Effects of exercise on glycogen synthetase in red and white skeletal muscle.
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Animals↗
Biomedical subjects
D R Lamb
Publications and source records attributed to D R Lamb.
Exercise: effects on hexokinase activity in red and white skeletal muscle.
Single bouts of exercise increase hexokinase activity in red and white skeletal muscle of guinea pigs. Multiple bouts of exercise cause two-fold increases. In contrast to other enzymes associated with glycolysis, hexokinase activity is higher in red than in white skeletal muscle.
Animals↗
Proximity of the opposite sex and spontaneous activity in the adult laboratory rat.
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Animals↗
Exercise training, indomethacin, and isoproterenol-induced myocardial necrosis in the rat.
It was hypothesized that endurance exercise training would attenuate isoproterenol-induced myocardial necrosis in the rat by increasing the concentration of prostacyclin in the myocardial vasculature. Rats were randomly assigned to exercise and control groups. Exercisers ran on a motorized treadmill 1 h.d-1, 5 d.week-1 for 14 weeks. Immediately following the training program subgroups of rats were injected with 4 mg.kg-1 indomethacin or saline. One day later, all rats were given a subcutaneous injection of isoproterenol (20 mg.kg-1); after another 24 h they were sacrificed. A decrease of myocardial creatine kinase (CK) activity was used as a marker for myocardial necrosis. Endurance exercise training attenuated the isoproterenol-induced decrease in myocardial CK relative to control by approximately 37% (exercise: 16.4 +/- 0.6 U.mg-1 protein; control: 10.5 +/- 0.6 U.mg-1 protein; p less than 0.05). Pretreatment with indomethacin decreased myocardial CK in the exercise-trained rats (indomethacin: 15.4 +/- 0.8 U.mg-1 protein; saline: 17.7 +/- 0.7 U.mg-1 protein; p less than 0.05), but not in the controls (indomethacin: 10.3 +/- 1.0 U.mg-1 protein; saline: 10.8 +/- 0.6 U.mg-1 protein; p greater than 0.05). The concentration of myocardial 6-keto-PGF1 alpha, a marker for prostacyclin, was not altered by exercise but, as expected, was reduced by indomethacin pretreatment (p less than 0.05). Thus, exercise training reduces myocardial damage caused by isoproterenol, but the evidence does not support the hypothesis that prostacyclin mediated this effect of training. Further research is needed to determine the extent to which exercise training-induced alterations in sensitivity to PGI2 or TXA2 affect myocardial damage from isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)
6-Ketoprostaglandin F1 alpha↗
Relationship between plasma concentrations of immunoreactive beta-endorphin and food intake in rats.
Periods of increased food intake in male rats were characterized by significant elevations in the plasma concentrations of immunoreactive beta-endorphin (beta-ep). Administration of 2-deoxy-D-glucose (400 mg/kg) produced rapid and concurrent increases in both food intake and plasma beta-ep. Administration of insulin (10 units/kg) produced large delayed increases in food intake but only modest delayed increases in plasma beta-ep. Spontaneous nocturnal feeding was associated with increased plasma beta-ep. Increases in daytime food intake in rats subjected to 24 hr of food deprivation were also characterized by elevated plasma beta-ep. In all cases examined, those feeding behaviors in male rats which were subject to inhibition by naloxone were characterized by elevated concentration of plasma beta-ep.
Animals↗
Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats.
The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.
Animals↗
Anabolic steroids in athletics: how well do they work and how dangerous are they?
The use of anabolic drugs by athletes who wish to increase lean body mass and improve muscular strength is widespread, especially among elite weight-trained athletes. The current regimens used for steroid doping include combinations of injectable and oral preparations of steroids at doses 10 to 40 times greater than those prescribed therapeutically. Most of the scientific studies of steroid use by healthy male athletes have used steroid doses substantially lower than those used by many athletes. Analysis of these studies suggests that most persons will gain an average of 2.2 kg of lean body weight during steroid administration but that there exist great individual differences in strength changes induced by steroids. Approximately 50% of the investigations show significant improvements in strength measurements with steroid treatment, whereas the remainder show indefinite effects. There is no substantial evidence to support the use of anabolic steroids for improving aerobic work capacity. Anabolic steroids cause interrupted growth and virilization in children, birth defects in the unborn, severe virilization in women, and testicular atrophy and reduced blood levels of gonadotropins and testosterone in adult males. In addition, the oral preparations of anabolic steroids are associated with liver dysfunction, including carcinoma and peliosis hepatis, and a number of other disorders including unpredictable changes in mood, aggression, and libido. Although there have been only rare reports of severe or life-threatening side effects in athletes who have abused steroids, such side effects may not appear obvious until 20 years or more of widespread steroid abuse.
Administration, Oral↗
Optimal use of fluids of varying formulations to minimise exercise-induced disturbances in homeostasis.
The rationale underlying the development of various formulations of beverages for consumption before, during, and/or after physical exercise is that such formulations should minimise some of the disturbances in physiological homeostasis that occur during exercise and thereby prevent injury and/or enhance performance. Exercise- and dehydration-induced increases in core temperature, body fluid osmolality, heart rate, losses of plasma and other body fluid volumes, and carbohydrate depletion are probably the most important homeostatic disturbances that can be ameliorated by fluid consumption. With the exception of athletes subject to hyponatraemia after consumption of ordinary water during prolonged activity, changes in electrolyte concentrations in the body fluids of most athletes do not justify the inclusion of electrolytes in fluid replacement beverages to be consumed during exercise. However, small amounts of sodium added to water does speed gastric emptying and fluid absorption from the intestine. Recent evidence suggests that a precompetition meal high in easily digested carbohydrates should be consumed not later than 5 to 6 hours before competition. There is little published research on the optimal composition of this meal. Water ingestion 30 to 60 minutes before exercise seems to be of benefit to temperature regulation and cardiovascular homeostasis if the exercise is of moderate intensity (50 to 65% VO2max), but probably has little effect at the higher intensities of athletic performance. There is no systematic evidence to support the inclusion of calcium or sodium chloride in drinks consumed an hour or 2 before exercise. Furthermore, if glucose solutions are fed 15 to 45 minutes before prolonged exercise, they will probably cause a fall in blood glucose during exercise and may adversely affect performance. These adverse effects are not present when fructose is consumed before exercise. Contrary to the adverse effects of glucose feedings 15 to 60 minutes before exercise, the consumption of 18 to 50% solutions of glucose or glucose polymers 5 minutes before prolonged exercise seems to have potential for improving endurance performance. Similarly, the inclusion of caffeine in beverages consumed 60 minutes before prolonged exercise improves athletic performance for many subjects. Others may be hypersensitive to the effects of caffeine and are adversely affected by its use. For exercise leading to exhaustion in less than 30 minutes, neither caffeine nor carbohydrate ingestion is effective in minimising homeostatic perturbations or improving exercise performance.(ABSTRACT TRUNCATED AT 400 WORDS)
Drinking↗