Effects of continuous versus intermittent exercise, obesity, and gender on growth hormone secretion.

CONTEXT: Obesity attenuates spontaneous GH secretion and the GH response to exercise. Obese individuals often have low fitness levels, limiting their ability to complete a typical 30-min bout of continuous exercise. An alternative regimen in obese subjects may be shorter bouts of exercise interspersed throughout the day. OBJECTIVE: The objective of the study was to examine whether intermittent and continuous exercise interventions evoke similar patterns of 24-h GH secretion and whether responses are attenuated in obese subjects or affected by gender. DESIGN: This was a repeated-measures design in which each subject served as their own control. SETTING: This study was conducted at the University of Virginia General Clinical Research Center. SUBJECTS: Subjects were healthy nonobese (n = 15) and obese (n = 14) young adults. INTERVENTIONS: Subjects were studied over 24 h at the General Clinical Research Center on three occasions: control, one 30-min bout of exercise, and three 10-min bouts of exercise. MAIN OUTCOME MEASURES: Twenty-four hour GH secretion was measured. RESULTS: Compared with unstimulated 24-h GH secretion, both intermittent and continuous exercise, at constant exercise intensity, resulted in severalfold elevation of 24-h integrated serum GH concentrations in young adults. Basal and pulsatile modes of GH secretion were attenuated both at rest and during exercise in obese subjects. CONCLUSIONS: The present data suggest that continuous and intermittent exercise training should be comparably effective in increasing 24-h GH secretion.

Growth hormone response to graded exercise intensities is attenuated and the gender difference abolished in older adults.

We investigated the joint impact of age, gender, and exercise intensity on growth hormone (GH) secretion. At a university center, nine young men, eight young women, seven older men, and six older women were each tested on six randomly ordered occasions [control (C) and 5 exercise conditions (Ex)]. Serum GH concentrations were measured by immunochemiluminometry [10-min samples: 0700-0900 (baseline); 0900-1300 (C or Ex + recovery)]. Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction, and GH secretion was modeled by deconvolution analyses. Subjects exercised from 0900 to 0930 at graded intensities [standardized to individual lactate threshold (LT)] of 25 and 75% of the difference between rest and LT, LT, and 25 and 75% of the difference between LT and peak oxygen consumption. Data were analyzed via mixed-effects ANOVA for repeated measures with post hoc contrasts. We found that 1) Ex elevated IGHC above C in all four cohorts, 2) 1.75 LT Ex resulted in maximal IGHC, 3) IGHC differed by gender in young (women > men) but not older adults, 4) older adults secreted 50% less GH during graded exercise, 5) Ex selectively augmented the mass of GH secreted per burst, and 6) higher Ex + recovery IGHC in young women was due to higher baseline IGHC, rather than greater stimulated GH secretion. We conclude that young women manifest a greater absolute and incremental IGHC response to exercise than postmenopausal women and men of any age. Age diminishes the GH response to exercise and abolishes the young-adult gender difference. Attenuation of GH responses to all exercise intensities in older adults has implications for exercise prescription because higher exercise intensities may be required to stimulate GH release in older adults.

Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance.

Little is known about the effects of exercise intensity on compensatory changes in glucose-stimulated insulin secretion (GSIS) when adjusted for adipose, liver and skeletal muscle insulin resistance (IR). Fifteen participants (8F, Age: 49.9±3.6yr; BMI: 31.0±1.5kg/m2; VO2peak: 23.2±1.2mg/kg/min) with prediabetes (ADA criteria, 75g OGTT and/or HbA1c) underwent a time-course matched Control, and isocaloric (200kcal) exercise at moderate (MIE; at lactate threshold (LT)), and high-intensity (HIE; 75% of difference between LT and VO2peak). A 75g OGTT was conducted 1 hour post-exercise/Control, and plasma glucose, insulin, C-peptide and free fatty acids were determined for calculations of skeletal muscle (1/Oral Minimal Model; SMIR), hepatic (HOMAIR), and adipose (ADIPOSEIR) IR. Insulin secretion rates were determined by deconvolution modeling for GSIS, and disposition index (DI; GSIS/IR; DISMIR, DIHOMAIR, DIADIPOSEIR) calculations. Compared to Control, exercise lowered SMIR independent of intensity (P<0.05), with HIE raising HOMAIR and ADIPOSEIR compared with Control (P<0.05). GSIS was not reduced following exercise, but DIHOMAIR and DIADIPOSEIR were lowered more following HIE compared with Control (P<0.05). However, DISMIR increased in an intensity based manner relative to Control (P<0.05), which corresponded with lower post-prandial blood glucose levels. Taken together, pancreatic insulin secretion adjusts in an exercise intensity dependent manner to match the level of insulin resistance in skeletal muscle, liver and adipose tissue. Further work is warranted to understand the mechanism by which exercise influences the cross-talk between tissues that regulate blood glucose in people with prediabetes.

