Inverse Association between Exercising Blood Pressure Response and Left Ventricular Chamber Size and Mass in Women Who Habitually Resistance Train.

Exercise is a major modifiable lifestyle factor that leads to temporarily increased systolic blood pressure (SBP), which is thought to influence left ventricular mass normalized to body surface area (LVM/BSA). This relationship has never been studied in women who habitually perform resistance exercise. PURPOSE: To determine if a direct correlation exists between the SBP response to resistance exercise (change from rest; eSBP) and LVM/BSA in young healthy women who habitually resistance train. METHODS: Leg extension resistance exercise was performed while continuously monitoring blood pressure using finger plethysmography. LVM was estimated using echocardiography. Data are shown as mean ± SD. RESULTS: Thirty-one women participated (age 23 ± 3 years, height 164 ± 7 cm, body mass 63.7 ± 10.3 kg). Resting SBP (110 ± 8 mmHg, r = 0.355, p = 0.049) was shown to be directly correlated to LVM/BSA (72.0 ± 28.4 g/m2). Conversely, eSBP (30.8 ± 14.6 ∆mmHg, r = -0.437, p = 0.014) was inversely related to LVM/BSA. eSBP was not correlated to interventricular septum width (0.88 ± 0.12 cm, r = -0.137, p = 0.463) or posterior wall thickness (0.91 ± 0.15 cm, r = -0.084, p = 0.654). eSBP was inversely related to left ventricle internal diameter during diastole (LVIDd) (4.25 ± 0.33 cm, r = -0.411, p = 0.021). CONCLUSION: Counter to the hypothesis, these data suggest an inverse association between eSBP during resistance exercise and LVM/BSA in healthy young women who resistance train. This relationship is due to a smaller LVIDd with greater eSBP.

Impact of a family history of hypertension and physical activity on left ventricular mass.

BACKGROUND: A positive family history of hypertension (FHH) (+FHH) is associated with elevated left ventricular mass (LVM). Regular physical activity (PA) may eliminate differences in LVM between +FHH and negative family history of hypertension (-FHH) adults. The aim of this study was to determine if a +FHH is associated with a greater LVM compared to a -FHH group within a sample of young, mostly active healthy adults with and without statistically controlling for PA. METHODS: Healthy young (18-32 y) participants self-reported FHH status and habitual moderate and vigorous PA frequency. Participants then underwent an echocardiogram. RESULTS: Of the 61 participants, 32 (M=11, W=21; non-active=8) reported -FHH and the remaining 29 (M=13, W=16; non-active=2) reported a +FHH. Mann-Whitney tests found the +FHH group had greater LVM (-FHH 129.5±41.8, +FHH 155.2±42.6 g, P=0.015) and LVM/body surface area (BSA) (-FHH 73.5±17.4, +FHH 88.4±17.3 g/m2, P=0.004). Separate ANCOVA models accounting for moderate and vigorous PA found that FHH status independently predicted LVM/BSA and PA frequencies were significant modifiers (ANCOVA controlling moderate PA: FHH status P=0.004, partial η2=0.133; moderate PA P=0.020, partial η2=0.089), (ANCOVA controlling vigorous PA: FHH status P=0.004, partial η2=0.132; vigorous PA P=0.007, partial η2=0.117). CONCLUSIONS: This analysis suggests that physically active young adults with a +FHH have elevated LVM compared to their -FHH counterparts. This finding is independent of their habitual moderate and vigorous physical activity frequencies.

Oxygen Consumption and Blood Pressure Are Not Influenced by Use of a Backpack Hip Strap.

