, EA,
Garetto LP,
Goodman MN,
and
Ruderman NB.
Enhanced muscle glucose metabolism after exercise: modulation by local factors.
Am J Physiol Endocrinol Metab
246:
E476-E482,
1984
17.
Vist, GE,
and
Maughan RJ.
The effect of osmolality and carbohydrate coingestion on the rate of gastric emptying of liquids in man.
J Physiol (Lond)
486:
523-531,
1995
18.
Wallberg-Henriksson
Glucose transport into skeletal muscle. Influence of contractile activity, insulin, catecholamines and diabetis mellitus.
Acta Physiol Scand
131, Suppl564:
29-47,
1987.
19.
Wisen, O,
Hellstrom PM,
and
Johansson C.
Meal energy density as a determinant of postprandial gastrointestinal adaptation in man.
Scand J Gastroenterol
28:
737-743,
1993[Web of Science][Medline].
20.
Zawadzki, KM,
Yaspelkis BB, III,
and
Ivy JL.
Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise.
J Appl Physiol
72:
1854-1859,
1992
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