Work organization, sleep and metabolic syndrome among long-haul truck drivers.

BACKGROUND: The work organization of long-haul truck drivers in the USA contains factors that have been shown to degrade sleep. In combination, these factors generate elevated cardiometabolic risk by inducing components of the metabolic syndrome (MetS). However, the prevalence and severity of MetS and the degree to which such factors differentially influence MetS among these drivers are unknown. AIMS: To determine the prevalence and severity of MetS among US long-haul truck drivers and to determine the predictive value of demographic, work organization and sleep variables in MetS diagnosis and severity. METHODS: A non-experimental, descriptive, cross-sectional study, designed to collect survey, anthropometric and biometric data from US long-haul truck drivers. Descriptive analyses were performed for demographic, work organization, sleep and MetS measures. Logistic and linear regression analyses examined potential predictive relationships between demographic, work organization and sleep variables and MetS diagnosis and severity. RESULTS: The study population was 262. Nearly 60% of drivers met MetS diagnosis criteria. Over 80% had a waist circumference >102 cm, 50% had triglyceride levels of ≥150 mg/dl, 66% had an high-density lipoprotein of <40 mg/dl, 28% had a blood pressure of ≥135/80 mm Hg and 17% had a fasting glucose of ≥110 mg/dl. Driving experience and work day sleep quality were associated with MetS prevalence and severity. CONCLUSIONS: The prevalence and severity of MetS among this sample of US long-haul truck drivers were high. Preventive efforts should focus on experienced drivers and work day sleep quality.

Some sex hormone profiles are consistent over time in normal menstruating women: implications for sports injury epidemiology.

PURPOSE: It is unclear whether sex hormone profiles obtained in two consecutive months are consistent within women. Month-to-month consistency in daily, nadir, peak and mean hormone concentrations during the early follicular and luteal phases in recreationally active, young eumenorrheic women was prospectively examined. METHODS: 60 healthy, non-smoking women who reported normal and consistent menstrual cycles lasting 26-32 days for the past 6 months were followed prospectively to obtain serum samples for the first 6 days of menses and for 8 days after a positive ovulation test over two consecutive months. Month-to-month consistency of daily concentrations of oestradiol (pg/ml), progesterone (ng/ml), testosterone (ng/dl), sex hormone-binding globulin (nmol/l) and free androgen index were determined using linear mixed models. Month-to-month consistency in nadir, peak and mean concentrations were then assessed using intraclass correlation coefficients and SEM to more precisely examine intraindividual consistency. RESULTS: Linear mixed models revealed stable hormone concentrations across cycles and cycles by day. Reliability estimates for nadir, peak, mean menses and mean postovulatory concentrations range from 0.56 to 0.86 for oestradiol, 0.44 to 0.91 for progesterone, 0.60 to 0.86 for testosterone, 0.88 to 0.97 for sex hormone-binding globulin and 0.78 to 0.91 for free androgen index. CONCLUSIONS: Hormone profiles were reproducible over two consecutive months. To reduce month-to-month intraindividual variations and improve measurement consistency, it is recommended that multiple samples be taken over consecutive days as opposed to a single sample.

Plasma protein carbonyl response to increasing exercise duration in aerobically trained men and women.

