Cardioprotective Effects of Mitochondria-Targeted Peptide SBT-20 in two Different Models of Rat Ischemia/Reperfusion.

PURPOSE: Dysfunctional mitochondria are considered to be the major source of intracellular reactive oxygen species and play a central role in the pathophysiology of myocardial ischemia/reperfusion. This study sought to determine effects of mitochondria-targeted cytoprotective peptide SBT-20 on myocardial infarct size in two different models of ischemia/reperfusion. METHODS: For in vivo studies, anesthetized Sprague Dawley rats were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. Rats received saline (control), low dose SBT-20 (0.3 mg/kg/h) or high dose SBT-20 (3 mg/kg/h) treatment (n = 15 rats in each group). Saline or SBT-20 were delivered into the jugular vein starting 5 min after coronary artery occlusion and were continued for one hour post coronary artery reperfusion. Body temperature, heart rate and blood pressure were monitored during the procedure. At the end of 3 h reperfusion, the ischemic risk area, no-reflow area, and infarct size were measured. In separate in vitro studies, isolated rat hearts were exposed to 20 min global ischemia, followed by SBT-20 administration (1 µM) or no SBT-20 (control) throughout the 2 h reperfusion. In vitro studies were conducted in cells and heart mitochondria to ascertain the mitochondrial effects of SBT-20 on mitochondrial respiration and reactive oxygen species production. RESULTS: In the in vivo study, the ischemic risk areas (as a percentage of the left ventricle) were similar among the saline (49.5 ± 2.3 %), low dose SBT-20 (48.6 ± 2.1 %), and high dose SBT-20 groups (48.7 ± 3.0 %). Treatment with SBT-20 significantly reduced infarct size ( as a percentage of risk area) in low dose (62.1 ± 4.4 %) and high dose (64.0 ± 4.9 %) compared with saline treatment (77.6 ± 2.6 %, p = 0.001 for both doses). There was no difference in infarct size between low and high dose SBT-20 treatment. The no-reflow areas (as a percentage of the risk area) were comparable among the saline (23.9 ± 1.7 %), low dose SBT-20 (23.7 ± 2.8 %), and high dose groups (25.0 ± 2.1 %). Body temperature, heart rate and blood pressure were comparable among the 3 groups at baseline, during ischemia, and at the end of 3 h of reperfusion. In the in vitro study, infarct size was reduced from 43.3 ± 2.6 % in control group (n = 11) to 17.2 ± 2.8 % in the SBT-20 treatment group (n = 5, p < 0.05). There were no benefits of SBT-20 on recovery of left ventricular developed pressure, coronary flow, or maximal rates of contraction/relaxation. In cell studies, treatment with SBT-20 significantly improved maximal mitochondrial respiration in response to an H2O2 challenge. In isolated mitochondria, reactive oxygen species production was significantly blunted following treatment with SBT-20. CONCLUSIONS: In summary, SBT-20 significantly reduced infarct size in two different models of myocardial injury, but did not affect hemodynamics or no-reflow area in rat heart. The reduction in injury is postulated to involve stabilization of mitochondrial function and reduced mitochondrial production of ROS.

Mitochondrial therapy improves limb perfusion and myopathy following hindlimb ischemia.

Critical limb ischemia is a devastating manifestation of peripheral arterial disease with no effective strategies for improving morbidity and mortality outcomes. We tested the hypothesis that cellular mitochondrial function is a key component of limb pathology and that improving mitochondrial function represents a novel paradigm for therapy. BALB/c mice were treated with a therapeutic mitochondrial-targeting peptide (MTP-131) and subjected to limb ischemia (HLI). Compared to vehicle control, MTP-131 rescued limb muscle capillary density and blood flow (64.7±11% of contralateral vs. 39.9±4%), and improved muscle regeneration. MTP-131 also increased electron transport system flux across all conditions at HLI day-7. In vitro, primary muscle cells exposed to experimental ischemia demonstrated markedly reduced (~75%) cellular respiration, which was rescued by MTP-131 during a recovery period. Compared to muscle cells, endothelial cell (HUVEC) respiration was inherently protected from ischemia (~30% reduction), but was also enhanced by MTP-131. These findings demonstrate an important link between ischemic tissue bioenergetics and limb blood flow and indicate that the mitochondria may be a pharmaceutical target for therapeutic intervention during critical limb ischemia.

Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics.

Mitochondria influence cardiac electrophysiology through energy- and redox-sensitive ion channels in the sarcolemma, with the collapse of energetics believed to be centrally involved in arrhythmogenesis. This study was conducted to determine if preservation of mitochondrial membrane potential (ΔΨm) contributes to the antiarrhythmic effect of exercise. We utilized perfused hearts, isolated myocytes, and isolated mitochondria exposed to metabolic challenge to determine the effects of exercise on cardiac mitochondria. Hearts from sedentary (Sed) and exercised (Ex; 10 days of treadmill running) Sprague-Dawley rats were perfused on a two-photon microscope stage for simultaneous measurement of ΔΨm and ECG. After ischemia-reperfusion, the collapse of ΔΨm was commensurate with the onset of arrhythmia. Exercise preserved ΔΨm and decreased the incidence of fibrillation/tachycardia (P < 0.05). Our findings in intact hearts were corroborated in isolated myocytes exposed to in vitro hypoxia-reoxygenation, with Ex rats demonstrating enhanced redox control and sustained ΔΨm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H2O2 Mitochondria from Ex rats sustained respiration with lower rates of H2O2 emission than Sed rats. Exercise helps sustain postischemic mitochondrial bioenergetics and redox homeostasis, which is associated with preserved ΔΨm and protection against reperfusion arrhythmia. The reduction of fatal ventricular arrhythmias through exercise-induced mitochondrial adaptations indicates that mitochondrial therapeutics may be an effective target for the treatment of heart disease.

Why Does Exercise "Trigger" Adaptive Protective Responses in the Heart?

Numerous epidemiological studies suggest that individuals who exercise have decreased cardiac morbidity and mortality. Pre-clinical studies in animal models also find clear cardioprotective phenotypes in animals that exercise, specifically characterized by lower myocardial infarction and arrhythmia. Despite the clear benefits, the underlying cellular and molecular mechanisms that are responsible for exercise preconditioning are not fully understood. In particular, the adaptive signaling events that occur during exercise to "trigger" cardioprotection represent emerging paradigms. In this review, we discuss recent studies that have identified several different factors that appear to initiate exercise preconditioning. We summarize the evidence for and against specific cellular factors in triggering exercise adaptations and identify areas for future study.

The "Goldilocks Zone" from a redox perspective-Adaptive vs. deleterious responses to oxidative stress in striated muscle.

Consequences of oxidative stress may be beneficial or detrimental in physiological systems. An organ system's position on the "hormetic curve" is governed by the source and temporality of reactive oxygen species (ROS) production, proximity of ROS to moieties most susceptible to damage, and the capacity of the endogenous cellular ROS scavenging mechanisms. Most importantly, the resilience of the tissue (the capacity to recover from damage) is a decisive factor, and this is reflected in the disparate response to ROS in cardiac and skeletal muscle. In myocytes, a high oxidative capacity invariably results in a significant ROS burden which in homeostasis, is rapidly neutralized by the robust antioxidant network. The up-regulation of key pathways in the antioxidant network is a central component of the hormetic response to ROS. Despite such adaptations, persistent oxidative stress over an extended time-frame (e.g., months to years) inevitably leads to cumulative damages, maladaptation and ultimately the pathogenesis of chronic diseases. Indeed, persistent oxidative stress in heart and skeletal muscle has been repeatedly demonstrated to have causal roles in the etiology of heart disease and insulin resistance, respectively. Deciphering the mechanisms that underlie the divergence between adaptive and maladaptive responses to oxidative stress remains an active area of research for basic scientists and clinicians alike, as this would undoubtedly lead to novel therapeutic approaches. Here, we provide an overview of major types of ROS in striated muscle and the divergent adaptations that occur in response to them. Emphasis is placed on highlighting newly uncovered areas of research on this topic, with particular focus on the mitochondria, and the diverging roles that ROS play in muscle health (e.g., exercise or preconditioning) and disease (e.g., cardiomyopathy, ischemia, metabolic syndrome).

