Microvascular Reactivity Is Greater Following Blood Flow Restriction Resistance Exercise Compared with Traditional Resistance Exercise.

ABSTRACT: Perlet, MR, Hosick, PA, Licameli, N, and Matthews, EL. Microvascular reactivity is greater following blood flow restriction resistance exercise compared with traditional resistance exercise. J Strength Cond Res XX(X): 000-000, 2024-Chronic blood flow restriction (BFR) resistance exercise can improve muscular strength, hypertrophy, and microvasculature function, but the acute microvascular effects are unknown. We aimed to test the effects of acute BFR resistance exercise on postexercise microvascular reactivity in an exercising muscle and nonexercising muscle compared with traditional resistance exercise (TRE). Twenty-five adults (men = 14, women = 11, age: 22 ± 3 years, body mass: 71.69 ± 14.49 kg, height: 170 ± 10 cm) completed barbell back squat 1-repetition maximum (1RM) testing followed by 2 randomized and counterbalanced resistance exercise visits separated by ≥48 hours. The 2 visits involved either BFR (4 sets of 30-15-15-15 repetitions at 30% 1RM, with 60-second rest intervals) or TRE (4 sets of 10 repetitions at 70% 1RM, 60-second rest intervals). During each exercise visit, a pre- and postbarbell back squat vascular occlusion test was performed using near-infrared spectroscopy to measure skeletal muscle oxygen (SmO2) in the vastus lateralis (VL) and flexor carpi radialis (FCR). Two-way repeated-measures ANOVA found an interaction effect (p = 0.020) for SmO2 reactivity in the VL. Post hoc analysis found greater reactive hyperemia postexercise in the VL for the BFR condition (p < 0.001) but not the TRE condition (p ≥ 0.05). There were no time, condition, or interaction effects (all p > 0.05) for the same analysis in the FCR. This analysis suggests that BFR, but not TRE, lead to acutely improved microvasculature function. Moreover, it suggests that the effects of BFR resistance exercise are local to the exercised or occluded limb and not systemic.

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.

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.

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.

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.

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.

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.

Heme oxygenase, a novel target for the treatment of hypertension and obesity?

Heme oxygenase (HO) is the rate-limiting enzyme in the metabolism of heme-releasing bioactive molecules carbon monoxide (CO), biliverdin, and iron, each with beneficial cardiovascular actions. Biliverdin is rapidly reduced to bilirubin, a potent antioxidant, by the enzyme biliverdin reductase, and iron is rapidly sequestered by ferritin in the cell. Several studies have demonstrated that HO-1 induction can attenuate the development of hypertension as well as lower blood pressure in established hypertension in both genetic and experimental models. HO-1 induction can also reduce target organ injury and can be beneficial in cardiovascular diseases, such as heart attack and stroke. Recent studies have also identified a beneficial role for HO-1 in the regulation of body weight and metabolism in diabetes and obesity. Chronic HO-1 induction lowers body weight and corrects hyperglycemia and hyperinsulinemia. Chronic HO-1 induction also modifies the phenotype of adipocytes in obesity from one of large, cytokine producing to smaller, adiponectin producing. Finally, chronic induction of HO-1 increases oxygen consumption, CO(2), and heat production and activity in obese mice. This review will discuss the current understanding of the actions of the HO system to lower blood pressure and body weight and how HO or its metabolites may be ideal candidates for the development of drugs that can both reduce blood pressure and lower body weight.

The interaction of obesity and puberty on substrate utilization during exercise: a gender comparison.

The study evaluated the interactions of puberty and obesity on substrate oxidation of overweight girls (n = 38) and boys (N = 35; BMI > 85th percentile) matched for gender, age, and puberty (pre/pubertal) with normal weight girls and boys. Metabolic rates (VO(2)) were obtained during rest and at 4, 5.6 and 8 k/h. Carbohydrate oxidation rates (mg/kgFFM/min) adjusted for % predicted VO(2max), were higher for prepubertal OW children than pubertal children (p < .03). Fat oxidation rates were higher for NW prepubertal boys compared with other boys. Results indicate that OW children, regardless of gender or pubertal status, increase their carbohydrate oxidation rate to compensate for higher than normal metabolic rates. The effects of obesity on the substrate use is marginally related to puberty.

Importance of proper scaling of aerobic power when relating to cardiometabolic risk factors in children.

BACKGROUND: The relationship between cardiometabolic risk factors (CMRF) and aerobic power (VO(2max)) scaled as mL O(2) per kilogram body mass is controversial because mass includes both fat and fat-free mass, and fat mass is independently associated with the CMRF. AIM: To examine common units used to scale VO(2max) and their relationships to mean blood pressure (MBP), total cholesterol (TC), HDL cholesterol, triglycerides (TG), insulin resistance (HOMA-IR) and cumulative risk score (z-score). SUBJECTS: 1784, 8-18 year-old youths, 938 girls and 886 boys. METHODS: Fasting blood samples were obtained. VO(2max) was estimated in mL/min from cycle ergometry and scaled to body mass (kg), fat free mass (kg(FFM)), body surface area (m(2)), height (cm) and allometric (mL/kg(0.67)/min). RESULTS: Unadjusted correlations between CMRF and many of the scaled VO(2max) units were significant (p < 0.0001), especially for MBP, HOMA-IR, HDL and z-score, with lower correlations for TC and TG. After adjusting for ancestry, sex, height and body fat associations were greatly weakened (r < 0.09), except for MBP. CONCLUSIONS: On a population basis, the physical characteristics of the child, especially body fat, are more related to CMRF than any scaled units of VO(2max); thus care is needed when relating fitness and health issues.

Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor kappa b pathway.

UNLABELLED: Acute exposure to lipopolysaccharide (LPS) can cause hypoglycemia and insulin resistance; the underlying mechanisms, however, are unclear. We set out to determine whether insulin resistance is linked to hypoglycemia through Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappaB (NFkappaB), a cell signaling pathway that mediates LPS induction of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha). LPS induction of hypoglycemia was blocked in TLR4(-/-) and MyD88(-/-) mice but not in TNFalpha(-/-) mice. Both glucose production and glucose utilization were decreased during hypoglycemia. Hypoglycemia was associated with the activation of NFkappaB in the liver. LPS inhibition of glucose production was blocked in hepatocytes isolated from TLR4(-/-) and MyD88(-/-) mice and hepatoma cells expressing an inhibitor of NFkappaB (IkappaB) mutant that interferes with NFkappaB activation. Thus, LPS-induced hypoglycemia was mediated by the inhibition of glucose production from the liver through the TLR4, MyD88, and NFkappaB pathway, independent of LPS-induced TNFalpha. LPS suppression of glucose production was not blocked by pharmacologic inhibition of the insulin signaling intermediate phosphatidylinositol 3-kinase in hepatoma cells. Insulin injection caused a similar reduction of circulating glucose in TLR4(-/-) and TLR4(+/+) mice. These two results suggest that LPS and insulin inhibit glucose production by separate pathways. Recovery from LPS-induced hypoglycemia was linked to glucose intolerance and hyperinsulinemia in TLR4(+/+) mice, but not in TLR4(-/-) mice. CONCLUSION: Insulin resistance is linked to the inhibition of glucose production by the TLR4, MyD88, and NFkappaB pathway.

Core temperature influences on the relationship between exercise-induced leukocytosis and cortisol or TNF-alpha.

INTRODUCTION: The extent to which exercise in the heat modifies leukocytosis and the relationship between the leukocytosis and tumor necrosis factor-alpha (TNF-alpha) or cortisol is not well understood. Thus, this study attempted to determine the combined effect of exercise and differing elevations in core temperature on exercise-induced leukocytosis and to examine associations between any leukocytosis and cortisol orTNF-alpha. METHODS: Eight male subjects completed two 40-min trials while immersed in 25 and 38.5 degrees C water. Leukocytes, TNF-alpha, and cortisol were determined at baseline, immediately post-, and 2 h post-exercise. RESULTS: Both trials resulted in significant 13-33% increases in total leukocytes, mostly driven by a 24-30% increase in neutrophils. A significant relationship was found between the change in core temperature (T(re)) during exercise and the increase in total leukocytes (r = 0.561). Similarly, the change in T(re) was related to the change in cortisol (r = 0.557) and TNF-alpha (r = 0.483). Yet the exercise-induced change in cortisol was not significantly correlated to any changes in leukocytes. There was a trend for the relationships between the exercise-induced change in TNF-alpha and the changes in total leukocytes (r = 0.491) and neutrophils (r = 0.479). DISCUSSION: These results suggest that although neither cortisol nor TNF-alpha are strong predictors of the leukocyte response during exercise or recovery, each factor may be one of many potential modifiers of the total leukocyte response.

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.

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.

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 resistance exercise on humoral markers of oxidative stress.

UNLABELLED: Previous research attempts to identify an oxidative stress response to acute resistance exercise have yielded mixed results. Inconsistencies in the current literature base probably reflect study-to-study variance in resistance exercise protocols; where high volume and short recovery elicit the most identifiable oxidative stress response. PURPOSE: This study examined the effect of resistance exercise intensity on blood oxidative stress. METHODS: To elicit a blood oxidative stress, 10 subjects undertook two different back squat protocols: 1) a hypertrophy protocol of four sets, 10 repetitions with 90 s of rest at 75% one-repetition max (1RM); and 2) a strength protocol of 11 sets, three repetitions with 5 min of rest at 90% 1RM. The resistance exercise protocols were standardized for total volume and completed in a randomized crossover fashion with 1 wk between trials. Blood drawn before (PRE), immediately following exercise (IP), and 60 min following exercise (60POST) was analyzed for markers of oxidative stress and damage. RESULTS: In response to both hypertrophy and strength exercise protein carbonyls were significantly elevated IP and 60POST while plasma lipid hydroperoxides were not. Following the hypertrophy protocol, trolox equivalent antioxidant capacity was elevated IP while urate lower than baseline. At the 60POST time point plasma ferric reducing ability of plasma was elevated following the hypertrophy protocol. Based on protein carbonyl data, a similar oxidative stress was incurred following both hypertrophy and strength protocols. CONCLUSION: Normalization for time of blood draw following the two protocols indicates that the magnitude of blood oxidative protein damage was identical between the protocols. These findings demonstrate that both resistance exercise protocols elicited a blood oxidative stress in a time-dependent fashion.

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.