Effect of increased physical activity on fructose-induced glycemic response in healthy individuals.

BACKGROUND/OBJECTIVES: The purpose of the current study was to determine whether increased physical activity (PA) altered glycemic control while ingesting an energy-balanced high-fructose diet. SUBJECTS/METHODS: Twenty-two normal-weight men and women (age: 21.2±0.6 years; body mass index: 22.6 ±0.6 kg/m(2)) participated in a randomized, cross-over design study in which they ingested an additional 75 g of fructose for 14 days while either maintaining low PA (FR+inactive) (<4500 steps/day) or high PA (FR+active) (>12,000 steps/day). Before and following the 2-week loading period, a fructose-rich meal challenge was administered and blood was sampled at baseline and for 6 h after the meal and analyzed for glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), c-peptide, glucose and insulin concentrations. RESULTS: Plasma insulin, glucose, c-peptide, GIP and GLP-1 concentrations significantly increased in response to the test meal on all test visits (P<0.05). C-peptide incremental area under the curve (AUC) decreased by 10,208 ±120 pmol/l × min for 6 h from pre to post Fr+active intervention (P=0.02) leading to a decrease in plasma insulin total AUC (pre: 58,470.2±6261.0 pmol/l; post: 49,444.3±3883.0 pmol/l; P=0.04) resulting in a decrease Δpeak[Insulin] (P=0.009). Following the FR+active intervention, GIP total AUC significantly decreased (P=0.005) yet only males had a lower total GLP-1 AUC after both interventions (P=0.049). There were no sex differences in GIP levels. CONCLUSIONS: Increased PA attenuates the deleterious effects on glycemic control caused by a high-fructose diet. These changes in glycemic control with PA are associated with decreases in insulin and GIP concentrations.

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.

Satiety, but not total PYY, Is increased with continuous and intermittent exercise.

OBJECTIVE: This study determined the hormonal and subjective appetite responses to exercise (1-h continuous versus intermittent exercise throughout the day) in obese individuals. DESIGN AND METHODS: Eleven obese subjects (>30 kg/m(2) ) underwent three 12-h study days: control condition [sedentary behavior (SED)], continuous exercise condition [(EX) 1-h exercise], and intermittent exercise condition [(INT) 12 hourly, 5-min bouts]. Blood samples (every 10 min) were measured for serum insulin and total peptide YY (PYY) concentrations, with ratings of appetite (visual analog scale [VAS): every 20 min]. Both total area under the curve (AUC), and subjective appetite ratings were calculated. RESULTS: No differences were observed in total PYY AUC between conditions, but hunger was reduced with INT (INT < EX; P < 0.05), and satiety was increased with both SED and INT conditions (INT > EX and SED > EX; P < 0.05). A correlation existed between the change in total PYY and insulin levels (r = -0.81; P < 0.05), and total PYY and satiety (r = 0.80; P < 0.05) with the EX condition, not the SED and INT conditions. CONCLUSIONS: The total PYY response to meals is not altered over the course of a 12-h day with either intermittent or continuous exercise; however, intermittent exercise increased satiety and reduced hunger to a greater extent than continuous exercise in obese individuals.

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.

Limb venous compliance responses to lower body negative pressure in humans with high blood pressure.

This study tested the hypothesis that limb venous responses to baroreceptor unloading are altered in individuals with high blood pressure (HBP) compared with normotensive (NT) controls. Calf venous compliance was assessed in 20 subjects with prehypertension and stage-1 hypertension (mean arterial pressure, MAP: 104±1 mm Hg) and 13 NT controls (MAP: 86±2 mm Hg) at baseline and during lower body negative pressure (LBNP), using venous occlusion plethysmography. Baroreflex sensitivity (BRS) was measured using the sequence technique and total peripheral resistance (TPR) was estimated from finger plethysmography. Baseline venous compliance was not different between groups, but the HBP group had lower baseline lnBRS (2.22±0.14 vs 2.7±0.18 ms mm Hg(-1)) and greater baseline TPR (3828±138 vs 3250±111 dyn sec(-1) cm(-5) m(2), P<0.05). Calf venous compliance was reduced in response to LBNP only in the NT group (P<0.05). The HBP group had a greater increase in TPR (ΔTPR) compared with the NT group (+1649±335 vs +718±196 dyn sec(-1) cm(-5) m(2), P<0.05). In conclusion, the early stages of hypertension are characterized by an attenuated venoconstrictor response to baroreceptor unloading, which may compensate for an exaggerated vasoconstrictor response and protect against further increases in blood pressure.

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.

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.

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.

Cardiac autonomic function and baroreflex changes following 4 weeks of resistance versus aerobic training in individuals with pre-hypertension.

