Ergogenic properties of metformin in simulated high altitude.

Metformin augments glucose/glycogen regulation and may acutely promote fatigue resistance during high-intensity exercise. In hypobaric environments, such as high altitude, the important contribution of carbohydrates to physiological function is accentuated as glucose/glycogen dependence is increased. Because hypoxia/hypobaria decreases insulin sensitivity, replenishing skeletal muscle glycogen in high altitude becomes challenging and subsequent physical performance may be compromised. We hypothesized that in conditions where glycogen repletion was critical to physical outcomes, metformin would attenuate hypoxia-mediated decrements in exercise performance. On three separate randomly ordered occasions, 13 healthy men performed glycogen-depleting exercise and ingested a low-carbohydrate dinner (1200 kcals, <10% carbohydrate). The next morning, in either normoxia or hypoxia (FiO2 =0.15), they ingested a high-carbohydrate breakfast (1225 kcals, 70% carbohydrate). Placebo (719 mg maltodextrin) or metformin (500 mg BID) was consumed 3 days prior to each hypoxia visit. Subjects completed a 12.5 km cycle ergometer time trial 3.5 hours following breakfast. Hypoxia decreased resting and exercise oxyhemoglobin saturation (P<.001). Neither hypoxia nor metformin affected the glucose response to breakfast (P=.977), however, compared with placebo, metformin lowered insulin concentration in hypoxia 45 minutes after breakfast (64.1±6.6 µU/mL vs 48.5±7.8 µU/mL; mean±SE; P<.001). Post-breakfast, pre-exercise vastus lateralis glycogen content increased in normoxia (+33%: P=.025) and in hypoxia with metformin (+81%; P=.006), but not in hypoxia with placebo (+27%; P=.167). Hypoxia decreased time trial performance compared with normoxia (P<.01). This decrement was similar with placebo (+2.6±0.8 minutes) and metformin (+1.6±0.3 minutes). These results indicate that metformin promotes glycogen synthesis but not endurance exercise performance in healthy men exposed to simulated high altitude.

Acute {beta}-adrenergic stimulation does not alter mitochondrial protein synthesis or markers of mitochondrial biogenesis in adult men.

Exercise-induced expression of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) is dramatically inhibited in mice pretreated with a beta-adrenergic receptor (beta-AR) antagonist, suggesting that beta-ARs play an important role in the regulation of skeletal muscle PGC-1alpha expression, and potentially, mitochondrial biogenesis. Accordingly, we hypothesized that acute beta-AR stimulation would induce transcriptional pathways involved in skeletal muscle mitochondrial biogenesis in humans. Whole body protein turnover (WBPT), myofibrillar protein synthesis (MyPS), skeletal muscle mitochondrial protein synthesis (MiPS), and mitochondrial biogenic signaling were determined in samples of vastus lateralis obtained on two separate occasions in 10 young adult males following 1 h of continuous intravenous administration of saline (CON) or a nonspecific beta-AR agonist [isoproterenol (ISO): 12 ng.kg fat free mass(-1).min(-1)], combined with coinfusion of [1,2](13)C-leucine. beta-AR stimulation induced appreciable increases in heart rate and systolic blood pressure (both P < 0.001) but did not affect mitochondrial biogenic signaling (no change in PGC-1alpha, TFAM, NRF-1, NRF-2, COX, or NADHox expression via RT-PCR; P > 0.05). Additionally, MiPS [CON: 0.099 +/- 0.028, ISO: 0.074 +/- 0.046 (mean +/- SD); P > 0.05] and MyPS (CON: 0.059 +/- 0.008, ISO: 0.055 +/- 0.009; P > 0.05), as well as measures of WBPT were unaffected. On the basis of this investigation, we conclude that acute intravenous beta-AR stimulation does not increase mitochondrial protein synthesis or biogenesis signals in skeletal muscle.

Phosphorylation of the JAK2-STAT5 pathway in response to acute aerobic exercise.