Endothelial function following glucose ingestion in adults with prediabetes: Role of exercise intensity.

OBJECTIVE: To determine whether high intensity exercise (HIE) would improve endothelial function more than an isocaloric bout of moderate intensity exercise (MIE) following glucose ingestion in adults with prediabetes. METHODS: Twelve subjects with prediabetes completed all three conditions: time-course matched control and isocaloric exercise (∼200 kcal) at moderate (MIE; at lactate threshold) and high intensity (HIE; 75% of difference between lactate threshold and VO2 peak). Brachial artery flow-mediated dilation (FMD) was measured before exercise (baseline), within 30 min postexercise, and 1 and 2 hr following a 75 g oral glucose tolerance test (OGTT). Plasma F2-isoprostanes were also assessed during the protocol (i.e., baseline to 2 hr OGTT) as a biomarker of oxidative stress. RESULTS: MIE reduced postexercise F2-isoprostanesAUC compared with time-course matched control and HIE. Although exercise had no statistical effect on FMD postexercise or during the OGTT, elevations in FMDAUC after MIE and HIE were associated with reduced postexercise F2-isoprostanesAUC . CONCLUSIONS: Exercise at either intensity had no effect on FMD immediately postexercise following glucose administration. However, individuals with reduced oxidative stress responses to exercise had greater exercise-induced improvement in FMD. Further work is required to identify the mechanism by which exercise alters oxidative stress to enhance endothelial function.

Comparing Simple Insulin Sensitivity Indices to the Oral Minimal Model Postexercise.

PURPOSE: This study aims to establish whether changes in indices of insulin sensitivity (Si) derived from fasting glucose and an oral glucose tolerance test (OGTT) are comparable to Si determined by the oral minimal model (OMM) in response to acute moderate-intensity exercise (MIE) and high-intensity exercise (HIE). METHODS: Eighteen prediabetic subjects completed three conditions: control (no exercise), ∼ 200 kcal of MIE (∼ 50% of VO2peak), and ∼ 200 kcal of HIE (∼ 80% VO2peak). One hour postexercise (or control), subjects underwent a 75-g OGTT; plasma glucose and insulin were measured to determine Si using several OGTT-based indices (OMM, Belfiore index, Cederholm index, Matsuda index, Gutt index, oral glucose insulin sensitivity index, Stumvoll metabolic clearance rate, Stumvoll insulin sensitivity index, 1/mean OGTT insulin, and 1/insulin incremental area under the curve) and fasting indices (1/homeostatic model assessment for insulin resistance, 1/adipose tissue insulin resistance, 40/fasting insulin, and Quantitative Insulin Sensitivity Check Index). ANOVA and Pearson's correlations were used to examine relationships between changes in Si (ΔSi) among various indices compared to the OMM. RESULTS: Exercise resulted in a significant increase in Si, according to OGTT-based indices ranging from 11% to 51% (MIE, P < 0.04) and from 8% to 85% (HIE, P < 0.05). Fasting indices showed no change in response to MIE (P > 0.29) and a decrease in Si following HIE (P < 0.001). OGTT-based and fasting indices underpredicted ΔSi-OMM by ∼ 40% and ∼ 90% following MIE and HIE, respectively. ΔSi-OMM following MIE was moderately correlated with ΔSi estimated by OGTT-based indices, but not fasting indices. In contrast, ΔSi-OMM following HIE was not significantly correlated with any Si index. CONCLUSIONS: Insulin sensitivity increases postexercise, according to most Si models. However, there is high variability between indices under each condition, and these measures only correlate with the OMM following MIE. Caution should be exerted when drawing conclusions about the insulin-sensitizing effects of exercise based on OGTT and fasting indices.

