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Biomedical subjects

R D Fell

Publications and source records attributed to R D Fell.

36 records · Page 2Linked to original sources
PubMed1985

Effect of contractile activity on rat skeletal muscle beta-adrenoceptor properties.

The effect of fiber type and endurance exercise training on skeletal muscle beta-adrenoceptor properties were assessed using a direct radioligand binding technique. Six separate muscles, composed of a variety of different fiber types, were examined in treadmill trained and sedentary rats. In trained animals, sarcolemmal preparations from heart and slow twitch soleus muscle exhibited a significantly greater receptor concentration than membranes from white fast twitch glycolytic fibers of the vastus lateralis. No significant changes were observed between trained and sedentary rat muscle beta-adrenoceptor density (beta max, fmole/mg protein) or affinity (Kd, nM) within each muscle type, despite significantly increased myocardial/body weight ratios and skeletal muscle enzyme adaptations associated with the exercise program. These results suggest that muscle beta-adrenoceptor properties may be influenced in part by the motor nerve innervation to that muscle, and are further discussed with respect to a possible relationship between exercise intensity and receptor regulation.

Animals↗
PubMed1984

Cigarette smoking, exercise and high density lipoprotein cholesterol.

Cigarette smoking is associated with depressed levels of HDL-C, whereas exercise is associated with elevated levels of HDL-C. The purpose was to determine effects of smoking and exercise on blood lipids and lipoproteins in middle-aged males. It was hypothesized that smoking may attenuate the effects of exercise to elevate HDL-C. A total of 269 males (70 smokers) met all criteria for inclusion in the study population. Age, height, weight, body fatness via hydrostatic weighing, daily caloric consumption and alcohol intake, and smoking habits and history were determined. Interviews concerning physical activity patterns were conducted and cardiovascular responses to treadmill exercise were determined. Subjects were grouped as sedentary (low activity), participants in vigorous recreational activities (moderate activity) and joggers/runners (high activity). Analysis of covariance with adjustments for factors which may affect blood lipids and lipoproteins was employed. Smokers demonstrated lower HDL-C and higher total cholesterol levels than nonsmokers. High activity subjects demonstrated significantly higher HDL-C levels than the low and moderate groups which did not differ. High activity smokers did not differ from low activity nonsmokers with respect to HDL-C. This supports the proposed hypothesis. Nonsmokers were higher in weight and body fatness than smokers even though smokers consumed 288 more calories per day on the average. This suggests that smoking may account for a significant number of calories through altered metabolism or some other means.

Adult↗
PubMed1984

Cigarette smoking, physical activity, and alcohol consumption: relationship to blood lipids and lipoproteins in premenopausal females.

A total of 164 premenopausal female subjects were randomly selected for evaluation from a much larger pool of volunteers. The relationships between blood lipid and lipoprotein levels as dependent variables and cigarette smoking, physical activity, and alcohol consumption were determined from partial regression coefficients. A lower HDL-C level (10.1 mg/dL) was seen in smokers v nonsmokers. For each ounce of alcohol consumed, HDL-C level was higher by 2.8 mg/dL, and greater physical activity was associated with a higher HDL-C level of 8.6 mg/dL. An analysis of covariance with covariance adjustments for age and body fat revealed that smokers who regularly exercise or consume alcohol had significantly lower HDL-C levels than nonsmokers with similar habits. Subjects who both exercise and consume alcohol demonstrated higher HDL-C levels than those who indulge in one or the other separately. Results suggest that cigarette smoking may attenuate the effects of chronic exercise or alcohol consumption, or of both, to raise HDL-C levels. Also, chronic exercise and alcohol consumption may exert an additive effect, raising HDL-C level.

Adult↗
PubMed1983

Tissue effects of iron deficiency in the rat.

Measurements of succinate dehydrogenase and mitochondrial glycerol-3-phosphate dehydrogenase activities, iron, cytochrome c and myoglobin, were made on various hind-leg muscles, fast-twitch red and white muscle and heart and liver of male Wistar rats fed an iron-deficient diet on weaning. Rats fed the same diet and given 20 mg iron intraperitoneally as iron-dextran (Imferon) served as controls. For iron-repletion studies anemic rats (hemoglobin less than 7 g/dl) were given a single injection of 10 mg iron (Imferon) and the time course of change in the above parameters was followed up to 22 days after injection. The iron concentration of most iron-deficient muscles dropped to approx. 35% of control, the heart to 60% and liver to 13%. On repletion, the iron concentration of all tissues increase significantly by 4 days. While the levels of cytochrome c and myoglobin approximated the iron levels in muscle, they did not change significantly in the heart. Succinate dehydrogenase activity dropped profoundly in muscle, to 10-30% of control; on repletion, the activity increased significantly. Mitochondrial glycerol-3-phosphate dehydrogenase activity showed only small changes in iron-deficient tissues.

