Metabolic responses to exercise after fasting

1986 ◽  
Vol 61 (4) ◽  
pp. 1363-1368 ◽  
Author(s):  
G. L. Dohm ◽  
R. T. Beeker ◽  
R. G. Israel ◽  
E. B. Tapscott

Fasting before exercise increases fat utilization and lowers the rate of muscle glycogen depletion. Since a 24-h fast also depletes liver glycogen, we were interested in blood glucose homeostasis during exercise after fasting. An experiment was conducted with human subjects to determine the effect of fasting on blood metabolite concentrations during exercise. Nine male subjects ran (70% maximum O2 consumption) two counterbalanced trials, once fed and once after a 23-h fast. Plasma glucose was elevated by exercise in the fasted trial but there was no difference between fed and fasted during exercise. Lactate was significantly higher (P less than 0.05) in fasted than fed throughout the exercise bout. Fat mobilization and utilization appeared to be greater in the fasted trial as evidenced by higher plasma concentrations of free fatty acids, glycerol, and beta-hydroxybutyrate as well as lower respiratory exchange ratio in the fasted trial during the first 30 min of exercise. These results demonstrate that in humans blood glucose concentration is maintained at normal levels during exercise after fasting despite the depletion of liver glycogen. Homeostasis is probably maintained as a result of increased gluconeogenesis and decreased utilization of glucose in the muscle as a result of lowered pyruvate dehydrogenase activity.

1991 ◽  
Vol 71 (5) ◽  
pp. 1807-1812 ◽  
Author(s):  
I. Tabata ◽  
F. Ogita ◽  
M. Miyachi ◽  
H. Shibayama

The effects of low blood glucose concentration during low-intensity prolonged physical exercise on the hypothalamus-pituitary-adrenocortical axis were investigated in healthy young men. In experiment 1, six subjects who had fasted for 14 h performed bicycle exercise at 50% of their maximal O2 uptake until exhaustion. At the end of the exercise, adrenocorticotropic hormone (ACTH) and cortisol increased significantly. However, this hormonal response was totally abolished when the same subjects exercised at the same intensity while blood glucose concentrations were maintained at the preexercise level. In experiment 2, in addition to ACTH and cortisol, the possible changes in plasma concentration of corticotropin-releasing factor (CRF) were investigated during exercise of the same intensity performed by six subjects. As suggested by a previous study (Tabata et al. Clin. Physiol. Oxf. 4: 299–307, 1984), when the blood glucose concentrations decreased to less than 3.3 mM, plasma concentrations of CRF, ACTH, and cortisol showed a significant increase. At exhaustion, further increases were observed in plasma CRF, ACTH, and cortisol concentrations. These results demonstrate that decreases in blood glucose concentration trigger the pituitary-adrenocortical axis to enhance secretion of ACTH and cortisol during low-intensity prolonged exercise in humans. The data also might suggest that this activation is due to increased concentration of CRF, which was shown to increase when blood glucose concentration decreased to a critical level of 3.3 mM.


1982 ◽  
Vol 243 (1) ◽  
pp. R179-R184 ◽  
Author(s):  
W. W. Winder ◽  
M. A. Beattie ◽  
R. T. Holman

Endurance exercise training produces major adaptations in hormonal and metabolic responses to exercise. This study was designed to determine whether the differences in hormone response persist in the fasted condition when liver glycogen is depleted. Rats were run on a motor-driven rodent treadmill 5 days/wk for periods up to 2 h/day for 10 wk. Trained and nontrained rats were then fasted 24 h and were run for periods ranging from 0- to 60 min. At the end of 60 min of exercise muscle glycogen was higher in trained rats (2.9 +/- 0.3 vs. 1.1 +/- 0.1 mg/g). Blood glucose was maintained at higher levels in trained rats throughout the course of the exercise (3.2 +/- 0.1 vs. 2.3 +/- 0.1 mM after 60 min). Plasma concentrations of glucagon and epinephrine increased in both groups during the exercise but were significantly lower in trained animals. Differences between trained and nontrained animals in stress hormone responses to exercise persist in the fasted state and appear to be a consequence of the capacity of trained animals to maintain higher blood glucose levels.


