Effects of acute exercise and detraining on insulin action in trained men

Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] underwent sequential hyperinsulinemic euglycemic clamps on three occasions: 1) in the "habitual state" 15 h after the last training bout (C), 2) after 60 min of bicycle exercise at 72 +/- 3% of VO2max performed in the habitual state (E), and 3) 5 days after the last ordinary training session (detrained, DT). Sensitivity for insulin-mediated whole-body glucose uptake was not affected by acute exercise [insulin concentrations eliciting 50% of maximal insulin-mediated glucose uptake being 44 +/- 2 (C) vs. 46 +/- 3 (E) microU/ml] but was decreased after detraining (54 +/- 2 microU/ml, P less than 0.05) to levels comparable to those found in untrained subjects [Am. J. Physiol. 254 (Endocrinol. Metab. 17): E248-E259, 1988]. Near-maximal insulin-mediated glucose uptake (responsiveness) was higher than in untrained subjects and not influenced by acute exercise or detraining [13.4 +/- 1.2 (C), 12.2 +/- 0.9 (E), and 12.2 +/- 0.3 (DT) mg.min-1.kg-1]. Calculated by indirect calorimetry, the glucose-to-glycogen conversion was not influenced by E but was reduced during detraining (P less than 0.05) yet remained higher than previously found in untrained subjects (P less than 0.05). However, only on E days did muscle glycogen increase during insulin infusion. Glycogen synthase activity was increased on E and decreased on DT compared with C days.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise improves import of 8-oxoguanine DNA glycosylase into the mitochondrial matrix of skeletal muscle and enhances the relative activity

Exercise has been shown to modify the level/activity of the DNA damage repair enzyme 8-oxoguanine-DNA glycosylase (OGG1) in skeletal muscle. We have studied the impact of regular physical training (8 weeks of swimming) and detraining (8 weeks of rest after an 8-week training session) on the activity of OGG1 in the nucleus and mitochondria as well as its targeting to the mitochondrial matrix in skeletal muscle. Neither exercise training nor detraining altered the overall levels of reactive species; however, mitochondrial levels of carbonylated proteins were decreased in the trained group as assessed by electron spin resonance and biochemical approaches. Importantly, nuclear OGG1 activity was increased by daily exercise training, whereas detraining reversed the up-regulating effect of training. Interestingly, training decreased the outer-membrane-associated mitochondrial OGG1 levels, whereas detraining reversed this effect. These results suggest that exercise training improves OGG1 import into the mitochondrial matrix, thereby increasing OGG1-mediated repair of oxidized guanine bases. Taken together, our data suggest that physical inactivity could impair the mitochondrial targeting of OGG1; however, exercise training increases OGG1 levels/activity in the nucleus and specific activity of OGG1 in mitochondrial compartments, thereby augmenting the repair of oxidized nuclear and mitochondrial DNA bases.     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

Effects of detraining on cardiovascular responses to exercise: role of blood volume

In this study we determined whether the decline in exercise stroke volume (SV) observed when endurance-trained men stop training for a few weeks is associated with a reduced blood volume. Additionally, we determined the extent to which cardiovascular function could be restored in detrained individuals by expanding blood volume to a similar level as when trained. Maximal O2 uptake (VO2max) was determined, and cardiac output (CO2 rebreathing) was measured during upright cycling at 50-60% VO2max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692 ml; P less than 0.01) during upright exercise, due primarily to a 12% lowering (P less than 0.01) of plasma volume (PV; Evans blue dye technique). SV was reduced by 12% (P less than 0.05) and VO2max declined 6% (P less than 0.01), whereas heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P less than 0.01) and 8% (P less than 0.05), respectively. When blood volume was expanded to a similar absolute level in the trained and detrained state (approximately 5,500 +/- 200 ml) by infusing a 6% dextran solution in saline, the effects of detraining on cardiovascular response were reversed. SV and VO2max were increased (P less than 0.05) by PV expansion in the detrained state to within 2-4% of trained values. Additionally, HR and TPR during submaximal exercise were lowered to near trained values. These findings indicate that the decline in cardiovascular function following a few weeks of detraining is largely due to a reduction in blood volume, which appears to limit ventricular filling during upright exercise.     

