Relationship between effort sense and ventilatory response to intense exercise performed with reduced muscle glycogen

2011 ◽  
Vol 112 (6) ◽  
pp. 2149-2162 ◽  
Author(s):  
Ryo Yamanaka ◽  
Takahiro Yunoki ◽  
Takuma Arimitsu ◽  
Chang-shun Lian ◽  
Afroundeh Roghayyeh ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Ventilatory Response ◽  
Intense Exercise ◽  
Effort Sense

scholarly journals Substrates for muscle glycogen synthesis in recovery from intense exercise in man.

1991 ◽  
Vol 434 (1) ◽  
pp. 423-440 ◽  
Author(s):  
J Bangsbo ◽  
P D Gollnick ◽  
T E Graham ◽  
B Saltin
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Intense Exercise ◽  
Muscle Glycogen Synthesis

Glucose ingestion before and during intense exercise

1981 ◽  
Vol 50 (4) ◽  
pp. 766-771 ◽  
Author(s):  
A. Bonen ◽  
S. A. Malcolm ◽  
R. D. Kilgour ◽  
K. P. MacIntyre ◽  
A. N. Belcastro
Keyword(s):  
Blood Glucose ◽  
Muscle Glycogen ◽  
Respiratory Exchange Ratio ◽  
Intense Exercise ◽  
Pilot Studies ◽  
Persistent Effect ◽  
Considerable Portion ◽  
Glucose Ingestion ◽  
Insulin Responses ◽  
Glucose Group

Glucose and insulin responses were compared in glycogen depleted subjects when glucose (1.5 g/kg) was ingested 15 min before (n = 7) or during (min 3-5) intense exercise (80% VO2 max; n = 8). A nonexercise group (n = 8) and a no-glucose group (n = 8) were also included for comparisons. A 36- to 44-h fast, combined with exhaustive exercise to deplete muscle glycogen, (congruent to 80% in pilot studies) suggested that the subjects initiated exercise with substantially depleted hepatic and muscle glycogen reserves. With no glucose ingestion, blood glucose decreased during exercise (P less than 0.05) and blood lactate (HLa congruent to 3.8 mM) and the respiratory exchange ratio (R) remained low (0.83); with glucose ingestion before or during exercise, HLa concentrations were doubled (7.3 mM) and R was greater (0.90-0.92; P less than 0.05). Although insulin concentrations decreased rapidly to basal levels within 10 min after the onset of exercise in the preexercise glucose group (P less than 0.05), blood glucose continued to decrease throughout exercise. No such decrease occurred in the subjects who ingested glucose during exercise, nor did insulin concentrations change markedly in this group (P greater than 0.05). The HLa and R data indicated that a considerable portion of glucose was metabolized during exercise. Differences in the preexercise insulin environment appear to exert a persistent effect on glucose uptake throughout exercise.

Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans

1985 ◽  
Vol 59 (5) ◽  
pp. 1350-1354 ◽  
Author(s):  
D. S. King ◽  
D. L. Costill ◽  
W. J. Fink ◽  
M. Hargreaves ◽  
R. A. Fielding
Keyword(s):  
Muscle Glycogen ◽  
Respiratory Exchange Ratio ◽  
Muscle Metabolism ◽  
Submaximal Exercise ◽  
Intense Exercise ◽  
O2 Uptake ◽  
Heat Acclimatization ◽  
Fuel Selection ◽  
Muscle Ph ◽  
Male Subjects

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.

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.

Metabolic, catecholamine, and endurance responses to caffeine during intense exercise

1996 ◽  
Vol 81 (4) ◽  
pp. 1658-1663 ◽  
Author(s):  
M. Jackman ◽  
P. Wendling ◽  
D. Friars ◽  
T. E. Graham
Keyword(s):  
Muscle Glycogen ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Muscle Metabolism ◽  
Intense Exercise ◽  
Muscle Lactate ◽  
Caffeine Ingestion ◽  
Norepinephrine Concentration ◽  
Before And After ◽  
Exercise Period

Jackman, M., P. Wendling, D. Friars, and T. E. Graham.Metabolic, catecholamine, and endurance responses to caffeine during intense exercise. J. Appl. Physiol. 81(4): 1658–1663, 1996.—This study examined the possible effects of caffeine ingestion on muscle metabolism and endurance during brief intense exercise. We tested 14 subjects after they ingested placebo or caffeine (6 mg/kg) with an exercise protocol in which they cycled for 2 min, rested 6 min, cycled 2 min, rested 6 min, and then cycled to voluntary exhaustion. In each exercise the intensity required the subject’s maximal O2 consumption. Eight subjects had muscle and venous blood samples taken before and after each exercise period. The caffeine ingestion resulted in a significant increase in endurance (4.12 ± 0.36 and 4.93 ± 0.60 min for placebo and caffeine, respectively) and resulted in a significant increase in plasma epinephrine concentration throughout the protocol but not in norepinephrine concentration. During the first two exercise bouts, the power and work output were not different; blood lactate concentrations were not affected significantly by caffeine ingestion, but during the exercise bouts muscle lactate concentration was significantly increased by caffeine. The net decrease in muscle glycogen was not different between treatments at any point in the protocol, and even at the time of fatigue there was at least 50% of the original glycogen concentration remaining. The data demonstrated that caffeine ingestion can be an effective ergogenic aid for exercise that is as brief as 4–6 min. However, the mechanism is not associated with muscle glycogen sparing. It is possible that caffeine is exerting actions directly on the active muscle and/or the neural processes that are involved in the activity.

Muscle glycogen synthesis in recovery from intense exercise in humans

1997 ◽  
Vol 273 (2) ◽  
pp. E416-E424 ◽  
Author(s):  
J. Bangsbo ◽  
K. Madsen ◽  
B. Kiens ◽  
E. A. Richter
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Knee Extensor ◽  
Intense Exercise ◽  
Muscle Lactate ◽  
Muscle Glycogen Synthesis ◽  
Arterial Plasma ◽  
Exercise Muscle ◽  
Exercise In Humans

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.

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