Short-term aerobic exercise training increases postprandial pancreatic polypeptide but not peptide YY concentrations in obese individuals.

OBJECTIVE: Short-term exercise training improves glycemic control, but the effect of short-term training on postprandial satiety peptide responses or perceived satiety remains unknown. We tested the hypothesis that short-term aerobic exercise training (15 days) would alter postprandial pancreatic and gut peptide (pancreatic polypeptide (PP) and peptide YY (PYY)) responses and perceived appetite and satiety in obese individuals. SUBJECTS: Thirteen healthy obese men and women (age: 42±2 years; body mass index: 30-45 kg m(-2)). MEASUREMENTS: Subjects were studied before and after 15 days of training (walking 1 h at 70-75% VO(2peak)). On the study day, subjects consumed 1500 kcal as six meals (250 kcal: 9 g protein, 40 g carbohydrate, 6 g fat), while blood samples and satiety measurements were taken at baseline and every 20 min for 12 h. Blood was analyzed for PP, PYY, glucose and insulin levels. Appetite and satiety was assessed with a visual analog scale throughout the day. RESULTS: Incremental area under the curve (iAUC) for PP increased significantly with training (pre: 2788±753; post: 3845±830 pg ml(-1)·per min for 12 h; P<0.001), but there was no difference in the PP response to each meal. The initial PP response to the first meal increased (ΔPP(min 20-0): pre 86±25; post 140±36 pg ml(-1); P<0.05) with training. PYY iAUC showed no significant changes with training but showed a significant main effect of time across meals, with the largest response being to the first meal (P<0.005). There were no changes in satiety, glucose or insulin levels with training. CONCLUSION: Short-term exercise training increases postprandial PP concentrations in obese individuals; however, PYY levels and glycemic control remain unaffected. Both PP and PYY show meal-induced increases at all meals, but PYY has a greater response at the first meal with reduced responses at subsequent meals.

Regulation of blood flow by aspirin following muscle ischemia.

BACKGROUND: The vascular endothelium secretes a balance of dilator and constrictor substances which regulate vascular tone. During ischemic stress, this balance changes. After a short period of ischemia, a protective mechanism known as reactive hyperemia (RH) contributes to a post-ischemic increase in blood flow. The agents regulating this phenomenon remain controversial. AIM: The purpose of this study was to examine whether aspirin regulates vascular endothelial function following ischemia. METHODS: Sixteen healthy volunteers presented for two visits, each serving as their own control, and randomized to receive 500 mg aspirin or placebo. Forearm blood flow (FBF) was measured at baseline and during reactive hyperemia (RH) which was induced by five minutes of arterial occlusion. Blood samples were analyzed for vWF and lipids. RESULTS: After ischemia, RH was attenuated when subjects were pre-medicated with 500 mg aspirin compared to placebo: AUC[aspirin] = 1450 +/- 201 mL/100 mL tissue/min vs. AUC[pIacebo] = 2207 +/- 294 mL/100 mL tissue/min; (p < 0.05). Separation of the subjects with high HDL or low HDL levels resulted in a similar peak FBF response with placebo, but in the high-HDL group only, aspirin ingestion attenuated peak FBF after ischemia compared to the placebo condition (22.6 +/- 1.7 m/100 mL tissue/min vs. 33.5 +/- 3.2 mL/100 mL tissue/min, respectively) (p < 0.05). CONCLUSIONS: Aspirin partially regulates the RH response following ischemia compared to placebo, and this effect appears to be more profound when adjusting for plasma HDL concentration in healthy individuals. This suggests that the post-ischemic RH response may be partially mediated by arachidonic acid-derived mediators such as the prostaglandins.

Plasticity of heart rate signalling and complexity with exercise training in obese individuals with and without type 2 diabetes.