The purpose of this study was to determine the effect of aerobic exercise duration on plasma protein carbonyl concentrations, a marker of protein oxidation, in aerobically trained men and women. Eight men (age: 27 +/- 4 years, VO (2peak): 4.09 +/- 0.26 L x min (-1); mean +/- SD) and 7 women (age: 27 +/- 6 years, VO (2peak): 2.33 +/- 0.24 L x min (-1)) exercised on an electrically-braked cycle ergometer at 70 % VO (2peak) for 30, 60 or 120 minutes on three separate days. Plasma samples collected before and immediately, 30- and 60-minutes post-exercise were analyzed for protein carbonyls. Mean oxygen uptake was greater for men in all conditions (2.75 +/- 0.03 L x min (-1); 38 +/- 0.43 ml x kg (-1) x min (-1)) compared to women (1.57 +/- 0.03 L x min (-1); 24.1 +/- 0.47 ml x kg (-1) x min (-1)). Total work performed during the exercise sessions was also greater for men than for women during the 30 (368 +/- 11 versus 223 +/- 7 kJ), 60 (697 +/- 17 versus 423 +/- 18 kJ), and 120-minute conditions (1173 +/- 44 versus 726 +/- 28 kJ) (Mean +/- SEM). Although these comparisons were significant (p < 0.0001), sex differences in total work performed and mean VO (2) did not result in sex differences in protein carbonyls. However, a condition by time interaction was observed with greater post-exercise values following the 120-minute condition compared to both the 30- and 60-minute conditions. Protein carbonyl concentration was greatest immediately post-exercise for both men and women and generally declined in a linear trend through one hour of recovery. These data suggest that protein carbonyl concentration is elevated by cycling exercise performed at 70 % VO (2peak), is greater following longer duration rides, begins to recover within one hour following exercise, and is not different between men and women.

Neuroendocrine control of GH release during acute aerobic exercise.

GH secretion declines with aging and is decreased in conditions such as obesity. Several physiologic factors alter pulsatile GH secretion, including age, gender, body composition, regional distribution of fat and in particular abdominal visceral fat, sleep, nutrition, exercise and serum concentrations of gonadal steroids, insulin and IGF-I. Acute aerobic exercise is a powerful stimulus to GH release. Available studies suggest that intensity and duration of acute exercise, fitness, and training state may all influence, in part, the GH response to exercise. Intensity of exercise plays a key role in GH response to exercise. In the present paper we will discuss the GH response during acute aerobic exercise with a focus on exercise intensity and GH release. We will also provide an overview of the neuroendocrine control of exercise-induced GH release. Finally, information related to the effects of aging and gender on the GH response to exercise will be provided.

E2 supplementation selectively relieves GH's autonegative feedback on GH-releasing peptide-2-stimulated GH secretion.

Female gender confers resistance to GH autonegative feedback in the adult rat, thereby suggesting gonadal or estrogenic modulation of autoregulation of the somatotropic axis. Here we test the clinical hypothesis that short-term E2 replacement in ovariprival women reduces GH's repression of spontaneous, GHRH-, and GH-releasing peptide (GHRP)-stimulated GH secretion. To this end, we appraised GH autoinhibition in nine healthy postmenopausal volunteers during a prospective, randomly ordered supplementation with placebo vs. E [1 mg micronized 17 beta-E2 orally twice daily for 6-23 d]. The GH autofeedback paradigm consisted of a 6-min pulsed i.v. infusion of recombinant human GH (10 microg/kg square-wave injection) or saline (control) followed by i.v. bolus GHRH (1 microg/kg), GHRP-2 (1 microg/kg), or saline 2 h later. Blood was sampled every 10 min and serum GH concentrations were measured by chemiluminescence. Poststimulus GH release was quantitated by multiparameter deconvolution analysis using published biexponential kinetics and by the incremental peak serum GH concentration response (maximal poststimulus value minus prepeak nadir). Outcomes were analyzed on the logarithmic scale by mixed-effects ANOVA at a multiple-comparison type I error rate of 0.05. E2 supplementation increased the (mean +/- SEM) serum E2 concentration from 43 +/- 1.8 (control) to 121 +/- 4 pg/ml (E2) (158 +/- 6.6 to 440 +/- 15 pmol/liter; P < 0.001), lowered the 0800 h (preinfusion) serum IGF-I concentration from 127 +/- 7.7 to 73 +/- 3.6 microg/liter (P < 0.01), and amplified spontaneous pulsatile GH production from 7.5 +/- 1.1 to 13 +/- 2.3 microg/liter per 6 h (P = 0.020). In the absence of exogenously imposed GH autofeedback, E2 replacement enhanced the stimulatory effect of GHRP-2 on incremental peak GH release by 1.58-fold [95% confidence interval, 1.2- to 2.1-fold] (P = 0.0034) but did not alter the action of GHRH (0.83-fold [0.62- to 1.1-fold]). In the E2-deficient state, bolus GH infusion significantly inhibited subsequent spontaneous, GHRH-, and GHRP-induced incremental peak GH responses by, respectively, 33% (1-55%; P = 0.044 vs. saline), 79% (68-86%; P < 0.0001), and 54% (32-69%; P = 0.0002). E2 repletion failed to influence GH autofeedback on either spontaneous or GHRH-stimulated incremental peak GH output. In contrast, E2 replenishment augmented the GHRP-2-stimulated incremental peak GH response in the face of GH autoinhibition by 1.7-fold (1.2- to 2.5-fold; P = 0.009). Mechanistically, the latter effect of E2 mirrored its enhancement of GH-repressed/GHRP-2-stimulated GH secretory pulse mass, which rose by 1.5-fold (0.95- to 2.5-fold over placebo; P = 0.078). In summary, the present clinical investigation documents the ability of short-term oral E2 supplementation in postmenopausal women to selectively rescue GHRP-2 (but not spontaneous or GHRH)-stimulated GH secretion from autonegative feedback. The secretagogue specificity of E's relief of GH autoinhibition suggests that this sex steroid may enhance activity of the hypothalamopituitary GHRP-receptor/effector pathway.

