The impact of supervised weight loss and intentional weight regain on sex hormone binding globulin and testosterone in premenopausal women.

What is the impact of intentional weight loss and regain on serum androgens in women? We conducted an ancillary analysis of prospectively collected samples from a randomized controlled trial. The trial involved supervised 10% weight loss (8.5 kg on average) with diet and exercise over 4-6 months followed by supervised intentional regain of 50% of the lost weight (4.6 kg on average) over 4-6 months. Participants were randomized prior to the partial weight regain component to either continuation or cessation of endurance exercise. Analytic sample included 30 obese premenopausal women (mean age of 40 ± 5.9 years, mean baseline body mass index (BMI) of 32.9 ± 4.2 kg/m(2)) with metabolic syndrome. We evaluated sex hormone binding globulin (SHBG), total testosterone (T), free androgen index (FAI), and high molecular weight adiponectin (HMWAdp). Insulin, homeostasis model assessment (HOMA), and quantitative insulin sensitivity check index (QUICKI), and visceral adipose tissue (VAT) measured in the original trial were reanalyzed for the current analytic sample. Insulin, HOMA, and QUICKI improved with weight loss and were maintained despite weight regain. Log-transformed SHBG significantly increased from baseline to weight loss, and then significantly decreased with weight regain. LogFAI and logVAT decreased similarly and increased with weight loss followed by weight regain. No changes were found in logT and LogHMWAdp. There was no significant difference in any tested parameters by exercise between the groups. SHBG showed prominent sensitivity to body mass fluctuations, as reduction with controlled intentional weight regain showed an inverse relationship to VAT and occurred despite stable HMWAdp and sustained improvements with insulin resistance. FAI showed opposite changes to SHBG, while T did not change significantly with weight. Continued exercise during weight regain did not appear to impact these findings.

Prior exercise and postprandial incretin responses in lean and obese individuals.

PURPOSE: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) help regulate postprandial triacylglycerol (TAG) and insulin concentrations, but the effects of acute aerobic exercise on GLP-1 or GIP responses are unclear. The purpose of this study was to determine whether reductions in postprandial TAG and insulin with exercise are associated with GLP-1 and GIP responses. METHODS: Thirteen normal-weight (NW) and 13 obese (Ob) individuals participated in two, 4-d trials in random order including an exercise (EX) and a no exercise (NoEX) trial. Diet was controlled during both trials. The EX trial consisted of 1 h of treadmill walking (55%-60% of V˙O2peak) during the evening of day 3 of the trial, 12 h before a 4-h mixed meal test on day 4, during which frequent blood samples were collected to assess postprandial lipemia, glycemia, insulin, C-peptide, GIP, and GLP-1 responses. Insulin secretion was estimated using the insulinogenic index, and insulin clearance was estimated using the ratio of insulin to C-peptide. RESULTS: Postprandial TAG were 29% lower after EX in Ob individuals (P < 0.05) but were not significantly altered in NW individuals (P > 0.05). The drop in postprandial HDL cholesterol was attenuated with EX in Ob individuals (P < 0.05). Insulin responses were 14% lower after EX in Ob individuals (P < 0.05), and this was associated with reduced insulin secretion (P < 0.05), with no change in insulin clearance (P > 0.05). Glucose, C-peptide, GIP, and GLP-1 were not different between trials. CONCLUSION: A 1-h bout of moderate-intensity aerobic exercise the night before a mixed meal attenuates TAG and insulin responses in Ob but not NW individuals, an effect not associated with altered GLP-1 or GIP responses.

The effect of fasting on indicators of muscle damage.

