Effects of exercise on maternal glycogen storage patterns and fetal outcome in mature rats

1992 ◽  
Vol 70 (12) ◽  
pp. 1634-1638 ◽  
Author(s):  
M. F. Mottola ◽  
J. H. Plust ◽  
P. D. Christopher ◽  
C. L. Schachter

The purpose of the present study was to examine the effects of exercise on maternal glycogen storage patterns and fetal outcome in mature (approximately 12 months of age) Sprague–Dawley rats. The exercise consisted of treadmill running at 30 m∙min−1, on a 10° incline, for 60 min, 5 days per week, for 4 weeks prior to pregnancy, which continued until day 19 of gestation. In mature animals, chronic exercise increased (p < 0.05) liver glycogen concentration in both pregnant and nonpregnant rats. In pregnant exercised animals, the glycogen concentration of the maternal liver increased almost twofold (p < 0.05) compared with the sedentary pregnant group. There was no difference in the amount of glycogen stored in the gastrocnemius or soleus muscles in response to training, pregnancy, or chronic maternal exercise in the mature rat. In the pregnant groups, there were fewer (p < 0.05) viable fetuses and more (p < 0.05) resorption sites than in young rats. In addition, exercise during pregnancy in the mature animal decreased (p < 0.05) fetal body weight. These results demonstrate that a conflict may exist between maternal exercise and fetal demands for energy in the mature rat. This conflict seems to favour the maternal system, as evidenced by the enhanced maternal liver glycogen storage and the negative effect on fetal growth.Key words: age, exercise, pregnancy, glycogen storage patterns.

2000 ◽  
Vol 25 (6) ◽  
pp. 443-452 ◽  
Author(s):  
P.E. Houghton ◽  
M.F. Mottola ◽  
J.H. Plust ◽  
C.L. Schachter

The purpose was to determine the effects of exercise on fetal and placental glycogen storage patterns at 20 days gestation (term 21 days) in mature (approximately 12 months of age) Sprague-Dawley rats. The exercise protocol consisted of treadmill running at 30 m min−1, on a 10 incline, for 60 min, 5 days per week, for 4 weeks prior to conception, which continued until day 19 of pregnancy. Exercise produced a significant reduction in fetal body weight, placental weight, and fetal organ weights (heart, kidney, brain, and liver) compared to sedentary control animals (p < .05). However, when fetal body size was taken into account, these differences disappeared, except for the fetal brain:body weight ratio, which was larger in the exercised animals compared to controls (p < .05). Fetal liver glycogen concentrations were significantly lower in exercised animals compared to nonrunning control animals (p < .05). These results demonstrate that exercise of mature rats may compromise fetal development and hepatic glycogen storage in the fetus. Key words: age, exercise, pregnancy, fetal glycogen storage patterns


1991 ◽  
Vol 71 (3) ◽  
pp. 1015-1019 ◽  
Author(s):  
M. F. Mottola ◽  
P. D. Christopher

To examine the effects of maternal exercise on liver and skeletal muscle glycogen storage, female Sprague-Dawley rats were randomly divided into control, nonpregnant runner, pregnant nonrunning control, pregnant runner, and prepregnant exercised control groups. The exercise consisted of treadmill running at 30 m/min on a 10 degree incline for 60 min, 5 days/wk. Pregnancy alone, on day 20 of gestation, decreased maternal liver glycogen content and increased red and white gastrocnemius muscle glycogen storage above control values (P less than 0.05). In contrast, exercise in nonpregnant animals augmented liver glycogen storage and also increased red and white gastrocnemius glycogen content (P less than 0.05). By combining exercise and pregnancy, the decrease in liver glycogen storage in the pregnant nonexercised condition was prevented in the pregnant runner group and more glycogen was stored in both the red and white portions of the gastrocnemius than all other groups (P less than 0.05). Fetal body weight was greatest (P less than 0.05) in the pregnant runner group and lowest (P less than 0.05) in the prepregnant exercise control group. These results demonstrate that chronic maternal exercise may change maternal glycogen storage patterns in the liver and skeletal muscle with some alteration in fetal outcome.