INTRODUCTION: Several studies have explored the effect of backpack carriage on physiologic responses while walking, but few have focused specifically on the influence of the use of a hip strap on these responses. The aim of this study was to investigate the effect of a backpack hip strap on physiologic responses when walking at a moderate intensity while carrying a backpack with a standardized relative load of 30% of the wearer's body mass. METHODS: Twenty-three healthy, active participants carrying backpacks walked on a treadmill at a speed and grade that elicited 40-50% of their heart rate reserve. Participants completed 2 counterbalanced 30-min trials, one with the hip strap in the strapped condition and one with the hip strap unfastened. Metabolic, heart rate, blood pressure, and muscle oxygen saturation (SmO2) responses were recorded during both trials. For each variable, 5-min intervals were averaged at baseline, 5, 10, 15, 20, 25, and 30 min. A repeated measures ANOVA test was used to evaluate the differences between the conditions at each time point. Data reported are the values from the final 5-min interval (30 min) and are reported as mean±SD. RESULTS: No differences were found between strapped and unstrapped trials for oxygen consumption (strapped 21.9±4.2 mL·kg-1·min-1; unstrapped 22.0±4.4 mL·kg-1·min-1, P=0.842), Δmean arterial pressure (strapped +5±17 Δmm Hg; unstrapped +12±14 Δmm Hg, P=0.128) or muscle oxygen saturation of the quadriceps (strapped 86±15%; unstrapped 90±12%, P=0.359) and calf (strapped 73±19%; unstrapped 81±12%, P=0.888). CONCLUSIONS: These results suggest that wearing a hip strap does not influence physiologic responses up to 30 min of moderate intensity walking while carrying 30% of the wearer's mass.

Young healthy adults with a family history of hypertension have increased microvascular reactivity but decreased macrovascular function.

OBJECTIVE: To determine whether, like hypertensives, normotensive adults with a family history of hypertension (+FHH) display lower microvascular reactivity and conduit artery function than normotensive adults without a family history of hypertension (-FHH). METHODS: A forearm vascular occlusion test was performed on healthy normotensive adults while resting in the supine position. A near-infrared spectroscopy sensor placed on the forearm measured skeletal muscle oxygen saturation kinetics to determine microvascular reactivity. Simultaneously, an ultrasound probe placed on the brachial artery above the occlusion cuff was used to assess flow-mediated dilation; a test of macrovascular function. RESULTS: Twenty-two participants were included in this investigation (-FHH n = 13, +FHH n = 9). Following cuff release, the resaturation slope (1st 10 s median ± SD, -FHH 2.76 ± 2.10, +FHH 5.59 ± 2.47%/s; p = .036) was greater in +FHH when accounting for the magnitude and rate of the decrease in skeletal muscle oxygen saturation during occlusion. Conversely, flow-mediated dilation (median ± SD, -FHH 5.96 ± 5.22, +FHH 4.10 ± 3.17%∆; p = .031) was lower in +FHH when accounting for baseline artery diameter and shear rate. CONCLUSIONS: Young +FHH adults have altered microvascular and macrovascular reactivity compared with young -FHH adults.

Mild dehydration following voluntary water intake reduction does not affect anaerobic power performance.

BACKGROUND: Dehydration is common among athletes. The negative impact of dehydration on aerobic performance is well characterized. However, little is known about the effect of dehydration on anaerobic performance particularly when dehydration results from insufficient water intake, not water loss due to body temperature regulation. The purpose of this study was to examine the effect of dehydration on anaerobic performance following voluntary water intake reduction. METHODS: Fifteen healthy adults completed two exercise sessions, euhydrated (EUD) and dehydrated (DEH). Sessions consisted of baseline anthropometric and blood lactate measurement followed by a 30-second Wingate test and three vertical jump trials to measure anaerobic performance. Additional blood lactate measurements were taken immediately and at 5, 10, and 15 minutes after taking the Wingate test. RESULTS: The dehydration protocol resulted in a reduction in body mass (EUD 69.1±17.2 kg, DEH 68.1±16.6 kg, P=0.039). The 30-s Wingate peak power (EUD 971±302 W, DEH 960±316 W, P=0.578) was not different between conditions, nor was the vertical jump height (EUH 26.4±4.5 cm, DEH 26.6±3.6 cm, P=0.778). Blood lactate (P<0.001) was elevated immediately following the 30-s Wingate test which remained throughout the trial. There were no differences in blood lactate between conditions. CONCLUSIONS: Acute anaerobic power and exercise performance is not negatively affected by voluntary dehydration.