Many studies have tested the consumption of foods and supplements to reduce exercise-induced muscle damage, but fasting itself is also worthy of investigation due to reports of beneficial effects of caloric restriction and/or intermittent fasting on inflammation and oxidative stress. This preliminary investigation compared indicators of exercise-induced muscle damage between upper-body untrained participants (N=29, 22yrs old (SD=3.34), 12 women) who completed 8h water-only fasts or ate a controlled diet in the 8h prior to five consecutive laboratory sessions. All sessions were conducted in the afternoon hours (i.e., post meridiem) and the women completed the first session while in the follicular phase of their menstrual cycles. Measures of muscle pain, resting elbow extension, upper arm girth, isometric strength, myoglobin (Mb), total nitric oxide (NO), interleukin 1beta (IL1b), and tumor necrosis factor alpha (TNFa) were collected before and after eccentric contractions of the non-dominant elbow flexors were completed. The fasting group's loss of elbow extension was less than the post-prandial group (p<.05, eta(2)=.10), but the groups did not change differently across time for any other outcome measures. However, significantly higher NO (p<.05, eta(2)=.22) and lower TNFa (p<.001, eta(2)=.53) were detected in the fasting group than the post-prandial group regardless of time. These results suggest intermittent fasting does not robustly inhibit the signs and symptoms of exercise-induced muscle damage, but such fasting may generally affect common indirect markers of muscle damage.

Sex differences in exercise-induced muscle pain and muscle damage.

UNLABELLED: There is uncertainty about sex differences in exercise-induced muscle pain and muscle damage due to several methodological weaknesses in the literature. This investigation tested the hypothesis that higher levels of exercise-induced muscle pain and muscle damage indicators would be found in women than men when several methodological improvements were executed in the same study. Participants (N = 33; 42% women) with an average age of 23 years (SD = 2.82) consented to participate. After a familiarization session, participants visited the laboratory before and across 4 days after eccentric exercise was completed to induce arm muscle pain and muscle damage. Our primary outcomes were arm pain ratings and pressure pain thresholds. However, we also measured the following indicators of muscle damage: arm girth; resting elbow extension; isometric elbow flexor strength; myoglobin (Mb); tumor necrosis factor (TNFa); interleukin 1beta (IL1b); and total nitric oxide (NO). Temporary induction of muscle damage was indicated by changes in all outcome measures except TNFa and IL1b. In contrast to our hypotheses, women reported moderately lower and less frequent muscle pain than men. Also, women's arm girth and Mb levels increased moderately less than men's, but the differences were not significant. Few large sex differences were detected. PERSPECTIVE: Lower muscle pain among women than men was detected with corresponding, but nonsignificant sex differences in other muscle damage indicators. Methodological advances may have improved alignment of these results with the nonhuman animal findings. This line of research continues to show exceptions to the generalization that women experience greater pain than men.

Exercise and weight loss improve exercise capacity independent of cardiac function in metabolic syndrome.

Hypertension, diabetes and obesity cause cardiac diastolic dysfunction (DD) which could reduce exercise capacity. Our aim was to determine if 10% weight loss by exercise at 60% VO(2max) five days/week (approximately -375 kcal/session) and caloric restriction (approximately -600 kcal/d) over 6 months improves exercise capacity and DD in Metabolic syndrome (MetS). Eighteen subjects (40 +/- 1y, women = 6, BMI = 33.5 +/- 1.0 kg/m(2)) successfully completed the study. Maximal treadmill stress echocardiography was performed at baseline and post weight loss to determine VO(2max), resting and stress DD as the ratio of peak early diastolic mitral inflow velocity (E) to tissue Doppler early diastolic annular decent (E'). After weight loss (mean = 9.5 +/- 0.2%), all metabolic parameters improved. Resting and stress E/E' values remained normal before and after weight loss. Exercise intolerance is likely due to general deconditioning and not cardiac dysfunction in early MetS as VO(2max) increases significantly with lifestyle while cardiac function remains unchanged.

Exercise and the metabolic syndrome with weight regain.

