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.

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.

One of the most debilitating effects of primary aging is the decline in aerobic exercise capacity. One of its causes is an age-related decline in peak exercise stroke volume. This study's main purpose was to determine the cardiovascular adaptations to aging that most influence peak exercise stroke volume in the elderly. We hypothesized that increased left ventricular (LV) filling and mild concentric LV remodeling would be associated with an increase in peak exercise stroke volume corrected for lean body mass (LBM) and that an increased augmentation index (AI), which is a marker of arterial stiffness, would be associated with a decrease. A second aim was to determine the adaptations to aging that most influence LV concentric remodeling in the elderly. We hypothesized that AI would be a predictor of LV mass/LBM and the LV posterior wall thickness-to-LV radius ratio (h/r). We performed a cross-sectional study of cardiac and vascular adaptations to aging in 52 sedentary, elderly subjects. LV filling [as measured by the early-to-late transmitral flow velocity ratio (E/A)] was inversely correlated with and was an independent predictor of peak exercise stroke volume/LBM and was also a predictor of LV remodeling. AI was a predictor of LV remodeling (LV mass/LBM) but not of peak exercise stroke volume/LBM. We conclude that 1) maintenance of LV filling (E/A <1) is associated with a higher peak exercise stroke volume/LBM in very elderly subjects and thus may be a useful adaptation that enhances stroke volume during peak exercise, 2) LV remodeling and AI are less influential on peak exercise stroke volume/LBM, and 3) AI was the most important predictor of LV remodeling.

To determine the mechanisms underlying increased aerobic power in response to exercise training in octogenarians, we studied mildly frail elderly men and women randomly assigned to an exercise group (n = 22) who participated in a training program of 6 mo of physical therapy, strength training, and walking followed by 3 mo of more intense endurance exercise at 78% of peak heart rate or a control sedentary group (n = 24). Peak O2 consumption (V(O2 peak)) increased 14% in the exercise group (P < 0.0001) but decreased slightly in controls. Training induced 14% increase (P = 0.027) in peak exercise cardiac output (Q), determined via acetylene re-breathing, and no change in arteriovenous O2 content difference. The increase in Q was mediated by increases in heart rate (P = 0.009) and probably stroke volume (P = 0.096). Left ventricular stroke work also increased significantly. In the men, the increase in V(O2 peak) was exclusively due to a large increase in peak Q (22%). In the women, the gain in V(O2 peak) was due to small increases in Q and O2 extraction from skeletal muscles. Pulse pressure normalized for stroke volume and arterial elastance during peak effort did not change with training. Controls showed no changes. The results suggest that, although frail octogenarians have a diminished capacity for improvement in aerobic power in response to exercise training, this adaptation is mediated mostly by an increase in Q during peak effort. Furthermore, Q likely plays a greater role in the adaptive increase in V(O2 peak) in old men than old women.

BACKGROUND:Epidemiologic studies suggest that estrogen replacement therapy (ERT) is protective against vascular disease. ERT confers this benefit by lowering lipid levels and improving arterial function. However, its effect on the microvasculature in vivo is unknown. Thus the purposes of this study were to evaluate effect of estrogen status on the hyperemic response of the microvasculature in vivo in postmenopausal women and to compare the hyperemic response of the microvasculature in postmenopausal women taking ERT with that of premenopausal women.METHODS:We measured forearm microvasculature flow velocity by using a laser Doppler in a cross section of 64 healthy premenopausal and postmenopausal women 23 to 72 years old. Microvasculature blood flow velocity was measured at baseline. throughout 2 minutes of ischemia, and immediately after the ischemic period was terminated (i.e., during the peak hyperemic response).RESULTS:The peak of the hyperemic flow velocity (PHFV) in the postmenopausal women who were taking long-term ERT at usual doses was greater than that of postmenopausal women who were not currently taking ERT (p < .0001). Moreover, the PHFV of postmenopausal women taking ERT was similar to that of premenopausal women. Multivariate regression analysis showed estrogen status and baseline flow velocity to be independent predictors of PHFV.CONCLUSIONS:Current, long-term ERT at usual replacement doses is associated with improved microvascular responses in postmenopausal women, which may explain some of its beneficial vascular effects.

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.