Increasing mitochondrial membrane phospholipid content lowers the enzymatic activity of electron transport complexes.

Activities of the enzymes involved in cellular respiration are markedly influenced by the composition of the phospholipid environment of the inner mitochondrial membrane. Contrary to previous suppositions, we show that fusion of mitochondria isolated from healthy cardiac muscle with cardiolipin or dioleoylphosphatidylcholine results in a 2-6-fold reduction in the activity of complexes I, II, and IV. The activity of complex III was unaffected by increased phospholipid levels. Phospholipid content had an indiscriminate yet detrimental effect on the combined activities of complexes I+III and II+III. These results have strong implications for therapeutic lipid replacement strategies, in which phospholipid modification of the mitochondria is proposed to enhance mitochondrial function.

Both a traditional and modified Daniel Fast improve the cardio-metabolic profile in men and women.

BACKGROUND: The Daniel Fast involves dietary modification similar to a purified vegan diet. Although improvements in several health-specific biomarkers have been noted with this plan, the removal of animal products results in a significant reduction in both dietary protein and saturated fatty acid intake, which results in a loss of lean body mass and a reduction in HDL-cholesterol. METHODS: We assigned 29 men and women to either a traditional or modified Daniel Fast for 21 days and measured anthropometric and biochemical markers of health pre and post intervention. The modified Daniel Fast was otherwise identical to the traditional plan but included one serving per day of lean meat and dairy (skim milk), providing approximately 30 grams per day of additional protein. RESULTS: Compared to baseline, both plans resulted in similar and significant improvements in blood lipids, as well as a reduction in inflammation. CONCLUSIONS: Modification of dietary intake in accordance with either a traditional or modified Daniel Fast may improve risk factors for cardiovascular and metabolic disease.

Redox-dependent increases in glutathione reductase and exercise preconditioning: role of NADPH oxidase and mitochondria.

AIMS: We have previously shown that exercise leads to sustainable cardioprotection through a mechanism involving improved glutathione replenishment. This study was conducted to determine if redox-dependent modifications in glutathione reductase (GR) were involved in exercise cardioprotection. Furthermore, we sought to determine if reactive oxygen species generated by NADPH oxidase and/or mitochondria during exercise were triggering events for GR modulations. METHODS AND RESULTS: Rats were exercised for 10 consecutive days, after which isolated hearts were exposed to ischaemia/reperfusion (25 min/120 min). Exercise protected against infarction and arrhythmia, and preserved coronary flow. The GR inhibitor BCNU abolished the beneficial effects. GR activity was increased following exercise in a redox-dependent manner, with no change in GR protein levels. Because fluorescent labelling of GR protein thiols showed lower amounts of reduced thiols after exercise, we sought to determine the source of intracellular reactive oxygen species that may be activating GR. Subsets of animals were exercised immediately after treatment with either NADPH-oxidase inhibitors apocynin or Vas2870, or with mitoTEMPO or Bendavia, which reduce mitochondrial reactive oxygen species levels. The cardioprotective effects of exercise were abolished if animals exercised in the presence of NADPH oxidase inhibitors, in clear contrast to the mitochondrial reagents. These changes correlated with thiol-dependent modifications of GR. CONCLUSION: Adaptive cardioprotective signalling is triggered by reactive oxygen species from NADPH oxidase, and leads to improved glutathione replenishment through redox-dependent modifications in GR.

A 21-day Daniel fast with or without krill oil supplementation improves anthropometric parameters and the cardiometabolic profile in men and women.