Cardiorespiratory fitness and the relationship between body fat and resting testosterone in men.

Objective: To examine the effect of cardiovascular fitness, i.e. VO2max, on the relationship between weight status and resting testosterone level (RTL) in males.Materials and methods: A subset of male participants from the 2003-2004 National Health and Nutrition Examination Survey were analyzed by weight status, i.e. normal, overweight, obese, and all participants. Bivariate correlation coefficients were computed for RTL, percent body fat (BF%), and VO2max. Partial correlation coefficients were computed between RTL and BF% controlling for VO2max and between RTL and VO2max controlling for BF%.Results: Bivariate correlations between RTL and BF%, and RTL and VO2max were significant in all groups. The partial correlation coefficients between RTL and BF% controlling for VO2max were significant in the normal and all participants group. When RTL and VO2max were analyzed controlling for BF% only the all participants group remained significant.Conclusion: Cardiovascular fitness or weight status may independently influence RTL in males.

Bioelectrical impedance analysis does not detect an increase in total body water following isotonic fluid consumption.

PURPOSE: To determine if single-frequency foot-to-foot bioelectrical impedance analysis (BIA) can detect acute changes in total body water (TBW) following consumption of isotonic saline. All participants ate a sodium-free meal at 4 h prior to the data collection visit and had euhydration confirmed using urine specific gravity at the beginning of the experimental visit. Subjects drank 466 mL of isotonic saline (Na+ 140 mmol·L-1) following baseline measures. Blood sampling and BIA were performed at baseline and every 30 min for 3 h after saline consumption. Ten healthy participants completed this study. Plasma volume (5%Δ, p < 0.001) and serum sodium concentration (1%Δ, p < 0.001) increased by 60 min and 90 min, respectively. Body mass (p < 0.001) displayed a biphasic response increasing to a peak at 30 min (+0.38Δkg) and then decreasing to its minimum at 180 min (-0.35Δkg). BIA impedance (p = 0.678) was unaffected by the saline administration. BIA-derived TBW (p = 0.039) decreased from baseline starting at 150 min (0.21Δkg). Novelty Athletes and coaches wishing to achieve hyperhydration can do so through the consumption of isotonic fluid. 50 kHz foot-to-foot BIA-derived TBW is inadequate for measuring hyperhydration. Future studies should examine the physiological and performance effects of such a hyperhydration protocol.

The Effect of a Backpack Hip Strap on Energy Expenditure While Walking.

Objective To examine the effect of backpack hip strap use on walking energy expenditure while carrying a loaded backpack. Background Previous studies have demonstrated that energy cost increases as the mass of the load carried increases. However, few investigations have focused on backpack carriage design. Methods Fifteen young, healthy, male subjects walked at a self-selected pace for 10 minutes in two backpack loading conditions: with a hip strap (strapped) and without a hip strap (nonstrapped). Oxygen consumption (VO2), rating of perceived exertion (RPE), respiratory exchange ratio (RER), and heart rate (HR) were monitored throughout each 10-minute trial. Change scores from the 4th to 10th minute were calculated for each variable. A t test was used to evaluate the difference between conditions for each variable. Results The changes in VO2 (-0.62 ± 0.40 vs. 0.33 ± 0.23, p = .04) and RPE (1 ± 0.25 vs. 2 ± 0.21, p < .01) from the 4th to the 10th minute were different for the strapped versus nonstrapped condition. There was no difference in the change in RER (0.04 ± 0.01 vs. 0.03 ± 0.01, p > .05) or HR (3.53 ± 0.93 vs. 4.07 ± 1.39, p > .05) for the strapped versus unstrapped condition. Conclusions Wearing a hip strap reduced the energy expenditure and perceived exertion in as little as 10 minutes of walking compared to the nonstrapped condition. Future work should consider the effect of a hip strap on these variables while hiking for extended periods. Application Wearing a hip strap may increase the comfort and reduce the energy required of wearing a backpack. This is useful information for backpack designers, military personnel, and recreational hikers.

