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)     

Comparison of effects of exercise and diuretic on left ventricular geometry, mass, and insulin resistance in older hypertensive adults

To compare the effects of exercise training and hydrochlorothiazide on left ventricular (LV) geometry and mass, blood pressure (BP), and hyperinsulinemia in older hypertensive adults, we studied 28 patients randomized either to a group (age 66.4 +/- 1.3 yr; n = 16) that exercised or to a group (age 65.3 +/- 1.2 yr; n = 12) that received hydrochlorothiazide for 6 mo. Endurance exercise training induced a 15% increase in peak aerobic power. The reduction in systolic BP was twofold greater with thiazide than with exercise (26.6 +/- 12.2 vs. 11.5 +/- 10.9 mmHg). Exercise and thiazide reduced LV wall thickness, LV mass index (14% in each group), and the LV wall thickness-to-radius ratio (h/r) similarly (exercise: before 0.48 +/- 0.2, after 0.42 +/- 0.01; thiazide: before 0.47 +/- 0.04, after 0.40 +/- 0.04; P = 0.017). The reductions in systolic BP and h/r were correlated in the exercise group (r = 0.70, P = 0.005) but not in the thiazide group. Exercise training reduced glucose-stimulated hyperinsulinemia (before: 13.65 +/- 2.6 vs. 9.84 +/- 1.5 mU.ml(-1).min; P = 0.04) and insulin resistance. Thiazide did not affect plasma insulin levels. The results suggest that although exercise is less effective in reducing systolic BP than thiazide, it can induce regression of LV hypertrophy similar in magnitude to thiazide. Unlike hydrochlorothiazide, exercise training can improve insulin resistance and aerobic capacity in older hypertensive people.     

Effect of endurance exercise training on ventilatory function in older individuals

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.     

Effects of chronic and acute exercise on cardiovascular beta-adrenergic responses.

beta-Adrenergic receptor density and responsiveness may be increased in experimental animals by physical conditioning, and the opposite effects have been observed after a single bout of exercise. To determine whether the chronic and acute effects of exercise include similar alterations in cardiovascular function in humans, we characterized heart rate, blood pressure, and distal lower extremity blood flow responses to graded-dose isoproterenol infusion in 15 young healthy subjects before and after exercise training and with and without a single preceding bout of prolonged exercise of either low or high intensity (61 +/- 1 or 82 +/- 1% maximal heart rate). VO2max was increased 18% after exercise training (43.2 +/- 2.7 to 51.1 +/- 3.3 ml.kg-1.min-1; P less than 0.001). Despite a concomitant fall in resting heart rate (59 +/- 3 to 50 +/- 2 beats/min; P less than 0.001), chronotropic and lower extremity blood flow responses to isoproterenol remained unchanged. Similarly, 1 h of acute high-intensity treadmill exercise altered baseline heart rate (58 +/- 4 to 74 +/- 5 beats/min; P less than 0.02), but neither low- nor high-intensity acute exercise influenced heart rate or lower extremity blood flow responses to isoproterenol. In contrast, the systolic pressure response to isoproterenol was blunted after high- but not low-intensity prolonged exercise (P less than 0.02). These data indicate that cardiac chronotropic (primarily beta 1) and vascular (beta 2) adrenergic agonist responses are not altered in humans by training or acute exercise. The systolic blood pressure response to beta-adrenergic stimulation is decreased by a single bout of high-intensity prolonged exercise by mechanisms that remain to be defined.     

Enhanced inotropic response to dobutamine in strength-trained subjects with left ventricular hypertrophy.

To determine whether strength-trained individuals with physiological concentric left ventricular (LV) hypertrophy exhibit enhanced inotropic responses to catecholamines, we studied 11 bodybuilders, aged 33.0 +/- 2 (SE) yr old, and 10 sedentary healthy subjects, aged 31.3 +/- 2.4 yr old, at baseline and during infusion of incremental doses of dobutamine after atropine. The bodybuilders had larger LV mass, posterior wall and septal wall thicknesses, and wall thickness-to-radius ratio, assessed with two-dimensional echocardiography, than did the sedentary subjects. There was a significant correlation between LV mass and lean body mass irrespective of training status. Baseline LV fractional shortening was similar in the two groups. There was a greater inotropic response to dobutamine in the strength-trained individuals, as evidenced by a steeper slope of the fractional shortening-end-systolic wall stress relationship with a higher y-axis intercept and by a shallower end-systolic wall stress-end systolic diameter relationship without changes in end-diastolic diameter. The heart rate response to dobutamine was attenuated in the strength-trained athletes. There was a significant correlation (r = 0.604, P < 0.05) between the inotropic sensitivity to dobutamine and LV mass normalized for lean body mass in the bodybuilders. The data suggest that concentric LV physiological hypertrophy in the resistance-trained individuals is associated with enhanced inotropic but not chronotropic responses to catecholamines.     