Anemia, Hypochromic↗
PubMed1983

Exercise training and glucose uptake by skeletal muscle in rats.

Glucose uptake rates at various insulin concentrations were compared in perfused hindlimbs of sedentary and endurance exercise-trained (treadmill-running) rats. Rates of glucose uptake by hindlimb muscles were approximately 50% higher in the trained than in the untrained animals on the day after the trained rats' last training session. However, by the 2nd day after the trained rats' last training session (40-46 h without exercise), there were no significant differences in glucose uptake rates between the trained and the sedentary rats' hindlimb muscles either in the absence of insulin, at physiological insulin levels, or at a maximally effective insulin concentration. A bout of exercise, consisting of swimming to fatigue on the day before study, and muscle contraction induced by electrical stimulation, both resulted in significant increases in glucose uptake by the rats' perfused hindlimbs; the magnitude of these increases were similar in the trained and untrained rats. We conclude that differences in muscle glucose uptake between trained and untrained rats are due to residual effects of the last exercise session and that training does not result in a long-term adaptive increase in sensitivity of muscle to insulin.

Animals↗
PubMed1982

Adrenaline reactivation of muscle phosphorylase after deactivation during phasic contractile activity.

The increase in % phosphorylase a associated with muscle contraction is reversed after a few minutes despite continued contractile activity. The present study was undertaken to determine whether adrenaline can activate phosphorylase after deactivation has occurred during prolonged stimulation of contraction. We found that adrenaline reactivates phosphorylase and glycogenolysis in rat fast-twitch and slow-twitch muscles that have been stimulated to contract for 15 min. The reactivation of glycogenolysis by adrenaline could have importance in fight-or-flight situations that call for an increase in exercise intensity.

Animals↗
PubMed1982

Metabolite changes in individual rat muscle fibers during stimulation.

Rat plantaris and soleus muscles were stimulated intensely in vivo for 1 and 15 min, freeze-clamped, and freeze-dried, and individual fibers were dissected free. Fibers, assigned to four groups on the basis of lactate dehydrogenase and malate dehydrogenase, were each separately analyzed for ATP, P-creatine, glycogen, glucose, glucose-6-phosphate (glucose-6-P), lactate, citrate, and malate. Some fibers were also analyzed for fructose 1,6-phosphate, total adenylate and total creatine. Although each group as a whole showed significant and often large differences in control composition and response to stimulation, individual fibers varied enough to create an almost continuous spectrum of metabolite levels from one extreme to the other. The data suggest that the slowest twitch fibers were the most active in the control state. Stimulation for 1 min caused a small increase in ATP in all groups with a large decrease in P-creatine in "fast white" fibers and a modest decrease in the rest. After 15-min stimulation, fast white fibers had lost 60% of initial ATP and 97% of initial P-creatine, whereas in other fiber types these compounds underwent little further change. Metabolite changes with stimulation were also greatest in fast white fibers. Glucose-6-P rose 15-fold in 1 min, then fell to below control by 15 min when glycogen had been exhausted; lactate rose two to six times more than in other types. Glucose rose in all groups to levels at 15 min, compatible with equilibrium with blood plasma.

Adenosine Triphosphate↗
PubMed1982

Effect of muscle glycogen content on glucose uptake following exercise.

This study examined the effects of raising muscle glycogen by carbohydrate feeding and of keeping muscle glycogen low by carbohydrate restriction following exhausting exercise on the ability of perfused skeletal muscle to take up glucose and to synthesize glycogen. Muscle glycogen concentration was more than twice as high in the rats fed carbohydrate as in those not given carbohydrate. Muscle glycogen synthesis during a 30-min perfusion with glucose and insulin was significantly greater in the animals with low muscle glycogen. Furthermore the muscles with low glycogen content converted a greater proportion of the glucose taken up to glycogen and less to lactate than did the muscles with high glycogen content. In rats subjected to exhausting exercise on the preceding day, the rate of glucose uptake by perfused skeletal muscle was significantly higher (60-80%) at the same insulin concentration in animals in which muscle glycogen was kept low than in those in which glycogen was raised by carbohydrate feeding.