Sex-Dependent Effects of HO-1 Deletion from Adipocytes in Mice.

Induction of heme oxygenase-1 (HO-1) has been demonstrated to decrease body weight and improve insulin sensitivity in several models of obesity in rodents. To further study the role of HO-1 in adipose tissue, we created an adipose-specific HO-1 knockout mouse model. Male and female mice were fed either a control or a high-fat diet for 30 weeks. Body weights were measured weekly and body composition, fasting blood glucose and insulin levels were determined every six weeks. Adipocyte-specific knockout of HO-1 had no significant effect on body weight in mice fed a high-fat diet but increased body weight in female mice fed a normal-fat diet. Although body weights were not different in females fed a high fat diet, loss of HO-1 in adipocytes resulted in significant alterations in body composition. Adipose-specific HO-1 knockout resulted in increased fasting hyperglycemia and insulinemia in female but not male mice on both diets. Adipose-specific knockout of HO-1 resulted in a significant loss of HO activity and a decrease in the protein levels of adiponectin in adipose tissue. These results demonstrate that loss of HO-1 in adipocytes has greater effects on body fat and fasting hyperglycemia in a sex-dependent fashion and that expression of HO-1 in adipose tissue may have a greater protective role in females as compared to males.

Mice with hyperbilirubinemia due to Gilbert's syndrome polymorphism are resistant to hepatic steatosis by decreased serine 73 phosphorylation of PPARα.

Gilbert's syndrome in humans is derived from a polymorphism (TA repeat) in the hepatic UGT1A1 gene that results in decreased conjugation and increased levels of unconjugated bilirubin. Recently, we have shown that bilirubin binds directly to the fat-burning nuclear peroxisome proliferator-activated receptor-α (PPARα). Additionally, we have shown that serine 73 phosphorylation [Ser(P)73] of PPARα decreases activity by reducing its protein levels and transcriptional activity. The aim of this study was to determine whether humanized mice with the Gilbert's polymorphism (HuUGT*28) have increased PPARα activation and reduced hepatic fat accumulation. To determine whether humanized mice with Gilbert's mutation (HuUGT*28) have reduced hepatic lipids, we placed them and C57BL/6J control mice on a high-fat (60%) diet for 36 wk. Body weights, fat and lean mass, and fasting blood glucose and insulin levels were measured every 6 wk throughout the investigation. At the end of the study, hepatic lipid content was measured and PPARα regulated genes as well as immunostaining of Ser(P)73 PPARα from liver sections. The HuUGT*28 mice had increased serum bilirubin, lean body mass, decreased fat mass, and hepatic lipid content as well as lower serum glucose and insulin levels. Also, the HuUGT*28 mice had reduced Ser(P)73 PPARα immunostaining in livers and increased PPARα transcriptional activity compared with controls. A chronic but mild endogenous increase in unconjugated hyperbiliubinemia protects against hepatic steatosis through a reduction in Ser(P)73 PPARα, causing an increase in PPARα transcriptional activity.

Biliverdin Reductase A Attenuates Hepatic Steatosis by Inhibition of Glycogen Synthase Kinase (GSK) 3ß Phosphorylation of Serine 73 of Peroxisome Proliferator-activated Receptor (PPAR) α.