Weight loss improves metabolic syndrome (MetS) factors, but risk may return with weight regain. This study was designed to determine if exercise training can maintain improvements in MetS risk factors during weight regain. In a randomized control trial,102 overweight or obese (body mass index 25.0-39.9 kg/m(2)) men and women (age 21-52 yr), with characteristics of the MetS, lost 10% of body weight with supervised walking/jogging at 60% of maximal oxygen consumption (Vo(2 max)) (-400 kcal/session), 5 days/wk, and caloric restriction (-600 kcal/day) over a 4- to 6-mo period. After weight loss, 77 remaining subjects underwent programmed weight regain (+50% of lost weight) for 4-6 mo with random assignment to two groups: no exercise (NoEX) or continued supervised exercise (EX). Blood pressure, regional fat, glucose homeostasis, lipids, and inflammatory markers were assessed at baseline, post-weight loss, and post-weight regain. Groups were compared by two-way repeated-measures ANOVA on the 67 subjects. After weight loss (9.7 +/- 0.2% of body weight), significant (P < 0.05) improvements were observed in almost all parameters assessed. Following weight regain (54.4 +/- 1.6% of lost weight), the NoEX group exhibited deterioration in most metabolic markers, while the EX group maintained improvements in Vo(2 max), blood pressures, glucose homeostasis, high- and low-density lipoprotein cholesterol (HDL-C and LDL-C), oxidized LDL, and other markers of inflammation, but did not maintain improvements in triglyceride and cholesterol concentrations or abdominal fat. Results of this design of controlled human weight regain suggest that aerobic exercise can counter the detrimental effects of partial weight regain on many markers of disease risk.

The effects of resistance training on metabolic health with weight regain.

To determine whether resistance training effectively maintains improvements in cardiometabolic syndrome risk factors during weight regain, 9 individuals lost 4% to 6% of their body weight during an 8- to 12-week diet- and aerobic exercise-induced weight loss phase followed by a controlled weight regain phase (8-12 weeks), during which they regained approximately 50% of the lost weight while participating in a supervised resistance training program. Following weight loss (6.0%+/-0.3%), body mass index, body fat percentage, waist circumference, all abdominal adipose tissue depots, total cholesterol, low-density lipoprotein cholesterol, insulin, and homeostasis model assessment (HOMA) were significantly reduced, while quantitative insulin-sensitivity check index (QUICKI) and cardiorespiratory fitness (maximal oxygen consumption) significantly increased. During weight regain (48.3%+/-3.3% of lost weight), body fat percentage, waist circumference, and maximal oxygen consumption were maintained and muscular strength and lean body mass significantly increased. Abdominal adipose tissue depots, insulin, HOMA, and QUICKI did not significantly change after weight regain. Resistance training was effective in maintaining improvements in metabolic health during weight regain.

Predicting postprandial lipemia in healthy adults and in at-risk individuals with components of the cardiometabolic syndrome.

To determine whether a single-point triglyceride (TG) concentration could estimate the 8-hour postprandial lipemic (PPL) response, men and women performed baseline PPL (n=188) and postexercise PPL (n=92) trials. Correlations were generated between TG concentrations at baseline and at various time points after a high-fat meal vs 8-hour area under the TG curve (TG-AUC) and peak TG level. Stepwise multiple regression and bootstrap simulations using TG level and additional predictor variables of sex, age, percentage of body fat, training status, and maximal oxygen consumption indicated that the 4-hour TG concentrations accounted for >90% of the variance in TG-AUC and peak TG responses during the PPL trials. Equations were confirmed by cross-validation in healthy as well as at-risk individuals with components of the cardiometabolic syndrome. Our data suggest that the 4-hour TG value is highly related to the total 8-hour PPL response and can be used for accurate estimation of PPL in a clinical or research setting.

Serum markers of bone turnover are increased by modest weight loss with or without weight-bearing exercise in overweight premenopausal women.

