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.

Comparison between blood and urinary fluid balance indices during dehydrating exercise and the subsequent hypohydration when fluid is not restored.

Blood serum osmolality (S (OSM)) is the gold standard to assess body fluid balance. Urine specific gravity (U (SG)) is also a body fluid balance index but it is not invasive. However, U (SG) capability to detect the minimal level of dehydration that affects athletic performance (i.e., 2 %) remains untested. We collected urine and blood samples in eighteen euhydrated trained athletes in the morning and that evening while dehydrating by 1, 2, and 3 % of body mass by cycling (60 % VO2peak) in the heat (32 °C, 46 % rh, 2.5 m s(-1) air flow). At 9:00 pm, subjects left the laboratory and went to bed after ingesting 0.7 ± 0.2 L of a sports drink. The next morning, subjects awoke 3 % hypohydrated, and blood and urine samples were collected and test terminated. We found that 2 % dehydration increased S (OSM) and U (SG) above exercise-baseline values (P < 0.05). The next morning, S (OSM) and U (SG) remained elevated compared to the first morning while euhydrated (287 ± 5 vs. 282 ± 3 mOsmol kg(-1) H(2)O and 1.028 ± 0.003 vs. 1.017 ± 0.005, respectively, P < 0.05). However, when comparing 3 % dehydration (end of exercise) to 3 % hypohydration (next morning), U (SG) increased (1.025 ± 0.003 to 1.028 ± 0.003; P < 0.05) while S (OSM) decreased (295 ± 5 to 287 ± 5 mOsmol kg(-1) H(2)O; P < 0.05). In summary, during exercise-induced dehydration, U (SG) is as sensitive as S (OSM) to detect low levels of dehydration (i.e., 2 %). Both indices maintain the ability to detect a 3 % overnight hypohydration although S (OSM) approaches euhydration values, while U (SG) remains a superior index to detect hypohydration.

In a hot-dry environment racewalking increases the risk of hyperthermia in comparison to when running at a similar velocity.

The purpose of this study was to determine if in a hot-dry environment, racewalking increases intestinal temperature (T(int)) above the levels observed when running either at the same velocity or at a similar rate of heat production. Nine trained racewalkers exercised for 60 min in a hot-dry environment (30.0 ± 1.4°C; 33 ± 8% relative humidity; 2.4 m s(-1) air speed) on three separate occasions: (1) racewalking at 10.9 ± 1.0 km h(-1) (Walk), (2) running at the same velocity (RunVel) and (3) running at 13 ± 1.8 km h(-1) to obtain a similar [Formula: see text] than during Walk (Run[Formula: see text]). As designed, energy expenditure rate was similar during Walk and Run[Formula: see text], but lower during RunVel (842 ± 78 and 827 ± 75 vs. 713 ± 55 W; p < 0.01). Final T(int) was lower during RunVel than during both Walk and Run[Formula: see text] (38.4 ± 0.3 vs. 39.2 ± 0.4 and 39.0 ± 0.4°C; p < 0.01). Heart rate and sweat rate were also lower during RunVel than during Walk and Run[Formula: see text] (i.e. heart rate 159 ± 13 vs. 179 ± 11 and 181 ± 11 beats min(-1) and sweat rate 0.8 ± 0.3 vs. 1.1 ± 0.3 and 1.1 ± 0.3 L h(-1); p < 0.01). However, we could not detect differences in skin temperature among trials. In conclusion, our data indicate that in a hot-dry environment racewalking increases the risk of hyperthermia in comparison with when running at a similar velocity. However, exercise mode (walking vs. running) had no measurable impact on T(INT) or heat dissipation when matched for energy expenditure.

Sweat sodium concentration during exercise in the heat in aerobically trained and untrained humans.