BACKGROUND: The Daniel Fast is a vegan diet that prohibits the consumption of animal products, refined foods, white flour, preservatives, additives, sweeteners, flavorings, caffeine, and alcohol. Following this dietary plan for 21 days has been demonstrated to improve blood pressure, LDL-C, and certain markers of oxidative stress, but it has also been shown to lower HDL-C. Krill oil supplementation has been shown to increase HDL-C. METHODS: We investigated the effects of following a Daniel Fast dietary plan with either krill oil supplementation (2 g/day) or placebo supplementation (coconut oil; 2 g/day) for 21 days. The subjects in this study (12 men and 27 women) were heterogeneous with respect to body mass index (BMI) (normal weight, overweight, and obese), blood lipids (normolipidemic and hyperlipidemic), blood glucose (normal fasting glucose, impaired fasting glucose, and type 2 diabetic), and blood pressure (normotensive and hypertensive). RESULTS: Krill oil supplementation had no effect on any outcome measure (all p > 0.05), and so the data from the krill oil group and the placebo group were collapsed and analyzed to examine the effects of following a 21-day Daniel Fast. Significant reductions were observed in LDL-C (100.6 ± 4.3 mg/dL vs. 80.0 ± 3.7 mg/dL), the LDL:HDL ratio (2.0 ± 0.1 vs. 1.7 ± 0.1), fasting blood glucose (101.4 ± 7.5 mg/dL vs. 91.7 ± 3.4 mg/dL), fasting blood insulin (7.92 ± 0.80 µU/mL vs. 5.76 ± 0.59 µU/mL), homeostasis model assessment of insulin resistance (HOMA-IR) (2.06 ± 0.30 vs. 1.40 ± 0.21), systolic BP (110.7 ± 2.2 mm Hg vs. 105.5 ± 1.7 mm Hg), and body weight (74.1 ± 2.4 kg vs. 71.5 ± 2.3 kg) (all p < 0.05). CONCLUSION: Following a Daniel Fast dietary plan improves a variety of cardiometabolic parameters in a wide range of individuals in as little as 21 days, and these improvements are unaffected by krill oil supplementation. TRIAL REGISTRATION: Clinicaltrial.govNCT01378767.

A dietary supplement containing chlorophytum borivilianum and velvet bean improves sleep quality in men and women.

BACKGROUND: Impaired sleep quality is commonplace within industrialized societies, as evidenced by the increasing number of prescription sleep aids available. Certain herbal preparations have been suggested to provide a natural benefit to sleep; however, limited controlled data are available documenting this benefit. In the present study we tested the effect of an experimental dietary supplement, containing the active ingredients Chlorophytum borivilianum and Velvet bean, on sleep quality using the Pittsburgh Sleep Quality Index (PSQI). METHODS: Eighteen healthy and active men and women, with evidence of impaired sleep quality, consumed the supplement daily for 28 days. The PSQI was administered before and after the intervention period. As indicators of safety, resting heart rate and blood pressure were measured, and a complete blood count, comprehensive metabolic panel, and lipid panel were determined. RESULTS: Sleep quality was influenced by the supplement, as evidenced by an improvement in every category of the PSQI questionnaire (P < 0.05), with most category scores improving approximately 50% from pre to post intervention. No adverse outcomes were noted with use of the supplement, as indicated by no change in resting heart rate, blood pressure, or any bloodborne parameter. CONCLUSIONS: An investigational dietary supplement containing the active ingredients Chlorophytum borivilianum and Velvet bean improves sleep quality in men and women. Additional placebo controlled trials are needed to corroborate these findings in individuals with self-reported sleeping difficulty.

Impact of short-term dietary modification on postprandial oxidative stress.