Weight loss improves metabolic fitness and reduces morbidity and mortality; however, weight reduction also reduces bone mineral density (BMD) and increases bone turnover. Weight-bearing aerobic exercise may preserve bone mass and maintain normal bone turnover during weight reduction. We investigated the impact of weight-bearing and nonweight-bearing exercise on serum markers of bone formation and breakdown during short-term, modest weight loss in overweight premenopausal women. Subjects (n = 36) were assigned to 1 of 3 weight-loss interventions designed to produce a 5% reduction in body weight over 6 weeks: (i) energy restriction only (n = 11; DIET); (ii) energy restriction plus nonweight-bearing exercise (n = 12, CYCLE); or (iii) energy restriction plus weight-bearing exercise (n = 13, RUN). Bone turnover markers were measured in serum collected at baseline and after weight loss. All groups achieved a ~5% reduction in body weight (DIET = 5.2%; CYCLE = 5.0%; RUN = 4.7%). Osteocalcin (OC) and C-terminal telopeptide of type I collagen (CTX) increased with weight loss in all 3 groups (p < 0.05), whereas bone alkaline phosphatase was unaltered by the weight-loss interventions. At baseline, OC and CTX were positively correlated (r = 0.36, p = 0.03), but the strength of this association was diminished (r = 0.30, p = 0.06) after weight loss. Modest weight loss, regardless of method, resulted in a significant increase in both OC and CTX. Low-impact, weight-bearing exercise had no effect on serum markers of bone formation or resorption in premenopausal women during weight loss. Future studies that examine the effects of high-impact, weight-bearing activity on bone turnover and BMD during weight loss are warranted.

Correlation of Normal Diastolic Cardiac Function With VO in the Metabolic Syndrome.

Morbid obesity and diabetes cause diastolic dysfunction that can be detected by Doppler echocardiography. Patients with the metabolic syndrome could demonstrate early diastolic dysfunction that may influence effort tolerance. A total of 32 patients (17 men) who fulfilled >/=2 of the 5 metabolic syndrome criteria were studied. The average age of patients was 37+/-2 years. All patients were overweight/obese (mean body mass index of 34.4+/-0.7 kg/m(2)), 15 had blood pressure >130/85 mm Hg, 19 had elevated triglyceride levels (>150 mg/dL), and 17 had low high-density lipoprotein cholesterol levels (men <40 mg/dL, women <50 mg/dL). Maximal exercise was performed using Bruce treadmill protocol with standard stress echocardiography and tissue Doppler. Maximal oxygen consumption (VO(2max)) was measured using indirect calorimetry. Left ventricular filling pressure was indirectly derived from dividing pulse Doppler early mitral inflow velocity (E) by tissue Doppler early diastolic mitral annular motion (E') or E/E'. The group's average treadmill time was 8.06+/-0.28 minutes, VO(2max) was 28.6+/-1.1 mL/kg/min, and 8.2+/-0.3 metabolic equivalents. None had evidence of myocardial ischemia or systolic or diastolic dysfunction with exercise. Mean "resting" E/E' and "post-exercise" E/E' were 7.01+/-0.04 and 7.41+/-0.41, respectively. There was no significant correlation between resting E/E' and VO(2max) (r=-0.266; P=.14). The post-exercise E/E' significantly correlated with VO(2max) (r=-0.483; P=.005) and metabolic equivalents (r=-0.487; P=.005). Diastolic function is preserved in early metabolic syndrome. Even in the normal diastolic function range, exercise E/E' is inversely related to VO(2max). Further longitudinal studies are needed to determine whether they develop diastolic dysfunction and related heart failure.

Interaction of exercise training and n-3 fatty acid supplementation on postprandial lipemia.