The purpose of this study was to determine whether sweat sodium concentration ([Na(+)](sweat)) during exercise in the heat differs between aerobically trained and untrained individuals. On three occasions, ten endurance-trained (Tr) and ten untrained (UTr) subjects (VO2peak = 4.0 ± 0.8 vs. 3.4 ± 0.7 L min(-1), respectively; P < 0.05) cycled in a hot-ventilated environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s(-1)) at three workloads (i.e., 40, 60, and 80% VO2peak). Whole-body (SR(WB)) and back sweat rates (SR(BACK)) were measured. At the conclusion of the study, Na(+) in sweat and blood samples was analyzed to calculate Na(+) secretion and reabsorption rates. SR(WB) and SR(BACK) were highly correlated in Tr and UTr (r = 0.74 and 0.79, respectively; P < 0.0001). In both groups, SR(BACK) increased with the increases in exercise intensity (P < 0.05). Likewise, [Na(+)](sweat) increased with the exercise intensity in both groups (P < 0.05) and it tended to be higher in Tr than in UTr at 60 and 80% VO2peak (~22 mmol L(-1) higher; P = 0.06). However, when normalized for SR(BACK), [Na(+)](sweat) was not different between groups. In both groups, Na(+) secretion and reabsorption rates increased with the increases in SR(BACK) (P < 0.05). However, Na(+) reabsorption rate was lower in the Tr than in the UTr (mean slope = 48 vs. 82 ηmol cm(-2) min(-1); P = 0.03). In conclusion, using a cross-sectional study design, our data suggest that aerobic fitness level does not reduce sweat Na(+) secretion or enhance Na(+) reabsorption during prolonged exercise in the heat that induced high sweat rates.

Relevance of individual characteristics for thermoregulation during exercise in a hot-dry environment.

The aim of this study was to investigate the relevance of individual characteristics for thermoregulation during prolonged cycling in the heat. For this purpose, 28 subjects cycled for 60 min at 60% VO(2peak) in a hot-dry environment (36 ± 1°C; 25 ± 2% relative humidity, airflow 2.5 m/s). Subjects had a wide range of body mass (99-43 kg), body surface area (2.2-1.4 m(2)), body fatness (28-5%) and aerobic fitness level (VO(2peak) = 5.0-2.1 L/min). At rest and during exercise, rectal and mean skin temperatures were measured to calculate the increase in body temperature (ΔT (body)) during the trial. Net metabolic heat production (M (NET)) and potential heat loss (by means of evaporation, radiation and convection) were calculated. Although subjects exercised at the same relative intensity, ΔT (body) presented high between-subjects variability (range from 0.44 to 1.65°C). ΔT (body) correlated negatively with body mass (r = -0.49; P < 0.01), body surface area (r = -0.47; P < 0.01) and T(body) at rest (r = -0.37; P < 0.05), but it did not significantly correlate with body fatness (r = 0.12; P > 0.05). ΔT (body) positively correlated with the body surface area/mass ratio (r = 0.46; P < 0.01) and the difference between M (NET) and potential heat loss (r = 0.56; P < 0.01). In conclusion, a large body size (mass and body surface area) is beneficial to reduce ΔT (body) during cycling exercise in the heat. However, subjects with higher absolute heat production (more aerobically fit) accumulate more heat because heat production may exceed potential heat loss (uncompensability).

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) H(2)O), 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 < 0.05). However, urine electrolyte concentrations were not different between groups. A higher percentage of rugby players than runners (56 vs. 11%; P = 0.03) could be cataloged as hypohydrated by U(sg) (i.e., >1.020) despite S (osm) being below 290 mOsmol kg(-1) H(2)O 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).

Restoration of blood pH between repeated bouts of high-intensity exercise: effects of various active-recovery protocols.

To determine which active-recovery protocol would reduce faster the high blood H(+) and lactate concentrations produced by repeated bouts of high-intensity exercise (HIE). On three occasions, 11 moderately trained males performed 4 bouts (1.5 min) at 163% of their respiratory compensation threshold (RCT) interspersed with active-recovery: (1) 4.5 min pedalling at 24% RCT (S(HORT)); (2) 6 min at 18% RCT (M(EDIUM)); (3) 9 min at 12% RCT (L(ONG)). The total work completed during recovery was the same in all three trials. Respiratory gases and arterialized-blood samples were obtained during exercise. At the end of exercise, L(ONG) in comparison to S(HORT) and M(EDIUM) increased plasma pH (7.32 +/- 0.02 vs. approximately 7.22 +/- 0.03; P < 0.05), while reduced lactate concentration (8.5 +/- 0.9 vs. approximately 10.9 +/- 0.8 mM; P < 0.05). Ventilatory equivalent for CO(2) was higher in L(ONG) than S(HORT) and M(EDIUM) (31.4 +/- 0.5 vs. approximately 29.6 +/- 0.5; P < 0.05). Low-intensity prolonged recovery between repeated bouts of HIE maximized H(+) and lactate removal likely by enhancing CO(2) unloading.

