Effects of a Caffeine-Containing Energy Drink on Simulated Soccer Performance

[Background] To investigate the effects of a caffeine-containing energy drink on soccer performance during a simulated game. A second purpose was to assess the post-exercise urine caffeine concentration derived from the energy drink intake. [Methodology/Principal Findings] Nineteen semiprofessional soccer players ingested 630±52 mL of a commercially available energy drink (sugar-free Red Bull®) to provide 3 mg of caffeine per kg of body mass, or a decaffeinated control drink (0 mg/kg). After sixty minutes they performed a 15-s maximal jump test, a repeated sprint test (7×30 m; 30 s of active recovery) and played a simulated soccer game. Individual running distance and speed during the game were measured using global positioning satellite (GPS) devices. In comparison to the control drink, the ingestion of the energy drink increased mean jump height in the jump test (34.7±4.7 v 35.8±5.5 cm; P<0.05), mean running speed during the sprint test (25.6±2.1 v 26.3±1.8 km · h−1; P<0.05) and total distance covered at a speed higher than 13 km · h−1 during the game (1205±289 v 1436±326 m; P<0.05). In addition, the energy drink increased the number of sprints during the whole game (30±10 v 24±8; P<0.05). Post-exercise urine caffeine concentration was higher after the energy drink than after the control drink (4.1±1.0 v 0.1±0.1 µg · mL−1; P<0.05). [Conclusions/significance] A caffeine-containing energy drink in a dose equivalent to 3 mg/kg increased the ability to repeatedly sprint and the distance covered at high intensity during a simulated soccer game. In addition, the caffeinated energy drink increased jump height which may represent a meaningful improvement for headers or when players are competing for a ball

Effects of athletes' muscle mass on urinary markers of hydration status

To determine if athletes’ muscle mass affects the usefulness of urine specific gravity (U sg) as a hydration index. Nine rugby players and nine endurance runners differing in the amount of muscle mass (42 ± 6 vs. 32 ± 3 kg, respectively; P = 0.0002) were recruited. At waking during six consecutive days, urine was collected for U sg analysis, urine osmolality (U osm), electrolytes (U[Na+], U[K+] and U[Cl−]) and protein metabolites (U [Creatinine], U [Urea] and U [Uric acid]) concentrations. In addition, fasting blood serum osmolality (S osm) was measured on the sixth day. As averaged during 6 days, U sg (1.021 ± 0.002 vs. 1.016 ± 0.001), U osm (702 ± 56 vs. 554 ± 41 mOsmol kg−1 H2O), U [Urea] (405 ± 36 vs. 302 ± 23 mmol L−1) and U [Uric acid] (2.7 ± 0.3 vs. 1.7 ± 0.2 mmol L−1) were higher in rugby players than runners (P 1.020) despite S osm being below 290 mOsmol kg−1 H2O in all participants. A positive correlation was found between muscle mass and urine protein metabolites (r = 0.47; P = 0.04) and between urine protein metabolites and U sg (r = 0.92; P < 0.0001). In summary, U sg specificity to detect hypohydration was reduced in athletes with large muscle mass. Our data suggest that athletes with large muscle mass (i.e., rugby players) are prone to be incorrectly classified as hypohydrated based on U sg

Skeletal muscle water and electrolytes following prolonged dehydrating exercise

We studied if dehydrating exercise would reduce muscle water (H2Omuscle) and affect muscle electrolyte concentrations. Vastus lateralis muscle biopsies were collected prior, immediately after, and 1 and 4 h after prolonged dehydrating exercise (150 min at 33 ± 1 °C, 25% ± 2% humidity) on nine endurance-trained cyclists (VO2max = 54.4 ± 1.05 mL/kg/min). Plasma volume (PV) changes and fluid shifts between compartments (Cl− method) were measured. Exercise dehydrated subjects 4.7% ± 0.3% of body mass by losing 2.75 ± 0.15 L of water and reducing PV 18.4% ± 1% below pre-exercise values (P < 0.05). Right after exercise H2Omuscle remained at pre-exercise values (i.e., 398 ± 6 mL/100 g dw muscle−1) but declined 13% ± 2% (342 ± 12 mL/100 g dw muscle−1; P < 0.05) after 1 h of supine rest. At that time, PV recovered toward pre-exercise levels. The Cl− method corroborated the shift of fluid between extracellular and intracellular compartments. After 4 h of recovery, PV returned to preexercise values; however, H2Omuscle remained reduced at the same level. Muscle Na+ and K+ increased (P < 0.05) in response to the H2Omuscle reductions. Our findings suggest that active skeletal muscle does not show a net loss of H2O during prolonged dehydrating exercise. However, during the first hour of recovery H2Omuscle decreases seemly to restore PV and thus cardiovascular stability

Increased blood cholesterol after a high saturated fat diet is prevented by aerobic exercise training