Non-alcoholic fatty liver disease is the most rapidly growing form of liver disease and if left untreated can result in non-alcoholic steatohepatitis, ultimately resulting in liver cirrhosis and failure. Biliverdin reductase A (BVRA) is a multifunctioning protein primarily responsible for the reduction of biliverdin to bilirubin. Also, BVRA functions as a kinase and transcription factor, regulating several cellular functions. We report here that liver BVRA protects against hepatic steatosis by inhibiting glycogen synthase kinase 3ß (GSK3ß) by enhancing serine 9 phosphorylation, which inhibits its activity. We show that GSK3ß phosphorylates serine 73 (Ser(P)73) of the peroxisome proliferator-activated receptor α (PPARα), which in turn increased ubiquitination and protein turnover, as well as decreased activity. Interestingly, liver-specific BVRA KO mice had increased GSK3ß activity and Ser(P)73 of PPARα, which resulted in decreased PPARα protein and activity. Furthermore, the liver-specific BVRA KO mice exhibited increased plasma glucose and insulin levels and decreased glycogen storage, which may be due to the manifestation of hepatic steatosis observed in the mice. These findings reveal a novel BVRA-GSKß-PPARα axis that regulates hepatic lipid metabolism and may provide unique targets for the treatment of non-alcoholic fatty liver disease.

Chronic treatment with a carbon monoxide releasing molecule reverses dietary induced obesity in mice.

Chronic, low level treatment with a carbon monoxide releasing molecule (CO-RM), CORM-A1, has been shown to prevent the development of obesity in response to a high fat diet. The objective of this study was to test the hypothesis that chronic, low level treatment with this CO-RM can reverse established obesity via a mechanism independent of food intake. Dietary induced obese mice were treated with CORM-A1, the inactive compound iCORM-A1, or saline every 48 hours for 30 weeks while maintained on a high fat (60%) diet. Chronic treatment with CORM-A1 resulted in a 33% decrease from initial body weight over the 30 week treatment period while treatment with iCORM and saline were associated with 18 and 25% gain in initial body weight over the same time frame. Chronic treatment with CORM-A1 did not affect food intake or activity but resulted in a significant increase in metabolism. CORM-A1 treatment also resulted in lower fasting blood glucose, improvement in insulin sensitivity and decreased heptatic steatosis. Chronic treatment with CO releasing molecules can reverse dietary induced obesity and normalize insulin resistance independent of changes in food intake or activity. These findings are likely though a mechanism which increases metabolism.

Biliverdin reductase isozymes in metabolism.

The biliverdin reductase (BVR) isozymes BVRA and BVRB are cell surface membrane receptors with pleiotropic functions. This review compares, for the first time, the structural and functional differences between the isozymes. They reduce biliverdin, a byproduct of heme catabolism, to bilirubin, display kinase activity, and BVRA, but not BVRB, can act as a transcription factor. The binding motifs present in the BVR isozymes allow a wide range of interactions with components of metabolically important signaling pathways such as the insulin receptor kinase cascades, protein kinases (PKs), and inflammatory mediators. In addition, serum bilirubin levels have been negatively associated with abdominal obesity and hypertriglyceridemia. We discuss the roles of the BVR isozymes in metabolism and their potential as therapeutic targets.

Heme oxygenase-1 promotes migration and ß-epithelial Na+ channel expression in cytotrophoblasts and ischemic placentas.

Preeclampsia is thought to arise from inadequate cytotrophoblast migration and invasion of the maternal spiral arteries, resulting in placental ischemia and hypertension. Evidence suggests that altered expression of epithelial Na(+) channel (ENaC) proteins may be a contributing mechanism for impaired cytotrophoblast migration. ENaC activity is required for normal cytotrophoblast migration. Moreover, ß-ENaC, the most robustly expressed placental ENaC message, is reduced in placentas from preeclamptic women. We recently demonstrated that heme oxygenase-1 (HO-1) protects against hypertension in a rat model of placental ischemia; however, whether HO-1 regulation of ß-ENaC contributes to the beneficial effects of HO-1 is unknown. The purpose of this study was to determine whether ß-ENaC mediates cytotrophoblast migration and whether HO-1 enhances ENaC-mediated migration. We showed that placental ischemia, induced by reducing uterine perfusion suppressed, and HO-1 induction restored, ß-ENaC expression in ischemic placentas. Using an in vitro model, we found that HO-1 induction, using cobalt protoporphyrin, stimulates cytotrophoblast ß-ENaC expression by 1.5- and 1.8-fold (10 and 50 µM). We then showed that silencing of ß-ENaC in cultured cytotrophoblasts (BeWo cells), by expression of dominant-negative constructs, reduced migration to 56 ± 13% (P < 0.05) of control. Importantly, HO-1 induction enhanced migration (43 ± 5% of control, P < 0.05), but the enhanced migratory response was entirely blocked by ENaC inhibition with amiloride (10 µM). Taken together, our results suggest that ß-ENaC mediates cytotrophoblast migration and increasing ß-ENaC expression by HO-1 induction enhances migration. HO-1 regulation of cytotrophoblast ß-ENaC expression and migration may be a potential therapeutic target in preeclamptic patients.