Whole organ transplantation and glucose regulation.

Pancreas transplantation has gained clinical acceptance since its initial application more than 30 years ago. A constellation of surgical, pharmacologic, and metabolic alterations occur with transplantation, particularly if pancreatic transplantation is performed in addition to renal transplantation in a uremic diabetic. Increasingly sophisticated studies have allowed analysis of the performance of the transplanted organ and have enhanced our basic understanding of insulin's complex interplay in peripheral glucoregulatory processes.

Impaired insulin secretion and increased insulin sensitivity in familial maturity-onset diabetes of the young 4 (insulin promoter factor 1 gene).

Diabetes resulting from heterozygosity for an inactivating mutation of the homeodomain transcription factor insulin promoter factor 1 (IPF-1) is due to a genetic defect of beta-cell function referred to as maturity-onset diabetes of the young 4. IPF-1 is required for the development of the pancreas and mediates glucose-responsive stimulation of insulin gene transcription. To quantitate islet cell responses in a family harboring a Pro63fsdelC mutation in IPF-1, we performed a five-step (1-h intervals) hyperglycemic clamp on seven heterozygous members (NM) and eight normal genotype members (NN). During the last 30 min of the fifth glucose step, glucagon-like peptide 1 (GLP-1) was also infused (1.5 pmol x kg(-1) x min(-1)). Fasting plasma glucose levels were greater in the NM group than in the NN group (9.2 vs. 5.9 mmol/l, respectively; P < 0.05). Fasting insulin levels were similar in both groups (72 vs. 105 pmol/l for NN vs. NM, respectively). First-phase insulin and C-peptide responses were absent in individuals in the NM group, who had markedly attenuated insulin responses to glucose alone compared with the NN group. At a glucose level of 16.8 mmol/l above fasting level, GLP-1 augmented insulin secretion equivalently (fold increase) in both groups, but the insulin and C-peptide responses to GLP-1 were sevenfold less in the NM subjects than in the NN subjects. In both groups, glucagon levels fell during each glycemic plateau, and a further reduction occurred during the GLP-1 infusion. Sigmoidal dose-response curves of glucose clearance versus insulin levels during the hyperglycemic clamp in the two small groups showed both a left shift and a lower maximal response in the NM group compared with the NN group, which is consistent with an increased insulin sensitivity in the NM subjects. A sharp decline occurred in the dose-response curve for suppression of nonesterified fatty acids versus insulin levels in the NM group. We conclude that the Pro63fsdelC IPF-1 mutation is associated with a severe impairment of beta-cell sensitivity to glucose and an apparent increase in peripheral tissue sensitivity to insulin and is a genetically determined cause of beta-cell dysfunction.