The effect of combining omega-3 fatty acid (n-3 FA) supplementation and exercise training treatment on postprandial lipemia (PPL) has not been studied. The purpose of this study was to examine the interaction of n-3 FA and exercise training in attenuating PPL after a high-fat meal. Previously sedentary, overweight, subjects (n=22; 12 women, 10 men, BMI 26.6+/-0.7 kg/m2) were randomly assigned to one of two treatment groups: n-3 FA supplementation alone (FO, n=10) or n-3 FA supplementation plus exercise training (FO+ExTr, n=12). Both groups consumed 4 g/d n-3 FA, and one group also exercise trained for 45 min/d, 5d/week of brisk walking and (or) jogging at 60% VO2 max. Before and after 4 weeks of treatment, subjects performed a baseline PPL and a PPL following a single session of exercise (ExPPL). PPL was assessed by triglyceride (TG) area under the curve (AUC) and peak TG response (TGpeak). A two-way analysis of variance (ANOVA) with repeated measures was used to compare results from treatments for baseline and exercise trials. FO alone reduced PPL and Ex PPL, and FO+ExTr attenuated the ExPPL response measured as total AUC and TGpeak. There was no significant main effect for group or group by time interaction for baseline PPL or ExPPL. Fasting high-density lipoprotein cholesterol (HDL-C) and HDL2-C (i.e., subfraction 2) concentrations were significantly increased in the FO+ExTr group after the treatments. These results suggest that n-3 FA supplementation reduced PPL in sedentary subjects. Exercise training has no interference or additive effects with n-3 FA supplementation in attenuating PPL, but combined treatments may be additive in raising high-density lipoprotein cholesterol.

Influence of sex, high-fat diet, and exercise training on potassium currents of swine coronary smooth muscle.

Potassium channels in vascular smooth muscle (VSM) control vasodilation and are potential regulatory targets. This study evaluated effects of sex differences, exercise training (EX), and high-fat diet (HF) on K(+) currents (I(K)) of coronary VSM cells. Yucatan male and female swine were assigned to either sedentary confinement (SED), 16 wk of EX, 20 wk of HF, or 20 wk of HF with 16 wk of EX (HF-EX). VSM cells of normal-diet SED animals exhibited three components of I(K): 4-aminopyridine-sensitive I(K(KV)), TEA-sensitive I(K(BK)), and 4-aminopyridine + TEA-insensitive I(K). Females exhibited significantly higher basal I(K) than males in the same group. EX increased basal I(K) in males and females. HF reduced I(K) in males and females and nullified effects of EX. Endothelin-1 increased I(K) significantly in males but not in females. In the presence of endothelin-1, 1) I(K(KV)) was similar in SED males and females and EX increased I(K(KV)) to a greater extent in males than in females and 2) I(K(BK)) was greater in SED females than in males and EX increased I(K(BK)) to a greater extent in males, resulting in I(K(BK)) similar to EX females. Importantly, HF nullified effects of EX on I(K(KV)) and I(K(BK)). These data indicate that basal I(K) of SED female swine is inherently greater than that shown in SED males and that males require EX to achieve comparable levels of I(K). Importantly, HF reduced I(K) in males and females and nullified effects of EX, suggesting HF abrogates beneficial effects of EX on coronary smooth muscle.

Exercise and diet induced weight loss improves measures of oxidative stress and insulin sensitivity in adults with characteristics of the metabolic syndrome.

Obesity and insulin resistance (IR) increase the risk for coronary heart disease; however, much of this risk is not attributable to traditional risk factors. We sought to determine whether weight loss associated with supervised aerobic exercise beneficially alters biomarkers of oxidative stress and whether these alterations are associated with improvements in measures of insulin resistance. Twenty-five sedentary and overweight to obese [body mass index (BMI) = 33.0 +/- 0.8 kg/m(2)] individuals, with characteristics of the metabolic syndrome, participated in a 4- to 7-mo weight loss program that consisted of energy restriction (reduced by approximately 500 kcal/day) and supervised aerobic exercise (5 days/wk, 45 min/day at 60% Vo(2 max); approximately 375 kcal/day). IR and insulin sensitivity were assessed by the calculation of the homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI), respectively. Oxidative stress was assessed by oxidized LDL (oxLDL), myeloperoxidase (MPO), and low- and high- density lipoprotein (LDL and HDL) lipid hydroperoxide concentrations in serum. Indexes for antioxidative status included apolipoprotein A1 (apoA1) concentrations and paraoxonase-1 (PON1) activity and protein concentrations. Exercise- and diet-induced weight loss ( approximately 10%) significantly (P < 0.05) increased insulin sensitivity and reduced IR, oxLDL, and LDL lipid hydroperoxides but did not alter HDL lipid hydroperoxides or MPO concentrations. Lifestyle modification impacted systemic antioxidative status by increasing apoA1 concentrations and reducing serum PON1 protein and activity. Changes in oxidative stress were not associated with alterations in HOMA or QUICKI. Diet- and exercise-induced weight loss ( approximately 10%) improves measures of insulin sensitivity and beneficially alters biomarkers of oxidative status.