Contrasting negative-feedback control of endogenously driven and exercise-stimulated pulsatile growth hormone secretion in women and men.

GH represses its own secretion via rapid and reversible feedback exerted at key hypothalamic loci. The primary mechanisms include stimulation of somatostatin release and inhibition of GHRH outflow. Autoinhibition is prominent in the adult male rat but diminutive in the female animal. The sex contrast reflects important differences in central neuropeptide signaling in this species. No comparable insights into gender-specific control of GH autofeedback are available in the human. To examine this issue, we quantitated acute recombinant human (rh)GH-induced inhibition of baseline (resting) and aerobic exercise-stimulated GH secretion in healthy young men (n = 8) and early follicular-phase women (n = 6). Each subject underwent four fasting, morning inpatient infusion studies in a prospectively randomized, placebo-controlled, double-blind, within-subject cross-over design. The feedback paradigm comprised 6-min bolus iv infusion of saline or rhGH (10 microg/kg) followed in 120 min by rest or submaximal aerobic (individually calibrated) bicycle ergometry for 30 min. Concomitantly, blood was sampled every 10 min for 6 h, and sera were submitted to immunochemiluminometric GH assay (sensitivity 0.005 microg/liter). Biexponential deconvolution analysis was applied to estimate stimulated GH secretory-burst mass (microg/liter per 90 min after onset of exercise or rest). Women and men had statistically comparable serum estradiol but unequal testosterone concentrations. Repeated-measures ANOVA documented a significant three-way interaction among gender, stimulus type (rest or exercise), and feedback status (saline or rhGH injection) in determining GH secretory-burst mass (P = 0.008). There were prominent two-factor interactions among gender and exercise (P < 0.001); gender and rhGH-induced negative feedback (P = 0.002); and exercise and rhGH feedback (P = 0.006). Gender comparisons disclosed that women, compared with men, maintain 20-fold higher GH secretory-burst mass at rest (P < 0.001); 40-fold less stimulation of pulsatile GH release by exercise than rest (P < 0.001); and 20-fold greater inhibition of GH secretory-burst mass by rhGH than saline at rest (P < 0.05). Observed feedback contrasts by sex were specific, inasmuch as gender did not affect absolute estimates of exercise-stimulated GH secretion (microg/liter/90 min); nadir GH concentrations (microg/liter) enforced by rhGH infusion; and the time latency (min) to manifest maximal inhibition after rhGH injection. In summary, the present clinical investigation unmasks: 1) markedly greater fractional feedback inhibition of pulsatile GH secretion by rhGH in young women than men; and 2) partial resistance of the aerobic-exercise stimulus to GH autofeedback in both women and men. We postulate that sex-steroid-specific control of somatostatin and GHRH outflow may mediate the former gender contrasts, whereas unknown (gender-independent) factors may determine the capability of exercise to significantly antagonize GH autoinhibition.

Impact of abdominal visceral fat, growth hormone, fitness, and insulin on lipids and lipoproteins in older adults.