Aerobically trained individuals have greater increases in rectal temperature than untrained ones during exercise in the heat at similar relative intensities.

To determine if the increases in rectal temperature (T(REC)) during exercise in the heat at a given percent of VO2peak depend on a subject's aerobic fitness level. On three occasions, 10 endurance-trained (Tr) and 10 untrained (UTr) subjects (VO2peak: 60 +/- 6 vs. 44 +/- 3 mL kg(-1) min(-1), P < 0.05) cycled in a hot-dry environment (36 +/- 1 degrees C; 25 +/- 2% humidity, airflow 2.5 m s(-1)) at three workloads (40, 60, and 80% VO2peak). At the same percent of VO2peak, on average, Tr had 28 +/- 5% higher heat production but also higher skin blood flow (29 +/- 3%) and sweat rate (20 +/- 7%; P = 0.07) and lower skin temperature (0.5 degrees C; P < 0.05). Pre-exercise T(REC) was lower in the Tr subjects (37.4 +/- 0.2 vs. 37.6 +/- 0.2; P < 0.05) but similar to the UTr at the end of 40 and 60% VO2peak trials. Thus, exercise T(REC) increased more in the Tr group than in the UTr group (0.6 +/- 0.1 vs. 0.3 +/- 0.1 degrees C at 40% VO2peak and 1.0 +/- 0.1 vs. 0.6 +/- 0.3 degrees C at 60% VO2peak; P < 0.05). At 80% VO2peak not only the increase in T(REC) (1.7 +/- 0.1 vs. 1.3 +/- 0.3 degrees C) but also the final T(REC) was larger in Tr than in UTr subjects (39.15 +/- 0.1 vs. 38.85 +/- 0.1 degrees C; P < 0.05). During exercise in the heat at the same relative intensity, aerobically trained individuals have a larger rise in T(REC) than do the untrained ones which renders them more hyperthermic after high-intensity exercise.

Respiratory compensation and blood pH regulation during variable intensity exercise in trained versus untrained subjects.

To determine whether endurance-trained cyclists (T; n = 10) have a superior blood-respiratory buffering for metabolic acidosis relative to untrained subjects (UT; n = 10) during variable intensity exercise (VAR). On three occasions, T and UT pedaled for 24 min alternating high- and low-intensities as percentage of their second ventilatory threshold (VT2): VAR(LOW) 87.5-37.5% VT2, VAR(MODERATE) 125-25% VT2, and VAR(HIGH) 162.5-12.5% VT2 to complete the same amount of work. Before and just after each VAR trial, maximal cycling power (P(MAX)) was assessed. For each trial, the respiratory compensation for exercise acidosis (ventilatory equivalent for CO2) and the final blood pH, lactate and bicarbonate concentrations were similar for T and UT subjects. However, after VAR(HIGH), UT reduced P(MAX) (-14 +/- 1%; P < 0.05) while T did not. Our data suggest that endurance training confers adaptations to withstand the low pH provoked by VAR without losing cycling power, although this response is not due to differences in blood-respiratory buffering.