Effects of exercise-training and detraining on fat cell lipolysis in men and women

The effects of training and detraining on adipose tissue lipolysis were studied in 19 healthy subjects (7 women and 12 men) who were submitted to a 20-week aerobic training program. Thereafter, subjects refrained from exercise for a period of 50 days. Suprailiac fat biopsies were performed before training, after training, and at the end of the detraining period. Mean fat cell diameter and epinephrine stimulated lipolysis (ESL) were assessed on collagenase isolated fat cells. Body density through underwater weighing and skinfolds at seven different sites were also obtained. Training significantly increased ESL (P less than 0.05) in men but not in women. However, ESL values in men returned to pretraining values after the exercise restriction period. No significant changes in women lipolysis were observed under any conditions. Changes in lipolysis were not correlated with changes in body fatness. However, a significant correlation was observed between the increase in ESL produced by training and the subsequent decrease caused by detraining (r = -0.53; P less than 0.05). The present results suggest that lipolysis in fat cells from the female subjects seems to be insensitive to changes in energy expenditure. Moreover, the present study demonstrates that there are high and low responders in adipocytes ESL to variations in habitual energy expenditure.     

Effect of high intensity interval training on 2,3-diphosphoglycerate at rest and after maximal exercise

The purpose of this study was to examine the effect of intense interval training on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels at rest and after maximal exercise. Eight normal men, mean +/- SE = 24.2 +/- 4.3 years, trained 4 days X week-1 for a period of 8 weeks. Each training session consisted of eight maximal 30-s rides on a cycle ergometer, with 4 min active rest between rides . Prior to and after training the subjects performed a maximal 45-s ride on an isokinetic cycle ergometer at 90 rev X min-1 and a graded leg exercise test ( GLET ) to exhaustion on a cycle ergometer. Blood samples were obtained from an antecubital vein before, during and after the GLET only. Training elicited significant increases in the amount of work done during the 45-s ride (P less than 0.05), and also in maximal oxygen uptake (VO2 max: Pre = 4.01 +/- 0.13; Post = 4.29 +/- 0.07 1 X min-1; P less than 0.05) during exercise and total recovery VO2 (Pre = 19.14 +/- 0.09; Post = 21.45 +/- 0.10 1 X 30 min-1; P less than 0.05) after the GLET . After training blood lactate was higher, base excess lower and pH lower during and following the GLET (P less than 0.05 for all variables).(ABSTRACT TRUNCATED AT 250 WORDS)     

Detraining in the older adult: effects of prior training intensity on strength retention

In this study, we assessed the influence of training intensity on strength retention and loss incurred during detraining in older adults. In a previous study, untrained seniors (age = 71.0 +/- 5.0; n = 61) were randomly divided into 3 exercise groups and 1 control group. Exercise groups trained 2 days per week for 18 weeks with equivalent volumes and acute program variables but intensities of 2 x 15 repetitions maximum (RM), 3 x 9RM, or 4 x 6RM. Thirty of the original training subjects (age 71.5 +/- 5.2 years) participated in a 20-week detraining period. A 1RM for 8 exercises was obtained pre- and posttraining and at 6 and 20 weeks of detraining. The total of 1RM for the 8 exercises served as the dependent variable. Analysis of variance procedures demonstrated significant increases in strength with training (44-51%; p < 0.05), but no group effect. All training groups demonstrated significant strength decreases at both 6 and 20 weeks of detraining independent of prior training intensity (all group average 4.5% at 6 weeks and 13.5% at 20 weeks; p < 0.04). However, total-body strength was significantly greater than pretraining values after the detraining period (all group average 82% at 6 weeks and 49% at 20 weeks; p < 0.001). The results suggest that when older adults participate in progressive resistance exercise for 18 weeks, then stop resistance training (i.e., detrain), strength losses occur at both 6 and 20 weeks of detraining independent of prior resistance training intensity. However, despite the strength losses, significant levels of strength are retained even after 20 weeks of detraining. The results have important implications for resistance-trained older adults who could undergo planned or unplanned training interruptions of up to 5 months.     