BACKGROUND:It is not known whether exercise training can induce a reduction of blood pressure (BP) and a regression of left ventricular hypertrophy (LVH) in older hypertensive subjects. This study was designed to determine whether endurance exercise training, by lowering BP, can induce regression of LVH and left ventricular (LV) concentric remodeling in older hypertensive adults.METHODS:We studied 11 older adults with mild to moderate hypertension (BP 152.0 +/- 2.5/91.3 +/- 1.5 mm Hg, mean +/- SE), 65.5 +/- 1.2 years old, who exercised for 6.8 +/- 3.8 months. Seven sedentary hypertensive (BP 153 +/- 3/89 +/- 2 mm Hg) subjects, 68.5 +/- 1 years old, served as controls. LV size and geometry and function were assessed with the use of two-dimensional echocardiography.RESULTS:Exercise training increased aerobic power by 16% (p < .001), and it decreased systolic (p < .05) and diastolic (p < .05) BP, LV wall thickness (from 12.8 +/- 0.4 mm to 11.3 +/- 0.3 mm; p < .05), and the wall thickness-to-radius (h/r) ratio (from 0.48 +/- 0.02 to 0.41 +/- 0.01; p < .05). There were no significant changes in the controls. The changes in LV mass index (deltaLVMI) were different between the two groups. LV mass index decreased in the exercise group (deltaLVMI - 14.3 +/- 3.3 g) but not in the controls (deltaLVMI 1.4 +/- 4.1 g; p = .009). A multiple stepwise regression analysis showed that among clinical and physiological variables including changes in resting systolic BP, aerobic power, body mass index, and systolic BP during submaximal and maximal exercise, only the reduction in resting systolic BP correlated significantly with a regression of concentric remodeling (delta h/r ratio r = .80; p = .003). The other variables did not add to the ability of the model to predict changes in the h/r ratio.CONCLUSIONS:The data suggest that exercise training can reduce BP and induce partial regression of LVH and LV concentric remodeling in older adults with mild or moderate hypertension.

We hypothesized that abnormal endothelium-dependent vasodilation (EDD) found in older otherwise healthy subjects can be attenuated with long-term endurance training. Ten endurance-trained men, 68.5 +/- 2.3 yr old, and 10 healthy sedentary men, 64.7 +/- 1.4 yr old, were studied. Aerobic exercise capacity (VO(2 max)), fasting plasma cholesterol, insulin, and homocysteine concentrations were measured. Master athletes had higher VO(2 max) (42 +/- 2.3 vs. 27 +/- 1.4 ml. kg(-1). min(-1), P < 0.001), slightly higher total cholesterol (226 +/- 8 vs. 199 +/- 8 mg/dl, P = 0.05), similar insulin, and higher homocysteine (10.7 +/- 1.3 vs. 9.2 +/- 1.4 micromol/ml, p = 0.02) concentrations. Brachial arterial diameter, determined with vascular ultrasound, during the hyperemic response was greater in the master athletes than in controls (P = 0.005). Peak vasodilatory response was 109.1 +/- 2 vs. 103.6 +/- 2% (P < 0.05) in the athletes and controls, respectively. Endothelium-independent vasodilation in response to nitroglycerin was similar between the two groups. The increased arterial diameter during the hyperemic response correlated significantly with the VO(2 max) in the entire population (r = 0.66, P < 0.002). Our results suggest that long-term endurance exercise training in older men is associated with systemic enhanced EDD, which is even detectable in the conduit arteries of untrained muscle.

To determine whether endurance exercise training can alter the beta-adrenergic-stimulated inotropic response in older women, we studied 10 postmenopausal healthy women (65.4 +/- 0.9 yr old) who exercised for 11 mo. Left ventricular (LV) function was evaluated with two-dimensional echocardiography during infusion of isoproterenol after atropine. Maximal O(2) consumption increased 23% in response to training (from 1.35 +/- 0.06 to 1.66 +/- 0.07 l/min; P = 0.004). Training had no effect on baseline LV function, end-diastolic diameter, LV wall thickness, or LV mass. The increase in LV systolic function in response to isoproterenol was unaffected by training. Furthermore, neither the systolic shortening-to-end-systolic wall stress relationship nor the end-systolic wall stress-to-end-systolic diameter relationship during isoproterenol infusion changed with training. We conclude that older postmenopausal women can increase their maximal O(2) consumption with exercise training without eccentric LV hypertrophy or enhancement of beta-adrenergic-mediated LV contractile function. These observations provide an explanation for the finding that maximal cardiac output and stroke volume are not increased in older women in response to training.