Synergy of L-arginine and growth hormone (GH)-releasing peptide-2 on GH release: influence of gender.

We test the hypotheses that 1) growth hormone (GH)-releasing peptide-2 (G) synergizes with L-arginine (A), a compound putatively achieving selective somatostatin withdrawal and 2) gender modulates this synergy on GH secretion. To these ends, 18 young healthy volunteers (9 men and 9 early follicular phase women) each received separate morning intravenous infusions of saline (S) or A (30 g over 30 min) or G (1 microg/kg) or both, in randomly assigned order. Blood was sampled at 10-min intervals for later chemiluminescence assay of serum GH concentrations. Analysis of covariance revealed that the preinjection (basal) serum GH concentrations significantly determined secretagogue responsiveness and that sex (P = 0.02) and stimulus type (P < 0.001) determined the slope of this relationship. Nested ANOVA applied to log-transformed measures of GH release showed that gender determines 1) basal rates of GH secretion, 2) the magnitude of the GH secretory response to A, 3) the rapidity of attaining the GH maximum, and 4) the magnitude or fold (but not absolute) elevation in GH secretion above preinjection basal, as driven by the combination of A and G. In contrast, the emergence of the G and A synergy is sex independent. We conclude that gender modulates key facets of basal and A/G-stimulated GH secretion in young adults.

Synergy of L-arginine and GHRP-2 stimulation of growth hormone in men and women: modulation by exercise.

We investigated the ability of exercise, a multipathway, potent, physiological stimulus for GH release, to alter the synergistic interaction of L-arginine (A) and GH-related peptide (GHRP)-2 (G) observed at rest and the ability of gender to further modulate this putative interaction. Subjects (9 men and 9 early follicular phase women) completed 30 min of constant load aerobic exercise in combination with intravenous infusions of saline (S), A (30 g over 30 min), G (1 microg/kg bolus), or both (AG) in separate study sessions in randomly assigned order. Measures of GH release were logarithmically transformed for statistical analysis. Similar to rest, exercise maintained the rank order (AG > G > A > S) of effective stimulation of GH release for the key response measures in men or women, a gender disparity in the time to reach the maximal serum GH concentration, the calculated endogenous GH half-life, and the observed effect of preinfusion (basal) serum GH concentrations on determining secretagogue responsiveness. Exercise potentiated the individual stimulatory actions of A and G, while blunting the relative magnitude of the synergistic (supra-additive) interaction observed at rest. We infer from the present data that 1) exercise is likely to induce release of both GHRH and somatostatin, 2) L-arginine may facilitate the effect of exercise by limiting somatostatin release, 3) GHRP-2 could further enhance the stimulatory impact of exercise by opposing central actions of somatostatin and/or heightening endogenous GHRH release, and 4) gender strongly controls the relative but not absolute magnitude of A/G synergy both at rest and after exercise.

Intensity of acute exercise does not affect serum leptin concentrations in young men.

PURPOSE: We examined the effects of exercise intensity on serum leptin levels. METHODS: Seven men (age = 27.0 yr; height = 178.3 cm; weight = 82.2 kg) were tested on a control (C) day and on 5 exercise days (EX). Subjects exercised (30 min) at the following intensities: 25% and 75% of the difference between the lactate threshold (LT) and rest (0.25 LT, 0.75 LT), at LT, and at 25% and 75% of the difference between LT and VO2peak (1.25 LT, 1.75 LT). RESULTS: Kcal expended during the exercise bouts ranged from 150 +/- 11 kcal (0.25 LT) to 529 +/- 45 kcal (1.75 LT), whereas exercise + 3.5 h recovery kcal ranged from 310 +/- 14 kcal (0.25 LT) to 722 +/- 51 kcal (1.75 LT). Leptin area under the curve (AUC) (Q 10-min samples) for all six conditions (C + 5 Ex) was calculated for baseline (0700-0900 h) and for exercise + recovery (0900-1300 h). Leptin AUC for baseline ranged from 243 +/- 33 to 291 +/- 56 ng x mL(-1) x min; for exercise + recovery results ranged from 424 +/- 56 to 542 +/- 99 ng x mL(-1) x min. No differences were observed among conditions within either the baseline or exercise + recovery time frames. Regression analysis confirmed positive relationships between serum leptin concentrations and percentage body fat (r = 0.94) and fat mass (r = 0.93, P < 0.01). CONCLUSION: We conclude that 30 min of acute exercise, at varying intensity of exercise and caloric expenditure, does not affect serum leptin concentrations during exercise or for the first 3.5 hours of recovery in healthy young men.