Estimation of the mitochondrial redox state in human skeletal muscle during exercise

The mitochondrial redox (NAD+/NADH) state can be used as a reflection of oxygen availability within the mitochondrion. Previous studies using isolated muscle preparations suggest that active muscle is not hypoxic during lactate production, whereas experiments with humans come to the opposite conclusion. Six men exercised for 5 min at 75% maximal O2 consumption (VO2max) and then at 100% VO2max to exhaustion. Ammonia, oxoglutarate (alpha-ketoglutarate), and glutamate, as well as lactate, were measured in biopsies (vastus lateralis) taken at the end of each exercise. The three former metabolites were used to determine the mass action ratio of glutamate dehydrogenase and thus were used as an estimate of the mitochondrial redox state. Muscle lactate increased (P less than 0.05) to 14.5 and 24.5 mmol/kg wet wt after 75 and 100% VO2max, respectively. At both exercise intensities, muscle ammonia rose (P less than 0.05), glutamate fell (P less than 0.05) to only 30-35% of rest levels, and oxoglutarate declined (P less than 0.05). Despite the high levels of muscle lactate accumulation, the estimated mitochondrial redox rate rose 300% (P less than 0.05) in both exercise bouts. This response should increase the activity of key oxidative enzymes and promote increased VO2. Furthermore the data do not support the concept that muscle lactate is formed because of tissue hypoxia.     

Effect of training/detraining on submaximal exercise responses in humans

Human subjects participated in a training/detraining paradigm which consisted of 7 wk of intense endurance training followed by 3 wk of inactivity. In previously sedentary subjects, training produced a 23.9 +/- 7.2% increase in maximal aerobic power (V02max) (group S). Detraining did not affect group S V02max. In previously trained subjects (group T), the training/detraining paradigm did not affect V02max. In group S, training produced an increase in vastus lateralis muscle citrate synthase (CS) activities (nmol.mg protein-1. min-1) from 67.1 +/- 14.5 to 106.9 +/- 22.0. Detraining produced a decrease in CS activity to 80 +/- 14.6. In group T, pretraining CS activity (139.5 +/- 14.9) did not change in response to training. Detraining, however, produced a decrease in CS activity (121.5 +/- 7.8 to 66.8 +/- 5.9). Group S respiratory exchange ratios obtained during submaximal exercise at 60% V02max (R60) decreased in response to training (1.00 +/- 0.02 to 0.87 +/- 0.02) and increased (0.96 +/- 0.02) after detraining. Group T R60 (0.91 +/- 0.01) was not affected by training but increased (0.89 +/- 0.02 to 0.95 +/- 0.02) after detraining. R60 was correlated to changes in CS activity but was unrelated to changes in V02max. These data support the hypothesis that the mitochondrial content of working skeletal muscle is an important determinant of substrate utilization during submaximal exercise.     

Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 +/- 1 yr; peak oxygen uptake = 50 +/- 2 ml.kg(-1).min(-1)) performed 4-6 x 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by approximately 35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining (P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained approximately 20% higher compared with baseline during detraining (P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.     

Effects of beta 1- vs. beta 1- beta 2-blockade on training adaptations in rat skeletal muscle

The effect of selective vs. nonselective beta-blockade on fast-twitch [extensor digitorum longus (EDL)] and slow-twitch [soleus (SOL)] muscle enzyme activities following endurance training were characterized. Citrate synthase (CS), lactate dehydrogenase (LDH), and beta-hydroxyacyl-CoA dehydrogenase (HAD) activities were compared in SOL and EDL muscles of trained (T), metoprolol-trained (MT), propranolol-trained (PT), and sedentary (C) rats. Following 8 wk of treadmill running (1 h/day, 5 days/wk at approximately 30 m/min), LDH activity was depressed approximately 20% (P less than 0.05) in both SOL and EDL in only the PT rats, indicating inhibition of beta 2-mediated anaerobic glycolysis. EDL CS activity was similarly elevated in all three trained groups compared with sedentary controls. In SOL muscle, however, a drug attenuation effect was observed so that CS activity was increased only in the T (P less than 0.01) and MT (P less than 0.05) groups. HAD enzyme activity was increased somewhat (P less than 0.10) in SOL muscle in only the T group, but more so (P less than 0.05) in EDL in all three trained groups. The above findings suggest a training-induced selectivity effect not only with respect to beta 1-vs. beta 1-beta 2-blockers, but also with respect to muscle fiber type.     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

Myogenin and oxidative enzyme gene expression levels are elevated in rat soleus muscles after endurance training.