Moderate exercise training does not worsen left ventricle remodeling and function in untreated severe hypertensive rats.

Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. This study set out to evaluate cardiac adaptations induced by moderate exercise training in normotensive and untreated severe hypertensive rats. Four groups of animals were studied: normotensive (Ctl) and severe hypertensive (HT) Wistar rats were assigned to be sedentary (Sed) or perform a moderate exercise training (Ex) over a 10-wk period. Severe hypertension was induced in rat by a two-kidney, one-clip model. At the end of the training period, hemodynamic parameters and LV morphology and function were assessed using catheterism and conventional pulsed Doppler echocardiography. LV histology was performed to study fibrosis infiltrations. Severe hypertension increased systolic blood pressure to 202 +/- 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 +/- 0.02 vs. 0.44 +/- 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alteration (early-to-atrial wave ratio = 2.02 +/- 0.11 vs. 1.63 +/- 0.12). Blood pressure was not altered by exercise training, but arterial stiffness was reduced in trained hypertensive rats (pulse pressure was 75 +/- 7 vs. 62 +/- 3 mmHg in HT-Sed and HT-Ex groups, respectively). Exercise training induced eccentric hypertrophy in both Ex groups by increasing LV cavity without alteration of LV systolic function. However, LV hypertrophy index was significantly decreased in normotensive rats only (0.34 +/- 0.02 vs. 0.30 +/- 0.02 in Ctl-Sed and Ctl-Ex groups, respectively). Moreover, exercise training improved LV passive filling in Ctl-Ex rats but not in Ht-Ex rats. In this study, exercise training did not reduce blood pressure and induced an additional physiological hypertrophy in untreated HT rats, which was slightly blunted when compared with Ctl rats. However, cardiac function was not worsened by exercise training.     

Skeletal muscle adaptations to endurance training in 60- to 70-yr-old men and women.

Previous studies of endurance exercise training in older men and women generally have found only minimal skeletal muscle adaptations to training. To evaluate the possibility that this may have been due to an inadequate training stimulus, we studied 23 healthy older (64 +/- 3 yr) men and women before and after they had trained by walking/jogging at 80% of maximal heart rate for 45 min/day 4 days/wk for 9-12 mo. This training program resulted in a 23% increase in maximal O2 consumption. Needle biopsy samples of the lateral gastrocnemius muscle were obtained before and after training and analyzed for selected histochemical and enzymatic characteristics. The percentage of type I muscle fibers did not change with training. The percentage of type IIb fibers, however, decreased from 19.1 +/- 9.1 to 15.1 +/- 8.1% (P less than 0.001), whereas the percentage of type IIa fibers increased from 22.1 +/- 7.7 to 29.6 +/- 9.1% (P less than 0.05). Training also induced increases in the cross-sectional area of both type I (12%; P less than 0.001) and type IIa fibers (10%; P less than 0.05). Capillary density increased from 257 +/- 43 capillaries/mm2 before training to 310 +/- 48 capillaries/mm2 after training (P less than 0.001) because of increases in the capillary-to-fiber ratio and in the number of capillaries in contact with each fiber. Lactate dehydrogenase activity decreased by 21% (P less than 0.001), whereas the activities of the mitochondrial enzymes succinate dehydrogenase, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase increased by 24-55% in response to training (P less than 0.001-0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

One- and two-dimensional echocardiography in bodybuilders using anabolic steroids

The object of this study was to investigate the possible concentric increase in the left ventricular (LV) wall thickness by intensive strength training and to differentiate between the specific effect of the strength training itself and the influence of anabolic drugs. In this study 21 top-level bodybuilders [users of anabolic steroids (A): n = 14; non-users (N): n = 7] underwent one-dimensional and two-dimensional echocardiography as well as a cycle ergometer test. In both groups blood pressure at rest and during ergometric exercise was within the normal range. In spite of the same amount of time being spent on training, A showed significantly better power results than N. Total heart volume (A = 11.3 +/- 0.9 ml.kg-1; N = 11.9 +/- 0.9 ml.kg-1) and LV muscle mass were almost identical in A and N and correlated significantly with body weight and lean body mass respectively. The body dimension-related diastolic LV diameter was significantly lower in A (0.567 +/- 0.062 mm.kg-1) than in N (0.639 +/- 0.040 mm.kg-1). An increase in the LV posterior wall (p less than 0.01) and septum thickness (ns) resulted in increased LV wall thickness:diameter (p less than 0.01) and LV muscle mass:volume (p less than 0.05) ratios in A (0.458 +/- 0.590; 1.38 +/- 0.25 g.ml-1) in comparison to N (0.356 +/- 0.077; 1.16 +/- 0.17 g.ml-1). The septal:posterior wall thickness ratio was similar for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of sildenafil on coronary active and reactive hyperemia