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow.

To test the hypothesis that heightened sympathetic outflow precedes and predicts the magnitude of the growth hormone (GH) response to acute exercise (Ex), we studied 10 men [age 26.1 +/- 1.7 (SE) yr] six times in randomly assigned order (control and 5 Ex intensities). During exercise, subjects exercised for 30 min (0900-0930) on each occasion at a single intensity: 25 and 75% of the difference between lactate threshold (LT) and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT). Mean values for peak plasma epinephrine (Epi), plasma norepinephrine (NE), and serum GH concentrations were determined [Epi: 328 +/- 93 (SE), 513 +/- 76, 584 +/- 109, 660 +/- 72, and 2,614 +/- 579 pmol/l; NE: 2. 3 +/- 0.2, 3.9 +/- 0.4, 6.9 +/- 1.0, 10.7 +/- 1.6, and 23.9 +/- 3.9 nmol/l; GH: 3.6 +/- 1.5, 6.6 +/- 2.0, 7.0 +/- 2.0, 10.7 +/- 2.4, and 13.7 +/- 2.2 microg/l for 0.25, 0.75, 1.0, 1.25, and 1.75LT, respectively]. In all instances, the time of peak plasma Epi and NE preceded peak GH release. Plasma concentrations of Epi and NE always peaked at 20 min after the onset of Ex, whereas times to peak for GH were 54 +/- 6 (SE), 44 +/- 5, 38 +/- 4, 38 +/- 4, and 37 +/- 2 min after the onset of Ex for 0.25-1.75LT, respectively. ANOVA revealed that intensity of exercise did not affect the foregoing time delay between peak NE or Epi and peak GH (range 17-24 min), with the exception of 0.25LT (P < 0.05). Within-subject linear regression analysis disclosed that, with increasing exercise intensity, change in (Delta) GH was proportionate to both DeltaNE (P = 0.002) and DeltaEpi (P = 0.014). Furthermore, within-subject multiple-regression analysis indicated that the significant GH increment associated with an antecedent rise in NE (P = 0.02) could not be explained by changes in Epi alone (P = 0.77). Our results suggest that exercise intensity and GH release in the human may be coupled mechanistically by central adrenergic activation.

Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men.

We examined the relationship between energy expenditure (in kcal) and epinephrine (Epi), norepinephrine (NE), and growth hormone (GH) release. Ten men [age, 26 yr; height, 178 cm; weight, 81 kg; O(2) uptake at lactate threshold (LT), 36.3 ml. kg(-1). min(-1); peak O(2) uptake, 49.5 ml. kg(-1). min(-1)] were tested on six randomly ordered occasions [control, 5 exercise: at 25 and 75% of the difference between LT and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT) (0900-0930)]. From 0700 to 1300, blood was sampled and assayed for GH, Epi, and NE. Carbohydrate (CHO) expenditure during exercise and fat expenditure during recovery rose proportionately to increasing exercise intensity (P = 0.002). Fat expenditure during exercise and CHO expenditure during recovery were not affected by exercise intensity. The relationship between exercise intensity and CHO expenditure during exercise could not be explained by either Epi (P = 1.00) or NE (P = 0.922), whereas fat expenditure during recovery increased with Epi and GH independently of exercise intensity (P = 0. 028). When Epi and GH were regressed against fat expenditure during recovery, only GH remained statistically significant (P < 0.05). We conclude that a positive relationship exists between exercise intensity and both CHO expenditure during exercise and fat expenditure during recovery and that the increase in fat expenditure during recovery with higher exercise intensities is related to GH release.