BACKGROUND: We have recently reported that short-term (21-day) dietary modification in accordance with a stringent vegan diet (i.e., a Daniel Fast) lowers blood lipids as well as biomarkers of oxidative stress. However, this work only involved measurements obtained in a fasted state. In the present study, we determined the postprandial response to a high-fat milkshake with regards to blood triglycerides (TAG), biomarkers of oxidative stress, and hemodynamic variables before and following a 21-day Daniel Fast. METHODS: Twenty-two subjects (10 men and 12 women; aged 35 ± 3 years) completed a 21-day Daniel Fast. To induce oxidative stress, a milkshake (fat = 0.8 g·kg-1; carbohydrate = 1.0 g·kg-1; protein = 0.25 g·kg-1) was consumed by subjects on day one and day 22 in a rested and 12-hour fasted state. Before and at 2 and 4 h after consumption of the milkshake, heart rate (HR) and blood pressure were measured. Blood samples were also collected at these times and analyzed for TAG, malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein products (AOPP), nitrate/nitrite (NOx), and Trolox Equivalent Antioxidant Capacity (TEAC). RESULTS: A time effect was noted for HR (p = 0.006), with values higher at 2 hr post intake of the milkshake as compared to pre intake (p < 0.05). Diastolic blood pressure was lower post fast as compared to pre fast (p = 0.02), and a trend for lower systolic blood pressure was noted (p = 0.07). Time effects were noted for TAG (p = 0.001), MDA (p < 0.0001), H2O2 (p < 0.0001), AOPP (p < 0.0001), and TEAC (p < 0.0001); all concentrations were higher at 2 h and 4 h post intake compared to pre intake, except for TEAC, which was lower at these times (p < 0.05). A condition effect was noted for NOx (p = 0.02), which was higher post fast as compared to pre fast. No pre/post fast × time interactions were noted (p > 0.05), with the area under the curve from pre to post fast reduced only slightly for TAG (11%), MDA (11%), H2O2 (8%), and AOPP (12%), with a 37% increase noted for NOx. CONCLUSION: Partaking in a 21-day Daniel Fast does not result in a statistically significant reduction in postprandial oxidative stress. It is possible that a longer time course of adherence to the Daniel Fast eating plan may be needed to observe significant findings.

Effects of 2-nitrooxy ethyl 2-amino 3-methylbutanoate gel on resistance exercise performance and blood nitrate/nitrite in resistance trained men.

Nitric oxide dietary supplements are popular within the sport community. Our recent work involving the oral intake of 2-nitrooxy ethyl 2-amino 3-methylbutanoate demonstrated an approximately 6.7% increase in circulating nitrate/nitrite. However, no measures of exercise performance were obtained. The present study used a topical form of this molecule to determine the impact on exercise performance and blood nitrate/nitrite. Fourteen resistance trained men (24 ± 1 years old) reported to the laboratory on 2 occasions to undergo exercise testing, which consisted of arm curl isometric force and muscular endurance (3 sets to fatigue using 80, 65, and 50% of 1 repetition maximum [1RM]: total of 9 sets). The gel (2-nitrooxy ethyl 2-amino 3-methylbutanoate; mixed in tea tree oil) or placebo (tea tree oil) was applied topically by the subjects for 7 days before each test day, with 7-10 days separating the randomly ordered conditions. Blood samples, arm circumference, and perceived "muscle pump" were taken before and immediately after exercise on both test days. The heart rate and perceived exertion were measured after each set. No statistically significant differences were noted between conditions for performance variables (p > 0.05). However, when using a load of 50% of 1RM, 6.2% more repetitions were performed when using the gel as compared with when using the placebo; 19.9% more repetitions were performed by 8 subjects noted to be "responders" to gel treatment. Blood lactate and muscle pump significantly increased with exercise (p < 0.0001) but were not different between conditions (p > 0.05). Minimal change was noted in nitrate/nitrite, and the heart rate and perceived exertion were nearly identical between conditions (p > 0.05). These findings indicate that 2-nitrooxy ethyl 2-amino 3-methylbutanoate gel has a modest (6.2%), nonstatistically significant effect on exercise performance, in particular when using a load of 50% 1RM-with greater benefit noted in selected individuals. Studies inclusive of a larger sample size are needed to extend these initial findings.

Biochemical and anthropometric effects of a weight loss dietary supplement in healthy men and women.