The intent of this study was to determine whether endurance exercise training regulates increases in metabolic enzymes, which parallel modulations of myogenin and MyoD in skeletal muscle of rats. Adult Sprague-Dawley rats were endurance trained (TR) 5 days weekly for 8 wk on a motorized treadmill. They were killed 48 h after their last bout of exercise. Sedentary control (Con) rats were killed at the same time as TR animals. Myogenin, MyoD, citrate synthase (CS), cytochrome-c oxidase (COX) subunits II and VI, lactate dehydrogenase (LDH), and myosin light chain mRNA contents were determined in soleus muscles by using RT-PCR. Myogenin mRNA content was also estimated by using dot-blot hybridization. Protein expression levels of myogenin and MyoD were measured by Western blots. CS enzymatic activity was also measured. RT-PCR measurements showed that the mRNA contents of myogenin, CS, COX II, COX VI, and LDH were 25, 20, 17, 16, and 18% greater, respectively, in TR animals compared with Con animals (P < 0.05). The ratio of myogenin to MyoD mRNA content estimated by RT-PCR in TR animals was 28% higher than that in Con animals (P < 0.05). Myosin light chain expression was similar in Con and TR muscles. Results from dot-blot hybridization to a riboprobe further confirmed the increase in myogenin mRNA level in TR group. Western blot analysis indicated a 24% greater level of myogenin protein in TR animals compared with Con animals (P < 0.01). The soleus muscles from TR animals had a 25% greater CS enzymatic activity than the Con animals (P < 0.01). Moreover, myogenin mRNA and protein contents were positively correlated to CS activity and mRNA contents of CS, COX II, and COX VI (P < 0.05). These data are consistent with the hypothesis that myogenin is in the pathway for exercise-induced changes in mitochondrial enzymes.     

运动训练和停训对鲈鲤幼鱼游泳能力的影响

为探讨运动训练和停训对鲈鲤Percocypris pingi幼鱼运动能力的影响,将480尾(体质量为2.18g±0.12g,体长为5.33cm±0.09cm)鲈鲤幼鱼随机分为4组(每组120尾):对照组(C)、无氧训练组(An)、4BL·s^-1组(BL为体长)(H)和2BL·s^-1组(L)(H组和L组每天均训练8h),在15℃±2℃条件下持续训练30d后停训。分别在训练前(T0)、训练30d后(T30)、停训20d后(DT20)和停训50d后(DT50)测定鲈鲤幼鱼的临界游泳速度(Ucrit)和1.5Ucrit条件下的耐受时间。结果显示:(1)持续运动训练显著提高了鲈鲤幼鱼的有氧和无氧运动能力,而力竭运动训练只提高了鲈鲤幼鱼的无氧运动能力;(2)停训20d后,L组的Ucrit显著高于An组和C组,An组、H组和C组间的差异无统计学意义,而An组和H组的耐受时间仍显著高于对照组,L组和C组间的差异无统计学意义;(3)停训50d后,实验组和C组间Ucrit和耐受时间的差异均无统计学意义。因此,运动训练显著提高了鲈鲤幼鱼的有氧和无氧运动能力,但不同训练方式的提升效果及其维持时间不同。     

Effects of chronic beta-adrenergic blockade on exercise training in dogs

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of exercise on the serum concentrations of FSH, LH, progesterone, and estradiol.