We examined the relationship between abdominal visceral fat (AVF) and plasma concentrations of lipids and lipoproteins in 19 females (F) (not on estrogen) and 31 males (M) over the age of 60 (age = 66.8 years). In addition, the effects of growth hormone (GH) release, fitness (Vo(2) peak), insulin, and glucose concentrations (both fasting and in response to an oral glucose tolerance test) on lipids were examined. Subjects were categorized by low (L) and high (H) AVF (L < 130 cm(2), H > 130 cm(2)), fat mass (FM) (above or below median value), and AVF corrected for fat mass. Factorial analysis of variance (ANOVA) showed that when subjects were divided by AVF and FM, similar results were observed with H > L (P <.05) for very-low-density lipoprotein-cholesterol (VLDL-C), triglycerides (TG), VLDL-TG, apolipoprotein (apo)-B, apo-B VLDL, cholesterol (Chol)/high-density lipoprotein (HDL), LDL/HDL, apoB/A1 and L > H for HDL, HDL(2), HDL(3), apo A1, and LDL/apo-B LDL. Gender differences were also observed with F > M for Chol, LDL, HDL, and HDL(2). When AVF was corrected for FM, these gender differences were still present. After correcting for FM, differences remained between H and L AVF groups for VLDL, TG, VLDL-TG, apo-B, apo-B LDL, apo-B VLDL, apoB/A1 (P <.05). Twenty-four hour integrated GH concentration (IGHC) was inversely related to VLDL, TG, VLDL TG, LDL TG, apoB, apoB VLDL, apoB LDL, Chol/HDL, LDL/HDL, and apoB/A1 in F, but not M (P <.05). Vo(2) peak was directly related to Chol, LDL, HDL(3), and apoB LDL with stronger relationships observed in F. Fasting insulin was related to lipids and lipoproteins in both men and women. These data suggest that, in older adults, elevated levels of AVF, FM, and AVF corrected for FM are associated with unfavorable lipid-lipoprotein profiles and extend similar findings reported in younger males and females with elevated AVF. These data also support previous findings indicating that AVF is a primary determinant of GH release.

Gender governs the relationship between exercise intensity and growth hormone release in young adults.

We previously reported that in young adult males growth hormone (GH) release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498-504, 1999). To investigate the effects of gender and exercise intensity on GH release, eight women (24.3 +/- 1.3 yr, 171 +/- 3.2 cm height, 63.6 +/- 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900-0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700-1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men.

Growth hormone release during acute and chronic aerobic and resistance exercise: recent findings.

Exercise is a potent physiological stimulus for growth hormone (GH) secretion, and both aerobic and resistance exercise result in significant, acute increases in GH secretion. Contrary to previous suggestions that exercise-induced GH release requires that a "threshold" intensity be attained, recent research from our laboratory has shown that regardless of age or gender, there is a linear relationship between the magnitude of the acute increase in GH release and exercise intensity. The magnitude of GH release is greater in young women than in young men and is reduced by 4-7-fold in older individuals compared with younger individuals. Following the increase in GH secretion associated with a bout of aerobic exercise, GH release transiently decreases. As a result, 24-hour integrated GH concentrations are not usually elevated by a single bout of exercise. However, repeated bouts of aerobic exercise within a 24-hour period result in increased 24-hour integrated GH concentrations. Because the GH response to acute resistance exercise is dependent on the work-rest interval and the load and frequency of the resistance exercise used, the ability to equate intensity across different resistance exercise protocols is desirable. This has proved to be a difficult task. Problems with maintaining patent intravenous catheters have resulted in a lack of studies investigating alterations in acute and 24-hour GH pulsatile secretion in response to resistance exercise. However, research using varied resistance protocols and sampling techniques has reported acute increases in GH release similar to those observed with aerobic exercise. In young women, chronic aerobic training at an intensity greater than the lactate threshold resulted in a 2-fold increase in 24-hour GH release. The time line of adaptation and the mechanism(s) by which this training effect occurs are still elusive. Unfortunately, there are few studies investigating the effects of chronic resistance training on 24-hour GH release. The decrease in GH secretion observed in individuals who are older or have obesity is associated with many deleterious health effects, although a cause and effect relationship has not been established. While exercise interventions may not restore GH secretion to levels observed in young, healthy individuals, exercise is a robust stimulus of GH secretion. The combination of exercise and administration of oral GH secretagogues may result in greater GH secretion than exercise alone in individuals who are older or have obesity. Whether such interventions would result in favourable clinical outcomes remains to be established.

Effects of exercise intensity on postprandial improvement in glucose disposal and insulin sensitivity in prediabetic adults.

