Adaptations in beta-adrenergic cardiovascular responses to training in older women.

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.

Estrogen increases hyperemic microvascular blood flow velocity in postmenopausal 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.

Effect of endurance exercise training on left ventricular size and remodeling in older adults with hypertension.

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.

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.

Enhanced endothelium-dependent vasodilation in older endurance-trained men.

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.

Effects of age and gender on the cardiovascular responses to isoproterenol.

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.

Effects of age and gender on cardiovascular responses to phenylephrine.

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.

Beta-adrenergic-mediated improvement in left ventricular function by exercise training in older 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 beta-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 (sigma es) relationship and an upward shift of the sigma es-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. beta-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.

Prescribing exercise intensity for older women.

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 VO2max 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: VO2max and maximal HR were determined during treadmill walking. The HR and VO2 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 VO2max. 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 %VO2max, and plasma lactate levels were also relatively low, suggesting that older women are able to exercise at a higher percentage of VO2max 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 VO2max.

Loss of cardiovascular adaptations after physical inactivity.

The main objective of this article is to focus on the loss of cardiovascular adaptations after cessation of exercise. A brief description of the nature of adaptive changes to chronic exercise is given to provide a background and understanding of physiologic mechanisms underlying cardiovascular adaptations to exercise training and their clinical implications.

Exercise training enhances cardiac function in response to an afterload stress in older men.

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.

Cardiovascular adaptations to 10 days of cycle exercise.

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.

Mitochondrial enzymes increase in muscle in response to 7-10 days of cycle exercise.

Endurance exercise training induces a significant increase in the respiratory capacity of skeletal muscle. This is reflected by a training-induced increase in mitochondrial enzyme activity. One consequence of this adaptation is that there is a decreased reliance on carbohydrate utilization with a concomitant increase in fat utilization, resulting in an improvement in endurance capacity. Recently it has been reported that 7-14 days of cycle ergometer exercise training does not induce an increase in mitochondrial enzyme levels in skeletal muscle but, nevertheless, results in smaller decreases in phosphocreatine and glycogen and smaller increases in Pi and lactate in muscle in response to the same exercise after compared with before training. However, previous studies in rats have shown that an adaptive increase in mitochondrial enzymes is already evident after only 2 days of exercise training. In view of this discrepency, the present study was performed to reevaluate the effect of short-term training (7-10 days) on mitochondrial enzymes in skeletal muscle of humans. Twelve subjects [6 men and 6 women, 27 +/- 5 (SE) yr old] underwent 7 (n = 5) or 10 days (n = 7) of cycle ergometer exercise for 2h/day at 60-70% of peak O2 consumption. Peak O2 consumption was increased by 9% (from 2.97 +/- 0.16 to 3.24 +/- 0.17 l/min) in response to training. Blood lactate levels were lower at the same absolute work rates after than before training. The activities of citrate synthase, beta-hydroxyacyl-CoA dehydrogenase, mitochondrial thiolase, and carnitine acetyltransferase were increased by approximately 30% in response to training. The results of the present study provide evidence that in humans, as in rats, the adaptive increase in mitochondrial enzymes in skeletal muscle occurs fairly rapidly in response to exercise training. They provide no support for the claim that this adaptive response is delayed for > 2 wk after the onset of training.

Effects of ovariectomy and exercise training on muscle GLUT-4 content and glucose metabolism in rats.

The present study examined the effects of 6 wk of ovarian endocrine deficiency on skeletal muscle GLUT-4 glucose transporter protein and glucose transport activity in sedentary and endurance-trained rats. Female Wistar rats (10 wk old) underwent bilateral ovariectomy (OVX) or sham surgery followed by a 5-wk swim-training protocol. OVX resulted in no significant changes in glycogen or GLUT-4 glucose transporter concentration in the soleus, epitrochlearis, or flexor digitorum brevis (FDB) muscles or in basal and maximally insulin-stimulated 2-deoxy-D-[1,2-3H]glucose (2-[3H]DG) transport in the soleus or epitrochlearis, suggesting that moderate-duration ovarian hormone deficiency does not significantly impair insulin action in skeletal muscle. In contrast, OVX decreased the maximal activation of 2-[3H]DG transport in the FDB by in vitro electrical stimulation. OVX had no significant effect on the training-induced changes in oxidative enzyme activities, GLUT-4 protein expression, glycogen content, or insulin-stimulated 2-[3H]DG transport in the soleus or epitrochlearis. These findings provide the first evidence that ovarian hormone deficiency decreases contraction-stimulated glucose transport in skeletal muscle.