Inhalation of carbon monoxide is ineffective as a long-term therapy to reduce obesity in mice fed a high fat diet.

BACKGROUND: Previous studies have demonstrated that induction of heme oxygenase-1 results in weight loss in several rodent models of obesity. However, the specific role of the heme oxygenase-1 metabolite, carbon monoxide (CO), in this response has yet to be established. We recently reported that chronic treatment with CO releasing molecules results in prevention of weight gain in mice fed a high fat diet. In the present study, we sought to determine the effect of chronic CO inhalation on the development and reversal of high fat diet induced obesity. RESULTS: CO inhalation at both levels initially resulted in a prevention and reversal of body weight and fat mass over the first 10 weeks of treatment, however, this effect was not sustained. CO inhalation in the prevention groups also had an early effect to lower fasting blood glucose but this effect also was not sustained. CONCLUSIONS: Our results demonstrate that CO inhalation has a transient effect to prevent and reduce body weight which is not sustained chronically in mice fed a high fat diet. These results suggest that chronic CO inhalation therapy is not an effective treatment to induce long term weight loss.

Effect of resveratrol and quercetin supplementation on redox status and inflammation after exercise.

Resveratrol and quercetin function as antioxidants and anti-inflammatories in vitro, but these mechanisms have been minimally examined in combination in exercising humans. The purpose of this investigation was to examine supplementation as a countermeasure against oxidative stress and inflammation in response to exercise. Fourteen athletes were randomly assigned, in a double-blind crossover design, to a resveratrol and quercetin combination (RQ) (120 mg resveratrol and 225 mg quercetin for 6 days and 240 mg resveratrol and 450 mg quercetin on day 7 just prior to exercise) or to placebo (P). There was a 1-week washout between trials. Blood was taken at baseline, pre-exercise, immediately after exercise, and 1 h after exercise. Plasma was analyzed for oxidative stress (F2-isoprostanes and protein carbonyls), antioxidant capacity (ferric-reducing ability of plasma (FRAP), Trolox equivalent antioxidant capacity (TEAC), oxygen radical absorptive capacity (ORAC)), and inflammation (cytokine interleukin (IL)-8 and C-reactive protein (CRP)). Statistical design utilized a 2 × 3 ANOVA and Student's t test. Pre-exercise values were not different from baseline for any measure. The postexercise increase in F2-isoprostanes was significantly less (p = 0.039 interaction) with RQ (68%) than with P (137%). Protein carbonyls, FRAP, ORAC, and TEAC significantly increased after exercise but were not affected by treatment. IL-8 and CRP increased significantly immediately after exercise but were not affected by treatment. These data indicate that RQ significantly reduces exercise-induced lipid peroxidation without associated changes in inflammation or plasma antioxidant status.

Heme oxygenase inhibition increases blood pressure in pregnant rats.