BACKGROUND: A single bout of exercise improves postprandial glycemia and insulin sensitivity in prediabetic patients; however, the impact of exercise intensity is not well understood. The present study compared the effects of acute isocaloric moderate (MIE) and high-intensity (HIE) exercise on glucose disposal and insulin sensitivity in prediabetic adults. METHODS: Subjects (n=18; age 49±14 y; fasting glucose 105±11 mg/dL; 2 h glucose 170±32 mg/dL) completed a peak O2 consumption/lactate threshold (LT) protocol plus three randomly assigned conditions: 1) control, 1 hour of seated rest, 2) MIE (at LT), and 3) HIE (75% of difference between LT and peak O2 consumption). One hour after exercise, subjects received an oral glucose tolerance test (OGTT). Plasma glucose, insulin, and C-peptide concentrations were sampled at 5- to 10-minute intervals at baseline, during exercise, after exercise, and for 3 hours after glucose ingestion. Total, early-phase, and late-phase area under the glucose and insulin response curves were compared between conditions. Indices of insulin sensitivity (SI) were derived from OGTT data using the oral minimal model. RESULTS: Compared with control, SI improved by 51% (P=.02) and 85% (P<.001) on the MIE and HIE days, respectively. No differences in SI were observed between the exercise conditions (P=.62). Improvements in SI corresponded to significant reductions in the glucose, insulin, and C-peptide area under the curve values during the late phase of the OGTT after HIE (P<.05), with only a trend for reductions after MIE. CONCLUSION: These results suggest that in prediabetic adults, acute exercise has an immediate and intensity-dependent effect on improving postprandial glycemia and insulin sensitivity.

Effect of an herbal/botanical supplement on recovery from delayed onset muscle soreness: a randomized placebo-controlled trial.

BACKGROUND: We examined the effects of a proprietary herbal/botanical supplement (StemSport, Stemtech, San Clemente, CA.) suggested to increase circulating stem cells, decrease inflammation, and attenuate exercise induced muscle damage on recovery from delayed onset muscle soreness (DOMS). METHODS: Sixteen subjects (male = 7, female = 9; age 23.8 ± 10 years; height 171.9 ± 10 cm, mass 72.2 ± 15 kg) were randomized in a crossover, double-blind, placebo controlled trial to receive a placebo or StemSport supplement (6150 mg/day) for 14 days. DOMS was induced on day 7 for both placebo and active conditions in the non-dominant elbow flexor group with repeated eccentric repetitions. Muscle swelling (biceps girth), elbow flexor isometric strength (hand held dynamometer), muscle pain/tenderness (visual analog scale), range of motion (active elbow flexion and extension), and inflammation (hsCRP, IL6, and TNF-α) were measured at baseline and at 24 h, 48 h, 72 h, and 168 h (1 week) post eccentric exercise. The crossover washout period was ≥14 days. RESULTS: No significant condition-by-time interactions between placebo and StemSport supplementation were observed with regard to measures of pain (p = 0.59), tenderness (p = 0.71), isometric strength (p = 0.32), elbow flexion (p = 0.45), muscle swelling (p = 0.90), or inflammation (p > 0.90). Decrements in elbow extension range of motion 48 h post-exercise were less after StemSport supplementation (Δ elbow extension 48 h post; StemSport, -2.0 deg; placebo, -10 deg; p = 0.003). CONCLUSIONS: These data suggest that compared to placebo, StemSport supplementation does not improve outcome measures related to muscle recovery after acute upper-arm induced DOMS.

Effect of exercise training intensity on abdominal visceral fat and body composition.

UNLABELLED: The metabolic syndrome is a complex clustering of metabolic defects associated with physical inactivity, abdominal adiposity, and aging. PURPOSE: To examine the effects of exercise training intensity on abdominal visceral fat (AVF) and body composition in obese women with the metabolic syndrome. METHODS: Twenty-seven middle-aged obese women (mean +/- SD; age = 51 +/- 9 yr and body mass index = 34 +/- 6 kg x m(-2)) with the metabolic syndrome completed one of three 16-wk aerobic exercise interventions: (i) no-exercise training (Control): seven participants maintained their existing levels of physical activity; (ii) low-intensity exercise training (LIET): 11 participants exercised 5 d x wk(-1) at an intensity < or = lactate threshold (LT); and (iii) high-intensity exercise training (HIET): nine participants exercised 3 d x wk(-1) at an intensity > LT and 2 d x wk(-1) < or = LT. Exercise time was adjusted to maintain caloric expenditure (400 kcal per session). Single-slice computed tomography scans obtained at the L4-L5 disc space and midthigh were used to determine abdominal fat and thigh muscle cross-sectional areas. Percent body fat was assessed by air displacement plethysmography. RESULTS: HIET significantly reduced total abdominal fat (P < 0.001), abdominal subcutaneous fat (P = 0.034), and AVF (P = 0.010). There were no significant changes observed in any of these parameters within the Control or the LIET conditions. CONCLUSIONS: The present data indicate that body composition changes are affected by the intensity of exercise training with HIET more effectively for reducing total abdominal fat, subcutaneous abdominal fat, and AVF in obese women with the metabolic syndrome.