Gender-related differences in left ventricular filling dynamics in older subjects after endurance exercise training.

The present study was designed to determine if gender affects the adaptive response to endurance exercise training of left ventricular filling dynamics in older individuals. Recently, it was shown that gender influences the cardiovascular responses to endurance exercise training in older subjects. Older men improve left ventricular systolic performance and increase maximal cardiac output in response to endurance exercise training, whereas older women do not. Twelve men (65 +/- 1 years old; mean +/- SE) and 10 women (64 +/- 1) were studied before and after 9 months of endurance exercise training. Maximal O2 uptake was determined during treadmill exercise. Left ventricular filling dynamics and ejection fraction (EF) at rest and during supine exercise were assessed by Tc-99m radionuclide ventriculography. When expressed relative to body weight, maximal O2 uptake (VO2 max) was increased by 24% (27.3 +/- 1.5 to 34.0 +/- 1.5 ml/kg/min; p < .01) in men and 27% (21.9 +/- 1.0 to 27.8 +/- 1.0 ml/kg/min; p < .01) in women in response to endurance exercise training. In men, the time-to-peak filling rate (TPFR) decreased (-19.8 +/- 6.7 ms; p < .05) during exercise at a comparable heart rate in response to training. In contrast, the change in TPFR in women (+2.7 +/- 6.0 ms) was small and insignificant. Peak filling rate (PFR) at rest and during exercise was similar before and after training in men and women. The change in left ventricular systolic reserve at a comparable heart rate from pre-to posttraining improved in men (delta EF 4 +/- 3%; p < .05), but not in women (-2 +/- 3%). The results indicate that the adaptive response of left ventricular filling dynamics to endurance exercise training is influenced by gender in older subjects. Older men show improvement in left ventricular filling dynamics, whereas older women do not.

Endurance exercise training decreases capillary basement membrane width in older nondiabetic and diabetic adults.

The objectives of these studies were to 1) evaluate the relationships among age, glucose intolerance, and skeletal muscle capillary basement membrane (CBM) width (CBMW) and 2) determine the effects of exercise training on CBMW by comparing values of young (28 +/- 4 yr) and older (63 +/- 7 yr) athletes with those of age-matched sedentary control subjects and by measuring CBMW in older men and women before and after a 9-mo endurance-exercise training program. CBMW was measured in tissue samples obtained from the gastrocnemius muscle. CBMW in sedentary 64 +/- 3-yr-old subjects was 25% thicker than in sedentary 24 +/- 3-yr-old subjects. CBMW was similar in young and older athletes and was thinner than the CBMW of age-matched sedentary control subjects. There were no differences in CBMW among older sedentary individuals with normal or impaired glucose tolerance or mild non-insulin-dependent diabetes mellitus. Nine months of endurance exercise training reduced CBMW in older men and women by 30-40%, to widths that were not different from those of the young subjects; this response was independent of glucose tolerance status. These findings suggest that habitual exercise prevents the thickening of the skeletal muscle CBM that is characteristic of advancing age. Moreover, the thickening of the CBM appears to be readily reversed as a result of exercise training, even in older individuals.

Enhanced beta-adrenergic-mediated cardiovascular responses in endurance athletes.