Weight-bearing, aerobic exercise increases markers of bone formation during short-term weight loss in overweight and obese men and women.

We investigated the impact of weight-bearing, aerobic exercise- and diet-induced weight loss on markers of bone turnover during a larger study of changes in metabolic fitness during short-term weight reduction using a repeated-measures, within-subject experimental design. Subjects (N = 19) underwent 6 weeks of energy restriction (reduced by approximately 3140 kJ/d) and aerobic exercise ( approximately 1675 kJ/d, walking or jogging at 60% maximum oxygen consumption) to induce a 5% reduction in body weight. Bone turnover markers and hormones were measured in serum collected at baseline and after 6 weeks of weight loss. Despite a 5% reduction in body weight at week 6, markers of bone formation, osteocalcin, and bone alkaline phosphatase, were significantly increased, and resorption markers, C-terminal cross-links of type I collagen and soluble receptor activator of nuclear factor kappaB ligand, were unchanged after 6 weeks of energy restriction and exercise. The concentration of leptin was significantly reduced after weight loss, but insulin-like growth factor I (IGF-I) and cortisol levels were unaffected. In conclusion, weight-bearing, aerobic exercise training may favorably affect the balance between bone resorption and formation during weight loss.

Short-term lifestyle modification alters circulating biomarkers of endothelial health in sedentary, overweight adults.

Obesity and inactivity are associated with endothelial dysfunction that may contribute to the development of atherosclerosis. We examined the effects of a short-term lifestyle intervention on circulating biomarkers of endothelial health. Nineteen overweight or obese (mean body mass index (BMI): 28.9 +/- 0.7 kg/m2) men and women underwent 6 weeks of body mass reduction induced by moderate energy restriction (approximately 750 kcal/d; 1 kcal = 4.184 kJ) and aerobic training (approximately 400 kcal/d). Fasting serum samples were collected at baseline and after reduction in body mass (week 6) to assess concentrations of nitrotyrosine (NT), secretory phospholipase A2 (sPLA2), and soluble intracellular adhesion molecule-1 (sICAM-1). Body mass was significantly reduced from 81.3 +/- 2.8 to 77.3 +/- 2.6 kg (p < 0.05). Circulating concentrations of NT and sICAM-1 were significantly reduced with treatment (approximately 25% and approximately 10%, respectively), whereas sPLA2 levels were significantly elevated (approximately 45%). Elevations in sPLA2 were negatively correlated with changes in NT (r = -0.58, p = 0.047); reductions in NT did not correlate significantly with reductions in sICAM-1. It appears that circulating markers of endothelial health are susceptible to short-term exercise interventions with modest reduction in body mass, and such a lifestyle modification may improve endothelial health by reducing protein nitration products and cellular adhesion.

Lipoprotein subfraction changes after continuous or intermittent exercise training.