Effects of gender on exercise-induced growth hormone release.

We examined gender differences in growth hormone (GH) secretion during rest and exercise. Eighteen subjects (9 women and 9 men) were tested on two occasions each [resting condition (R) and exercise condition (Ex)]. Blood was sampled at 10-min intervals from 0600 to 1200 and was assayed for GH by chemiluminescence. At R, women had a 3.69-fold greater mean calculated mass of GH secreted per burst compared with men (5.4 +/- 1.0 vs. 1.7 +/- 0.4 microg/l, respectively) and higher basal (interpulse) GH secretion rates, which resulted in greater GH production rates and serum GH area under the curve (AUC; 1,107 +/- 194 vs. 595 +/- 146 microg x l(-1) x min, women vs. men; P = 0.04). Compared with R, Ex resulted in greater mean mass of GH secreted per burst, greater mean GH secretory burst amplitude, and greater GH AUC (1,196 +/- 211 vs. 506 +/- 90 microg x l(-1) x min, Ex vs. R, respectively; P < 0.001). During Ex, women attained maximal serum GH concentrations significantly earlier than men (24 vs. 32 min after initiation of Ex, respectively; P = 0.004). Despite this temporal disparity, both genders had similar maximal serum GH concentrations. The change in AUC (adjusted for unequal baselines) was similar for men and women (593 +/- 201 vs. 811 +/- 268 microg x l(-1) x min), but there were significant gender-by-condition interactive effects on GH secretory burst mass, pulsatile GH production rate, and maximal serum GH concentration. We conclude that, although women exhibit greater absolute GH secretion rates than men both at rest and during exercise, exercise evokes a similar incremental GH response in men and women. Thus the magnitude of the incremental secretory GH response is not gender dependent.

Impact of acute exercise intensity on pulsatile growth hormone release in men.

To investigate the effects of exercise intensity on growth hormone (GH) release, 10 male subjects were tested on 6 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 (exercise+ recovery). 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 (0.25LT and 0.75LT, respectively), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT and 1.75LT, respectively). No differences were observed among conditions for baseline IGHC. Exercise+recovery IGHC (mean +/- SE: C = 250 +/- 60; 0.25LT = 203 +/- 69; 0.75LT = 448 +/- 125; LT = 452 +/- 119; 1.25LT = 512 +/- 121; 1.75LT = 713 +/- 115 microg x l(-1) x min(-1)) increased linearly with increasing exercise intensity (P < 0.05). Deconvolution analysis revealed that increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and GH production rate [production rate increased from 16. 5 +/- 4.5 (C) to 32.1 +/- 5.2 microg x distribution volume(-1) x min(-1) (1.75LT), P < 0.05], with no changes in GH pulse frequency or half-life of elimination. We conclude that the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern in young men.

Validity of methods of body composition assessment in young and older men and women.

We examined the validity of percent body fat (%Fat) estimation by two-compartment (2-Comp) hydrostatic weighing (Siri 2-Comp), 3-Comp dual-energy X-ray absorptiometry (DEXA 3-Comp), 3-Comp hydrostatic weighing corrected for the total body water (Siri 3-Comp), and anthropometric methods in young and older individuals (n = 78). A 4-Comp model of body composition served as the criterion measure of %Fat (Heymsfield 4-Comp; S. B. Heymsfield, S. Lichtman, R. N. Baumgartner, J. Wang, Y. Kamen, A. Aliprantis, and R. N. Pierson Jr., Am. J. Clin. Nutr. 52: 52-58, 1990.). Comparison of the Siri 3-Comp with the Heymsfield 4-Comp model revealed mean differences of /= r = 0.997, total error values

The influence of anatomical boundaries, age, and sex on the assessment of abdominal visceral fat.

