Biomedical subjects
Publications and source records attributed to H W Bonner.
The effect of an acute exercise stress upon the acute toxicity of adriamycin was tested. Mice were forced to swim for 30 min following 18 or 23 mg/kg ip of adriamycin. Survival was checked daily for 30 days. The exercise stress did not appear to increase the toxicity of adriamycin in these animals.
Female Wistar rats were used to determine the effects of the chelating agents, EDTA and EGTA, on the in vitro 45Ca2+ accumulation by mitochondria isolated from the skeletal muscle of fatigued animals. The rats were divided into three groups: sedentary-rested (SR), trained-rested (TR), trained-exhausted (TE). The trained groups were exercised on a treadmill for 1 h daily, five times a week, for 22 weeks. At the conclusion of the training program, the TE group was rapidly exercised to exhaustion immediately following their daily 1-h run. In the TR group EDTA reduced 45Ca2+ binding while both EDTA and EGTA appeared to increase mitochondrial Ca2+ and Mg2+ content. In the TE group, EDTA reduced endogenous mitochondrial Ca2+ and Mg2+ content, while both EDTA and EGTA increased 45Ca2+ binding. Since chelating Ca2+ and Mg2+ from the membrane may affect the structure and function of the mitochondria, it is suggested that the use of chelating agents during the isolation of mitochondria from the skeletal muscle of trained rats be viewed with caution.
In order to ascertain the effects of long-term exercise training and long-term exhaustive exercise on mitochondrial 45Ca2+ uptake and related variables in rat skeletal muscle, female rats were randomly divided into three groups: sedentary-rested (SR), trained-rested (TR), and trained-exhausted (TE). The trained groups were exercised five times per week on a treadmill for 22 weeks. At the conclusion of the training period, the TE group was exercised to exhaustion following their daily 1 h run. The 45Ca2+ uptake and endogenous mitochodrial Ca2+ content of skeletal muscle followed stepwise increases of approximately 25% and 50%, respectively, across the groups, suggesting that long-term exercise induces the mitochondria to play an important role as a Ca2+ uptake buffer. A 75--83% reduction in 45Ca2+ binding in the TE group suggests a selective loss and partial saturation of membrane phospholipids with exhaustive exercise. The TE group had a two-fold greater content of mitochondrial Mg2+ than did the rested groups. It is speculated that the mitochondria accumulate Mg2+ during acute exercise to maintain the functional integrity of the membrane, thus offsetting the deleterious effects of excessive Ca2+ uptake
5-day-old neonatal offspring of exercised or non-exercised pregnant Sprague Dawley rats were used to prepare primary cultures of beating myocardial cells. The cells from the exercise group exhibited a slower beating rate for both single and aggregate cells; a larger cell size; an increased percentage of contracting cells; a greater capacity to form confluent monolayers, and a greater viability. It was concluded that exercise during the period of pregnancy produced morphological alterations in the myocardium of the progeny.
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The effect of exercise on the severity of isoproterenol-induced myocardial infarction was studied in male rats. Ninety-three rats were randomly divided into three groups. The exercise-isoproterenol (E-1) and exercise control (EC) groups exercised daily for thirty days on a treadmill at 1 mph, 2% grade while animals of the sedentary-isoproterenol (S-I) group remained sedentary. Eight animals were assigned to the sedentary control (SC) group which remained sedentary throughout the experimental period. Forty-eight hours after the final exercise period, S-I and E-I animals received a single subcutaneous injection of isoproterenol (250 mg/kg body weight). Animals of the S-I group exhibited significantly (Pp less than 0.05) greater mortality from the effects of isoproterenol than animals of the E-I group. Serum CPK activity for E-I animals was significantly (p less than 0.05) greater than for animals in the S-I and EC groups twenty hours following isoproterenol injection. No statistically significant differences were observed between the two isoproterenol treated groups for severity of the induced lesions, changes in heart weight, or heart weight to body weight ratios. The results indicated that exercise reduced the mortality associated with the effects of large dosages of isoproterenol but had little on the severity of the infarction.
Following a 25 muCi/Kg i/p. injection, 45Ca++ activity from the mitochondria and fragmented sarcoplasmic reticulum (FSR) of the superficial rectus femoris (FG-fibers) and combined soleus muscle (SO-fibers) of trained (T, N = 9) and untrained (UT, N = 8) male Wistar rats was determined. The FG mitochondrial 45Ca++ activity from rested animals was 3.9 (T) and 5.3 (UT) times greater than the FSR from this muscle group while the so-mitochondrial 45Ca++ activity was 13.2 (T) and 20.5 (UT) times greater when compared with the respective SO-FSR (p less than .01). The mitochondrial 45Ca++ content of the SO-fibers from rested animals was 58% UT, p less than .01) and 148% (T, p less than .001) greater than that of the FG mitochondria. After 20-26 weeks of exercise training the SO-mitochondrial 45Ca++ content of the rested-T animals was approximately 18% lower (p less than .05) while the T-FG-mitochondrial 45Ca++ content was 48% less than that of UT animals (p less than .01) with a concomitant 28% greater 45Ca++ activity in SO-FSR for the T-group as compared to UT (p less than .01). Following a rapidly exhaustive treadmill run the mitochondrial 45Ca++ content in the UT group was depressed by 21% in SO-fibers and 37% in FG-fibers (p less than .01) with no changes occurring in the T-group. Exhaustion produced no significant changes in the 45Ca++ activity of the FSR from either group of animals.
Mitochondrial and sarcoplasmic reticular 45Ca2+ uptake and Ca2+-ATPase activity were determined in skeletal muscle from exercise trained and non-trained rats at rest or following short-term exhaustive exercise. In trained rats exercised to exhaustion, mitochondrial 45Ca2+ uptake was significantly depressed when compared to non-trained rats at rest. Ca2+-ATPase activity of sarcoplasmic reticulum from trained rats exercised to exhaustion was significantly increased as compared to trained rats at rest. These data suggest that the disruptive influence of Ca2+ accumulation in mitochondria isolated following exhaustive exercise may be diminished as a result of training.
15 untrained women were subjected to a walking treadmill test to determine the influence of maximal exercise upon synthesis of erythrocyte 2,3 DPG. Although there was a 9.8% increase in the 2,3 DPG content following exercise, there was a concomitant 9.4% increase in the hemoglobin level; therefore, when 2,3 DPG is expressed as a ratio to hemoglobin (See Article), there was no significant change as a result of exercise stress. It was suggested that three additive factors produced during strenuous exercise; decreased pH; increased hemoglobin concentration; and increased CO2 production result in by-product inhibition of 2,3 DPG synthesis. It is concluded that 2,3 DPG does not provide a physiologic benefit in the adaptation of the oxygen transport system to exercise.
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