PURPOSE: This study compared total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) and their respective subfractions after completing 4 wk of either intermittent (INT-EX) or continuous (CON-EX) aerobic exercise training (TRAIN). METHODS: Untrained males (N = 7) and females (N = 11) completed 4 wk of TRAIN of supervised treadmill jogging occurring 5 d.wk(-1) for 30 min per session at 60% VO2max (75% HRmax). CON-EX was a single 30-min bout. INT-EX consisted of three 10-min bouts separated by 20 min of seated rest. Pre- and post-TRAIN fasting plasma samples were collected after subjects had followed 48 h of activity restriction and a 24-h repeated diet including a 12-h dietary fast. Postprandial lipemia was measured for 8 h following a standardized high-fat meal. RESULTS: Fasting triglycerides and very LDL-C were not affected by TRAIN, and TRAIN did not change postprandial area under the curve or peak in either group. With groups combined, TRAIN significantly decreased TC, total LDL-C, and the TC:HDL ratio, and increased HDL-C subfraction 2 and LDL mean particle size. Total intermediate-density lipoprotein cholesterol remained unchanged at post-TRAIN, and was not different between groups. CONCLUSIONS: To prevent dyslipidemia, our findings suggest that persons who are normolipidemic can improve the lipoprotein profile equally with CON-EX and INT-EX by lowered TC through the sum of changes in LDL-C subfractions, increased mean LDL particle size, and increased HDL-C subfraction 2 concentration.

Exercise plus n-3 fatty acids: additive effect on postprandial lipemia.

The purpose of this study was to examine changes in postprandial lipemia (PPL) in recreationally active males following aerobic exercise, omega-3 fatty acids (n-3FA) supplementation, and the combination of the two. PPL following a high-fat meal was measured in 10 recreationally active males (25 +/-1.5 years) under each of the following conditions: no exercise and no n-3 FA supplementation (control); exercise and no n-3FA supplementation (exercise); n-3FA supplementation and no exercise (n-3FA); and exercise and n-3 FA supplementation (combined). Blood was collected before the high-fat meal and at 2, 4, 6, and 8 hours after the meal to assess the PPL response. Supplementation consisted of 4.0 g of n-3FA per day for 5 weeks. Triglyceride (TG) peak response, the total area under the TG curve (TG-AUCT), and the incremental area under the TG curve (TG-AUCI) were used to define the PPL response. TG peak response was significantly reduced 38% by n-3FA supplementation and 50% by the combination of exercise and n-3FA supplementation. N-3FAs significantly reduced the TG-AUCT by 27% and by 42% when combined with exercise. When compared with the exercise trial, the TG-AUCT during the combined trial was significantly lower. Exercise, n-3FAs, and the combination significantly reduced the TG-AUCI by 40%, 42%, and 58%, respectively. These results suggest that the combination of exercise and n-3FA supplementation reduce PPL to a greater degree in recreationally active males when compared with the individual treatments.

Single sessions of intermittent and continuous exercise and postprandial lipemia.

PURPOSE: This study compared the effects of continuous (CON-EX) and intermittent (INT-EX) exercise on postprandial lipemia (PPL). METHODS: Subjects were 18 inactive males (N = 7) and females (N = 11), aged 25 +/- 1.8 yr (mean +/- SE), VO2max 38.4 +/- 1.5 (mL x kg(-1)x min(-1)), and BMI 23.2 +/- 0.8 (kg x m(-2)). After 48-h activity and 24-h dietary control periods, subjects consumed a high-fat meal (HFM) containing 1.5 g fat (88% of calories), 0.05 g protein, and 0.4 g carbohydrate per kilogram body weight for three trials: no exercise (NOEX), CON-EX, and INT-EX. Both exercise trials consisted of 30 min of treadmill running at 60% VO2max. INT-EX was conducted in a single session of three bouts, each lasting 10 min and separated by a 20-min rest period. Blood was collected before the HFM (0 h) and at 2, 4, 6, and 8 h post-HFM. Exercise trials were completed 12 h before the HFM. Trials were separated by 7-10 d and were performed in random order. RESULTS: Plasma analysis indicated TG incremental area under the curve (AUCI) and TG incremental peak (PeakI) were significantly lower in INT-EX compared with NOEX, but CON-EX was not different from INT-EX or NOEX. Compared with females, males had significantly higher AUCI and PeakI in both exercise trials, but genders were not different in the NOEX trial. No difference was discovered among trials in high density lipoprotein (HDL)Total-C, HDL2-C, and HDL3-C, or fasting total cholesterol (TC) or fasting TC:HDL ratio. Females had higher fasting HDLTotal-C, HDL2-C, and HDL3-C compared with males. No gender or trial difference was found for fasting TC or TC:HDL ratio. CONCLUSIONS: Our data suggest that a single bout of INT-EX is more effective than CON-EX for lowering PPL as compared with NOEX in inactive, normolipidemic individuals.

