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Beta-adrenoceptor adaptation to endurance training.

Endurance exercise is associated with various cardiovascular adaptations, and these may include changes in sympathoadrenal activity and end-organ responsiveness to norepinephrine (NE). Because beta-adrenoceptor function is a major determinant of sympathetic responsiveness, we used the lymphocyte beta-adrenoceptor as a model to study the effects of endurance training in 19 male subjects before, during, and after preparation for a marathon race. Before the subjects trained, resting beta-adrenoceptor density was positively correlated to resting heart rate (r = 0.47, p less than 0.05) but this correlation was not evident after training. Eleven of the 19 subjects completed the 3 1/2-month training period, and mean (+/- 1 SD) resting beta-adrenoceptor density fell from 1,593 +/- 333 to 1,197 +/- 332 sites per cell (p less than 0.02) after the training period. Two weeks after cessation of training, receptor density was at pretraining values of 1,547 +/- 209 sites per cell. During training, the subjects ran two 21-km races. Each of these was associated with decreases in beta-adrenoceptor density. Our results demonstrate the episodes of endurance running result in reductions in lymphocyte beta-adrenoceptor density. We conclude that down-regulation of beta-adrenoceptors is an important component of the response to endurance training.

Adult

Echocardiographic findings in strength- and endurance-trained athletes.

Assessment of echocardiographic measurements in athletes should take into account the specific sport and the quantity and quality of training. In addition, values corrected for body dimensions, especially the active body mass, should be used rather than absolute values. All parts of the athlete's heart are enlarged and its performance increases. Highly trained endurance athletes show the most enlarged hearts. Athlete's heart can be observed in athletes of all ages including the young. However, it is rarer than generally assumed. To differentiate between physiological and pathological myocardial changes, the relationship between heart size and ergometric performance as well as the echocardiographically measured ratio between left ventricular (LV) myocardial thickness and volume are useful; the latter remains unchanged, on the whole, in endurance- and strength-trained athletes. Concentric hypertrophy cannot be induced by strength training alone; additional factors, such as hypertension, aortic stenosis, cardiomyopathy or anabolic steroid use can play an important role. When corrected for body dimensions, non-endurance-trained, e.g. strength-trained, athletes have standard heart sizes even if considerable time is devoted to training. Findings in healthy untrained persons with large body dimensions also indicate no significant difference between the increase of echocardiographic measures caused by training and that caused by growth. An LV myocardial thickness of 13mm is seldom exceeded even in the highly endurance-trained or anabolic drug-free strength trained athletes under physiological conditions. However, the echocardiographic differentiation of cardiomyopathy can be difficult if an individual is highly trained and has large body dimensions. In such cases, LV end-diastolic diameter may be up to 66 to 70mm. The upper normal value of LV muscle mass is 170 g/m2 for a physiological heart enlargement. Future areas of investigation should include: adaptative changes; of the right ventricle; differences in the regression of the athlete's heart after cessation of training; the differentiation between echocardiographic changes; in highly endurance-trained or combined strength-endurance-trained persons and pathological changes; the importance of heart size and endurance sports performance; and finally the influence of genetic factors.

Cardiomegaly

Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume.

To determine the role of preload in maintaining the enhanced stroke volume of upright exercise-trained endurance athletes after deconditioning, six highly trained subjects undergoing upright and supine bicycle ergometry were characterized before and after 3, 8 and 12 weeks of inactivity that reduced oxygen uptake by 20%. During exercise, oxygen uptake, cardiac output by carbon dioxide rebreathing, cardiac dimensions by M-mode echocardiography, indirect arterial blood pressure and heart rate were studied simultaneously. Two months of inactivity resulted in a reduction in stroke volume, calculated as cardiac output/heart rate, during upright exercise (p less than 0.005) without a significant change during supine exercise. A concomitant decrease in the left ventricular end-diastolic dimension from the trained to the deconditioned state was observed in the upright posture (5.1 +/- 0.3 versus 4.6 +/- 0.3 cm; p = 0.02) but not with recumbency (5.4 +/- 0.2 versus 5.1 +/- 0.3 cm; p = NS). There was a strong correlation between left ventricular end-diastolic dimension and stroke volume (r greater than 0.80) in all subjects. No significant changes in percent fractional shortening or left ventricular end-systolic dimension occurred in either position after cessation of training. Estimated left ventricular mass was 20% lower after 3 and 8 weeks of inactivity than when the subjects were conditioned (p less than 0.05 for both). Thus, the endurance-trained state for upright exercise is associated with a greater stroke volume during upright exercise because of augmented preload. Despite many years of intense training, inactivity for only a few weeks results in loss of this adaptation in conjunction with regression of left ventricular hypertrophy.