Sildenafil, a selective inhibitor of phosphodiesterase type 5, produces relaxation of isolated epicardial coronary artery segments by causing accumulation of cGMP. Because shear-induced nitric oxide-dependent vasodilation is mediated by cGMP, this study was performed to determine whether sildenafil would augment the coronary resistance vessel dilation that occurs during the high-flow states of exercise or reactive hyperemia. In chronically instrumented dogs, sildenafil (2 mg/kg per os) augmented the vasodilator response to acetylcholine, with a leftward shift of the dose-response curve relating coronary flow to acetylcholine dose. Sildenafil caused a 6. 7 +/- 2.1 mmHg decrease of mean aortic pressure, which was similar at rest and during treadmill exercise (P < 0.05), with no change of heart rate, left ventricular (LV) systolic pressure, or LV maximal first time derivative of LV pressure. Sildenafil tended to increase myocardial blood flow at rest and during exercise (mean increase = 14 +/- 3%; P < 0.05 by ANOVA), but this was associated with a significant decrease in hemoglobin, so that the relationship between myocardial oxygen consumption and oxygen delivery to the myocardium (myocardial blood flow x arterial O(2) content) was unchanged. Furthermore, sildenafil did not alter coronary venous PO(2), indicating that the coupling between myocardial blood flow and myocardial oxygen demands was not altered. In addition, sildenafil did not alter the peak coronary flow rate, debt repayment, or duration of reactive hyperemia that followed a 10-s coronary occlusion. The findings suggest that cGMP-mediated resistance vessel dilation contributes little to the increase in myocardial flow that occurs during exercise or reactive hyperemia.     

The impact of endurance exercise training on left ventricular systolic mechanics

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 +/- 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 +/- 25 vs. 144 +/- 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 +/- 550 vs. 3,260 +/- 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 +/- 51 vs. 256 +/- 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 +/- 3% vs. 60 +/- 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S'Delta = 0.9 +/- 0.6 cm/s, P = 0.004; and basal septal S'Delta = 0.8 +/- 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (DeltaRV end-diastolic area vs. DeltaLV septal CS; r2 = 0.898, P < 0.001) and function (Deltapeak RV systolic velocity vs. DeltaLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.     

Cardiovascular responses of 70- to 79-yr-old men and women to exercise training

This study determined the effects of endurance or resistance exercise training on maximal O2 consumption (VO2max) and the cardiovascular responses to exercise of 70- to 79-yr-old men and women. Healthy untrained subjects were randomly assigned to a control group (n = 12) or to an endurance (n = 16) or resistance training group (n = 19). Training consisted of three sessions per week for 26 wk. Resistance training consisted of one set of 8-12 repetitions on 10 Nautilus machines. Endurance training consisted of 40 min at 50-70% VO2max and at 75-85% VO2max for the first and last 13 wk of training, respectively. The endurance training group increased its VO2max by 16% during the first 13 wk of training and by a total of 22% after 26 wk of training; this group also increased its maximal O2 pulse, systolic blood pressure, and ventilation, and decreased its heart rate and perceived exertion during submaximal exercise. The resistance training group did not elicit significant changes in VO2max or in other maximal or submaximal cardiovascular responses despite eliciting 9 and 18% increases in lower and upper body strength, respectively. Thus healthy men and women in their 70s can respond to prolonged endurance exercise training with adaptations similar to those of younger individuals. Resistance training in older individuals has no effect on cardiovascular responses to submaximal or maximal treadmill exercise.     