Single-slice abdominal computed tomography (CT) scanning has been used extensively for the measurement of abdominal visceral fat (AVF). Optimal anatomical scan location and pixel density ranges have been proposed and are specifically reported to allow for the replication and standardization of AVF measurements. Standardization of the anatomical boundaries for CT measurement of AVF and the influence of age and gender on results obtained with different boundary locations have received much less attention. To determine the influence of three boundary analysis methods (AVF-1, AVF-2, and AVF-3) on the measurement of AVF by CT, 54 older (60 years to 79 years) and 37 younger (20 years to 29 years) healthy men and women were examined. The measurement boundary for AVF-1 was the internal most aspect of the abdominal and oblique muscle walls, and the posterior aspect of the vertebral body. AVF-2 used fat measurements enclosed in a boundary formed by the midpoint of the abdominal and oblique muscle walls, and the most posterior aspect of the spinous process. AVF-3 used fat measurements enclosed in a boundary formed by the external border of the abdominal and oblique muscle walls, and the external border of the erector spinae. Greater AVF measures were obtained with AVF-2 and AVF-3 compared with AVF-1 (p < 0.0001). These differences were greater in older compared with younger subjects (p < 0.0001) and greater in women compared with men (p < 0.02). The significantly greater AVF measurements obtained with AVF-2 and AVF-3 resulted from the inclusion of larger amounts of fat that are not drained by the portal circulation. This included retroperitoneal, intermuscular, and intramuscular lipid droplets, which increase with aging. On the basis of these results, we recommend the AVF-1 anatomical boundaries for the measurement of AVF in clinical investigations, particularly with older subjects. These data demonstrate the importance of precise and reproducible anatomical boundaries for the measurement of AVF, particularly in longitudinal studies.

Body composition by DEXA in older adults: accuracy and influence of scan mode.

Dual energy x-ray absorptiometry (DEXA) measures bone mineral content (BMC), bone mineral density (BMD), fat-free mass (FFM), and provides estimates of percent body fat. Changes in scan mode geometry (pencil beam vs array) may impact these measures and body composition estimates using multi-compartment models. Forty-one adults, ages 59-79 yr, were scanned in each mode and also underwent hydrostatic weighing and measurement of total body water (tritiated water dilution). The effect of scan mode on measurement of DEXA BMC, BMD, FFM, and percent body fat (DEXA %Fat) was examined. The effect of scan mode on percentage body fat determined by a 4-compartment body composition model (4 Comp %Fat) and comparison of DEXA %Fat and 4 Comp %Fat were also examined. BMC and DEXA %Fat were greater (1.3% and 3.9%, respectively, P < 0.01), and BMD and FFM were lower (1.1% and 1.9%, respectively, P < 0.01) with the array scan mode. The 4 Comp %Fat was significantly greater (0.2%) when the array scan mode measurements of total body bone mineral were used; however, these differences were physiologically inconsequential. Comparison between DEXA %Fat and 4 Comp %Fat measures revealed a total error of +/-5.0% in the older adults examined. These results indicate significant scan mode differences in total body BMC, BMD, FFM, and DEXA %Fat measurements and demonstrate the importance of using a single DEXA scan mode for clinical investigation, particularly with longitudinal studies. For all investigations with DEXA, the scan mode should be reported. Furthermore, the error associated with using DEXA alone to estimate percent fat in an older population suggests that this technique is unacceptable in a research setting.

Postprandial lipemia in obese men with abdominal fat patterning.