UNLABELLED: Growth hormone (GH) is a powerful stimulator of the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5 (STAT5) pathway. Acute exercise is a known stimulus for GH secretion. PURPOSE: The purpose of this study was to determine the phosphorylation of the JAK2-STAT5 pathway in human skeletal muscle in response to acute aerobic exercise. METHODS: Eleven young (22.5 +/- 0.6, mean +/- SE), healthy, aerobically trained males performed 30 min of cycling at 70% V O2max. Blood samples were collected at 10- to 15-min intervals and analyzed for human GH, immunofunctional (IF) GH, GH binding protein, and insulin-like growth factor I (IGF-I). Muscle biopsies were taken from the vastus lateralis before exercise, immediately after exercise, as well as, 30 and 60 min postexercise. Muscle samples were analyzed for changes in JAK2 and STAT5 tyrosine phosphorylation, as well as changes in JAK2 and STAT5 protein content. RESULTS: Multivariate ANOVA with post hoc comparisons demonstrated that GH and IF GH were significantly elevated immediately after exercise compared with preexercise (P < 0.001). Exercise significantly increased the phosphorylation of JAK2 immediately after exercise (P = 0.004). A trend toward increasing levels of STAT5 phosphorylation was observed immediately after exercise (P = 0.08) and was significantly elevated 30 min after exercise (P = 0.002), compared with preexercise levels. Muscle JAK2 and STAT5 protein content did not change. CONCLUSION: The results demonstrate that the JAK2-STAT5 pathway is activated in response to acute aerobic exercise in human skeletal muscle and suggests that the exercise-induced release of GH may play a role in the activation of this pathway.

Adiponectin levels are reduced, independent of polymorphisms in the adiponectin gene, after supplementation with alpha-linolenic acid among healthy adults.

Our first aim was to determine whether an isocaloric intervention using alpha-linolenic acid (ALA) in the form of flaxseed oil would alter adiponectin levels among overweight, otherwise healthy, males and females, and our second aim was to test for any potential modification of this intervention by 2 single nucleotide polymorphisms (276 and 45) in the adiponectin gene. Subjects included healthy adult males and females (approximately 81% female; average age, 38 years) with increased waist circumference (mean, 99 cm) and body mass index (mean, 30 kg/m(2)) who were free of chronic disease, not taking medications, and sedentary. Subjects met weekly with a registered dietician for 8 weeks. The control subjects (n = 27) were instructed not to alter their habitual diet and the ALA group (n = 30) was instructed to follow an enriched ALA diet by using flaxseed oil capsules (increasing ALA to 5% of total energy intake) and to lower their dietary fat consumption by a commensurate amount. Diets were analyzed using the Food Intake and Analysis System (v. 3.0, University of Texas School of Public Health, 1998). Fasting blood samples were obtained before and after the 8-week intervention. We found significant decreases (P = .02) in adiponectin (10.12 microg/mL pre, 9.23 microg/mL post) in the ALA group as compared with the control group (7.93 microg/mL pre, 8.10 microg/mL post) after the intervention. We also saw a decline in adiponectin in all genotype groups with the greatest decline among those carrying the rare T allele of single nucleotide polymorphism 276. There were no significant changes in fasting insulin, glucose, or quantitative insulin sensitivity check index values as a result of this intervention. In conclusion, this study suggests that supplementing with ALA for 8 weeks may lower adiponectin levels among healthy individuals, and this effect appears to be independent of polymorphisms in the adiponectin gene. Although the change in adiponectin in response to the omega-3 fatty acids was not accompanied by any change in glucose, insulin, or quantitative insulin sensitivity check index, long-term implications of such a decrease should be considered in future studies.

Regulators of human white adipose browning: evidence for sympathetic control and sexual dimorphic responses to sprint interval training.