OBJECTIVE: To examine the responsiveness of cardiac autonomic function and baroreflex sensitivity (BRS) to exercise training in obese individuals without (OB) and with type 2 diabetes (ObT2D). DESIGN: Subjects were tested in the supine position and in response to a sympathetic challenge before and after a 16-week aerobic training program. All testing was conducted in the morning following a 12-h fast. SUBJECTS: A total of 34 OB and 22 ObT2D men and women (40-60 years of age) were studied. MEASUREMENTS: Heart rate variability (HRV) was measured at rest via continuous ECG (spectral analysis with the autoregressive approach) and in response to upright tilt. The dynamics of heart rate complexity were analyzed with sample entropy and Lempel-Ziv entropy, and BRS was determined via the sequence technique. Subjects were aerobically trained 4 times per week for 30-45 min for 16 weeks. RESULTS: Resting HR decreased and total power (lnTP, ms(2)) of HRV increased in response to exercise training (P<0.05). High frequency power (lnHF) increased in OB subjects but not in OBT2D, and no changes occurred in ln low frequency/HF power with training. Upright tilt decreased lnTP and lnHF and increased LF/HF (P<0.01) but there were no group differences in the magnitude of these changes nor were they altered with training in either group. Tilt also decreased complexity (sample entropy and Lempel-Ziv entropy; P<0.001), but there was no group or training effect on complexity. BRS decreased with upright tilt (P<0.01) but did not change with training. Compared to OB subjects the ObT2D had less tilt-induced changes in BRS. CONCLUSION: Exercise training improved HRV and parasympathetic modulation (lnHF) in OB subjects but not in ObT2D, indicating plasticity in the autonomic nervous system in response to this weight-neutral exercise program only in the absence of diabetes. HR complexity and BRS were not altered by 16 weeks of training in either OB or ObT2D individuals.

Muscle indices do not fully account for enhanced upper extremity bone mass and strength in gymnasts.

OBJECTIVES: Muscular forces are an important determinant of bone strength, but bone may also adapt to non-muscular loading. We tested the hypothesis that loads associated with childhood gymnastics yield high arm bone mass (BMC), bone size and bone strength, independent of arm lean mass (FFM) and muscle cross-sectional area (CSA). METHODS: Total body DXA and distal radius pQCT scans were performed on 33 post-menarcheal girls (19 ex/gymnasts, 14 non-gymnasts). Physical activity and calcium intake were assessed by questionnaire. For the non-dominant arm, pQCT measured bone strength indices and bone CSA (total, cortical) (4%, 33% sites); DXA measured arm FFM, arm BMC and skull BMC. Multiple regression analyses assessed gymnastic exposure, arm FFM, gynecological age and stature as predictors of bone parameters. RESULTS: Bone outcomes at loaded upper extremity sites were 10-42% greater in ex/gymnasts than non-gymnasts. Gymnastic exposure remained a consistent, significant predictor of upper extremity skeletal parameters after accounting for the effects of muscle parameters, gynecological age and height. CONCLUSIONS: Considering the effects of either arm FFM or muscle CSA, indices of bone mass, geometry and theoretical strength are disproportionately elevated after gymnastic exposure. Thus, non-muscular loading may be a distinct and important determinant of human skeletal structure.

Short-term exercise training improves aerobic capacity with no change in arterial function in obesity.

The aim of the study is to determine the effects of short-term high-intensity exercise on arterial function and glucose tolerance in obese individuals with and without the metabolic syndrome (MetSyn). Obese men and women (BMI > 30 kg/m(2); 39-60 years) with and without MetSyn (MetSyn, n = 13; Non-MetSyn, n = 13) participated in exercise training consisting of ten consecutive days of treadmill walking for 1 h/day at 70-75% of peak aerobic capacity. Changes in aerobic capacity, flow-mediated dilation (FMD), and arterial stiffness using central and peripheral pulse wave velocity (PWV) measurements were assessed pre- and post-training. These measurements were obtained fasting and 1-h post-test meal while the subjects were hyperglycemic. Aerobic capacity improved for both groups [Non-MetSyn 24.0 +/- 1.6 vs. 25.1 +/- 1.5 mL/(kg min); MetSyn 25.2 +/- 1.8 vs. 26.2 +/- 1.7 mL/(kg min), P < 0.05]. There was no change in body weight. FMD decreased by ~20% (P < 0.05) for both groups during acute hyperglycemia (MetSyn, n = 11; Non-MetSyn, n = 10), while hyperglycemia increased central PWV and not peripheral PWV. Exercise training did not change FMD in the fasted or challenged state. Central and peripheral PWV were not altered with training for either group (MetSyn, n = 13; Non-MetSyn, n = 13). A 10-day high-intensity exercise program in obese individuals improved aerobic capacity and glucose tolerance but no change in arterial function was observed. Acute hyperglycemia had a deleterious effect on arterial function, suggesting that persons with impaired glucose homeostasis may experience more opportunities for attenuated arterial function on a daily basis which could contribute to increased cardiovascular risk.

Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives.

The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre- or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2 +/- 1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136 +/- 2.9 vs. post 132 +/- 3.4; AE, pre 141 +/- 3.8 vs. post 136 +/- 3.4 mm Hg, P = 0.005; diastolic BP: RE, pre 78 +/- 1.3 vs post 74 +/- 1.6; AE, pre 80 +/- 1.6 vs. post 77 +/- 1.7 mm Hg, P = 0.001). Central PWV increased (P = 0.0001) following RE (11 +/- 0.9-12.7 +/- 0.9 ms(-1)) but decreased after AE (12.1 +/- 0.8-11.1 +/- 0.8 m s(-1). Peripheral PWV also increased (P = 0.013) following RE (RE, pre 11.5 +/- 0.8 vs. post 12.5 +/- 0.7 ms(-1)) and decreased after AE (AE, pre 12.6 +/- 0.8 vs post 11.6 +/- 0.7 m s(-1)). The VC area under the curve (VC(AUC)) increased more with RE than that with AE (RE, pre 76 +/- 8.0 vs. post 131.1 +/- 11.6; AE, pre 82.7 +/- 8.0 vs. post 110.1 +/- 11.6 ml per min per s per 100 ml, P = 0.001). Further, peak VC (VCpeak) increased more following resistance training compared to aerobic training (RE, pre 17 +/- 1.9 vs. post 25.8 +/- 2.1; AE, pre 19.2 +/- 8.4 vs post 22.9 +/- 8.4 ml per min per s per 100 ml, P = 0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.

Fatty acid kinetic responses to exercise. Effects of obesity, body fat distribution, and energy-restricted diet.

UNLABELLED: Upper body obesity (UB Ob) is associated with a reduced net free fatty acid (FFA) response to epinephrine compared with nonobese (Non Ob) and lower-body obese (LB Ob) women. Because catecholamines regulate some of the metabolic responses to exercise, we hypothesized that UB Ob would have a reduced net FFA response to exercise. Plasma FFA rate of appearance (Ra) ([1-14C]palmitate) and fatty acid oxidation (indirect calorimetry) were therefore measured during 2.5 h of stationary bicycle exercise (45% VO2 peak) in 13 UB Ob, 11 LB Ob, and 8 Non Ob premenopausal women. 10 UB Ob and 8 LB Ob women were retested after an approximately 8-kg weight loss. RESULTS: During exercise Non Ob and LB Ob women had greater increments in FFA availability (51 +/- 7 and 53 +/- 8 mmol, respectively) than UB Ob women (27 +/- 4 mmol, P < 0.05). Total exercise FFA availability and fatty acid oxidation were not different between Non Ob, LB Ob, and UB Ob women, however. Following weight loss (approximately 8 kg), the FFA response to exercise increased (P < 0.01) and remained greater (P < 0.05) in LB Ob than in UB Ob women. In conclusion, the FFA response to exercise was reduced in UB Ob women before and after weight loss, but no effects on fatty acid oxidation were apparent.

Oral arginine attenuates the growth hormone response to resistance exercise.

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.

Exercise is required for visceral fat loss in postmenopausal women with type 2 diabetes.