Effects of strength training on muscle strength characteristics, functional capabilities, and balance in middle-aged and older women

Progressive strength training can lead to substantial increases in maximal strength and mass of trained muscles, even in older women and men, but little information is available about the effects of strength training on functional capabilities and balance. Thus, the effects of 21 weeks of heavy resistance training--including lower loads performed with high movement velocities--twice a week on isometric maximal force (ISOmax) and force-time curve (force produced in 500 milliseconds, F0-500) and dynamic 1 repetition maximum (1RM) strength of the leg extensors, 10-m walking time (10WALK) and dynamic balance test (DYN.D) were investigated in 26 middle-aged (MI; 52.8 +/- 2.4 years) and 22 older women (O; 63.8 +/- 3.8 years). 1RM, ISOmax, and F0-500 increased significantly in MI by 28 +/- 10%, 20 +/- 19%, 31 +/- 34%, and in O by 27 +/- 8%, 20 +/- 16%, 18 +/- 45%, respectively. 10WALK (MI and O, p < 0.001) shortened and DYN.D improved (MI and O, p < 0.001). The present strength-training protocol led to large increases in maximal and explosive strength characteristics of leg extensors and in walking speed, as well to an improvement in the present dynamic balance test performance in both age groups. Although training-induced increase in explosive strength is an important factor for aging women, there are other factors that contribute to improvements in dynamic balance capacity. This study indicates that total body heavy resistance training, including explosive dynamic training, may be applied in rehabilitation or preventive exercise protocols in aging women to improve dynamic balance capabilities.     

Sympathetic activity and the heterogenous blood pressure response to exercise training in hypertensives.

To test whether changes in sympathetic nervous system (SNS) activity or insulin sensitivity contribute to the heterogeneous blood pressure response to aerobic exercise training, we used compartmental analysis of [3H]norepinephrine kinetics to determine the extravascular norepinephrine release rate (NE2) as an index of systemic SNS activity and determined the insulin sensitivity index (S(I)) by an intravenous glucose tolerance test, before and after 6 mo of aerobic exercise training, in 30 (63 +/- 7 yr) hypertensive subjects. Maximal O2 consumption increased from 18.4 +/- 0.7 to 20.8 +/- 0.7 ml x kg(-1) x min(-1) (P = 0.02). The average mean arterial blood pressure (MABP) did not change (114 +/- 2 vs. 114 +/- 2 mmHg); however, there was a wide range of responses (-19 to +17 mmHg). The average NE2 did not change significantly (2.11 +/- 0.15 vs. 1.99 +/- 0.13 microg x min(-1) x m(-2)), but there was a significant positive linear relationship between the change in NE2 and the change in MABP (r = 0.38, P = 0.04). S(I) increased from 2.81 +/- 0.37 to 3.71 +/- 0.42 microU x 10(-4) x min(-1) x ml(-1) (P = 0.004). The relationship between the change in S(I) and the change in MABP was not statistically significant (r = -0.03, P = 0.89). When the changes in maximal O2 consumption, percent body fat, NE2, and S(I) were considered as predictors of the change in MABP, only NE2 was a significant independent predictor. Thus suppression of SNS activity may play a role in the reduction in MABP and account for a portion of the heterogeneity of the MABP response to aerobic exercise training in older hypertensive subjects.     

Effects of intense exercise training on plasma catecholamines in coronary patients

This paper reports the effect of 12 mo of intense endurance exercise training on the plasma catecholamine response to exercise in 11 male patients [aged 50 +/- 8 yr (mean +/- SD)] with coronary artery disease. A substantial adaptation to training was attained as evidenced by a 42% increase in maximum O2 uptake capacity. At rest, heart rate was lower after training, but resting blood pressure and plasma catecholamines were unchanged. At the same absolute work rate, plasma norepinephrine and epinephrine levels, rate pressure product, and ischemic S-T segment depression were all significantly lower after training. A higher plasma norepinephrine level was attained at maximal exercise after training (2,049 +/- 654 before vs. 3,408 +/- 1,454 pg/ml after, P less than 0.025); this was associated with a higher systolic blood pressure (175 +/- 25 before vs. 188 +/- 22 mmHg after, P less than 0.025) and a higher rate-pressure product (25.3 X 10(3) +/- 4.5 X 10(3) before vs. 27.6 X 10(3) +/- 5.2 X 10(3) after, P less than 0.025). Despite the higher plasma norepinephrine level and rate pressure product, S-T segment depression at maximal exercise was unchanged. These findings suggest that some patients with coronary arterial disease can attain a higher myocardial O2 requirement, without electrocardiographic evidence of increased ischemia, after prolonged strenuous exercise training.     

Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8-12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.     

Effect of aging on response to exercise training in humans: skeletal muscle GLUT-4 and insulin sensitivity.