The conversion of white adipose to the highly thermogenic beige adipose tissue has been proposed as a potential strategy to counter the unfavorable consequences of obesity. Three regulators of this conversion have recently emerged but information regarding their control is limited, and contradictory. We present two studies examining the control of these regulators. Study 1: In 10 young men, the plasma concentrations of irisin and fibroblast growth factor 21 (FGF21) were determined prior to and during activation of the sympathetic nervous system via hypoxic gas breathing (FIO2 = 0.11). The measurements were performed twice, once with and once without prior/concurrent sympathetic inhibition via transdermal clonidine administration. FGF21 was unaffected by basal sympathetic inhibition (338±113 vs. 295±80 pg/mL; P = 0.43; mean±SE), but was increased during hypoxia mediated sympathetic activation (368±135); this response was abrogated (P = 0.035) with clonidine (269±93). Irisin was unaffected by sympathetic inhibition and/or hypoxia (P>0.21). Study 2: The plasma concentration of irisin and FGF21, and the skeletal muscle protein content of fibronectin type III domain containing 5 (FNDC5) was determined in 19 young adults prior to and following three weeks of sprint interval training (SIT). SIT decreased FGF21 (338±78 vs. 251±36; P = 0.046) but did not affect FNDC5 (P = 0.79). Irisin was decreased in males (127±18 vs. 90±23 ng/mL; P = 0.045) and increased in females (139±14 vs. 170±18). Collectively, these data suggest a potential regulatory role of acute sympathetic activation pertaining to the browning of white adipose; further, there appears to be a sexual dimorphic response of irisin to SIT.

Lipidomic analysis of human plasma reveals ether-linked lipids that are elevated in morbidly obese humans compared to lean.

BACKGROUND: Lipidomic analysis was performed to explore differences in lipid profiles between plasma from lean and obese subjects, followed by in vitro methods to examine a role for the identified lipids in endothelial cell pathophysiology. METHODS: Plasma was collected from 15 morbidly obese and 13 control subjects. Lipids were extracted from plasma and analyzed using LC/MS, and MS/MS to characterize lipid profiles and identify lipids that are elevated in obese subjects compared to lean. RESULTS: Orthogonal partial least squares-discriminant analysis (OPLS-DA) modelling showed that lipid profiles were significantly different in obese subjects compared to lean. Analysis of lipids that were driving group separation in the OPLS-DA model and that were significantly elevated in the obese group led to identification of a group of ether-linked phosphatidylcholine (PC) and phosphatidylethanolamine (PE) lipids of interest. Treatment of human coronary artery endothelial cells with the ether-linked phosphatidylethanolamine induced expression of cell adhesion molecules, a hallmark of endothelial cell activation. However, oxidized phosphatidylcholine products that can induce endothelial cell activation in vitro, were not significantly different between groups in vivo. CONCLUSION: These data suggest a role for ether-linked lipids in obesity associated dyslipidemia and vascular disease.

Cardiometabolic plasticity in response to a short-term diet and exercise intervention in young Hispanic and nonHispanic white adults.

BACKGROUND: Young adult Mexican Americans (MA) exhibit lower insulin sensitivity (Si) than nonHispanic whites (NHW), even when controlling for fitness and adiposity. It is unclear if MA are as responsive to the same lifestyle intervention as NHW. OBJECTIVE: We developed a model to examine cardiometabolic plasticity (i.e., changes in Si and plasma lipids) in MA compared to NHW adults in response to a diet-exercise intervention. DESIGN: Sedentary subjects (20 NHW: 11F, 9M, 23.0 y, 25.5 kg/m(2); 17 MA: 13F, 4M, 22.7 y, 25.4 kg/m(2)) consumed their habitual diets and remained sedentary for 7 days, after which fasting blood samples were obtained, and a 3-h intravenous glucose tolerance test (IVGTT) was performed with the insulin area under the curve (IAUC) used to estimate Si. Subjects then completed a 7-day diet/exercise intervention (diet: low saturated fat, low added sugar, high fiber; exercise: cycling, six total sessions lasting 40-45 min/session at 65% VO(2) max). Pre-intervention tests were repeated. RESULTS: Pre intervention IAUC was 28% higher (p<0.05) in MA (IAUC pre  =  2298 µU*180 min/mL) than in NHW (IAUC = 1795 µU*180 min/mL). Following the intervention, there was a significant reduction in IAUC in MA (29%) and NHW (32%), however, the IAUC remained higher (p<0.05) for MA (post  = 1635 µU*180 min/mL) than for NHW (post = 1211 µU*180 min/mL). Pre test plasma lipids were not different in MA compared to NHW. Plasma cholesterol and TG concentrations significantly improved in both groups, but concentrations of low density lipoprotein-cholesterol and small dense LDL particles significantly improved only in the NHW. CONCLUSION: With a short-term diet-exercise intervention, the magnitude of improvements in Si and serum cholesterol and TG in Hispanics are similar to those in NHW. However, because at the outset MA were less insulin sensitive compared to NHW, within the short timeframe studied the ethnic gap in insulin sensitivity remained.