A high saturated fatty acids diet (HSFAD) deteriorates metabolic and cardiovascular health 3 while aerobic training improves them. The aim of this study was to investigate in physically 4 inactive, overweight people if two weeks of HSFAD leads to hyperlipemia or insulin resistance 5 and if concurrent aerobic exercise training counteracts those effects. Fourteen overweight (BMI: 27.5±0.6 kg·m-26 ) healthy-young individuals (24.8±1.8 yr old) were randomly assigned to 7 a diet (D) or a diet plus exercise (D+E) group. During 14 consecutive days both groups increased dietary saturated fatty acids from 31±10 to 52±14 g·day-1 8 (P<0.001) while 9 maintaining total fat intake. Concurrent to the diet, the D+E group underwent 11 cycleergometer sessions of 55 min at 60% 2peak O · 10 V . Before and after intervention insulin sensitivity 11 was estimated and body composition, plasma lipid profile, free fatty acids (FFA) composition, resting blood pressure (BP) and 2peak O · 12 V were measured. Body weight and composition, 13 plasma FFA composition and insulin sensitivity remained unchanged in both groups. 14 However, total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) increased above pre-intervention values in the D group (147±8 to 161±9 mg·dL-115 , P=0.018 and 71±10 to 82±10 mg·dL-116 , P=0.034, respectively). In contrast, in the D+E group, TC and LDL-C remained unchanged (153±20 to 157±24 mg·dL-1 and 71±21 to 70±25 mg·dL-117 ). Additionally the D+E group lowered systolic BP (6±2 mmHg, P=0.029) and increased 2peak O · V (6±2 ml·kg-1·min-118 , 19 P=0.020). Increases in TC and LDL-C induced by 14 days of HSFAD can be prevented by 20 concurrent aerobic exercise training that in addition improves cardio-respiratory fitness

Comparison of glucose tolerance tests to detect the insulin sensitizing effects of a bout of continuous exercise

The aim of the present study was to determine which of the available glucose tolerance tests (oral (OGTT) vs. intravenous (IVGTT)) could more readily detect the insulin sensitizing effects of a bout of continuous exercise. Ten healthy moderately fit young men (V˙ O2peak of 45.4 ± 1.8 mL·kg−1·min−1; age 27.5 ± 2.7 yr) underwent 4 OGTT and 4 IVGTT on different days following a standardized dinner and overnight fast. One test was performed immediately after 55 min of cycle-ergometer exercise at 60% V˙ O2peak. Insulin sensitivity index was determined during a 50 min IVGTT according to Tura (CISI) and from a 120 min OGTT using the Matsuda composite index (MISI). After exercise, MISI improved 29 ± 10% without reaching statistical significance (p = 0.182) due to its low reproducibility (coefficient of variation 16 ± 3%; intra-class reliability 0.846). However, CISI significantly improved (50 ± 4%; p < 0.001) after exercise showing better reproducibility (coefficient of variation 13 ± 4%; intra-class reliability 0.955). Power calculation revealed that 6 participants were required for detecting the effects of exercise on insulin sensitivity when using IVGTT, whereas 54 were needed when using OGTT. The superior response of CISI compared with MISI suggests the preferential use of IVGTT to assess the effects of exercise on insulin sensitivity when using a glucose tolerance test

Higher insulin-sensitizing response after sprint interval compared to continuous exercise

This study investigated which exercise mode (continuous or sprint interval) is more eff ective for improving insulin sensitivity. 10 young, healthy men underwent a non-exercise trial (CON) and 3 exercise trials in a cross-over, randomized design that included 1 sprint interval exercise trial (SIE; 4 all-out 30-s sprints) and 2 continuous exercise trials at 46 % VO 2 peak (CE LOW ) and 77 % VO 2 peak (CE HIGH ). Insulin sensitivity was assessed using intravenous glucose tolerance test (IVGTT) 30 min, 24 h and 48 h postexercise. Energy expenditure was measured during exercise. Glycogen in vastus lateralis was measured once in a resting condition (CON) and immediately post-exercise in all trials. Plasma lipids were measured before each IV GTT . Only after CE HIGH did muscle glycogen concentration fall below CON (P < 0.01). All exercise treatments improved insulin sensitivity compared with CON, and this eff ect persisted for 48-h. However, 30-min post-exercise, insulin sensitivity was higher in SIE than in CE LOW and CE HIGH (11.5 ± 4.6, 8.6 ± 5.4, and 8.1 ± 2.9 respectively; P < 0.05). Insulin sensitivity did not correlate with energy expenditure, glycogen content, or plasma fatty acids concentration (P > 0.05). After a single exercise bout, SIE acutely improves insulin sensitivity above continuous exercise. The higher post-exercise hyperinsulinemia and the inhibition of lipolysis could be behind the marked insulin sensitivity improvement after SIE

Ingestion of a moderately high caffeine dose before exercise increases postexercise energy expenditure