Author(s):  
Yutaka Matsunaga ◽  
Kenya Takahashi ◽  
Yumiko Takahashi ◽  
Hideo Hatta

Abstract Background When a high-carbohydrate diet is ingested, whether as small frequent snacks or as large meals, there is no difference between the two with respect to post-exercise glycogen storage for a period of 24 h. However, the effect of carbohydrate intake frequency on glycogen recovery a few hours after exercise is not clear. Athletes need to recover glycogen quickly after physical exercise as they sometimes exercise multiple times a day. The aim of this study was to determine the effect of carbohydrate intake at different frequencies on glycogen recovery during the first few hours after exercise. Methods After 120 min of fasting, 6-week-old male ICR mice were subjected to treadmill running exercise (20 m/min for 60 min) to decrease the levels of muscle and liver glycogen. Mice were then given glucose as a bolus (1.2 mg/g of body weight [BW], immediately after exercise) or as a pulse (1.2 mg/g of BW, every 15 min × 4 times). Following this, the blood, tissue, and exhaled gas samples were collected. Results In the bolus group, blood glucose concentration was significantly lower and plasma insulin concentration was significantly higher than those in the pulse group (p < 0.05). The plantaris muscle glycogen concentration in the bolus group was 25.3% higher than that in the pulse group at 60 min after glucose ingestion (p < 0.05). Liver glycogen concentration in the pulse group was significantly higher than that in the bolus group at 120 min after glucose ingestion (p < 0.05). Conclusions The present study showed that ingesting a large amount of glucose immediately after exercise increased insulin secretion and enhanced muscle glycogen recovery, whereas frequent and small amounts of glucose intake was shown to enhance liver glycogen recovery.


1986 ◽  
Vol 60 (4) ◽  
pp. 1254-1258 ◽  
Author(s):  
K. I. Carlson ◽  
H. T. Yang ◽  
W. S. Bradshaw ◽  
R. K. Conlee ◽  
W. W. Winder

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22–60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.


2015 ◽  
Vol 128 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Mavin Macauley ◽  
Fiona E Smith ◽  
Peter E Thelwall ◽  
Kieren G Hollingsworth ◽  
Roy Taylor

In health, food carbohydrate is stored as glycogen in muscle and liver, preventing a deleterious rise in osmotically active plasma glucose after eating. Glycogen concentrations increase sequentially after each meal to peak in the evening, and fall to fasting levels thereafter. Skeletal muscle accounts for the larger part of this diurnal buffering capacity with liver also contributing. The effectiveness of this diurnal mechanism has not been previously studied in Type 2 diabetes. We have quantified the changes in muscle and liver glycogen concentration with 13C magnetic resonance spectroscopy at 3.0 T before and after three meals consumed at 4 h intervals. We studied 40 (25 males; 15 females) well-controlled Type 2 diabetes subjects on metformin only (HbA1c (glycated haemoglobin) 6.4±0.07% or 47±0.8 mmol/mol) and 14 (8 males; 6 females) glucose-tolerant controls matched for age, weight and body mass index (BMI). Muscle glycogen concentration increased by 17% after day-long eating in the control group (68.1±4.8 to 79.7±4.2 mmol/l; P=0.006), and this change inversely correlated with homoeostatic model assessment of insulin resistance [HOMA-IR] (r=−0.56; P=0.02). There was no change in muscle glycogen in the Type 2 diabetes group after day-long eating (68.3±2.6 to 67.1±2.0 mmol/mol; P=0.62). Liver glycogen rose similarly in normal control (325.9±25.0 to 388.1±30.3 mmol/l; P=0.005) and Type 2 diabetes groups (296.1±16.0 to 350.5±6.7 mmol/l; P<0.0001). In early Type 2 diabetes, the major physiological mechanism for skeletal muscle postprandial glycogen storage is completely inactive. This is directly related to insulin resistance, although liver glycogen storage is normal.


2003 ◽  
Vol 176 (2) ◽  
pp. 247-255 ◽  
Author(s):  
MR Pickard ◽  
AJ Leonard ◽  
LM Ogilvie ◽  
PR Edwards ◽  
IM Evans ◽  
...  

Maternal hypothyroidism impairs fetal growth in the rat, but the mechanisms by which this occurs are unknown. Since the fetus derives its glucose supply from the mother, and maternal thyroidectomy may disturb maternal and placental glucose metabolism, we postulated that maternal and/or placental glucose metabolic compromise may contribute to fetal growth retardation in hypothyroid dams. Feto-placental growth, tissue glycogen stores and glucose levels in sera and amniotic fluid were determined in rat dams partially thyroidectomized (TX) before pregnancy and in euthyroid controls. Fetal body weight at 16, 19 and 21 days gestation (d.g.) was related to pre-mating maternal serum total thyroxine (TT(4)) levels; permanent fetal growth retardation occurred in severely (TX(s); pre-mating maternal serum TT(4) 16.19 nM) - but not in moderately (TX(m)) - hypothyroid dams. In TX(s) dams, glycogen concentration was elevated in maternal liver and in the fetal side of the placenta at 16 and 19 d.g., and in the maternal side of the placenta at 19 and 21 d.g., despite maternal euglycemia. In contrast, fetal liver glycogen concentration was deficient in TX(m) dams at 19 d.g. and in TX(s) dams at 19 and 21 d.g., and fetal hypoglycemia occurred in TX(s) dams at 21 d.g. Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term. The mechanisms by which severe maternal hypothyroidism permanently retards rat fetal growth remain to be determined.