AIM: Cardiac autonomic modulation and baroreflex sensitivity (BRS) are altered in individuals with hypertension. Aerobic exercise (AE) training has been shown to improve both measures, yet little is known about the effects of resistance exercise (RE). The purpose of this study was to examine the heart rate variability (HRV) and BRS following 4 weeks of resistance or aerobic training in a population with borderline high blood pressure (BP). METHODS: Twenty-nine mild hypertensives were recruited and randomly assigned to 4 weeks of RE or AE training. Before and after training, resting measures of HRV frequencies and BRS were obtained. RESULTS: There was a significant decrease in resting systolic BP for both exercise training modes (RE 136 +/- 3.0 pre- to 132 +/- 3.4 post-training vs. AE 142 +/- 4.0 pre- to 137 +/- 3.6 mmHg post-training, P = 0.019). Diastolic BP decreased significantly following both exercise training modes (RE 78 +/- 1.31 pre to 74 +/- 1.1 post vs. AE 80 +/- 1.7 pre to 77 +/- 1.6 mmHg post, P = 0.002). A significant time by training mode interaction for low frequency : high frequency (HF) ratio (P = 0.017) with AE decreasing the ratio (275.21 +/- 67.28 to 161.26 +/- 61.49) and RE increasing this ratio (143.73 +/- 65.00 to 227.83 +/- 59.41). Natural log-transformed (ln) HRV values showed a time-by-training mode interaction for ln HF (P = 0.05) as ln HF increased (4.7 +/- 0.38 to 5.4 +/- 0.35 ms(2)) following AE and decreased (5.98 +/- 0.37 to 5.76 +/- 0.42 ms(2)) following RE. BRS increased following aerobic training and decreased after resistance training (6.74 +/- 1.2 to 7.94 +/- 1.3 and 10.44 +/- 1.2 to 9.1 +/- 1.2 ms mmHg(-1) respectively, P = 0.021). CONCLUSIONS: Aerobic exercise improved the autonomic nervous system (increasing vagal tone, reducing sympathovagal balance while increasing BRS) while RE showed no improvements in cardiac autonomic tone and decreased BRS.

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.

Regional differences in abdominal fat loss.

OBJECTIVE: This study determined if the magnetic resonance imaging (MRI) protocol used alters the estimation of change in abdominal fat with weight loss in obese type 2 diabetic women. This study also examined if there is a uniform fat loss across the abdomen. METHODS AND PROCEDURES: Thirty-three obese postmenopausal women with type 2 diabetes (age 50-70 years, body mass index>30 kg/m(2)) had a total abdominal MRI scan pre- and post weight loss intervention. Three different MRI analysis protocols were used and compared: a single slice at L(2)-L(3) vs five slices (centered at L(4)-L(5)) vs all abdominal slices. In addition, the total abdominal scan was divided into four regions (four slices each) with region 3 (critical region) including the traditionally studied L(2)-L(3), and regions 1 and 2 superior and region 4 inferior to critical region 3. Analysis of variance (ANOVA) with repeated measures was used to compare the influence of weight loss on abdominal fat measured both regionally and using the varying number of MR slices. RESULTS: At baseline, the ratio of visceral adipose tissue:subcutaneous adipose tissue (VAT:SAT) was significantly lower using the single-slice method compared to five slices and the total abdomen (P<0.01). Using the single-slice method, a lower %VAT was found than with the other methods (P<0.01). In regions 1, 2, 3, and 4, the absolute change in total fat was 122+/-50, 182+/-48, 182+/-55, and 155+/-40 cm(3), respectively. The regional difference in abdominal fat patterning revealed that the critical region (region 3) had a smaller VAT:SAT ratio than regions 1 and 2 (P<0.05), and the ratio at region 4 was smaller than region 3 (P<0.05). Weight loss resulted in a decrease in the VAT:SAT ratio (P<0.05) for regions 3 and 4 but not for regions 1 and 2. CONCLUSIONS: The number of MR slices analyzed yields differential result in relative VAT distribution. Regional differences in abdominal fat loss occur with a greater relative VAT loss in the critical region, thus if only the critical region is analyzed the overall VAT loss induced by weight loss intervention may be overestimated.

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.

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.

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.

Influence of resistance exercise training on glucose control in women with type 2 diabetes.