This study examined the effects of aerobic exercise without weight loss, a hypocaloric high monounsaturated fat diet, and diet plus exercise (D+E) on total abdominal and visceral fat loss in obese postmenopausal women with type 2 diabetes. Thirty-three postmenopausal women (body mass index, 34.6 +/- 1.9 kg/m(2)) were assigned to one of three interventions: a hypocaloric high monounsaturated fat diet alone, exercise alone (EX), and D+E for 14 wk. Aerobic capacity, body composition, abdominal fat distribution (magnetic resonance imaging), glucose tolerance, and insulin sensitivity were measured pre- and postintervention. Body weight ( approximately 4.5 kg) and percent body fat ( approximately 5%) were decreased (P < 0.05) with the D and D+E intervention, whereas only percent body fat ( approximately 2.3%) decreased with EX. Total abdominal fat and sc adipose tissue (SAT) were reduced with the D and D+E interventions (P < 0.05), whereas visceral adipose tissue (VAT) decreased with the D+E and EX intervention, but not with the D intervention. EX resulted in a reduction in total abdominal fat, VAT, and SAT (P < 0.05) despite the lack of weight loss. The reductions in total abdominal fat and SAT explained 32.7% and 9.7%, respectively, of the variability in the changes in fasting glucose levels, whereas the reductions in VAT explained 15.9% of the changes in fasting insulin levels (P < 0.05). In conclusion, modest weight loss, through either D or D+E, resulted in similar improvements in total abdominal fat, SAT, and glycemic status in postmenopausal women with type 2 diabetes; however, the addition of exercise to diet is necessary for VAT loss. These data demonstrate the importance of exercise in the treatment of women with type 2 diabetes.

Hormone-replacement therapy use, but not race, impacts the resting and exercise-induced GH response in postmenopausal women.

OBJECTIVE: This study examined the effect of hormone-replacement therapy (HRT) use on the incremental GH response to aerobic exercise in postmenopausal women and established whether racial differences in the GH response were seen at rest and in response to exercise. METHODS: 13 white (n = 6, HRT; n = 7, no HRT) and seven black women (no HRT) were studied on two occasions, a control day and an exercise day (30 min at 70% VO(2)max on a cycle ergometer). Blood was sampled every 10 min for a 4-h period and analyzed for GH using an ultrasensitive chemiluminescent assay. RESULTS: The mean 4-h GH concentration was higher on both study days in the HRT women than the non-HRT users. The integrated GH concentrations were greater in the HRT women both at rest and in response to exercise (rest, 352 +/- 53 min microg l(-1); exercise, 711 +/- 57 min microg l(-1); P < 0.01) than in the non-HRT women (rest, 157 +/- 87 min microg l(-1); exercise, 248 +/- 94 min microg l(-1)). The incremental GH response was greater in the HRT users than in the non-HRT women (358 +/- 130 versus 90.8 +/- 94 min microg l(-1), respectively; P < 0.05). GH-production rate during the 4-h period was greater in the HRT women than in the non-HRT women (P < 0.01), due to an increase in the GH mass secreted/pulse (P < 0.05), with no change in GH pulse number or GH half-life. No racial differences in the mean 4-h GH concentrations or integrated GH concentrations were found at rest or in response to exercise. CONCLUSION: HRT use resulted in a greater incremental exercise response compared with non-HRT users, due to changes in the secretory pulse characteristics in the HRT users. This study also demonstrated that no racial differences exist at rest and in response to exercise in the morning hours.

The effect of submaximal exercise on immuno- and bioassayable IGF-I activity in patients with GH-deficiency and healthy subjects.