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

OBJECTIVE: We studied the effects of exercise training alone or combined with dietary supplementation of omega-3 polyunsaturated fatty acids (Ω-3PUFA) and oleate on metabolic syndrome (MSyn) components and other markers of cardiometabolic health. METHODS: Thirty-six patients with MSyn underwent 24 weeks of high-intensity interval training. In a double-blind randomized design, half of the group ingested 500 mL/day of semi-skim milk (8 g of fat; placebo milk) whereas the other half ingested 500 mL/day of skim milk enriched with 275 mg of Ω-3PUFA and 7.5 g of oleate (Ω-3 + OLE). RESULTS: Ω-3 + OLE treatment elevated 30% plasma Ω-3PUFA but not significantly (P = 0.286). Improvements in VO2peak (12.8%), mean blood pressure (-7.1%), waist circumference (-1.8%), body fat mass (-2.9%), and trunk fat mass (-3.3%) were similar between groups. However, insulin sensitivity (measured by intravenous glucose tolerance test), serum concentration of C-reactive protein, and high-density lipoprotein improved only in the Ω-3 + OLE group by 31.5%, 32.1%, and 10.3%, respectively (all P < 0.05). Fasting serum triacylglycerol, glucose, and plasma fibrinogen concentrations did not improve in either group after 24 weeks of intervention. CONCLUSIONS: Diet supplementation with Ω-3PUFA and oleate enhanced cardiometabolic benefits of intense aerobic exercise training in patients with MSyn.

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 (V̇O2peak 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% V̇O2peak. 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.

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 × 10(-4) min(-1) (µU 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 insulin-sensitizing effects of a single bout of exercise that on the contrary, tends to enhance it.

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 while aerobic training improves them. The aim of this study was to investigate in physically inactive and overweight people if 2 weeks of HSFAD leads to hyperlipemia or insulin resistance and if concurrent aerobic exercise training counteracts those effects. Fourteen overweight (body mass index, 27.5 ± 0.6 kg·m(-2)), healthy, young individuals (aged 24.8 ± 1.8 years) were randomly assigned to 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) (p < 0.001) while maintaining total fat intake. Concurrent to the diet, the D + E group underwent 11 cycle-ergometer sessions of 55 min at 60% peak oxygen uptake (V˙O(2peak)). Before and after intervention, insulin sensitivity and body composition were estimated, and blood lipids, resting blood pressure, and VO(2peak) were measured. Body weight and composition, plasma free fatty acids composition and concentration, and insulin sensitivity remained unchanged in both groups. However, post-intervention total cholesterol (T(C)) and low-density lipoprotein cholesterol (LDL-C) increased above pre-intervention values in the D group (147 ± 8 to 161 ± 9 mg·dL(-1), p = 0.018 and 71 ± 10 to 82 ± 10 mg·dL(-1), p = 0.034, respectively). In contrast, in the D + E group, T(C) and LDL-C remained unchanged (153 ± 20 to 157 ± 24 mg·dL(-1) and 71 ± 21 to 70 ± 25 mg·dL(-1)). Additionally, the D + E group lowered systolic blood pressure (6 ± 2 mm Hg, p = 0.029) and increased VO(2peak) (6 ± 2 mL·kg(-1)·min(-1), p = 0.020). Increases in T(C) and LDL-C concentration induced by 14 days of HSFAD can be prevented by concurrent aerobic exercise training, which, in addition, improves cardiorespiratory fitness.

Fluid ingestion is more effective in preventing hyperthermia in aerobically trained than untrained individuals during exercise in the heat.

It is unclear if fluid ingestion during exercise in the heat alleviates the thermoregulatory and cardiovascular strain similarly in aerobically trained and untrained individuals. It is also unknown at what exercise intensity the effects of rehydration are greater. Ten aerobically trained (T) and 10 healthy untrained (UT) subjects ([Formula: see text]O(2peak), 60 ± 6 vs. 44 ± 3 mL O(2)·kg(-1)·min(-1), respectively; P < 0.05) pedalled in a hot, dry environment (36 ± 1 °C; 25% ± 2% relative humidity; airflow, 2.5 m·s(-1)) at 40%, 60%, and 80% [Formula: see text]O(2peak) while ingesting fluids (Fluid). The results were compared with those from our previous study [Mora-Rodriguez et al., Eur. J. Appl. Physiol. 109(5): 973-981 (2010)] with no fluid ingestion (No Fluid). Subjects were not heat-acclimated. At 40% [Formula: see text]O(2peak), Fluid reduced rectal temperature (T(RE)) in T and UT (0.31 ± 0.08 and 0.32 ± 0.07 °C; respectively). At 60% [Formula: see text]O(2peak), Fluid reduced T(RE) in T more than in UT (0.30 ± 0.10 °C vs. 0.18 ± 0.10 °C; P < 0.05) but had no effect at 80% [Formula: see text]O(2peak) in any group. At similar relative intensity, heart rates (HR) were similar between groups. Fluid lowered heart rate (i.e., HR) similarly in the T and UT at 40% and 60% [Formula: see text]O(2peak) (11% and 6%, respectively; P < 0.05) but not at 80% [Formula: see text]O(2peak) (P > 0.05). At similar metabolic heat production (i.e., 60% for T vs. 80% [Formula: see text]O(2peak) for UT), Fluid lowered T(RE) only in the T individuals (P < 0.05). In summary, rehydration during low- and moderate-intensity exercise reduces T(RE) and HR more than during high-intensity exercise (80% [Formula: see text]O(2peak)) in T and UT subjects. Fluid replacement is more effective on preventing the rise in T(RE) in T than in UT individuals during moderate-intensity exercise (60% [Formula: see text]O(2peak)), as well as when exercising at a similar heat production rate.