Adult

Resting echocardiographic parameters after cessation of regular endurance training.

Resting echocardiograms were examined in nonathletic healthy young men (controls, n = 16), in highly trained endurance athletes (n = 20), and in endurance athletes who stopped regular training (n = 40). The relative muscular wall thickness (Rel. MWTd), left ventricular internal diameters both in diastole and in systole (LVIDd, LVIDs), thus also the end-diastolic and end-systolic volumes (LVEDV, LVESV), and the stroke volume index (SVI) were greater in the endurance athletes still in training than in the nonathletes. The ejection fraction (EF), heart rate (HR), cardiac index (CI), and mean circumferential shortening velocity (Vcf) were significantly lower in the athletes. During the 60 days of detraining no change was seen in the Rel. MWTd, LVEDV, LVESV, and HR. The SVI became even greater; EF and Vcf rose up to the control level while CI exceeded it. The cardiovascular regulation is therefore assumed to undergo a peculiar shift during detraining in that a persisting cardiac enlargement and bradycardia is associated with a temporarily unstable autonomous control. This imbalance often leads to a hyperkinesis-like syndrome when an athlete stops endurance training abruptly.

Adult

Potential for strength and endurance training to amplify endurance performance.

The impact of adding heavy-resistance training to increase leg-muscle strength was studied in eight cycling- and running-trained subjects who were already at a steady-state level of performance. Strength training was performed 3 days/wk for 10 wk, whereas endurance training remained constant during this phase. After 10 wk, leg strength was increased by an average of 30%, but thigh girth and biopsied vastus lateralis muscle fiber areas (fast and slow twitch) and citrate synthase activities were unchanged. Maximal O2 uptake (VO2max) was also unchanged by heavy-resistance training during cycling (55 ml.kg-1.min-1) and treadmill running (60 ml.kg-1.min-1); however, short-term endurance (4-8 min) was increased by 11 and 13% (P less than 0.05) during cycling and running, respectively. Long-term cycling to exhaustion at 80% VO2max increased from 71 to 85 min (P less than 0.05) after the addition of strength training, whereas long-term running (10 km times) results were inconclusive. These data do not demonstrate any negative performance effects of adding heavy-resistance training to ongoing endurance-training regimens. They indicate that certain types of endurance performance, particularly those requiring fast-twitch fiber recruitment, can be improved by strength-training supplementation.

Adenosine Triphosphate

Serum hormone concentrations during prolonged training in elite endurance-trained and strength-trained athletes.

A study of 1 year was performed on nine elite endurance-trained athletes (swimmers) and on eight elite strength-trained athletes (weightlifters) in order to examine the effects of training on the endocrine responses and on physical performance capacity. The measurements for the determination of serum hormone concentrations were performed at about 4-month intervals during the course of the year. The primary findings demonstrated that during the first and most intensive training period of the year in preparing for the primary competitions similar but statistically insignificant changes were observed in the concentrations of serum testosterone, free testosterone and cortisol in both the endurance-trained and strength-trained groups. After that period the changes in hormonal response over the year were infrequent and minor. A significant (p less than 0.01) decrease occurred in the strength-trained group in serum-free testosterone during the second period, which was characterized by the highest overall amount of training. Over the entire year the concentrations of serum hormones remained statistically unaltered in both groups. Slight but statistically insignificant increases of 1.2% +/- 0.8% and 2.1% +/- 5.1% were observed in the competitive performances over the year in the endurance-trained and strength-trained groups, respectively. The present findings in the two groups of elite athletes, who differed greatly with regard to the type of physiological loading, demonstrated that the overall hormonal responses both during the most intensive and during prolonged training periods were rather similar and the infrequent small changes remained well within the normal physiological range.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise

Decreases in resting plasma beta-endorphin and depression scores after endurance training.

That endurance training changes resting plasma beta-endorphin (BE) at the same time that there are improvements in non-clinical depression was tested in medically healthy middle-aged men (40-60 years). Subjects were self-selected based on compliance into treatment (T, n = 10) and placebo (P, n = 6) groups. T attended an eight month fitness program. P had less than 50% attendance in the program. Treadmill tests at the pre and post program were used to estimate the Physical Fitness Score (PFS). The Minnesota Multiphasic Personality Inventory (MMPI) was used to measure depression. All psychological scores were within non-pathological, normal limits. BE was measured with the subjects fasting and resting in the early morning. BE, detected by radioimmunoassay, decreased (p less than .005) from pre 48.53 +/- 3.32 (SE) to post 31.73 +/- 4.43 pg/ml in T. The MMPI depression score also decreased in T (p less than .05) from pre 58.90 +/- 2.81 (SE) to post 53.20 +/- 1.48 T-score units. In contrast, the PFS increased in T (p less than .005) from pre 254.57 +/- 18.62 (SE) to post 304.94 +/- 15.95 PFS units. No pre to post program changes were detected in P. In conclusion, endurance training of eight months duration appeared to decrease the resting plasma BE concentrations and the MMPI depression scores of the middle-aged men in the present study.