We studied the effects of age and gender on cardiovascular responses to beta-adrenergic stimulation with the use of two-dimensional echocardiography in 16 young (aged 20-31) and 20 older (aged 60-75) healthy individuals. Following administration of atropine, each subject was given an infusion of isoproterenol at incremental doses from 0.010 to 0.030 microgram kg-1 min-1. The slopes of the fractional shortening-end-systolic wall stress (FS-sigma es) relationships were steeper in the young men (-0.87 +/- 0.28, n = 8) compared to the older men (-0.41 +/- 0.13, n = 10), and in the young women (-0.55 +/- 0.14, n = 8) compared to the older women (-0.38 +/- 0.13, n = 10). Furthermore, the magnitude of the age-associated differences in these slopes was larger in the men (old vs young) than in the women (old vs young) which, in the absence of changes in preload, suggests a greater decline in the contractile response to isoproterenol with advancing age in men compared to women. Furthermore, the men exhibited a greater attenuation of chronotropic response to isoproterenol than did the women. These observations suggest that gender plays a significant role in the age-associated decline in inotropic and chronotropic responses to beta-adrenergic stimulation, with men exhibiting a greater decline with aging than women.

BACKGROUND:The age-associated impairment in left ventricular (LV) systolic function appears to be mostly detectable during exercise or sympathetic stimulation. We hypothesized that the decline in cardiac function could be unmasked by an acute increase in afterload induced by phenylephrine. We further sought to examine whether the deterioration in cardiac function is influenced by gender.METHODS:We studied 17 young (20-31 years old) and 21 older healthy subjects (60-75 years old) who were given infusions of incremental doses of phenylephrine following cardiac muscarinic receptor blockade with atropine. Left ventricular systolic function was assessed with 2-D echocardiography.RESULTS:The young subjects exhibited a paradoxical increase in heart rate in response to alpha-adrenergic stimulation, but the older subjects did not (p < .01). The increase in systolic blood pressure in response to phenylephrine was influenced by age and gender (i.e., greater in the younger men and older women), whereas the increase in diastolic blood pressure was greater in the younger than the older subjects of both sexes. The changes in LV end-diastolic diameter with phenylephrine were unaffected by age or gender. The slope of the systolic shortening-end systolic wall stress relationship was significantly steeper in the older subjects, suggesting a decline in the contractile response to an acute increase in afterload with aging.CONCLUSIONS:This study's findings suggest that age can significantly influence the cardiovascular responses to alpha-adrenergic stimulation and that phenylephrine, by acutely increasing afterload, is effective in unmasking the age-associated deterioration in left ventricular systolic function. Further, it appears that the increase in systolic blood pressure in response to an alpha-adrenergic challenge is significantly influenced not only by age but also by gender.

1943 The effects of aging on the cardiovascular system have been well characterized in men. However, data on the effects of aging on the oxygen transport capacity of the cardiovascular system are lacking in women. Therefore, the present study was designed to characterize the effects of age on maximal O2 uptake (VO2max), cardiac output (Q max) and the arterio-venous O2 content difference (a-v O2 diff) in women 60 to 90 yrs of age. Fifty two elderly women (eld) 83 ± 4.4 (mean ± SD) yrs of age and 42 women 64 ± 4 yrs (YO) of age participated in this study. VO2 max was measured during treadmill exercise. Q max was assessed during treadmill exercise with the use of the acetylene rebreathing procedure. VO2 max was 35% lower in the elderly women (0.89 ± 0.20 L/min vs 1.36 0.0.20 L/min; p<0.01) compared to the YO group of women. The lower VO2 max was mediated predominately by a decrease in Qmax, 8.6 ± 1.90 L/min in the elderly group vs 11.4 ± 1.65 L/min in the YO group (p<0.01). A 20% decline in peak heart rate 127 ± 18 bpm in the eld group vs 159 ± 13 in the YO group (p<0.01) accounted for most of the decline in Q group. The a-v O2 diff decreased 12% in the elderly group compared to YO group (12.0 ± 1.7 mL O2/100 mL of blood vs 10.6 ± 2.2 mL O2/100 mL of blood; p<0.05). The results suggest that the decline in VO2 max in women between the ages of 60-90 is due predominately to a decrease in Q max and to a lesser extent in the a-v O2 diff. Supported by NIH grants AG-13629, AG-12235 and AG-05562