Animals↗
PubMed1982

Effects of beta-adrenergic receptor blockade on glycogenolysis during exercise.

The purpose of this study was to determine whether beta-adrenergic receptor blockade inhibits glycogen utilization in rats during exercise. Propranolol (1 mg/kg body wt) completely blocked the glycogenolytic effect of a large dose of epinephrine given by injection but did not prevent glycogen breakdown in skeletal muscle or liver during a bout of treadmill exercise. On the contrary, exercise resulted in greater glycogen depletion in plantaris muscles of beta-blocked rats than in those of control rats, probably as a result of decreased availability of fatty acids. Increasing the availability of exogenous substrates slowed the rate of skeletal muscle glycogen depletion during exercise. However, even with increased availability of exogenous substrates, beta-blockade did not result in reduced utilization of skeletal muscle or liver glycogen. In contrast to its effect on skeletal muscle, beta-blockade markedly reduced glycogen depletion in the heart during exercise. We conclude that beta-adrenergic stimulation is of major importance in mediating glycogenolysis in the heart but is not necessary for glycogenolysis in skeletal muscle or liver during prolonged exercise.

Adrenergic beta-Antagonists↗
PubMed1981

Physiological and biochemical effects of iron deficiency on rat skeletal muscle.

Young rats were made iron deficient by feeding them a low-iron diet for 8 wk. Iron deficiency resulted in a 50% decrease in cytochrome c and cytochrome oxidase and a 26% decrease in mitochondrial glycerol-3-phosphate dehydrogenase activity in skeletal muscle. Respiratory capacity of muscle homogenates was reduced 55%. After 8 days of iron treatment, respiratory capacity, cytochrome c, cytochrome oxidase, and glycerol-3-phosphate dehydrogenase had returned 50% toward normal. Maximum O2 uptake of contracting hindlimb muscles averaged 8.5 mumol O2.min-1.g-1 in control, 4.3 mumol O2.min-1.g-1 in iron-deficient, and 6.2 mumol O2.min-1.g-1 in the 8-day-iron-repleted rats. Muscle fatigue during 10 min of stimulation was greater in the iron-deficient group. Lactate concentration in red muscle was higher in iron-deficient than in control rats after stimulation. The muscle fatigue and lactate responses returned 50% toward normal during 8 days of iron treatment. We conclude that iron deficiency results in a decrease in skeletal muscle capacity for aerobic metabolism and, by this mechanism, increases susceptibility to fatigue.

Animals↗
PubMed1981

Adaptive responses of rats to prolonged treatment with epinephrine.

Rats were given a daily injection of L-epinephrine, 100 micrograms/100 g body wt, for 6 wk. The hearts of the epinephrine-treated animals were heavier (11.5%), and blood glucose and plasma insulin concentrations were lower than those of control rats. Acute responses to epinephrine were compared in the two groups. An increase in blood glucose and decreases in plasma insulin, liver glycogen, and muscle glycogen occurred in both groups. The magnitude of these responses were similar in the two groups except for the decrease in muscle glycogen, which was smaller in the chronic epinephrine-treatment group. There were no changes in respiratory capacity, citrate synthase or succinate dehydrogenase activities, or in cytochrome c concentration in skeletal muscle in response to 6 wk of epinephrine treatment. These results are compatible with the suggestion that catecholamines may play a role in some of the metabolic and cardiac adaptations to exercise training. However, they argue strongly against the hypothesis that catecholamines are responsible for inducing the increase in muscle mitochondria that occurs in response to exercise training.

Animals↗
PubMed1981

Effects of glycerol feeding before and after exhausting exercise in rats.

Rats were fed either 1 g of glycerol or 1 g of glucose following exercise to exhaustion. Glucose feeding resulted in a rapid increase in blood glucose, with attainment of peak hyperglycemia within 1 h and of peak muscle glycogen in about 2 h. Feeding 1 g of glycerol resulted in marked elevation of glycerol concentration in blood, liver, and muscle; the highest values, measured 1 h after glycerol feeding, ranged from 29 to 42 mumol/g tissue. Blood glucose and muscle glycogen increased slowly in the glycerol-fed rats and peaked much later than after glucose feeding. In perfused rat hindlimb muscles, negligible amounts of [14C]glycerol were incorporated into glycogen. These findings suggest that muscle is not able to utilize glycerol to a significant extent and that glucose derived from glycerol was the major substrate for muscle glycogen synthesis. Animals fed glycerol before a run to exhaustion were able to exercise significantly longer than control rats (153 +/- 11 min vs. 116 +/- 6 min). The glycerol-fed rats depleted their muscle and liver glycogen stores less rapidly than the controls and were protected against development of hypoglycemia during the exercise.