Depression

Endurance training and human alpha 2-adrenergic receptors on platelets.

Trained endurance athletes have a smaller rise in blood pressure, heart rate, and catecholamine response to stress when compared to an untrained, control population. Since pre-synaptic alpha 2-adrenergic receptors modulate the control of epinephrine release from nerve terminals, and since platelets are used as models of monoaminergic neurons, we investigated changes in the number and affinity binding of alpha 2-adrenergic receptors on platelets from endurance athletes and a sedentary population using the radiolabeled ligand yohimbine. We found, compared to a control, sedentary population, trained athletes had a 45% increase in the number of platelet alpha 2-adrenergic receptors (338 +/- 39 receptors/platelet vs 233 +/- 25 receptors/platelet, P less than 0.05) with no change in the dissociation constant (2.53 nM +/- 0.2 vs 2.24 nM +/- 0.2, NS) or the ED50 concentration for the competitive displacement of 2.5 nM yohimbine by epinephrine (2.8 X 10(-6) M vs 3.34 X 10(-6) M, NS). The increase in alpha 2-adrenergic receptors found in athletes may explain their decreased catecholamine response and concomitant physiologic responses to exertion.

Adult

Effects of respiratory muscle endurance training on ventilatory and endurance performance of moderately trained cyclists.

This study examined the effects of respiratory muscle endurance training (RMET) on ventilatory and endurance performance among moderately trained, male cyclists. Nine subjects initially completed two cycling VO2 max tests, two endurance cycling tests for time at 95% VO2 max, a 15-s MVV test, and an endurance breathing test for time at 100% MVV. Four subjects then underwent 3 weeks of strenuous RMET while five served as controls. Mean posttest 15-s MVV and endurance breathing time were significantly higher in the RMET group (243 +/- 14 l X min-1 and 804 +/- 94 s) than in the control group (205 +/- 6 l X min-1 and 48 +/- 8 s). No significant group differences in VO2 max or endurance cycling time at 95% VO2 max were observed following RMET. Results of this exploratory study indicated that RMET improved ventilatory power and endurance, but did not alter VO2 max or endurance cycling performance among moderately trained, male cyclists.

Adult

The influence of short-term endurance training on maximum oxygen uptake, submaximum endurance and the ability to perform brief, maximal exercise.

The hypothesis that endurance training impairs sprinting ability was examined. Eight male subjects undertook a 30-s sprint test on a cycle ergometer before and after 6 weeks of cycling training for endurance. Maximum oxygen uptake (VO2 max) and submaximum endurance were determined to evaluate the influence of the training regimen on endurance performance. Endurance was defined as the time to exhaustion at a relative exercise intensity of 85% VO2 max. Maximum oxygen uptake was increased by 18% post-training (3.29 +/- 0.29 1 min-1 versus 3.89 +/- 0.49 1 min-1; P less than 0.01), but endurance at the same absolute work rate as pre-training was increased by more than 200% (32.2 +/- 11.4 min versus 97.8 +/- 27.3 min; P less than 0.01). These improvements were accompanied by changes in the cardiovascular and metabolic responses to standard, submaximum exercise. Despite the improvements in endurance, neither performance during the cycle sprint test nor the increase in blood lactate concentration during the sprint was influenced by endurance training. For short-term cycling training, these findings reinforce the concept of training specificity whilst demonstrating that decrements in sprint performance are not a necessary consequence of improved endurance.

Adult

Aerobic capacity estimated by exercise vs cold-exposure: endurance training effects in rats.

Two widely used measures of aerobic capacity, the maximal rate of oxygen consumption elicited by exercise (VO2max(ex)) and that induced by cold-exposure (VO2max(cold)), were compared before and after a six-week endurance training period in rats. A laddermill was used to elicit by running VO2max(ex) in a few attempts without training. Endurance training was incremented to achieve 85% of the weekly measured VO2max(ex) during the 25 min/day, 5 days/week sessions. Additional rats were left untrained either as controls or for weekly VO2max(ex) measurement. Mean VO2max(ex) was significantly greater by 34% and 20% (VO2max(ex)Mb, 29% and 9%) in the trained and weekly run groups, respectively, but no differences were found in either VO2max(cold) or body mass. Both training and the measurement of VO2max by exercise were sufficient to elevate VO2max(ex) but the enhancement of cold-exposure VO2 reported by others after endurance training was not apparent in VO2max(cold). Thus, the thermogenically-based VO2max(cold) did not reflect the adaptation to endurance training shown by exercise-elicited VO2max. We conclude that VO2max(ex) and VO2max(cold) cannot be used interchangeably as measures of aerobic capacity.