BACKGROUND: We have recently noted an acute increase in circulating free fatty acids and glycerol, as well as resting metabolic rate, when men and women ingested the dietary supplement OxyELITE Pro™ in a single dose. We have also noted a reduction in appetite when subjects were treated with this supplement for 14 consecutive days. It is possible that such findings may favor body weight and fat loss over time. Therefore, the purpose of the present study was to determine the effects of this dietary supplement on weight loss and associated markers using an eight week intervention. METHODS: Exercise-trained subjects were randomly assigned in double blind manner to ingest either the dietary supplement (n = 16; aged 22.8 ± 0.7) or a placebo (n = 16; 22.5 ± 0.5) every day for eight weeks. Body weight, body composition, skinfold thickness, serum lipids, and appetite were measured as the primary outcome variables. As measures of supplement safety, a complete blood count and comprehensive metabolic panel were performed, and resting heart rate and blood pressure were measured (pre and post intervention). RESULTS: No interactions or main effects were noted for our primary outcome measures (P > 0.05). However, when comparing pre and post intervention values for the supplement, significant decreases were noted in appetite, body weight, body fat percentage, and skinfold thickness (P < 0.05), while increases were noted for total and HDL-C, as well as for resting heart rate (P < 0.05). No changes were noted for placebo from pre to post intervention (P > 0.05), with the exception of an increase in HDL-C (P < 0.05). Blood pressure and bloodborne safety variables were not differently impacted by supplement or placebo (P > 0.05), with the exception of monocytes, for which an interaction effect was noted (P = 0.04). CONCLUSION: These data indicate that the dietary supplement OxyELITE Pro™ may assist in weight and body fat loss in a sample of exercise-trained men and women. The supplement does not result in any adverse effects pertaining to resting blood pressure or bloodborne markers of safety; however a small increase in resting heart rate is observed.

A finished dietary supplement stimulates lipolysis and metabolic rate in young men and women.

BACKGROUND: Dietary supplements are often marketed to increase lipolysis and thermogenesis, with the proposed end result being weight loss and body fat reduction. It was the purpose of the present investigation to study the acute effects of a weight/fat loss supplement within a sample of healthy human subjects. METHODS: Twelve subjects (men 24.8 ± 4.3 yrs; women 22.8 ± 0.4 yrs) ingested a dietary supplement (OxyELITE Pro™) or a placebo, on two separate days in a double-blind, cross-over design. Blood samples were collected immediately before ingestion, and at 60 and 120 minutes post ingestion, and analyzed for plasma glycerol and free fatty acids (FFA). Breath samples were collected immediately before ingestion and at 30, 60, 90, and 120 minutes post ingestion, for a measure of kilocalorie expenditure using indirect calorimetry. Area under the curve (AUC) was calculated. Heart rate and blood pressure were recorded at all times and rate pressure product (RPP) was calculated. RESULTS: AUC was greater for supplement compared to placebo for glycerol (22.74 ± 1.98 µg · mL(-1) · 2 hr(-1) vs. 15.76 ± 1.36 µg · mL(-1) · 2 hr(-1); P = 0.001), FFA (1.62 ± 0.07 mmol · L(-1) · 2 hr(-1) vs. 0.78 ± 0.12 mmol · L(-1) · 2 hr(-1); P < 0.0001), and kilocalorie expenditure (149 ± 7 kcal · 2 hr(-1) vs. 122 ± 8 kcal · 2 hr(-1); P = 0.005). Heart rate (P = 0.02), systolic blood pressure (P < 0.0001), and RPP (P = 0.002) were higher for supplement compared to placebo. CONCLUSION: Ingestion of OxyELITE Pro™ resulted in an increase in blood markers of lipolysis, as well as metabolic rate, during a two-hour post ingestion time period. An increase in hemodynamic variables was also observed. These findings are in reference to a sample of healthy men and women who were naïve to treatment with the dietary supplement. Additional work is needed to determine if the acute changes observed here would persist with chronic use of the supplement and possibly lead to weight/body fat loss over time.

Hormonal response to lipid and carbohydrate meals during the acute postprandial period.