OBJECTIVE: Growth hormone (GH) increases during exercise, but the response of the insulin-like growth factor (IGF) system has not been as definitive. Therefore, we investigated the effect of the exercise-induced GH response on the circulating IGF-system in GH-deficient (GHD) and intact adults. DESIGN: Eight GHD adults were studied on 2 occasions, with (+GH) and without (-GH) GH administered (0.4 IU) during exercise (45 min of cycle ergometer exercise at the lactate threshold). Eight age-matched controls were only studied on one occasion. Blood samples were drawn at baseline, during and post-exercise. IGFBP-3 proteolysis was measured by an in vitro proteolytic activity assay, IGF-I bioactivity by novel IGF-I kinase receptor activation assay (KIRA) and other hormones by immunoassay. RESULTS: GH administration to GHD adults resulted in a serum GH peak similar to the exercise-stimulated GH response in GH intact controls, but exercise had only a small impact on the IGF system. IGF-I concentration was lower in controls but was only significantly lower than the +GH day. Neither IGF-I nor -II levels changed over time. IGFBP-1 demonstrated a time effect (P<0.01) in all groups, and a time x group interaction (P<0.01) with a rise at 75 min post-exercise, which was greater in the GHD subjects than controls. IGFBP-2 and -3 increased significantly (P<0.01) over time in the GHD subjects, but not in the controls. No change in IGFBP-3 proteolysis or IGF-I bioactivity was found during exercise or recovery in either group. CONCLUSION: Submaximal exercise induced minor changes in IGFBP-1, -2 and -3, without affecting IGFBP-3 proteolysis and IGF-I bioavailability. Thus the metabolic status during submaximal exercise does not require a change in plasma IGF-I bioavailability. Administration of GH to GHD adults does not result in changes in proteolysis or bioavailability.

Cortisol and growth hormone responses to exercise at different times of day.

Exercise of appropriate intensity is a potent stimulus for GH and cortisol secretion. Circadian and diurnal rhythms may modulate the GH and cortisol responses to exercise, but nutrition, sleep, prior exercise patterns, and body composition are potentially confounding factors. To determine the influence of the time of day on the GH and cortisol response to acute exercise, we studied 10 moderately trained young men (24.1 +/- 1.1 yr old; maximal oxygen consumption, 47.9 +/- 1.4 mL/kg.min; percent body fat, 13.2 +/- 0.6%). After a supervised night of sleep and a standard meal 12 h before exercise, subjects exercised at a constant velocity (to elicit an initial blood lactate concentration of approximately 2.5 mmol/L) on a treadmill for 30 min on 3 separate occasions, starting at 0700, 1900, and 2400 h. Blood samples were obtained at 5-min intervals for 1 h before and 5 h after the start of exercise; subjects were not allowed to sleep during this period. Subjects were also studied on 3 control days under identical conditions without exercise. There were no significant differences with time of day in the mean blood lactate and submaximal oxygen consumption values during exercise. The differences over time in serum GH and cortisol concentrations between the exercise day and the control day were determined with 95% confidence limits for each time of day. Exercise stimulated a significant increase in serum GH concentrations over control day values for approximately 105--145 min (P < 0.05) with no significant difference in the magnitude of this response by time of day. The increase in serum GH concentrations with exercise was followed by a transient suppression of GH release (for approximately 55--90 min; P < 0.05) after exercise at 0700 and 1900 h, but not at 2400 h. Although the duration of the increase in serum cortisol concentrations after exercise was similar (approximately 150--155 min; P < 0.05) at 0700, 1900, and 2400 h, the magnitude of this increase over control day levels was greatest at 2400 h. This difference was significant for approximately 130 min and approximately 40 min compared to exercise at 1900 and 0700 h, respectively (P < 0.05). The cortisol response to exercise at 0700 h was significantly greater than that at 1900 h for about 55 min (P < 0.05). A rebound suppression of cortisol release for about 50 min (P < 0.05) was observed after exercise at 2400 h, but not 0700 or 1900 h. Both baseline (before exercise) and peak cortisol concentrations were significantly higher at 0700 h than at 1900 or 2400 h (P < 0.01). We conclude that time of day does not alter the GH response to exercise; however, the exercise-induced cortisol response is modulated by time of day.

Insulin regulation of insulin-like growth factor binding protein-1 in obese and nonobese humans.