OBJECTIVE: The purpose of this study was to assess differences in measures of postprandial triglyceride (TG) clearance between obese men with abdominal fat patterning (OAF) and men of desirable weight (DW). It was hypothesized that the OAF men would have impaired postprandial TG clearance. EXPERIMENTAL DESIGN: A comparative design was used. SETTING: Data were collected in a research laboratory with access to blood analysis instrumentation. PARTICIPANTS: Fourteen healthy, physically active, normolipemic men (7 OAF and 7 DW) were studied. INTERVENTIONS: Each subject consumed an oral fat load (78 grams of fat) and blood samples were collected every hour for 8 hours. MEASURES: Measures of postprandial lipemia included: incremental TG area, total TG area, time to peak TG concentration, maximal change in TG concentration, and time to return to baseline TG concentration. RESULTS: OAF men had significantly greater total area under the TG curve (24.7 +/- 1.09 vs 16.1 +/- 1.3 mmol-L(-1).8 hours, p = 0.003) and greater maximum TG change (2.0 +/- 0.3 vs 1.2 +/- 0.2 mmol-L-1, p = 0.03) following the oral fat load. Additionally, the total area under the TG curve was positively correlated with baseline TG concentrations (r = 0.53) and inversely correlated with baseline HDL2 concentrations (r = 0.64). Baseline HDL2 concentrations were inversely correlated with time to return to TG baseline (r = 0.57). CONCLUSIONS: Normal fasting lipoprotein profiles and regular physical activity do not preclude OAF men from having pronounced postprandial lipemia.

The validity of regulating blood lactate concentration during running by ratings of perceived exertion.

We examined whether ratings of perceived exertion (RPE) observed during an incremental (response) protocol could be used to produce target blood [HLa] of 2.5 mM and 4.0 mM during a 30-min treadmill run at a constant RPE. RPE (15.3, 17.6, 19.1), oxygen uptake (VO2) (3.31, 3.96, 4.00 l.min-1), velocity (V) (198, 218, 223 m.min-1), and heart rate (HR) (179, 185, 190 bpm) at blood [HLa] of 2.5 mM and 4.0 mM, and peak were determined for nine subjects (5 males, 4 females) during incremental exercise. Subjects then completed two 30-min runs at the RPE corresponding to blood [HLa] of 2.5 mM (RPE 2.5 mM) and 4.0 mM (RPE 4.0 mM) measured during the incremental protocol. For both 30-min runs, VO2 was not different from VO2 corresponding to either 2.5 or 4.0 mM blood [HLa] during the incremental test. During the 30-min run at RPE 2.5 mM: (a) only during minutes 25-30 was the blood [HLa] significantly different than 2.5 mM (3.2 +/- 0.6 mM, P < 0.05), (b) for the first 20 min HR was significantly lower than the HR at 2.5 mM during the incremental protocol, and (c) V did not differ from V at 2.5 mM during the incremental protocol. During the 30-min run at RPE 4.0 mM: (a) blood [HLa] was not significantly different from 4.0 mM, (b) HR at every time point was significantly lower than HR 4.0 mM during the incremental protocol, and (c) V was decreased over time by an average of 24.6 m.min-1 (P < 0.05). Because RPE from the response protocol was able to produce a blood [HLa] close to the criterion value during each 30-min run, we conclude that RPE is a valid tool for prescribing exercise intensities corresponding to blood [HLa] of 2.5 mM and 4.0 mM.

Assessment of the aerosport TEEM 100 portable metabolic measurement system.

The present study evaluated the utility of a portable metabolic measurement system, the Aerosport TEEM 100. A total of 505 data points [242 from incremental (INC) and 263 from constant load (CL) exercise] were collected on 12 subjects (age = 25 +/- 4 yr), by placing the Aerosport TEEM 100 medium flow pneumotach and mouthpiece in-line with a validated system, the Rayfield system. When VO2 values were separated into categories (< 1.5, 1.5-2.0, 2.0-2.5, 2.5-3.0, > 3.0 l.min-1), there was a small but statistically significant difference between the two metabolic measurement systems for VO2, VCO2, VE, RER, %ECO2, and %EO2 during both INC and CL exercise and measurement error for VO2 ranged between 2% and 11%. Correlations for VO2 values during INC and CL exercise between the two systems were r = 0.95 (SEest +/- 0.18 l.min-1) and r = 0.96 (SEest +/- 0.29 l.min-1), respectively. Correlations for RER were r = 0.82 (SEest +/- 0.08) and r = 0.47 (SEest +/- 0.11), for INC and CL, respectively. Results from the present investigation indicate that the Aerosport TEEM 100 has utility for the assessment of VO2, but the estimation of carbohydrate and fat utilization from RER should be used with caution.