Nitrogen balance in older individuals in energy balance depends on timing of protein intake.

To explore whether nitrogen retention can differ on an isonitrogenous diet by changing when protein is consumed, we performed a short-term study in older individuals (64.5 ± 2.0 years) performing daily exercise while in energy balance. Participants consumed an isonitrogenous-isocaloric diet with the timing of a protein or carbohydrate beverage after exercise (protein after exercise [PRO], carbohydrate after exercise [CHO]) versus earlier in the day. Three-day mean energy balance (PRO: 202 ± 36 kcal and CHO: 191 ± 44 kcal; p = .68) did not differ between trials, but 3-day mean nitrogen balance was significantly more positive in the PRO (1.2 ± 0.32 g N) trial than the CHO trial (0.8 ± 0.45 g N; p < .05). Older individuals were better able to maintain nitrogen balance by simply changing when a portion of an identical amount of daily protein was consumed.

Effect of resistance exercise, with or without carbohydrate supplementation, on plasma ghrelin concentrations and postexercise hunger and food intake.

The effects of resistance exercise with and without carbohydrate (CHO) supplementation on hunger, postexercise food intake, and plasma ghrelin, an orexigenic gastric peptide, are poorly characterized. We examined the individual and combined effects of a resistance exercise bout and CHO consumption on plasma ghrelin and postexercise food intake. Twenty-one apparently healthy young male participants ([mean +/- SD] age = 20 +/- 1.8 years, body mass index = 24.8 +/- 3.3 kg/m(2)) completed in random order 3 treatment conditions: (1) ExCHO-80-minute resistance exercise bout while consuming CHO ( approximately 77 g CHO, 306 kcal); (2) ExPLA-identical exercise with a non=caloric placebo; and (3) NoExCHO-no-exercise trial of quiet sitting and CHO consumption. Blood samples were obtained before, during, and immediately postexercise, and 110 minutes after exercise. At 2 hours postexercise, they were provided a buffet of food from which they ate ad libitum. There was a significant time x treatment interaction for plasma ghrelin caused by a decline from pre- to postexercise in the 2 exercise conditions compared with an increase over time in the NoExCHO condition. At 110 minutes postexercise, ghrelin was 21% and 13% lower in ExCHO and ExPLA compared with NoExCHO (both Ps < .05). However, despite the lower ghrelin concentrations for the 2 exercise conditions, the subjective ratings of hunger were not lower for these conditions compared with the NoExCHO. There were no differences in absolute ad libitum energy intake from the buffet among the 3 conditions, but relative energy intake from the buffet accounting for the estimated cost of exercise was lowest among the 2 exercise conditions. We conclude that (1) weight lifting lowers plasma ghrelin concentrations during exercise and attenuates its rise during the postexercise period in young men and (2) the lower plasma ghrelin concentration is not associated with lower subjective feelings of hunger measured 100 minutes postexercise, but is associated with a lower relative food intake.

Does prior acute exercise affect postexercise substrate oxidation in response to a high carbohydrate meal?

