Dehydroepiandrosterone and a beta-agonist, energy transducers, alter antioxidant enzyme systems: influence of chronic training and acute exercise in rats.

We examined the influence of dehydroepiandrosterone (DHEA), a beta-agonist, and exercise training on enzymes that detoxify toxic oxygen species. Feeding 0.4% DHEA decreased hepatic cytosolic (c) selenium-dependent glutathione peroxidase (GPX), (-26%, P less than 0.0001) and increased hepatic mitochondrial (m) Mn superoxide dismutase (SOD), (+38%, P less than 0.001). DHEA decreased myocardial c-GPX (-21%, P less than 0.05) when compared to a beta-agonist (beta A; L644969 Merck and Co.) fed at 5 ppm but neither differed from the Control (C). In contrast, the beta A increased hepatic m-GPX (+25%, P less than 0.05). In skeletal muscle, DHEA and beta A decreased muscle c-GPX by 20 and 12%, respectively (P less than 0.0009). DHEA increased both muscle (+20%, P less than 0.01) and myocardial (+20%, P less than 0.05) c-glutathione S-transferase (GST) over beta A (+20%, P less than 0.01) but neither was significantly different from C. Similar to DHEA, chronic training (Tr) (1 h/day, 5 days/week at 27 m/min, 15% grade on treadmill) decreased hepatic c-GPX (-16%, P less than 0.003). Tr elevates muscle c-GPX (+36%, P less than 0.05) in C. Tr increased myocardial c-GPX by 28% in the beta A-treated rats, whereas Tr decreased myocardial c-GPX by 22% in the C (P less than 0.05, interaction). One hour of acute exercise (Ex) (70% VO2 max relative work load) decreased hepatic homogenate catalase (-12%, P less than 0.02) and increased hepatic m-Mn SOD (+28%, P less than 0.03). Ex decreased myocardial c-GST (P less than 0.05) only in the DHEA-treated rats. DHEA and Tr may improve efficiency of oxygen utilization at the tissue level with lower antioxidant enzyme activity in liver and locally protective up-regulation in muscle. beta A stresses oxygen utilization systems and liver responds by up-regulation of antioxidant enzymes. The increase in myocardial c-GPX activity in the beta A-treated group may be a protective effect against indirect catecholamine-induced myocardial necrosis which results from free radical generation.

Characteristics and performance of male citizen cross-country ski racers.

Forty-three male citizen or recreational cross-country (X-C) ski racers (aged 31 +/- 4.4 years) were tested to determine their weight (BW) and percent body fat (BF), maximal oxygen uptake (VO2max), quadriceps (Quad), hamstrings (Ham) and upper body (UBS) isokinetic strength (60 degrees, 180 degrees, 240 degrees/s), and Quad endurance. In addition, skiers filled out a questionnaire to determine their skiing experience and to see what other activities they participated in. All these variables were run through a stepwise regression procedure to see which characteristics best predicted performance in a 10 km X-C ski race. The relatively high VO2max of 56.6 ml O2/kg/min and low BF of 10.1% indicate this group to be a very fit subset of the general population. All the skiers were active in other sports on a year-round basis. Of the variables studied, UBS, VO2max, and Quad strength were all significant determinants of 10 km race performance, yielding a multiple R of 0.78. Quad endurance, Ham strength, BW, BF, and experience did not significantly contribute toward the prediction of performance. It is felt that a proper training program for the citizen X-C skier should strive to maximize upper body strength as well as one's aerobic capacity.

Usefulness of a branching treadmill protocol for evaluation of cardiac functional capacity.

A branching treadmill protocol was designed to measure functional capacity in patients with low work capacity and varying ability to walk at speeds used in traditional protocols. A comfortable walking pace is first selected (2.0 to 3.5 mph, 0.25 mph increments) and the workload is then increased every 2 minutes in 1 MET increments (a multiple of the resting oxygen uptake [1 MET = 3.5 ml O2/kg/min]) by adjusting grade. Nine trained (maximal MET = 7.6 +/- 1.6, mean +/- standard deviation) male subjects (age 59 +/- 7 years) with previous myocardial infarction and 9 trained (maximal MET = 11.7 +/- 2.5) male control subjects (age 56 +/- 8 years) completed submaximal and maximal workloads without handrail support. The measured oxygen consumption, volume of oxygen in ml/kg/min (VO2), was compared with the predicted VO2 cost of treadmill walking calculated from speed and grade. A linear regression analysis of predicted versus measured VO2 was performed. There were no significant differences between myocardial infarction and control regression lines. Therefore, a simplified prediction equation for estimated VO2 in myocardial infarction and control subjects is proposed. Overall VO2 prediction = 1.61 + 0.99 x. The main advantage of the branching protocol format is the selection of a stable, brisk walking pace compatible with age and gait, which may improve mechanical efficiency through impedance matching. The protocol is adaptable enough in design so that most patients can complete the exercise test without use of handrails, which is essential for an accurate estimate of VO2 from treadmill speed and grade.

Carnitine supplementation and depletion: tissue carnitines and enzymes in fatty acid oxidation.

Sixty-two male rats were randomly assigned into a 3 X 2 X 2 factorial design containing 12 groups according to carnitine treatment, exercise training (treadmill, 1 h, 5 times/wk, 8 wk, 26.8 m/min, 15% grade), and physical activity [rested for 60 h before they were killed or with an acute bout of exercise (1 h, 26.8 m/min, 15% grade) immediately before they were killed]. Isotonic saline was injected intraperitoneally 5 times/wk in the controls, whereas 750 mg/kg of L- or D-carnitine, respectively, were injected in the supplemented and depleted treatment groups. A significant increase in free and short-chain acyl carnitine concentration in skeletal muscle and heart was observed in L-carnitine supplemented rats, whereas a significant reduction in skeletal muscle, heart, and liver occurred in rats depleted of L-carnitine. Long-chain acyl carnitine in all tissues was not altered by carnitine treatment; training increased plasma and liver concentrations, whereas acute exercise decreased skeletal muscle and increased liver concentrations. An acute bout of exercise significantly increased short-chain acylcarnitine in liver, regardless of carnitine and/or training effects. beta-Hydroxyacyl-CoA dehydrogenase activity in skeletal muscle was induced by training but reduced by depletion. Carnitine acetyltransferase (CAT) was significantly increased in heart by L-carnitine supplementation, whereas it was reduced by depletion in skeletal muscle. Exercise training significantly increased CAT activity in skeletal muscle but not in heart, whereas acute exercise significantly increased activity in both tissues. Carnitine palmitoyltransferase activity was increased by acute exercise in the heart in only the supplemented and exercise-trained rats.