Effect of exercise on postprandial lipemia following a higher calorie meal in Yucatan miniature swine.

Exercise has been shown to attenuate the postprandial lipemic (PPL) response to a modest kcal high-fat meal in numerous human studies, but has not been fully examined in swine. In addition, the effects of exercise on a high-fat meal of larger magnitude have not been examined in humans or in swine. Thus, the purpose of this study was to examine the PPL response to a single, high-fat/cholesterol (HFC) meal (approximately 3,000 kcal, 1,300 kcal from fat) and determine if exercise attenuates the PPL response. Sedentary, female Yucatan miniature swine (n = 10) completed 3 PPL trials: (1) pre diet (PRE); (2) post HFC diet (POST); and (3) post HFC diet plus exercise (EX, 45 minutes at 75% heart rate maximum). Blood samples were collected before (0 hour) and at 2, 4, 6, and 8 hours after the single HFC meal for PPL analysis. Postheparin lipoprotein lipase (LPL) activity was assessed at 8 hours. While fasting LPL activity was significantly increased with the HFC diet, the PPL response to the HFC meal did not differ depending on diet. Furthermore, the PPL response was not significantly altered with a single session of exercise, perhaps because of the severity of the HFC meal, the sedentary nature of the swine, or because LPL activity was not elevated after exercise. These findings suggest that administration of a HFC meal of this magnitude (approximately 3,000 kcal, 1,300 kcal from fat) will promote significant elevations in postprandial triglyceride (TG) concentrations, overwhelm the adaptive response to a HFC diet (elevated LPL activity), and attenuate the beneficial effects of a single exercise session on this system.

Effects of acute 60 and 80% VO2max bouts of aerobic exercise on state anxiety of women of different age groups across time.

The purpose of this investigation was to study the effects of an acute bout of aerobic exercise on state anxiety of women while controlling for iron status (hemoglobin and serum ferritin). Participants were 24 active women, ages 18-20 years (n = 12) and 35-45 years (n = 12). In addition to a nonexercise control condition, participants completed one exercise bout at 60% maximal oxygen uptake (VO2max) and one at 80% VO2max. Each exercise session consisted of a 33-min bout in which participants exercised at their target intensities for a 20-min segment. Immediately before each exercise trial, participants were given the Spielberger State Anxiety Inventory (SAI). The SAI was again administered immediately following the exercise session and at 30, 60, and 90 min postexercise. Data were analyzed using an Age x Intensity x Time (2 x 3 x 5) repeated measures analysis of covariance (ANCOVA) with iron status serving as the covariate. The ANCOVA on state anxiety yielded significant effects for time (p < .0001, eta2(p) = .48), the Intensity x Time interaction (p = .0006, eta2(p) = .19), and the Intensity x Age interaction (p = .04, eta2(p) = .15). All three exercise conditions (including control) showed a decline in state anxiety across time, but the 80% VO2max condition showed a sharper decline. Intensity of exercise conditions did not differ in state anxiety at baseline or immediately after exercise, but a difference favoring the 80% VO2max condition over the control condition emerged at 30 min postexercise. After controlling for iron status, older women who exercised at 80% VO2max exhibited lower SAI scores compared to the control condition.