The objective of the study was to evaluate the effects of acute and chronic resistance training on glucose and insulin responses to a glucose load in women with type 2 diabetes. Subjects consisted of type 2 diabetic women (n = 7) and age-matched controls (n = 8) with normal glucose tolerance. All subjects participated in 3 oral glucose tolerance tests: pretraining, 12 to 24 hours after the first exercise session (acute) and 60 to 72 hours after the final training session (chronic). Exercise training consisted of a whole body resistance exercise program using weight-lifting machines 3 days per week for 6 weeks. Resistance training was effective in increasing strength of all muscle groups in all subjects. Integrated glucose concentration expressed as area under the curve (AUC) was 3,355.0 +/- 324.6 mmol/L. min pretraining, improved significantly (P <.01) after the acute bout of exercise (2,868 +/- 324.0 mmol/L. min), but was not improved with chronic training (3,206.0 +/- 337.0 mmol/L. min) in diabetic subjects. A similar pattern of significance was observed with peak glucose concentration (pre: 20.2 +/-1.4 mmol/L; acute: 17.2 +/- 1.7 mmol/L; chronic: 19.9 +/- 1.7 mmol/L). There were no significant changes in insulin concentrations after any exercise bout in the diabetic subjects. There were no changes in glucose or insulin levels in control subjects. An acute bout of resistance exercise was effective in improving integrated glucose concentration, including reducing peak glucose concentrations in women with type 2 diabetes, but not age-matched controls. There were no significant changes in insulin concentrations for either group. Resistance exercise offers an alternative to aerobic exercise for improving glucose control in diabetic patients. To realize optimal glucose control benefits, individuals must follow a regular schedule that includes daily exercise.

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.

Dose related association of impact activity and bone mineral density in pre-pubertal girls.

Impact activity is an important contributor to bone accrual. Children engaging in such activity have been shown to have greater bone mineral density (BMD) than their peers. This cross-sectional study was designed to quantify the association between BMD and impact activity in pre-pubescent girls, specifically examining for a dose-dependent relationship. Fifty 7-11-year-old Caucasian female gymnasts were grouped by hours of gymnastics participation during a 6-month period: LOW, 1-8 hours/week (hrs/wk); HIGH, >8 hrs/wk. They were compared with 20 controls, with height, weight, age, and Tanner stage averages matched to the gymnasts. Total body, forearm, hip, lumbar spine BMD, and body composition were measured by dual energy X-ray absorptiometry (DXA). Strength was measured by one repetition maximum testing, calcium intake was quantified by questionnaire, and physical activity was measured by questionnaire and activity monitors. Total and regional BMD were greater in the HIGH group than the controls (P<0.05). Furthermore, both total and forearm BMD were greater in the HIGH group than in the LOW group, and greater in the LOW group than in the controls (P<0.05). Simple regression analysis between hrs/wk of gymnastics activity versus total and regional BMD (using maturation-adjusted Z scores) yielded a positive slope for each site. R2 was greatest for hip BMD (R2 = 0.25), and least for lumbar spine (R2 = 0.10) (P<0.0001). In conclusion, in this group of pre-pubescent girls, we observed a dose-dependent relationship between BMD and hrs/wk of impact activity; even moderate doses of impact activity were associated with increased BMD.

Resting leptin responses to acute and chronic resistance training in type 2 diabetic men and women.

PURPOSE: To evaluate the plasma leptin levels approximately 24 h post-exercise in control and type 2 diabetic subjects and to establish if observed changes in leptin concentrations were acute or chronic effects of a resistance training program. METHODS: Thirty men and women (17 controls and 13 type 2, obese diabetics, age 40-55 y) had resting blood samples drawn at 08:00 h (12 h postprandial) at the beginning of the study (pre-training), 24 h after a three repetition maximal weight lifting bout (acute) and 72 h after their last training bout of 6 weeks of resistance training (chronic). The two groups were not matched with respect to body mass index and the control subjects were not normal weight. Subjects weight-trained three times a week, for 6 weeks, for 1 h, training both the upper and lower body. RESULTS: Serum leptin concentrations were significantly higher in the type 2 diabetics than in the control group at pre-training (41.4+/-8.9 vs 11.4+/-3.0 ng/ml, P<0.05, respectively). Compared to pre-training, the leptin levels decreased significantly (P<0.01) after acute exercise in the diabetics but not in the control subjects (diabetics 30.9+/-7.1 vs controls 10.6+/-2.6 ng/ml). Approximately 72 h after 6 weeks of exercise training, the leptin concentrations were no longer lower than the pre-training values in either group (36.9+/-8.8 vs 11.9+/-8.8 ng/ml, respectively, P=NS). When leptin concentrations were log transformed and adjusted for fat mass there were still significant changes in leptin levels over time and between the control and diabetic group (P<0.05). CONCLUSIONS: The type 2 diabetics showed a significant 30% reduction in resting leptin levels 24 h after a single bout of resistance exercise. This was an acute response to resistance exercise and not a chronic training effect (no difference between pre-training and chronic). The decreased resting leptin concentrations approximately 24 h post-acute exercise may be due to reduced glucose availability to the adipose tissue, particularly in the diabetic subjects. There is no chronic effect of resistance exercise on leptin concentrations.