Animals↗
PubMed1980

Preferential resynthesis of muscle glycogen in fasting rats after exhausting exercise.

Despite carbohydrate starvation (fasting or fat feeding) considerable glycogen accumulation, ranging from 20 to 30 mumol glucose/g, occurred in hindlimb muscles of rats following exhausting exercise that caused severe muscle and liver glycogen depletion and hypoglycemia. The largest increase in muscle glycogen occurred during the first 3 h after exercise when plasma levels of glucagon and epinephrine were very high and insulin concentration was low. The concentrations of glycogen attained in different hindlimb muscles in the fasting and fat-fed animals were between 50 and 100% of the values found in rats fed carbohydrate after the exhausting exercise. In rats fed carbohydrate following exercise, liver glycogen accumulation greatly exceeds muscle glycogen accumulation. A remarkable difference in the response of liver glycogen was seen in the carbohydrate starved rats. In contrast to the rapid increase in muscle glycogen, liver glycogen was still essentially completely depleted in the fasting and fat-fed rats 24 h after exercise. This indicates that the glucose made available via gluconeogenesis was preferentialy channeled away from liver glycogen synthesis into muscle glycogen.

Animals↗
PubMed1979

Liver glycogenolysis during exercise without a significant increase in cAMP.

Liver glycogenolysis may be controlled by glucagon or catecholamine-induced changes in cAMP or by cAMP-independent mechanisms. The purpose of these experiments was to determine whether an increase in liver cAMP occurs during exercise at a time when the rate of liver glycogenolysis is greatly accelerated. Rats were taught to run on a treadmill 10 min/day for 6 wk. They were then run continuously for periods of time ranging from 0 to 120 min at 0.8 mph up a 15% grade. Liver glycogen was depleted by the end of 90 min in fed animals and by 20 min in overnight-fasted animals. Liver cAMP was not significantly increased in fed animals during the first 60 min of exercise. The major increase in liver cAMP occurred after liver glycogen was depleted, at which time the rat must rely entirely on gluconeogenesis for maintenance of blood glucose. This increase in cAMP corresponded to large increases in plasma glucagon and catecholamines. We conclude that liver glycogenolysis in the rat can occur during exercise independently from significant detectable increases in cAMP concentrations.

Animals↗
PubMed1978

Adrenocortical function in response to myocardial necrosis in exercise-trained rats.

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone was determined in exercise-trained rats. Virgin, male rats, 100 days of age, were trained for an 11-wk period by treadmill running. Following the training program, rats were subjected to two subcutaneous injections of l-isoproterenol 24 h apart and killed 24 h after the second injection. All exercise-trained rats survived isoproterenol treatment, while 44% of the control rats died. Plasma corticosterone concentrations were elevated only in exercise-trained rats treated with isoproterenol. Control rats treated with isoproterenol had plasma corticosterone concentrations similar to that in control and exercise-treated rats given placebo injections. Exercise training reduced adrenocortical responsiveness to ACTH in vitro, but isoproterenol treatment increased in vitro responsiveness to ACTH in exercise-trained and control rats. Total unstimulated corticosterone secretion rates in vitro were similar. The reason for better rat survival in exercise-trained rats is unknown; however, improved energy metabolism, depressed aldosterone secretion, or both are suggested as reasons for the better survival of exercise-trained rats.

Adrenal Cortex↗
PubMed1977

Adrenocortical function in aging exercise-trained rats.

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone were determined in exercise-trained rats. Rats, 100, 200, and 300 days of age, were trained for a 10-wk period by treadmill running. Following the training program, rats were subjected to an acute bout of swimming. Acute swimming elevated plasma corticosterone concentrations in all age groups. At 170 days of age, the plasma corticosterone concentration following swimming was higher in exercise-trained rats than in controls. The opposite was true of acutely swum rats at 270 and 370 days of age. Acute swimming elevated the in vitro adrenal gland response to adrenocorticotropic hormone stimulation in control rats at all ages and in trained rats at 170 days of age. The in vivo relationship of epinephrine and the pituitary adrenal system is suggested as a mechanism which could have caused this response. The relationship of secretion rates to plasma corticosterone concentrations indicated that extra-adrenal mechanisms, such as decreased turnover, were also responsible for the elevated plasma corticosterone levels observed in response to acute swimming.

Adrenal Cortex↗