The purpose of this study was to compare the effects of short-term exercise training on insulin-responsive glucose transporter (GLUT-4) concentration and insulin sensitivity in young and older individuals. Young and older women [22.4 +/- 0.8 (SE) yr, n = 9; and 60.9 +/- 1. 0 yr, n = 10] and men (20.9 +/- 0.9, n = 9; 56.5 +/- 1.9 yr, n = 8), respectively, were studied before and after 7 consecutive days of exercise training (1 h/day, approximately 75% maximal oxygen uptake). The older groups had more adipose tissue, increased central adiposity, and a lower maximal oxygen uptake. Despite these differences, increases in whole body insulin action (insulin sensitivity index, determined with an intravenous glucose tolerance test and minimal-model analysis) with training were similar regardless of age, in both the women and men (mean increase of 2.2 +/- 0.3-fold). This was accompanied by similar relative increases in muscle (vastus lateralis) GLUT-4 protein concentration, irrespective of age (mean increase of 3.1 +/- 0.7-fold). Body mass did not change with training in any of the groups. These data suggest that older human skeletal muscle retains the ability to rapidly increase muscle GLUT-4 and improve insulin action with endurance training.     

Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization

Sympathetic nervous activation is a crucial compensatory mechanism in heart failure. However, excess catecholamine may induce cardiac dysfunction and beta-adrenergic desensitization. Although magnesium is known to be a cardioprotective agent, its beneficial effects on acute cardiac dysfunction remain to be elucidated. We examined the effects of magnesium on left ventricular (LV) dysfunction induced by a large dose of isoproterenol in dogs. Sixteen anesthetized dogs underwent a continuous infusion of isoproterenol (1 micro g.kg(-1).min(-1)) with or without a magnesium infusion (1 mg.kg(-1).min(-1)). The dose response to small doses of isoproterenol (0.025-0.2 micro g.kg(-1).min(-1)) was tested hourly. A large dose of isoproterenol decreased LV systolic function, increased the time constant of LV isovolumic relaxation, and suppressed the dose response to small doses of isoproterenol in a time-dependent manner. Magnesium significantly attenuated isoproterenol-induced LV systolic and diastolic dysfunction and preserved the dose response to isoproterenol. Serum-ionized calcium significantly decreased with a large dose of isoproterenol but was fully maintained at baseline level with magnesium. A large dose of isoproterenol increased serum lipid peroxide levels and serological markers of myocardial damage, which were significantly suppressed by magnesium. In conclusion, magnesium significantly attenuated excess isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization.     

Absence of left ventricular and arterial adaptations to exercise in octogenarians.

Recent evidence suggests that octogenarians exhibit attenuated adaptations to training with a small increase in peak O2 consumption (VO2) that is mediated by a modest improvement in cardiac output without an increase in arteriovenous O2 content difference. This study was designed to determine whether diminished increases in peak VO2 and cardiac output in the octogenarians are associated with absence of left ventricular and arterial adaptations to exercise training. We studied 22 octogenarians (81.9 +/- 3.7 yr, mean +/- SD) randomly assigned a group that exercised at an intensity of 82.5 +/- 5% of peak heart rate for 9 mo and 14 (age 83.1 +/- 4.1) assigned to a control group. Peak VO2 increased 12% in the exercise group but decreased slightly (-7%) in the controls. The exercise group demonstrated significant but small decreases in the heart rate (6%, P = 0.002) and the rate-pressure product (9%, P = 0.004) during submaximal exercise at an absolute work rate. Training induced no significant changes in the left ventricular size, geometry (wall thickness-to-radius ratio), mass, and function assessed with two-dimensional echocardiography or in arterial stiffness evaluated with applanation tonometry. Data suggest that the absence of cardiac and arterial adaptations may in part account for the limited gain in aerobic capacity in response to training in the octogenarians.     

Left ventricular systolic performance during prolonged strenuous exercise in female triathletes

BACKGROUND: The effect of prolonged strenuous exercise (PSE) on left ventricular (LV) systolic function has not been well studied in younger female triathletes. This study examined LV systolic function prior to, during and immediately following PSE (i.e., 40 km bicycle time trial followed by a 10 km run) in 13 younger (29 PlusMinus; 6 years) female triathletes. METHODS: Two-dimensional echocardiographic images were obtained prior to, at 30-minute intervals during and immediately following PSE. Heart rate, systolic blood pressure, end-diastolic and end-systolic cavity areas were measured at each time point. Echocardiographic and hemodynamic measures were also combined to obtain LV end-systolic wall stress and myocardial contractility (i.e., systolic blood pressure - end-systolic cavity area relation). RESULTS: Subjects exercised at an intensity equivalent to 90 PlusMinus; 3% of maximal heart rate. Heart rate, systolic blood pressure, systolic blood pressure - end-systolic cavity area relation and fractional area change increased while end-diastolic and end-systolic cavity areas decreased during exertion. CONCLUSIONS: PSE is associated with enhanced LV systolic function secondary to an increase in myocardial contractility in younger female triathletes.