BACKGROUND: During normal gestation, the placenta is a relatively hypoxic organ and, as such, is subject to significant oxidative stress. In the preeclamptic patient, inadequate remodeling of the maternal vasculature severely exacerbates placental oxidative stress, which has been shown to be an important component of maternal hypertension. There is emerging evidence that Heme Oxygenase-1 (HO-1) acts as an important regulator of placental and cardiovascular function during normal pregnancy. Here, we have examined the effect of Heme Oxygenase (HO) inhibition in late gestation on maternal blood pressure, angiogenic balance, and placental oxidative stress in pregnant rats. METHODS: HO activity was inhibited with tin mesoporphyrin (SnMP), which was administered on gestational day 14, and blood pressure was measured on gestational day 19. Placental angiogenic balance and plasma Vascular Endothelial Growth Factor (VEGF) were determined by sandwich enzyme-linked immunosorbent assay. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was measured by lucigenin chemilluminescence. RESULTS: In response to SnMP treatment, maternal mean arterial pressure (MAP) was significantly increased (99±1 vs. 113±2mm Hg; P < 0.05; n = 15 per group). Placental soluble fms-like tyrosine kinase-1 (sFlt-1) (631±47 vs. 648±26 pg/mg; P = 0.76) levels in the placenta were not affected by HO inhibition. Additionally, there was no significant difference in free VEGF in the maternal circulation (287±22 vs. 329±14 pg/ml; P = 0.11). There was, however, a significant decrease in placental VEGF (23±2 vs. 16±1 pg/mg; P < 0.05) and a significant increase in placental NADPH oxidase activity in SnMP-treated rats (2021±238 vs. 3005±301 RLU/min/mg; P < 0.05). CONCLUSIONS: Our results demonstrate that HO is an important regulator of blood pressure and an important antioxidant in the developing placenta.

Differences in the GH-IGF-I axis in children of different weight and fitness status.

OBJECTIVE: To determine if differences in the GH-IGF-I axis exist between children of high and low aerobic fitness who are obese or of normal weight. DESIGN: 124 children (ages 8-11) divided into four groups based on BMI and VO2max (mL O2/kg fat free mass(FFM)/min): normal weight--high-fit (NH), normal weight--low-fit (NL), obese--high-fit (OH), and obese--low-fit (OL). Height, weight, skinfolds, body mass index (BMI), body fat percentage and predicted VO2max (both ml/kg/min and ml/kg(FFM)/min) were assessed. Resting growth hormone (GH), total insulin-like growth factor 1 (total IGF-I), free insulin-like growth factor 1(free IGF-I), and insulin were measured using morning fasting blood samples. RESULTS: GH was greater in the NH group compared to the OL group only (p<0.01). No group differences existed for either total IGF-I (p=0.53) or free IGF-I (p=0.189). Insulin was greater in the OH and OL groups than the NH and NL groups (p<0.01). With groups combined (or overall), insulin and free IGF-I were related to fitness (insulin--ml/kg/min: r=-0.226, p<0.05 and ml/kg(FFM)/min: r=-0.212, p<0.05; free IGF-I--ml/kg/min: r=-0.219, p<0.01 and ml/kg(FFM)/min: r=-0.272, p<0.05). CONCLUSIONS: Fitness may contribute to the obesity related reduction of GH that may be involved with weight gain.

Bilirubin, renal hemodynamics, and blood pressure.

Bilirubin is generated from the breakdown of heme by heme oxygenase and the reduction of biliverdin by the enzyme biliverdin reductase. Several large population studies have reported a significant inverse correlation between plasma bilirubin levels and the incidence of cardiovascular disease. Protection from cardiovascular disease is also observed in patients with Gilbert's syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile. Despite the strong correlation between plasma bilirubin levels and the protection from cardiovascular disease, the mechanism by which increases in plasma bilirubin acts to protect against cardiovascular disease is unknown. Since the chronic antihypertensive actions of bilirubin are likely due to its renal actions, the effects of moderate increases in plasma bilirubin on renal hemodynamics as well as bilirubin's potential effects on renal tubule function will be discussed in this review. Mechanisms of action as well as the potential for antihypertensive therapies targeting moderate increases in plasma bilirubin levels will also be highlighted.