Animals

Reflex venomotor responses to lower body negative pressure following endurance training.

The effect of endurance training on reflex venomotor control during an orthostatic challenge was investigated in 11 sedentary male volunteers. An exercise (E) group (n = 6) underwent 12 weeks of endurance exercise training, whereas a control (C) group (n = 5) remained sedentary. Training significantly increased VO2max values in E (pre-training: 37.0 +/- 2.5 ml.kg-1.min-1; post training: 44.6 +/- 2.5 ml.kg-1.min-1), while C showed no significant change. During exposures to two levels of lower body negative pressure (-10 and -40 mm Hg), both C and E groups showed similar graded decreases in forearm venous volume (FVV). The magnitude of the FVV decreases did not differ between groups or when comparing pre-training and post-training values. We conclude that the reflex venoconstrictor response to LBNP was not affected by endurance training.

Adult

Attenuation of postexercise ketosis in fasted endurance-trained rats.

Endurance-trained animals and human subjects have been reported to exhibit a lesser degree of postexercise ketosis than nontrained controls. We have studied the mechanism of this adaptation. Trained (2 h/day, 6 wk) and nontrained rats were fasted overnight and then run at 16 m/min up a 15% grade for 90 min. Trained rats had lower blood 3-hydroxybutyrate during exercise and during a 90-min postexercise period than nontrained rats. Liver malonyl coenzyme A (CoA), carnitine, and glycogen were not significantly different in the two groups at any time during and after exercise. Therefore these factors cannot be responsible for the difference in ketonemia. Plasma free-fatty acids and hepatic adenosine 3',5'-cyclic monophosphate were elevated in nontrained rats with respect to trained rats. These two differences could conceivably be responsible for a different ketogenic rate. In addition, 3-ketoacid CoA transferase activity of gastrocnemius muscle was increased by training. The increase in ketone oxidizing enzymes of muscle may also be partially responsible for the training-induced attenuation of postexercise ketonemia in these fasted rats.

3-Hydroxybutyric Acid

A laboratory running test: metabolic responses of sprint and endurance trained athletes.

A laboratory-based sprint running test has been devised to examine the performance characteristics and metabolic responses of an individual to 30 seconds of maximal exercise. A non-motorised treadmill was used so that the individual was able to sprint at his own chosen speed and also to vary his speed as fatigue occurred. The treadmill was instrumented so that the chosen speeds as well as the equivalent distance travelled could be monitored by micro-computer throughout the test. The test-retest reliability of the procedure was investigated with 14 recreational runners who performed the test on different days. A good correlation (r = 0.93) was found between the values obtained for peak running speeds on the two occasions. In an attempt to establish whether or not this test could be used to identify the differences in the performance characteristics of highly trained individuals, the responses to the test of eleven sprint trained and eleven endurance trained athletes were examined. The sprint trained athletes covered a greater distance (162.2 +/- 5.95 m vis 153.51 +/- 12.32 m; p less than 0.01) and had higher blood lactate concentrations (16.52 +/- 1.23 mM vis 12.98 +/- 1.77 mM; p less than 0.01) than the endurance trained athletes. Therefore this laboratory sprint running test offers an additional way of investigating human responses to brief periods of high intensity exercise.

Adult

Heart and plasma atrial natriuretic peptide (ANP) in response to long-term endurance training in rats.

Long-term endurance training effects on heart and plasma ANP were investigated in male Wistar rats. Maximal O2 uptake (VO2max) was significantly higher in trained groups, when they are used as their own control. After 3, 4, and 5 weeks of endurance training, VO2max was respectively increased by 7.7% (p less than 0.05), 13.7% (p less than 0.01), and 18.4% (p less than 0.001). Plasma ANP and glomerular ANP receptor density showed no clear variations in trained rats. However, cardiac ANP content decreased significantly in left and right atrial tissues by 35-36% (p less than 0.05) after 5 weeks of training. ANP immunoreactivity was investigated to show the distribution of ANP within the atria. ANP was found in diffuse and granular forms. The diffuse pattern (immature ANP) disappeared in cardiocytes of trained rats, while the granular form persisted, especially in the left atrial tissue. These data suggest that chronic endurance training might cause a decrease in ANP synthesis with no change in ANP storage. Such results are in agreement with the hypothesis that the left atrium could be especially involved in long-term fluid volume control.