Insulin is the principal regulator of hepatic insulin-like growth factor binding protein-1 (IGFBP-1) production, mediating the rapid decrease in plasma IGFBP-1 in response to nutritional intake. In this study, we defined IGFBP-1 regulation by insulin in upper and lower body obesity, conditions associated with insulin resistance and chronic hyperinsulinemia. Overnight postabsorptive IGFBP-1 levels in obese and nonobese women showed an inverse, nonlinear relationship with plasma insulin concentrations. Maximum suppression of IGFBP-1 was seen at 70-90 pmol/L plasma insulin. Both groups of obese women had mean fasting plasma insulin concentrations above this threshold level and, consequently, markedly suppressed IGFBP-1 levels. To assess the dynamics of insulin regulated IGFBP-1, 10 obese and 8 nonobese women were studied during sequential saline infusion (0-90 min), hyperinsulinemia (insulin infusion; 90-210 min) and hypoinsulinemia (somatostatin + GH infusion; 210-330 min). Insulin infusion rapidly decreased plasma IGFBP-1 levels in nonobese subjects (60% decrease in 2 h), but had little or no further suppressive effect in obese subjects. Complete insulin withdrawal resulted in a significant rise in plasma IGFBP-1 concentrations in all subjects, but the response was blunted in obese compared to nonobese groups. In contrast to plasma IGFBP-1, IGF-I concentrations did not vary during hyper- and hypoinsulinemic infusion periods and were not significantly different between groups. Basal GH levels were significantly higher in nonobese when compared to obese women, but did not change with infusions. In conclusion, low IGFBP-1 levels in obesity are related to elevated insulin levels which are, in turn, related to body fat distribution and insulin resistance. The chronically depressed levels of IGFBP-1 may promote IGF bioactivity as well as its feedback regulation of GH secretion, thus contributing to the metabolic and mitogenic consequences of obesity. In addition, our findings imply that hepatic insulin sensitivity in terms of IGFBP-1 production is preserved despite peripheral insulin resistance in obesity.

Obesity attenuates the growth hormone response to exercise.

Resting serum GH concentrations are decreased in obesity. In nonobese (NonOb) individuals, acute exercise of sufficient intensity increases GH levels; however, conflicting data exist concerning the GH response to exercise in obese individuals. To examine the exercise-induced GH response in obese individuals, we studied 8 NonOb, 11 lower body obese (LBO), and 12 upper body obese (UBO) women before, during, and after 30 min (0800-0830 h) of treadmill exercise at 70% oxygen consumption peak. Blood samples were taken every 5 min (0700-1300 h) and were analyzed for GH concentrations with a sensitive (0.002 microg/L) chemiluminescence assay. The impact of 16 weeks of aerobic exercise training on the GH response to exercise was also examined in the obese women. In response to exercise, the 6-h integrated GH concentration was significantly greater (P < 0.05) in the NonOb women (1006 +/- 220 min/microg x L) than in either of the obese groups (LBO, 435 +/- 136; UBO, 189 +/- 26 min/microg x L). No differences were found between the LBO and UBO women. The increased integrated GH concentrations could be accounted for by a greater 6-h GH production rate [micrograms per L distribution volume (Lv)] in the NonOb women than in either of the obese groups (NonOb, 45.6 +/- 12.3; LBO, 16.9 +/- 1.2; UBO, 8.7 +/- 0.64 microg/Lv; P < 0.05). This increase was attributed to a greater mass of GH secreted per pulse in the NonOb women (NonOb, 10.8 +/- 2.5; LBO, 4.9 +/- 0.8; UBO, 4.0 +/- 0.5 microg/Lv; P < 0.05, NonOb vs. both obese groups). After 16 weeks of aerobic training, maximal oxygen consumption increased from 44.7 +/- 2.2 to 48.5 +/- 1.9 mL/kg fat-free mass x min; P < 0.05), but no significant change in body composition occurred in the 10 obese women who completed the training. No change was observed in the GH response to exercise after training (n = 10; pre, 379 +/- 144; post, 350 +/- 55 min/microg x L). In conclusion, the GH response to exercise was attenuated in the obese women compared to NonOb women. Short term aerobic training improved fitness, but did not increase the GH response to exercise.

Measurement of abdominal and visceral fat with computed tomography and dual-energy x-ray absorptiometry.