BACKGROUND: Optimizing the hormonal environment during the postprandial period in favor of increased anabolism is of interest to many active individuals. Data are conflicting regarding the acute hormonal response to high fat and high carbohydrate feedings. Moreover, to our knowledge, no studies have compared the acute hormonal response to ingestion of lipid and carbohydrate meals of different size. METHODS: We compared the hormonal response to lipid and carbohydrate meals of different caloric content during the acute postprandial period. Nine healthy men (22 ± 2 years) consumed in a random order, cross-over design one of four meals/beverages during the morning hours in a rested and fasted state: dextrose at 75 g (300 kcals), dextrose at 150 g (600 kcals), lipid at 33 g (300 kcals), lipid at 66 g (600 kcals). Blood samples were collected Pre meal, and at 0.5 hr, 1 hr, 2 hr, and 3 hr post meal. Samples were assayed for testosterone, cortisol, and insulin using ELISA techniques. Area under the curve (AUC) was calculated for each variable, and a 4 × 5 ANOVA was used to further analyze data. RESULTS: A meal × time effect (p = 0.0003) was noted for insulin, with values highest for the dextrose meals at the 0.5 hr and 1 hr times, and relatively unaffected by the lipid meals. No interaction (p = 0.98) or meal (p = 0.39) effect was noted for testosterone, nor was an interaction (p = 0.99) or meal (p = 0.65) effect noted for cortisol. However, a time effect was noted for both testosterone (p = 0.04) and cortisol (p < 0.0001), with values decreasing during the postprandial period. An AUC effect was noted for insulin (p = 0.001), with values higher for the dextrose meals compared to the lipid meals (p < 0.05). No AUC effect was noted for testosterone (p = 0.85) or cortisol (p = 0.84). CONCLUSIONS: These data indicate that 1) little difference is noted in serum testosterone or cortisol during the acute postprandial period when healthy men consume lipid and dextrose meals of different size; 2) Both testosterone and cortisol experience a drop during the acute postprandial period, which is similar to what is expected based on the normal diurnal variation--feeding with lipid or dextrose meals does not appear to alter this pattern; 3) dextrose meals of either 75 g or 150 g result in a significant increase in serum insulin, in particular at 0.5 hr and 1 hr post-ingestion; 4) lipid meals have little impact on serum insulin.

A blend of chlorophytum borivilianum and velvet bean increases serum growth hormone in exercise-trained men.

BACKGROUND: Several isolated ingredients have been proposed to increase growth hormone (GH) release, including Chlorophytum borivilianum and Velvet bean. A combination of these two ingredients has been packaged within an investigational dietary supplement. It was the purpose of the present investigation to determine the impact of acute ingestion of this supplement on circulating GH in healthy, exercise-trained men. METHODS: Fifteen men ingested the dietary supplement on two different days, separated by one week. Blood was collected from subjects before ingestion of the supplement and at 20, 40, 60, 80, 100, and 120 minutes post ingestion. GH was analyzed in serum samples using an ELISA method. Values for GH for each subject, at each collection time, were averaged over both test days and used in the main analysis. RESULTS: Serum GH increased over time, with higher values at 60 minutes (1.56 ± 0.65 ng · mL(-1); P = 0.04; +767%), 80 minutes (1.76 ± 0.69 ng · mL(-1); P = 0.02; +878%), and 100 minutes (1.48 ± 0.62 ng · mL(-1); P = 0.05; +722%) compared to pre ingestion (0.18 ± 0.04 ng · mL(-1)). A great deal of subject variability existed in the area under the curve (AUC) for GH, with pooled values ranging from 0.49 to 61.2 ng · mL(-1) · 2 hr(-1.) CONCLUSION: Acute ingestion of an investigational dietary supplement containing the active ingredients Chlorophytum borivilianum and Velvet bean results in an increase in circulating GH in exercise-trained men. Additional placebo controlled investigations are needed to extend these findings. Moreover, studies are needed to determine if chronic use of such supplementation leads to favorable changes in health-related parameters associated with increased circulating GH.