1984 ◽  
Vol 247 (5) ◽  
pp. R827-R832 ◽  
Author(s):  
W. Langhans ◽  
K. Pantel ◽  
W. Muller-Schell ◽  
E. Eggenberger ◽  
E. Scharrer

Prandial changes in plasma pancreatic glucagon, blood glucose, and liver glycogen levels were studied during the first meal after 12 h of food deprivation in rats. To determine whether pancreatic glucagon secretion is influenced by the composition of the diet, the experiments were performed in rats fed high-carbohydrate (HC), high-fat (HF), or high-protein (HP) diets. Plasma glucagon levels in the hepatic portal vein increased about 100% during meals in all feeding groups, whereas glucagon levels in the hepatic vein changed very little. Blood glucose concentration in the hepatic portal vein increased during meals in HC diet-fed rats but decreased in HF and in HP diet-fed rats. Blood glucose in the hepatic vein also increased in HC and HP diet-fed rats. In addition, liver glycogen content decreased during meals in HC and HP diet-fed rats and by 14 min after the meal in HF diet-fed rats. These results demonstrate that a considerable amount of the glucagon released during meals in HC, HF, and HP diet-fed rats remains in the liver. This is consistent with the hypothesis that the liver is important for the satiety effect of glucagon. The results also suggest that glucagon contributes to the meal-induced changes in hepatic carbohydrate metabolism observed in all groups.


1990 ◽  
Vol 258 (1) ◽  
pp. E203-E211 ◽  
Author(s):  
L. P. Turcotte ◽  
A. S. Rovner ◽  
R. R. Roark ◽  
G. A. Brooks

To evaluate the role played by gluconeogenesis in blood glucose homeostasis, female Sprague-Dawley rats were injected with mercaptopicolinic acid (MPA), a gluconeogenic inhibitor. Glucose kinetics were assessed by primed, continuous infusion of [U-14C]- and [6(-3)H]glucose via an indwelling jugular catheter at rest and during submaximal exercise at 13.4 m/min on level grade. Blood samples were taken from carotid catheters and analyzed for glucose and lactate concentrations and specific activities. Tissue glycogen samples were obtained from rats after exercise as well as from unexercised animals. When compared with the sham-injected animals, MPA-treated animals had 22% lower (5.92 +/- 0.36 vs. 7.62 +/- 0.21 mM) and 44% higher (1.90 +/- 0.11 vs. 1.32 +/- 0.09 mM) resting arterial glucose and lactate concentrations, respectively. Resting glucose appearance (Ra) rates were 20% lower in the MPA-treated animals (57.2 +/- 7.5 mumol.kg-1.min-1) than in the sham-injected animals (71.1 +/- 12.1 mumol.kg-1.min-1). During exercise, Ra increased to 174.7 +/- 32.8 mumol.kg-1.min-1 in sham-injected animals. In the MPA-treated animals, there was a 35% increase during the first 15 min of exercise, followed by a decrease to the resting values. MPA-treated animals had no measurable glucose recycling at rest or during exercise. Exercise decreased blood glucose concentration (35%) and increased blood lactate concentration (160%) in the MPA-treated animals. Exercising sham-injected animals had increased blood glucose (9.8%) but no change in blood lactate concentration. Moderate depletions in liver and skeletal muscle glycogen contents were observed after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)


Diabetes ◽  
1965 ◽  
Vol 14 (4) ◽  
pp. 186-193 ◽  
Author(s):  
T. W. Burns ◽  
R. Bregant ◽  
H. J. Van Peenan ◽  
T. E. Hood

1965 ◽  
Vol 31 (2) ◽  
pp. 127-137 ◽  
Author(s):  
P. J. BENTLEY ◽  
B. K. FOLLETT

SUMMARY River lampreys regulated their blood glucose concentration when injected with glucose. Mammalian insulin decreased the blood glucose concentration in the lamprey while adrenaline, cortisol and arginine vasotocin increased it. Glucagon had no effect initially but after a delay of 4 hr. decreased the blood glucose level. Insulin and cortisol increased the liver glycogen concentration. Adrenaline decreased the muscle glycogen concentration; vasotocin increased it. Treatment with alloxan increased the blood glucose concentration. Fat and glycogen in the lamprey are stored mainly in the skeletal muscles and their histochemical distribution in muscle is described. The results are discussed in relation to the metabolism of the migrating lamprey and the evolution of the control of carbohydrate metabolism in vertebrates.