These studies were undertaken to compare dual-energy x-ray absorptiometry (DXA) and computed tomography (CT) measurements of abdominal fat and to determine whether anthropometry could be combined with DXA to predict intraabdominal (visceral) fat mass in humans. Twenty-one volunteers underwent abdominal CT scans, DXA, and anthropometry. DXA- and CT-measured total abdominal fat were similar (8448 +/- 5005 and 8066 +/- 5354 mL, respectively; NS) and were highly correlated (r = 0.985, P < 0.001). The combination of anthropometry and DXA was a suboptimal predictor of CT-measured intraabdominal fat (r = 0.61, P < 0.05); however, the combination of a single CT slice (to assess the ratio of intraabdominal to total abdominal adipose tissue) and DXA-measured abdominal fat was an excellent predictor of CT-measured intraabdominal fat (r = 0.98, P < 0.001). We conclude that a single-slice CT scan (or other imaging technique) with or without DXA is required for accurate predictions of intraabdominal fat.

Differential health benefits of weight loss in upper-body and lower-body obese women.

Upper-body obesity (UB Ob) is more strongly associated with adverse health consequences; however, few obesity-treatment studies have examined outcome according to body-fat distribution. To examine whether diet and formal- or informal-exercise instruction causes differential changes in health and lipid profiles, ten LB Ob and nine UB Ob premenopausal women received dietary intervention (2.1 MJ-deficit/d for 16 wk) and were randomly assigned to either formal- or informal-exercise instruction. Weight loss was similar between groups (approximately 8 kg), and no change occurred in lean body mass or basal metabolic rate. Baseline cholesterol and triglycerides were greater (P < 0.01) in UB Ob than LB Ob women and decreased more (P < 0.01) in response to treatment in UB Ob women. Formal exercise instruction increased high-density-lipoprotein cholesterol (P < 0.05) especially in UB Ob women. Future studies on treatment of obesity should include consideration of regional fat distribution.

Assessment of body composition with use of dual-energy x-ray absorptiometry: evaluation and comparison with other methods.

Dual-energy x-ray absorptiometry (DEXA) is a relatively new method of assessing body composition in humans. In the current study, DEXA was analyzed for accuracy and precision by using both anthropomorphic phantoms and a combination of body composition techniques in humans. Satisfactory precision for measurement of total body fat, fat-free mass, and total body bone mineral could be demonstrated in vivo and in vitro. Predictions of lean body mass in humans on the basis of DEXA, total body water, and total body potassium were significantly different. The results of multiple regression analysis suggested that a component of total body water was related to body potassium, and another component was predicted by body fat. In addition, extracellular fluid volume, as measured by the bromide space technique, was significantly associated with both fat-free mass and fat mass as measured by DEXA. These findings have implications for the interpretation of body composition data in humans.

Antioxidant enzyme activity during prolonged exercise in amenorrheic and eumenorrheic athletes.

Exogenous 17 beta-estradiol (E2) has been shown to be associated with elevated levels of erythrocyte glutathione peroxidase (GPX) activity. The purpose of this study was to examine the influence of endogenous E2, as defined by menstrual status (amenorrhea v eumenorrhea), on activity of blood antioxidant enzymes at rest and during prolonged exercise. Six amenorrheic (AMc) and six eumenorrheic (EUc) athletes were subjected to a treadmill running test at 60% VO2max for 90 minutes. Serial blood samples were taken from a forearm vein at rest, 30, 60, and 90 minutes during exercise, and 15 minutes into recovery. Resting estrogen levels were significantly lower in AMc athletes at rest and during exercise as compared with EUc athletes, whereas plasma cortisol levels in AMc were significantly higher. GPX activity was significantly higher in AMc than EUc at rest (46.9 +/- 7.7 v 30.2 +/- 2.2 nmol/min x mg Hb, P less than .05, respectively) and throughout exercise. Glutathione reductase (GR) activity was similar between the two groups at rest and was significantly higher (P less than .01) in AMc than EUc during exercise. Plasma lipid peroxidation and catalase activity did not change significantly in response to exercise, nor were they different between AMc and EUc athletes. GPX activity was found to be negatively correlated with E2 (r = -.64, P less than .01) and positively correlated with cortisol (r = .69, P less than .01). It is tentatively concluded that the alteration of hormonal status in amenorrhea has an influence on the blood antioxidant enzyme system.