772 To determine whether endurance exercise training resulted in any improvements in the in left ventricular (LV) contractile responses to afterload stress, seven men were studied (26.1 ± 1.1 yrs; mean ± SE) before and after a 12-week exercise program. VO2max was measured(Pretraining: 47.0 ± 2.8 ml/kg·min, posttraining: 55.4 ± 3.2 ml/kg·min; p<0.01) during treadmill exercise. LV performance was evaluated by 2D-echocardiography. Subjects were given phenylephrine at graded doses (0.25 to 1.00 μg/kg·min) following the measurement of baseline at supine rest. Although heart rate did not exhibit any training-related differences in response to phenlyephrine, systolic and diastolic blood pressure were greater after training during the last 3 infusion stages. Training did not alter the LV end-systolic dimension response to increasing doses of phenylephrine in men. Training resulted in a lesser decrease in LVFS at a given increase in LVσes (slopes = -0.17 ± 0.07 vs. -0.05± 0.01; p<0.01). These results suggest that 12 weeks of aerobic training increases pressor responses to phenylephrine and improves the LV performance to afterload stress in young men.

To test the hypothesis that the training-induced improvement in the age-related decline in left ventricular (LV) function is mediated by enhanced inotropic responses to β-adrenergic stimulation, 10 sedentary healthy men, 65 ± 1 yr (mean ± SE) of age, exercised for 9 mo, which resulted in a 28% increase in aerobic exercise capacity. Training induced a greater increase in LV systolic shortening, assessed with two-dimensional echocardiography, in response to isoproterenol with a steeper slope of the fractional shortening-end-systolic wall stress (ςes) relationship and an upward shift of the ςes-systolic diameter relationship without an acute increase in heart rate or preload. The increase in the early-to-late diastolic flow velocity ratio, normalized for heart rate and preload, in response to isoproterenol was larger after training. LV systolic reserve and cardiac output during peak exercise were higher after training. β-Adrenergic blockade with esmolol HCl abolished the adaptive increases in LV systolic reserve capacity and cardiac output during peak exercise in the trained state. The results suggest that one of the underlying mechanisms responsible for the adaptive increase in LV systolic function in response to exercise training is an enhanced inotropic sensitivity to catecholamines. Furthermore, the enhanced inotropic responses are associated with increased diastolic filling.

OBJECTIVE: For the purpose of prescribing exercise intensity, the American College of Sports Medicine (ACSM) provides guidelines for relating the perceived level of exertion and the heart rate (HR) response during exercise, expressed either as a percentage of maximal HR or of HR reserve, to a percentage of maximal aerobic power (VO2max). However, because maximal HR and V̇O2max decline with age, it is possible that these guidelines are not appropriate for an older population. The purpose of this study was to evaluate in 60‐to 72‐year‐old women the relationships among the common methods of prescribing exercise intensity.DESIGN: Participants were 112 healthy but sedentary women, aged 66 ± 4 years, who performed treadmill walking at four speeds.SETTING: Subjects were recruited from the community, and exercise tests were performed at a university laboratory facility.MEASUREMENTS: V̇O2max and maximal HR were determined during treadmill walking. The HR and V̇O2 responses to walking 6 minutes at each of four speeds ranging from 67 to 107 m/min, along with ratings of perceived exertion (RPE) and plasma lactate levels, were determined on a separate day.RESULTS: The exercise bouts required an average of 55 ± 10%, 64 ± 12%, 77 ± 12%, and 91 ± 9% of V̇O2max. Corresponding HR values were 64 ± 8%, 70 ± 9%, 81 ± 10%, and 92 ± 7% of maximal HR, and they were within the expected ranges based on ACSM guidelines. HR values as a percentage of HR reserve were much lower than expected based on the guidelines. RPE values were lower than expected at a given %V̇O2max, and plasma lactate levels were also relatively low, suggesting that older women are able to exercise at a higher percentage of V̇O2max than levels currently recommended.CONCLUSIONS: The results indicate that HR expressed as a percentage of maximal HR is an appropriate method of prescribing exercise intensity in healthy, sedentary 60‐ to 72‐year‐old women. The HR reserve method is not recommended in this population because it will likely result in the exercise being performed at a higher than expected percentage of V̇O2max.