1995 ◽  
Vol 269 (2) ◽  
pp. E222-E230 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
S. M. Grant

This study investigated the hypothesis that training-induced reductions in exercise blood glucose utilization can occur independently of increases in muscle mitochondrial potential. To induce a training adaptation, eight active participants (23 +/- 1 yr, 80.6 +/- 3.7 kg, mean +/- SE) with a maximal oxygen consumption (VO2max) of 45.5 +/- 2.4 ml.kg-1.min-1, cycled at 59% VO2max for 2 h per day for 10 consecutive days. Measurements of blood glucose appearance (Ra) and disappearance (Rd), using a primed continuous infusion of [6,6-2H2]glucose, were made during 90 min of cycle exercise (59% VO2max) performance before and after training. Training resulted in a 25% decrease (P < 0.01) in mean glucose Ra during exercise (43.0 +/- 3.7 to 34.4 +/- 2.8 mumol.kg-1.min-1). Since blood glucose concentration was not different between training conditions, glucose metabolic clearance rate was also depressed (P < 0.05). Exercise-induced glycogen depletion in vastus lateralis muscle was reduced (P < 0.05) with training. Calculation of carbohydrate and fat oxidation based on the respiratory exchange ratio supported a shift toward greater preference for fat. Because training did not elicit changes in the maximal activities of citrate synthase and malate dehydrogenase, two enzymes of the citric acid cycle, it would appear that increases in mitochondrial potential are not necessary for the adaptations that occurred.


2005 ◽  
Vol 288 (1) ◽  
pp. E143-E147 ◽  
Author(s):  
Jill A. Fattor ◽  
Benjamin F. Miller ◽  
Kevin A. Jacobs ◽  
George A. Brooks

Catecholamine release is known to be regulated by feedforward and feedback mechanisms. Norepinephrine (NE) and epinephrine (Epi) concentrations rise in response to stresses, such as exercise, that challenge blood glucose homeostasis. The purpose of this study was to assess the hypothesis that the lactate anion is involved in feedback control of catecholamine concentration. Six healthy active men (26 ± 2 yr, 82 ± 2 kg, 50.7 ± 2.1 ml·kg−1·min−1) were studied on five occasions after an overnight fast. Plasma concentrations of NE and Epi were determined during 90 min of rest and 90 min of exercise at 55% of peak O2 consumption (V̇o2 peak) two times with exogenous lactate infusion (lactate clamp, LC) and two times without LC (CON). The blood lactate profile (∼4 mM) of a preliminary trial at 65% V̇o2 peak (65%) was matched during the subsequent LC trials. In resting men, plasma NE concentration was not different between trials, but during exercise all conditions were different with 65% > CON > LC (65%: 2,115 ± 166 pg/ml, CON: 1,573 ± 153 pg/ml, LC: 930 ± 174 pg/ml, P < 0.05). Plasma Epi concentrations at rest were different between conditions, with LC less than 65% and CON (65%: 68 ± 9 pg/ml, CON: 59 ± 7 pg/ml, LC: 38 ± 10 pg/ml, P < 0.05). During exercise, Epi concentration showed the same trend (65%: 262 ± 37 pg/ml, CON: 190 ± 34 pg/ml, LC: 113.2 ± 23 pg/ml, P < 0.05). In conclusion, lactate attenuates the catecholamine response during moderate-intensity exercise, likely by feedback inhibition.


1960 ◽  
Vol 198 (2) ◽  
pp. 371-374 ◽  
Author(s):  
E. Douglas Rees ◽  
William W. Winternitz ◽  
William F. Lattanzi

The blood ketone body concentrations of fasted and nonfasted rats fed a diet deficient in choline were determined and found to be similar to the concentrations obtained from a control group fed the same diet supplemented with choline. However, the animals on the choline-deficient diet had an 18–20% greater mean liver mass, and this could account for the failure to demonstrate the depressed level of blood ketone bodies which was anticipated on the basis of previous in vitro studies. Other possible explanations of this discrepancy are discussed. Despite a high hepatic fat content, the choline-deficient group had a normal concentration of liver glycogen. The nonfasting blood glucose concentration of the choline-deficient group (91.5 ± 5 mg %) was lower than that of the control group (102 ± 3 mg %). After 24 hours of fasting, the values were 52 ± 3 mg % and 61 ± 5 mg % for the choline-deficient and control group, respectively. The 72-hour fasting values were 43 ± 2 mg %, and 49 ± 2 mg %, respectively. Data showing the effect of diet composition on ketonemia, liver glycogen and blood glucose are presented and are in accord with previous studies.


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