BACKGROUND: Consumption of a mixed meal increases postprandial carbohydrate utilization and decreases fat oxidation. On the other hand, acute endurance exercise increases fat oxidation and decreases carbohydrate utilization during the post-exercise recovery period. It is possible that the resulting post-exercise increase in circulating nonesterified fatty acids could attenuate the ability of ingested carbohydrate to inhibit lipid oxidation. The purpose of this study was to determine whether prior exercise attenuates the usual meal-induced decline in lipid oxidation. METHODS: Six healthy, physically active young subjects (x age = 26.3 years, 4 males, 2 females) completed three treatments in random order after a ~10 h fast: (a) Exercise/Carbohydrate (Ex/CHO) - subjects completed a bout of exercise at 70% VO2peak (targeted net energy cost of 400 kcals), followed by consumption of a carbohydrate-rich meal; (b) Exercise/Placebo (Ex/Placebo) - subjects completed an identical bout of exercise followed by consumption of a placebo; and (c) No Exercise/Carbohydrate (NoEx/CHO) - subjects sat quietly rather than exercising and then consumed the carbohydrate-rich meal. Blood samples were obtained before and during the postprandial period to determine plasma glucose, insulin, and non-esterified fatty acids (NEFA). Respiratory gas exchange measures were used to estimate rates of fat and carbohydrate oxidation. RESULTS: Plasma NEFA were approximately two-fold higher immediately following the two exercise conditions compared to the no-exercise condition, while meal consumption significantly increased insulin and glucose in both Ex/CHO and NoEx/CHO. NEFA concentrations fell rapidly during the 2-h postprandial period, but remained higher compared to the NoEx/CHO treatment. Carbohydrate oxidation increased rapidly and fat oxidation decreased in response to the meal, with no differences in the rates of carbohydrate and fat oxidation during recovery between the Ex/CHO and NoEx/CHO conditions. CONCLUSION: The plasma NEFA concentration is increased during the post exercise period, which is associated with elevated fat oxidation when no meal is consumed. However, when a mixed meal is consumed immediately following exercise, the initially elevated plasma NEFA concentration decreases rapidly, and postexercise fat oxidation during this 2-h postexercise, postprandial period is no higher than that of the 2-h postprandial period without prior exercise.

Inflammatory markers are not altered by an eight week dietary alpha-linolenic acid intervention in healthy abdominally obese adult males and females.

Atherogenesis is thought to be mediated by local and/or systemic production of pro-inflammatory cytokines and omega-3 fatty acids have been implicated in reducing these inflammatory markers. The objective of this study was to determine the effect of an isocaloric diet supplemented with a plant-based dietary omega-3 fatty acid [alpha-linolenic acid (ALA)] on interleukin-6, C-reactive protein, serum amyloid A, and tumor necrosis factor-alpha. Subjects included healthy adult males and females (approximately 79% female, average age 38 years) with increased waist circumference (mean WC=99 cm) and body mass index (mean BMI=29.8 kg/m(2)) who were free of chronic disease, not taking medications, and sedentary. Control subjects (n=24) did not to alter their habitual diet and the ALA group (n=27) followed an enriched ALA diet by using flaxseed oil capsules (increasing ALA to 5% of total energy intake) and lowered their dietary fat consumption by a commensurate amount. Fasting blood samples were obtained before and after the 8-week intervention. We found no significant changes in the inflammatory factors after this 8-week dietary intervention. This study suggests there are no beneficial effects of an 8-week ALA intervention on these inflammatory factors among young, healthy, overweight/obese subjects whose inflammatory factors are not significantly elevated.

High resistance/low repetition vs. low resistance/high repetition training: effects on performance of trained cyclists.

In order to investigate the effects of a resistance training modality on cycling performance, 23 trained club-level cyclists were placed into high resistance/low repetition (H-Res), low resistance/high repetition (H-Rep), or cycling-only groups for a 10-week program. All 3 groups followed the same cycling plan, but the H-Res and H-Rep groups added resistance training. Testing pre and post consisted of a graded incremental lactate profile test on an ergometer, with blood lactate being sampled. VO2 values were measured to determine economy. Maximum strength testing of 4 strength exercises targeting the lower extremity musculature was conducted with the H-Res and H-Rep groups. There were significant gains in all 4 resistance training exercises (p < 0.05) for both H-Res and H-Rep, with the H-Res group having significantly greater gains than the H-Rep group had in the leg press exercise (p < 0.05). There were, however, no significant group x training differences (p > 0.05) found between the 3 training groups on the cycling test in lactate values or economy. It appears that for this population of cyclists, neither H-Res nor H-Rep resistance training provided any additional performance benefit in a graded incremental cycling test when compared with cycling alone over a training time of this length. It is possible that with this population, various factors such as acute fatigue, strength, and aerobic gains from the cycling training, in addition to well-developed bases of strength and conditioning from previous training, reduced differences between groups in both strength gains and cycling performance.