1999 ◽  
Vol 87 (5) ◽  
pp. 1678-1683 ◽  
Author(s):  
S. Brooke Bramlett ◽  
Jun Zhou ◽  
Ruth B. S. Harris ◽  
Stephen L. Hendry ◽  
Trudy L. Witt ◽  
...  

We investigated the effect of a single bout of exercise on leptin mRNA levels in rat white adipose tissue. Male Sprague-Dawley rats were randomly assigned to an exercise or control group. Acute exercise was performed on a rodent treadmill and was carried out to exhaustion, lasting an average of 85.5 ± 1.5 min. At the end of exercise, soleus muscle and liver glycogen were reduced by 88% ( P < 0.001). Acutely exercised animals had lower ( P< 0.05) leptin mRNA levels in retroperitoneal but not epididymal fat, and this was independent of fat pad weight. To test the hypothesis that β3-adrenergic-receptor stimulation was involved in the downregulation of leptin mRNA in retroperitoneal fat, a second experiment was performed in which rats were randomized into one of four groups: control, control + β3-antagonist, exercise, and exercise + β3-antagonist. A highly selective β3-antagonist (SR-59230A) or vehicle was given by gavage 30 min before exercise or control experiment. Exercise consisted of 55 min of treadmill running, sufficient to reduce liver and muscle glycogen by 70 and 80%, respectively (both P < 0.0001). Again, acute exercise reduced leptin mRNA in retroperitoneal fat (exercise vs. control; P < 0.05), but β3-antagonism blocked this effect (exercise + β3-antagonist vs. control + β3-antagonist; P = 0.42). Unexpectedly, exercise increased serum leptin. This would be consistent with the idea that there are releasable, preformed pools of leptin within adipocytes. We conclude that β3-receptor stimulation is a mechanism by which acute exercise downregulates retroperitoneal adipose tissue leptin mRNA in vivo.


1997 ◽  
Vol 22 (4) ◽  
pp. 384-393 ◽  
Author(s):  
Pamela E. Houghton ◽  
Michelle F. Mottola ◽  
Jamie Mezzapelli ◽  
Richard Vandermolen ◽  
Paul D. Christopher

The purpose was to determine if running 30 m/min on a 10° incline, 60 min/day for 5 days/week altered fetal glycogen storage in prepregnancy trained rats. Animals that exercised for 3 weeks prior to pregnancy either continued the same exercise program until Day 19 of gestation (pregnant running group [PR]), or ceased exercising at conception (pregnant controls [PC]). A separate set of animals did not exercise either before or during pregnancy (pregnant nonrunning control group [PNRC]). On Day 20 of gestation, fetal organs and placenta were weighed and analyzed for glycogen concentration. Glycogen concentrations were not different in either fetal liver, heart, or placenta of PR rats compared to PNRC animals. However, fetal liver glycogen concentration was significantly lower in the fetal heart and liver of PC animals compared to glycogen measured in both PNRC and PR animals (p < .0.5). These results suggest that exercise of this intensity does not compromise fetal glycogen storage in trained pregnant rats. However, chronic prepregnancy exercise and then abrupt cessation of exercise at conception may compromise fetal growth and development. Key words: exercise training, pregnancy, fetal glycogen


Author(s):  
Xiangyu Liu ◽  
Xiong Xue ◽  
Junsheng Tian ◽  
Xuemei Qin ◽  
Shi Zhou ◽  
...  

The objectives of this study were to compare the antidepressant effects between endurance and resistance exercise for optimizing interventions and examine the metabolomic changes in different types of skeletal muscles in response to the exercise, using a rat model of chronic unpredictable mild stress (CUMS)-induced depression. There were 32 male Sprague-Dawley rats randomly divided into a control group (C) and 3 experimental groups: CUMS control (D), endurance exercise (E), and resistance exercise (R). Group E underwent 30 min treadmill running, and group R performed 8 rounds of ladder climbing, 5 sessions per week for 4 weeks. Body weight, sucrose preference, and open field tests were performed pre and post the intervention period for changes in depressant symptoms, and the gastrocnemius and soleus muscles were sampled after the intervention for metabolomic analysis using the 1H-NMR technique. The results showed that both types of exercise effectively improved the depression-like symptoms, and the endurance exercise appeared to have a better effect. The levels of 10 metabolites from the gastrocnemius and 13 metabolites from the soleus of group D were found to be significantly different from that of group C, and both types of exercise had a callback effect on these metabolites, indicating that a number of metabolic pathways were involved in the depression and responded to the exercise interventions.


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