Animals

Hormone and bone mineral status in endurance-trained and sedentary postmenopausal women.

Serum hormone levels and bone mineral status were studied in 18 sedentary and 15 endurance-trained postmenopausal women (mean age, 62 yr). The endurance-trained women had lower body weight, lower body fat, and higher aerobic capacity than the sedentary women (P less than 0.05). There were no differences in current calcium intake between the 2 groups, as assessed by a 7-day food record, but carbohydrate intake (grams per kg BW) was higher in the endurance-trained women (P less than 0.001). Bone mineral density (BMD) of the spine (L1-L3), proximal femur, and radius did not differ between the 2 groups; however, when normalized for body weight, the BMDs of the spine and radius were higher in the endurance-trained than in the sedentary women. Serum estrone and PTH levels were lower, and 1,25-dihydroxyvitamin D and somatomedin-C levels were higher in the endurance-trained than in the sedentary women. Serum GH tended to be higher in the endurance-trained than in the sedentary women (P = 0.08), and there was a postexercise increase in serum GH in the endurance-trained, but not in the sedentary, women (P less than 0.01). The major effect of habitual exercise was on body weight and hormone status. Although leanness and low serum estrone levels are risk factors for osteoporosis, these were not associated with lower BMD in endurance-trained women. Endurance-trained women may have improved calcium absorption as a result of higher carbohydrate intake and higher serum 1,25-dihydroxyvitamin D levels.

Adult

Anabolic steroids alter the haemodynamic effects of endurance training and deconditioning in rats.

The haemodynamic effects of endurance training with or without anabolic steroid treatment (nandrolone decanoate, 5.0 mg kg-1 week-1) were studied before and after a six-week sedentary period in anaesthetized, open-chest rats during isoproterenol and CaCl2 loads. In comparison to the control group (CG I, n = 13) endurance training (TG I, n = 10) increased the resting stroke index significantly, end-diastolic pressure and during CaCl2 infusion the end-diastolic and end-systolic volumes. Peripheral resistance decreased in TG I during both inotropic loads but increased in CG I (P less than 0.01 between the groups). After combined endurance training and anabolic steroid treatment (TSG I, n = 16) the haemodynamic state was similar to that in CG I except peripheral resistance which was even higher than in CG I. The heart weight to body weight ratio was significantly greater both in TG I and TSG I than in CG I. After a six-week deconditioning period the haemodynamic values were essentially similar in endurance trained (TG II, n = 10) and in control rats (CG II, n = 12). After the sedentary period, in the simultaneously trained and anabolic steroid-treated group (TSG II, n = 13) stroke index and end-diastolic volume decreased more during isoproterenol load when compared with TG II or CG II (P less than 0.05 between the groups). Peripheral resistance was higher in the TSG II than in the two other groups. In conclusion, the enhanced pumping performance of the heart by increased left ventricular diastolic filling after endurance training is attenuated by simultaneous anabolic steroid treatment which further increases the peripheral resistance. Detraining reversed the main training effects in six weeks and simultaneous anabolic steroid treatment led to a decreased left ventricular filling and to elevated peripheral resistance after the sedentary period.

Anabolic Agents

The cardiovascular effects of deconditioning after endurance training in rats.

The haemodynamic effects of endurance training and physical deconditioning were studied in anaesthetized rats using aortic and left ventricular pressure recordings and volume measurements by thermodilution method during isoproterenol and CaCl2 loads. The resting stroke volume was significantly larger in the training group (TG I, n = 10) than in the control group (CG I, n = 13). During the CaCl2 infusion stroke index, end-diastolic and end-systolic volumes increased in the TG I, but decreased in the CG I. Both isoproterenol and CaCl2 decreased systemic vascular resistance in the TG I, but increased it in the CG I. After a six-week deconditioning following training period (TG II, n = 10) stroke index, end-diastolic and end-systolic volumes decreased during CaCl2 and isoproterenol infusions similarly to the control deconditioning group (CG II, n = 12). These responses differed significantly from those observed in the TG I. Peripheral resistance increased in both the CG II and the TG II. Cardiac hypertrophy observed during training was partly reversed after the deconditioning period. In conclusion, endurance training improves the pumping performance of the rat heart by enhancing the diastolic filling of the left ventricle and decreasing peripheral resistance during inotropic load. Left ventricular contractility is not affected. A six-week deconditioning period after endurance training returns the haemodynamic changes to sedentary levels.

Animals