To determine whether the adaptive increase in left ventricular systolic function in the trained state is mediated by enhanced responses to beta-adrenergic stimulation, we studied eight male endurance athletes [age 27 +/- 1.8 yr; maximal O2 uptake (VO2max) 60 +/- 0.9 (SE) ml x kg-1 x min-1] and eight sedentary men (age 27 +/- 1.4 yr; VO2max 43.1 +/- 1.7 ml x kg-1 x min-1). Left ventricular function was evaluated with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile in the basal state, after parasympathetic blockade by atropine, and during infusion of dobutamine. Cardiac output and stroke volume, determined with the acetylene rebreathing technique, during maximal exercise were significantly higher in the endurance athletes than in the sedentary men (28.9 +/- 1.7 vs. 23 +/- 1.23 1/min, P = 0.019, and 162 +/- 12 vs. 125 +/- 7 ml/min, P = 0.029). Endurance athletes showed physiological volume overload-left ventricular hypertrophy and greater enhancements of left ventricular systolic function and filling dynamics in response to dobutamine than did the sedentary men as reflected in 1) a steeper slope of the fractional shortening-end-systolic wall stress relationship (-0.986 +/- 0.16 vs. -0.508 +/- 0.054, P = 0.014, athletes vs. controls) and 2) a higher early-to-late transmitral diastolic Doppler velocity ratio (2.14 +/- 0.14 vs. 1.74 +/- 0.12, P = 0.016) at a comparable heart rate. Although endurance athletes had a significantly greater inotropic response to dobutamine, they demonstrated a markedly attenuated chronotropic response to beta1-adrenergic stimulation compared with sedentary subjects. Our findings suggest that, even with a blunted chronotropic response, endurance-trained young men show an augmented inotropic response to a beta1-adrenergic agonist that, along with physiological volume overload hypertrophy and increased diastolic filling, can contribute to a larger stroke volume during maximal exercise in the trained state.

Effect of 7-10 days of cycle ergometer exercise on skeletal muscle GLUT-4 protein content.

Previous studies in animals and humans have shown that endurance exercise-training protocols of several weeks to many months in duration induce adaptive increases in skeletal muscle GLUT-4 protein concentration. It is generally assumed that the increase in GLUT-4 concentration is a long-term adaptation to training. The present study examined whether 7-10 days of cycle ergometer exercise could induce increases in skeletal muscle GLUT-4 levels. Eight healthy subjects (4 men, 4 women) aged 31 +/- 2 (SE) yr exercised 2 h daily at 65-70% of peak O2 uptake (VO2peak) for either 7 (n = 3) or 10 (n = 5) consecutive days. Muscle biopsies (vastus lateralis) were obtained before initiation of the exercise program and 36-48 h after the final bout of exercise. Glucose transporter protein was quantitated by Western blotting using antiserum specific for GLUT-4. VO2peak was increased by 10% (from 3.0 +/- 0.2 to 3.3 +/- 0.2 l/min; P < 0.01) in response to the training. Body weight did not change (74.3 +/- 4.6 before vs. 75.0 +/- 4.2 kg after) as a result of training. Muscle GLUT-4 immunoreactivity was increased 98% (from 584 +/- 50 to 1,154 +/- 40 counts per minute 125I/25 micrograms protein; P < 0.001) in response to training. Increase in VO2peak and GLUT-4 protein were similar for 7 and 10 days of training. These results suggest that, given an adequate training stimulus, adaptations in skeletal muscle GLUT-4 protein occur very rapidly. Furthermore, the increase in GLUT-4 after 7-10 days of exercise is as large as that reported in studies employing long-term training protocols.

Effects of exercise training on alpha-adrenergic mediated pressor responses and baroreflex function in older subjects.

Endurance exercise training increases maximal O2 uptake (VO2max) in older subjects, and training also improves cardiac function in older men. Although the effects of training on beta-adrenergic responses have been investigated, little information is available regarding the effects of alpha-adrenergic responses and baroreflex function in older men and women. The purpose of the study was to determine whether endurance exercise training can affect alpha-adrenergic responses and baroreflex function in the elderly. We studied 13 men and women, 63 +/- 4 yrs old (mean +/- SE). VO2max was determined during treadmill exercise. Baroreflex function was determined from the change in heart rate (HR) relative to the change in systolic blood pressure (delta HR/delta SBP) during infusion of phenylephrine. VO2max was increased by 23% (1.9 +/- 0.16 vs 2.34 +/- 0.20 l/min; p < .01) in response to training. Maximal heart rate did not change, but HR during submaximal exercise at the same absolute exercise intensity was 17% lower after training. Resting heart rate was slower in the trained state. During alpha-adrenergic stimulation induced by graded doses of phenylephrine infusion, heart rate was lower after training because of training-induced bradycardia at rest. However, the elevation in systolic blood pressure (delta SBP) and mean blood pressure (delta MBP) from basal levels in response to a given dose of phenylephrine were significantly larger (delta SBP:18 +/- 3 vs 26 +/- 3 mmHg, p < .01; and delta MBP 10 +/- 2 vs 15 +/- 3 mmHg, p < .01) after than before training.(ABSTRACT TRUNCATED AT 250 WORDS)