Caffeine is an ergogenic aid widely used before and during prolonged exercise. Due to its prolonged biological half-life caffeine effects could remain after exercise. We aimed to investigate the metabolic, respiratory, and cardiovascular postexercise responses to preexercise graded caffeine ingestion. Twelve aerobically trained subjects (mean VO2max = 54 ± 7 ml · min–1 · kg–1) cycled for 60-min at 75% VO2max after ingesting placebo (0 mg of caffeine per kg of body weight) or 0.5, 1.5, 3.0 and 4.5 mg · kg–1 on five occasions. During the 3 hr postexercise, heart rate, blood pressure, glucose, lactate, and fatty acids were analyzed. None of these variables were statistically affected by preexercise caffeine ingestion between 0.5 and 4.5 mg · kg–1. However, ingestion of 4.5 mg · kg–1 of caffeine raised postexercise energy expenditure 15% above placebo (233 ± 58 vs. 202 ± 49 kcal/3 hr; p < .05). Ventilation and tidal volume were elevated after the 4.5 mg·kg–1 caffeine dose above placebo (9.2 ± 2.5 L · min–1 and 0.67 ± 0.29 L · breath–1 vs. 7.8 ± 1.5 L · min–1 and 0.56 ± 0.20 L · breath–1, respectively; p < .05). Ventilation correlated with tidal volume (r = .45; p < .05) and energy expenditure (r = .72; p < .05). In summary, preexercise ingestion of ergogenic caffeine doses do not alter postexercise cardiovascular responses. However, ingestion of 4.5 mg · kg–1 of caffeine raises 3-hr postexercise energy expenditure (i.e., 31 kcal) likely through increased energy cost of ventilation

Metformin does not attenuate the acute insulin-sensitizing effect of a single bout of exercise in individuals with insulin resistance

Combining metformin and exercise is recommended for the treatment of insulin resistance. However, it has been suggested that metformin blunts the insulin-sensitizing effects of exercise. We evaluated in a group of insulin-resistant patients the interactions between exercise and their daily dose of metformin. Ten insulin-resistant patients underwent insulin sensitivity assessment using intravenous glucose tolerance test after an overnight fast in the following conditions: (1) after taking their habitual morning dose of metformin (MET), (2) after 45 min of high intensity interval exercise having withheld metformin during 24 h (EX), and (3) after their habitual metformin dose plus an identical exercise bout (MET ? EX). During the exercise trials (EX and MET ? EX), energy expenditure and substrate oxidation were assessed by indirect calorimetry. In addition, 12-h postprandial blood glucose was measured in all three trials. Insulin sensitivity was similar between MET and EX [4.0 ± 0.8 and 4.1 ± 0.7 9 10-4 min-1 (lU mL)-1; P = 0.953] but was 43 % higher than both MET and EX after MET ? EX (NS; P = 0.081). Blood glucose disappearance rate was higher after MET ? EX than after MET or EX trials (1.7 ± 0.2,1.0 ± 0.1, and 1.2 ± 0.1 % min-1, respectively; P = 0.020). There was no difference in postprandial blood glucose concentration after the three meals that followed the trials (P = 0.446). Exercise energy expenditure was 9 % higher during MET ? EX than during EX (P = 0.015) partly due to increased carbohydrate oxidation. Our data suggest that habitual metformin treatment in insulin-resistant patients does not blunt the acute insulinsensitizing effects of a single bout of exercise that on the contrary, tends to enhance it

Effects of simultaneous or sequential weight loss diet and aerobic interval training on metabolic syndrome

Our purpose in this study was to investigate efficient and sustainable combinations of exercise and diet-induced weight loss (DIET), in order to combat obesity in metabolic syndrome (MetS) patients. We examined the impact of aerobic interval training (AIT), followed by or concurrent to a DIET on MetS components. 36 MetS patients (54 ± 9 years old; 33 ± 4 BMI; 27 males and 9 females) underwent 16 weeks of AIT followed by another 16 weeks without exercise from the fall of 2013 to the spring of 2014. Participants were randomized to AIT without DIET (E CON, n = 12), AIT followed by DIET (E-then-D, n = 12) or AIT concurrent with DIET (E + D, n = 12). Body weight decreased below E CON similarly in the E-then-D and E + D groups (~5 %). Training improved blood pressure and cardiorespiratory fitness (VO2peak) in all trials with no additional effect of concurrent weight loss. However, E + D improved insulin sensitivity (HOMA) and lowered plasma triglycerides and blood cholesterol below E CON and E-then-D (all P < 0.05). Weight loss in E-then-D in the 16 weeks without exercise lowered HOMA to the E + D levels and maintained blood pressure at trained levels. Our data suggest that a new lifestyle combination consisting of aerobic interval training followed by weight loss diet is similar, or even more effective on improving metabolic syndrome factors than concurrent exercise plus diet

Dietary supplementation with omegaâ 3 fatty acids and oleate enhances exercise training effects in patients with metabolic syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/133560/1/oby21552.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/133560/2/oby21552_am.pd