Adrenocortical responses to submaximal exercise in postmenopausal black and white women.

The purpose of this study was to determine whether racial differences exist in the dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), and cortisol concentrations of black and white postmenopausal women at rest and in response to submaximal exercise. Twenty-three postmenopausal women (13 white and 10 black) were studied on 2 occasions. On one occasion subjects rested quietly for 4 hours (control day), whereas on the other occasion after 50 minutes of rest, subjects exercised at 70% of Vo(2) peak for 30 minutes on a cycle ergometer (exercise day). Blood was sampled at rest, during exercise, and during recovery and assayed for DHEA, DHEAS, and cortisol concentrations. Resting DHEA and cortisol concentrations and integrated area under the curve (AUC) were similar between the black and white women; however, the black women had lower resting DHEAS concentrations compared with the white women (DHEAS, black: 1.32 +/- 0.29 v white: 2.18 +/- 0.25 micromol. L(-1), P <.05). Regardless of race, DHEA and cortisol AUC increased significantly above resting values (P <.01), but the exercise AUC for DHEA and cortisol were not different between the black and white women (DHEA: 607 +/- 133 and 824 +/- 108 min x nmol. L(-1); cortisol: 9,604 +/- 1,247 and 8,076 +/- 1,093 min x nmol. L(-1), respectively). No exercise-induced change in integrated DHEAS AUC was found in either group. In conclusion, racial differences exist in the resting DHEAS levels of postmenopausal women, but with no racial differences in resting DHEA and cortisol concentrations. Race had no impact on these adrenal hormone responses to submaximal exercise.

Racial differences in subcutaneous and visceral fat distribution in postmenopausal black and white women.

Most studies examining racial disparities in abdominal fat distribution have focused on premenopausal women. The purpose of this report was to determine if racial differences exist in the abdominal fat distribution in postmenopausal white and black women. Fifty-four women (33 white and 21 black) were scanned by magnetic resonance imaging (MRI) to determine abdominal fat distribution, were measured by hydrostatic weighing for percent body fat, and had their fasting blood lipids, glucose, and insulin levels measured. These women were matched for age (mean age, 53.5 +/- 0.9 years) and percent body fat (black: 39.6% +/- 2.3%, white: 37.3% +/- 1.2%). When adjusted for total body fat mass and hormone replacement therapy (HRT), total abdominal fat (white: 10,352.1 +/- 535.2, black: 11,220.4 +/- 670.1 cm(3)) was not statistically different between groups, but the visceral fat content was significantly higher in the white women (white: 2,943.5 +/- 220.4, black: 2,332.6 +/- 176.1 cm(3)). The percent visceral fat was also higher in these women (white: 30.5% +/- 1.3%, black: 22.1% +/- 1.6%, P <.01). Subcutaneous adipose tissue (SAT) was significantly higher in the black women (white: 7,408.6 +/- 450.2, black: 8,887 +/- 563.1 cm(3), P <.05). No significant differences were found in the insulin concentrations or the blood lipid profile of these women. Regardless of race, visceral fat was a significant predictor of log triglyceride, low-density lipoprotein-cholesterol (LDL-C), cholesterol/LDL-C, insulin levels, and insulin resistance. Race was only found to contribute to 8% of the variability of LDL-C. HRT use had no effect on abdominal fat distribution or the blood lipid profile in this cohort of women. In conclusion, disparities in abdominal fat distribution between black and white women continue to exist in the early postmenopausal years, and the regression results indicate that the absolute amount of visceral fat, and not the relative amounts of visceral fat, is the best predictor of the blood lipid profile and insulin sensitivity. HRT use did not result in differences in abdominal fat distribution in these women. Factors, such as genetics and lifestyle, must play a larger role in explaining the increased health risk in black women.