The effects of 30 min of exercise (74.1 +/- 3.0% (VO2), on the responses of progesterone (P), estradiol (E2), follicle stimulating hormone (FSH), and luteinizing hormone (LH) were investigated in 10 women. With such exercise significant increments occurred in P (37.6 +/- 9.5%) and E2 (13.5 +/- 7.5%) (P less than 0.05), whereas no changes were observed in FSH and LH (p greater than 0.05). Exercise in the luteal phase and during menses provoked similar changes in P, but E2 concentrations remained unchanged when exercise occurred during menses (p greater than 0.05). With 8-11 weeks of training the menstrual cycles were quite irregular and retesting of subjects in the same phase of the cycle was not possible. Yet, when subjects were retested after training, no changes occurred in P, E2 or LH (p greater than 0.05) but a decrement did occur in FSH (p less than 0.10). Thus, heavy exercise in untrained subjects provokes significant increments in ovarian hormones, whereas no such increments are observed in trained subjects exercising at the same absolute workload.     

Aerobic training effects on maximum oxygen consumption, lactate threshold and lactate disappearance during exercise recovery of dogs

1. Dogs were submitted to an aerobic training schedule and its maximum oxygen consumption, lactate threshold and lactate concentration during recovery were compared among the following conditions: not trained (UT), after 1 month of training (T1), after 2 months of training (T2) and after detraining (DT). 2. Maximum oxygen consumption increased significantly in relation to UT condition only at T2 condition. The detraining reversed this alteration. 3. Lactate threshold when expressed as Vo2 or absolute work load increased significantly after aerobic training (T2) but did not present any alteration when it was expressed as % of Vo2 max. 4. The lactate decreasing during recovery did not differ between the four experimental conditions (after 10 min). 5. The latency time for the lactate concentration to reach the top values was reduced by aerobic training (T2).     

Plasma LDH and CK activities after 400 m sprinting by well-trained sprint runners

Blood lactate concentration and the activities of plasma LDH and CK were determined in 13 well-trained middle distance runners after a 400-m sprint. It was found that there is a significant relationship between mean velocity in the 400-m sprint and plasma CK activity (r = -0.56, P less than 0.05), but the mean sprint velocity did not correlate with peak blood lactate concentration (r = -0.09) or plasma LDH activity (r = -0.40). There was a significant negative correlation between mean sprint velocity and H type LDH isozyme activity (r = -0.66, P less than 0.05), and a significant positive correlation with M type LDH isozyme activity (r = 0.66, P less than 0.05). These results suggest that the magnitude of enzyme efflux from tissue into blood may be depressed by training, and that in well-trained sprinters plasma CK and LDH isozyme activities may be better indicators of physical training and/or physical performance than peak blood lactate or plasma LDH activities.     

Exercise training improves left ventricular contractile response to beta-adrenergic agonist.

To determine whether endurance exercise training can improve left ventricular function in response to beta-adrenergic stimulation, young healthy sedentary subjects (10 women and 6 men) were studied before and after 12 wk of endurance exercise training. Training consisted of 3 days/wk of interval training (running and cycling) and 3 days/wk of continuous running for 40 min. The training resulted in an increase in maximal O2 uptake from 41.0 +/- 2 to 49.3 +/- 2 ml.kg-1.min-1 (P less than 0.01). Left ventricular function was evaluated by two-dimensional echocardiography under basal conditions and during beta-adrenergic stimulation induced by isoproterenol infusion. Fractional shortening (FS) under basal conditions was unchanged after training (36 +/- 1 vs. 36 +/- 2%). During the highest dose of isoproterenol, FS was 52 +/- 1% before and 56 +/- 1% after training (P less than 0.05). At comparable changes in end-systolic wall stress (sigma es), the increase in FS induced by isoproterenol was significantly larger after training (13 +/- 1 vs. 17 +/- 2%, P less than 0.01). Furthermore there was a greater decrease in end-systolic dimension at similar changes in sigma es in the trained state during isoproterenol infusion (-4.6 +/- 0.1 mm before vs. -7.0 +/- 0.1 mm after training, P less than 0.01). There were no concurrent changes in end-diastolic dimension between the trained and untrained states during isoproterenol infusion, suggesting no significant changes in preload at comparable levels of sigma es.(ABSTRACT TRUNCATED AT 250 WORDS)