G R Brodowicz

The Ohio State University, Columbus, Ohio, United States

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Publications (7)17.03 Total impact

  • G R Brodowicz, D R Lamb
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    ABSTRACT: 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)
    Archiv für Kreislaufforschung 01/1991; 86(1):40-8. · 5.90 Impact Factor
  • T S Baur, G R Brodowicz, D R Lamb
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    ABSTRACT: The aim was to determine if prostaglandin like activity might be involved in changes due to exercise training in the coronary flow responses to hypoxia. The coronary flow response to hypoxia was measured under constant perfusion pressure in isolated perfused hearts from 12 endurance exercise trained rats and 12 control rats. Eight hearts were perfused with a solution containing indomethacin, a cyclo-oxygenase inhibitor, to determine its effect on any training induced changes in the coronary flow response to hypoxic stress. 24 male Sprague-Dawley rats, 517 (SD 51) g, were used for this study. The animals were anesthetised and the hearts rapidly excised and perfused with a modified Langendorff perfusion system. Under constant perfusion pressure, the hearts of endurance exercise trained rats had a greater increase in coronary flow during hypoxia relative to normoxia than did hearts of untrained rats, at 13.52(2.15) v 9.56(1.05) ml.min-1.g-1 dry heart weight. Indomethacin treatment abolished this difference and lowered coronary flow: exercise -3.81(3.75) ml.min-1.g-1; control 0.38(2.44) ml.min-1.g-1. The inhibition by indomethacin of the endurance exercise training induced potentiation of the coronary fluid flow response to hypoxia suggests that prostacyclin or a related compound may be involved in this adaptation to exercise.
    Cardiovascular Research 10/1990; 24(9):733-6. · 5.81 Impact Factor
  • D R Lamb, G R Brodowicz
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    ABSTRACT: 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)
    Sports Medicine 01/1986; 3(4):247-74. · 5.32 Impact Factor
  • G. R. Brodowicz, D. R. Lamb, T. S. Baur, D. F. Connors
    Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/1984; 16(2).
  • Thomas S. Baur, David R. Lamb, G. R. Brodowicz
    Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/1984; 16(2).
  • Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/1983; 15(2).
  • Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/1983; 15(2).