Population variation and differences in serum leptin independent of adiposity: a comparison of Ache Amerindian men of Paraguay and lean American male distance runners.

BACKGROUND: Serum leptin variation is commonly associated with fat percentage (%), body mass index (BMI), and activity. In this investigation, we report population differences in mean leptin levels in healthy men as well as associations with fat % and BMI that are independent of these factors and reflect likely variation resulting from chronic environmental conditions. METHODS: Serum leptin levels, fat %, and BMI were compared between lean American distance runners and healthy Ache Native Americans of Paraguay. Mean levels were compared as were the regressions between fat %, BMI, and leptin. Comparisons were performed between male American distance runners (n = 13, mean age 32.2 +/- 9.2 SD) and highly active male New World indigenous population (Ache of Paraguay, n = 20, mean age 32.8 +/- 9.2) in order to determine whether significant population variation in leptin is evident in physically active populations living under different ecological circumstances independent of adiposity and BMI. RESULTS: While the Ache were hypothesized to exhibit higher leptin due to significantly greater adiposity (fat %, Ache 17.9 +/- 1.8 SD; runners 9.7 +/- 3.2, p < 0.0001), leptin levels were nonetheless significantly higher in American runners (Ache 1.13 ng/ml +/- 0.38 SD; runners 2.19 +/- 1.15; p < 0.007). Significant differences in the association between leptin and fat % was also evident between Ache and runner men. Although fat % was significantly related with leptin in runners (r = 0.90, p < 0.0001) fat % was negatively related in Ache men (r = -0.50, p < 0.03). CONCLUSION: These results illustrate that chronic ecological conditions in addition to activity are likely factors that contribute to population variation in leptin levels and physiology. Population variation independent of adiposity should be considered to be an important source of variation, especially in light of ethnic and population differences in the incidence and etiology of obesity, diabetes, and other metabolic conditions.

Effect of acute prior exercise on glycemic and insulinemic indices.

BACKGROUND: Acute exercise is associated with increased insulin sensitivity characterized by increased insulin-induced glucose transport for periods of up to 48 h after the bout of exercise. This suggests that the glycemic response to a meal may be altered by prior exercise. OBJECTIVE: We tested the hypothesis that the glycemic and insulinemic responses to a test food consumed following exercise would be lower than when consumed without prior exercise. DESIGN: Four lean males (age: 27 +/- 4 y) and 4 females (age: 23 +/- 3 y) completed 3 experimental conditions in random order: ExCHO-Subjects exercised on a cycle ergometer at 70% VO2peak with a net energy cost of 400 kcal, which was followed by consumption of a high carbohydrate (CHO) energy bar; NoExCHO-Same as ExCHO except subjects sat quietly rather than exercised; and NoExGlc-Same as NoExCHO except subjects consumed a 50 g glucose (glc) drink as the reference CHO for GI and insulinemic index (II) determination. For each condition, following exercise or rest, baseline venous blood samples were obtained. Postprandial blood samples were obtained at 15 min intervals for 2 h. RESULTS: Neither the 2-h glucose area under the curve (AUC) or the GI were different between ExCHO and NoExCHO. The insulin AUC for ExCHO was 28% lower than the insulin AUC for NoExCHO (p = 0.03). The calculated II for the ExCHO condition was 30% lower than that of NoExCHO (p = 0.05). CONCLUSIONS: An acute bout of prior exercise had no effect on the GI of an energy bar compared to that of the same food determined under the standard no-exercise conditions. However, prior exercise resulted in a lower 2-h insulin response to the CHO-rich energy bar.

Dissociation of the glycaemic and insulinaemic responses to whole and skimmed milk.