This study was designed to characterize cardiac adaptations to endurance exercise training in older healthy men by evaluation of changes in left ventricular function in response to an afterload stress in the presence of cardiac muscarinic receptor blockade. Eight men 65 +/- 2 (SE) yr old underwent 9 mo of endurance exercise training. Maximal O2 uptake (V(O2 max)) was determined during treadmill exercise. Left ventricular function was assessed with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile at baseline, after an intravenous bolus of atropine and during infusion of graded doses of phenylephrine. V(O2 max) was increased by 29% in response to training (28.9 +/- 1 to 37.3 +/- 1 ml x kg(-1) x min(-1)). Baseline end-diastolic diameter (EDD) was increased, with no change in left ventricular wall thickness-to-radius ratio, after training, suggestive of eccentric left ventricular hypertrophy. EDD, end-systolic dimension, and end-systolic wall stress (sigma(es)) increased similarly in response to phenylephrine before and after training. Fractional shortening (FS) decreased in response to phenylephrine before but not after training. When the changes in FS (delta FS) during phenylephrine infusion were plotted as a function of changes in sigma(es), delta FS were significantly higher after than before training (P = 0.003) at comparable increases in sigma(es), indicative of improved contractile function. This adaptive response was preload independent, because EDD did not differ between the trained and untrained states during phenylephrine infusion. Heart rate responses to phenylephrine were similar before and after training. Exercise training resulted in a higher (P = 0.028) early-to-late transmitral diastolic flow velocity ratio at virtually identical heart rates, suggestive of improved diastolic filling. The results suggest that endurance exercise training induces an enhancement of left ventricular systolic function in response to an afterload stress in older healthy men.

To determine the effects of aging on the cardiovascular sensitivity toβ-adrenergic stimulation, we assessed the cardiovascular responses to graded doses of isoproterenol (ISP) in 8 young (25 ± 1 yrs, mean± SE) and 9 older, healthy men (65 ± 2 yrs). All subjects were carefully screened for cardiovascular diseases. VO2max was measured(young: 46.7 ± 0.7 ml/kg·min, older: 28.0 ± 1.0 ml/kg·min; p<0.01) during treadmill exercise. LV performance was evaluated by 2D-echocardiography and pulsed Doppler profile. Subjects received graded doses of ISP (0.01 to 0.03 μg/kg·min) following vagal blockade by atropine. LV dimensions, heart rate (HR), systolic and diastolic blood pressures were not different between the two groups at baseline or in response to atropine. The young men exhibited a greater increase in LV fractional shortening (FS, 21.1 ± 1.1 vs. 12.3 ± 3.9%, p<0.01) and HR (50.5 ± 5.6 vs. 30.5 ± 3.9 bpm) in response to ISP compared to the older men. Both groups showed an inverse linear relationship (r=0.934 ± 0.019) between FS and end-systolic wall stress. Young men elicited a greater increase in LVFS at a given decrease in LV end-systolic wall stress (slopes = -0.74 ± 0.09 vs. -0.40 ± 0.05; p<0.01). In addition, LV filling dynamics corrected for HR and end-diastolic dimension were impaired in the older men. These findings suggest that older men exhibit a decline in LV systolic and diastolic performance, compared to young men, in response to β-adrenergic stimulation.

We hypothesized that 10 days of training would enhance cardiac output (CO) and stroke volume (SV) during peak exercise and increase the inotropic response to beta-adrenergic stimulation. Ten subjects [age 26 +/- 2 (SE) yr] trained on a cycle ergometer for 10 days. At peak exercise, training increased O2 uptake, CO, and SV (P < 0.001). Left ventricular (LV) size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training (P < 0.02), whereas LV wall thickness was unchanged. LV contractile performance was assessed by relating fractional shortening (FS) to the estimated end-systolic wall stress (sigmaES). Training increased the slope of the FS-sigmaES relationship (P < 0.05), indicating enhanced systolic function. The increase in slope correlated with increases in CO (r = -0.71, P < 0.05) and SV (r = -0.70, P < 0.05). The increase in blood volume also correlated with increases in CO (r = 0.80, P < 0.01) and SV (r = 0.85, P < 0.004). These data show that 10 days of training enhance the inotropic response to beta-adrenergic stimulation, associated with increases in CO and SV during peak exercise.