NIH ImageJ and Slice-O-Matic computed tomography imaging software to quantify soft tissue.

OBJECTIVE: To compare reliability and limits of agreement of soft tissue cross-sectional areas obtained using Slice-O-Matic and NIH ImageJ medical imaging software packages. RESEARCH METHODS AND PROCEDURES: Abdominal and midthigh images were obtained using single-slice computed tomography. Two trained investigators analyzed each computed tomography image in duplicate. Adipose tissue and skeletal muscle cross-sectional areas (centimeters squared) were calculated using standard Hounsfield unit ranges (adipose tissue: -190 to -30 and skeletal muscle: -29 to 150). Regions of interest included abdominal total area, total fat area, subcutaneous fat area, visceral fat area (AVF), and right and left thigh total area, fat area, and skeletal muscle area. RESULTS: For all images, intra-investigator coefficients of variation ranged from 0.2% to 3.4% and from 0.4% to 5.6% and inter-investigator coefficients of variation ranged from 0.9% to 4.8% and 0.2% to 2.6% for Slice-O-Matic and NIH ImageJ, respectively, with intra- and inter-investigator coefficients of reliability of R(2) = 0.99. Mean AVF values for investigators A and B ranged from 168 to 170 cm(2) using Slice-O-Matic and NIH ImageJ. Bland-Altman analyses revealed that Slice-O-Matic and NIH ImageJ results were comparable. The mean differences (95% confidence intervals) between the AVF cross-sectional areas obtained using the Slice-O-Matic and NIH ImageJ medical imaging software were +2.5 cm(2) (-5.7, +10.8 cm(2)) or +1.4% (-3.4%, +6.4%). DISCUSSION: These findings show that both the Slice-O-Matic and NIH ImageJ medical imaging software systems provide reliable measurements of adipose tissue and skeletal muscle cross-sectional areas.

The metabolic syndrome, hypertriglyceridemic waist, and cardiometabolic risk factor profile in obese women.

The hypertriglyceridemic waist (HTGW) and metabolic syndrome (MS) are associated with increased cardiometabolic risk. We evaluated the impact of the HTGW on cardiometabolic risk factors in obese women diagnosed with the MS. Thirty-six abdominally obese women with the MS as defined by the International Diabetes Federation (IDF) [(mean (SD); age 49 (11) y, ht 165 (6) cm, wt 95 (16) kg] participated. The HTGW was defined as follows: a waist circumference ≥80 cm and triglycerides ≥1.7 mM. Unpaired t-tests and Analysis of Covariance (ANCOVA) were employed to detect mean differences between women with MS plus or minus HTGW. Women with the MS plus HTGW had higher total cholesterol (16%, p=0.015), VLDL-cholesterol (97%, p<0.001), non-HDL-cholesterol (16%, p=0.002), insulin (40%, p=0.043), and abdominal visceral fat (24%, p=0.100), and lower total HDL-cholesterol (6%, p=0.024), HDL(3) (11%, p=0.031) and Quantitative Insulin Sensitivity Check Index (QUICKI) (5%, p=0.068) compared with women with the MS minus HTGW. Thus, the presence of the HTGW was accompanied by a worsened cardiometabolic risk factor profile in these obese women with the MS. In particular, women with the MS plus HTGW were more insulin resistant compared to women with the MS minus HTGW. In conclusion, the presence of the HTGW in obese women with the MS exacerbates insulin resistance and cardiometabolic risk factors.