In most carbohydrate-containing foods, the blood insulin response is predictable and is closely linked to the food's glycaemic index (GI). A single study, examining whole milk and fermented milk products made from whole milk, recently reported a large dissociation between the GI and insulinaemic index (II) in healthy normal adults. Because the fat component of a food may influence the GI and II, it is unclear if a similar dissociation may exist for skimmed milk in normal adults. We determined the GI and II of both skimmed and whole milk in nine healthy, male (n 6) and female (n 3) subjects (23.6 (sd 1.4) years). No significant (P>0.05) differences existed between GI and II for skimmed and whole milks. Significant (P<0.05) differences were observed between the actual and predicted areas under the insulin curves for both skimmed milk (predicted 1405 (sd 289) pmol x min/l; actual 6152 (sd 1177) pmol x min/l) and whole milk (predicted 1564 (sd 339) pmol x min/l; actual 5939 (sd 1095) pmol x min/l). Consequently, a large and similar dissociation of the GI and II existed for both whole milk (42 (sd 5) and 148 (sd 14)) and skimmed milk (37 (sd 9) and 140 (sd 13)). It is concluded that the dissociation of the GI and II in milk is not related to its fat content.

Comparison of two twelve week off-season combined training programs on entry level collegiate soccer players' performance.

Olympic-style lifts (OSL) and plyometric exercises (PE) are frequently combined with traditional resistance training (TRT) to improve athletic performance. The goal of this study was to directly compare the performance effect of TRT (30 minutes) combined with either OSL or nondepth-jump PE (15 minutes) on entry level competitive collegiate athletes. Ten female and 5 male competitive soccer players, divided into 2 groups, completed 12 weeks of tri-weekly training during their off-season. Countermovement vertical jump, 4 repetition maximum squat, 25-m sprint, and figure-8 drill on a 5-dot mat were conducted pre-, mid-, and postintervention. Significant improvements were made by both groups in each performance parameter over the 12-week period (p < 0.05), with no significant differences found between the training groups. Although these training modalities may achieve their results through slightly different mechanisms, the performance-related improvements may not be significantly different for entry-level collegiate athletes with little resistance training experience.

Circulating tumor necrosis factor alpha is higher in non-obese, non-diabetic Mexican Americans compared to non-Hispanic white adults.

Mexican Americans (MA) exhibit high risk for the insulin resistance syndrome characterized by subclinical inflammation and greater risk for type 2 diabetes compared with non-Hispanic white (NHW) adults. The reasons for this phenomenon remain obscure. Because the inflammatory cytokine, tumor necrosis factor-alpha (TNF alpha), is associated with insulin resistance in various models of obesity and diabetes, we sought to determine whether circulating concentrations of this cytokine and its soluble receptors are higher in MA than NHW, and also to determine if the TNF alpha system is related to the lower insulin sensitivity in MA. Fasting blood samples were used to determine concentrations of TNF alpha, soluble TNF receptors 1 (sTNFR1) and 2 (sTNFR2) in the same 13 MA (7 women, 6 men, age=27.0+/-2.0 years, BMI=23.0+/-0.7) and 13 NHW (7 women, 6 men, age=24.8+/-1.5 years, BMI=22.8+/-0.6) previously shown to exhibit differences in insulin sensitivity. Circulating TNF alpha was significantly higher (3.11+/-0.38 vs. 2.10+/-0.24 pg/ml, p<0.05) and sTNFR2 was significantly lower (1324+/-85 vs. 1925+/-127 pg/ml, p<0.05) among MA compared with NHW subjects. Soluble TNFR1 was not different between groups (MA: 970+/-111 pg/ml vs. NHW: 1218+/-73 pg/ml, p=0.07). TNF alpha, sTNFR1 and sTNFR2 were not correlated with HOMA-IR when the two groups were analyzed in aggregate. This study documents higher circulating TNF alpha concentrations in non-obese, non-diabetic MA, a population group at increased risk for the metabolic syndrome and the untoward effects of sub-clinical inflammation. The clinical implications of this difference, if any, are not yet known.