Salt and fluid loading: effects on blood volume and exercise performance.

During prolonged exercise, fluid and salt losses through sweating reduce plasma volume which leads to heart rate drift in association with hyperthermia and reductions in performance. Oral rehydration with water reduces the loss of plasma volume and lessens heart rate drift and hyperthermia. Moreover, the inclusion of sodium in the rehydration solution to levels that double those in sweat (i.e., around 90 mmol/l Na(+)) restores plasma volume when ingested during exercise, and expands plasma volume if ingested pre-exercise. Pre-exercise salt and fluid ingestion with the intention of expanding plasma volume has received an increasing amount of attention in the literature in recent years. In four studies, pre-exercise salt and fluid ingestion improved performance, measured as time to exhaustion, either during exercise in a thermoneutral or in a hot environment. While in a hot environment, the performance improvements were linked to lowering of core temperatures and heart rate, the reasons for the improved performance in a thermoneutral environment remain unclear. However, when ingesting pre-exercise saline solutions above 0.9% (i.e., > 164 mmol/l Na(+)), osmolality and plasma sodium increase and core temperature remain at dehydration levels. Thus, too much salt counteracts the beneficial effects of plasma volume expansion on heat dissipation and hence in performance. In summary, the available literature suggests that pre-exercise saline ingestion with concentrations not over 164 mmol/l Na(+) is an ergogenic aid for subsequent prolonged exercise in a warm or thermoneutral environment.

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.

Aerobic fitness determines whole-body fat oxidation rate during exercise in the heat.

The purpose of this study was to determine whole-body fat oxidation in endurance-trained (TR) and untrained (UNTR) subjects exercising at different intensities in the heat. On 3 occasions, 10 TR cyclists and 10 UNTR healthy subjects (peak oxygen uptake = 60 ± 6 vs. 44 ± 3 mL·kg-1·min-1; p < 0.05) exercised at 40%, 60%, and 80% peak oxygen uptake in a hot, dry environment (36 °C; 25% relative humidity). To complete the same amount of work in all 3 trials, exercise duration varied (107 ± 4, 63 ± 1, and 45 ± 0 min for 40%, 60%, and 80% peak oxygen uptake, respectively). Substrate oxidation was calculated using indirect calorimetry. Blood samples were collected at the end of exercise to determine plasma epinephrine ([EPI]plasma) and norepinephrine ([NEPI]plasma) concentrations. The maximal rate of fat oxidation was achieved at 60% peak oxygen uptake for the TR group (0.41 ± 0.01 g·min-1) and at 40% peak oxygen uptake for the UNTR group (0.28 ± 0.01 g·min-1). TR subjects oxidized absolutely (g·min-1) and relatively (% of total energy expenditure) more fat than UNTR subjects at 60% and 80% peak oxygen uptake (p < 0.05). At these exercise intensities, TR subjects also had higher [NEPI]plasma concentrations than UNTR subjects (p < 0.05). In the heat, whole-body peak fat oxidation occurs at higher relative exercise intensities in TR than in UNTR subjects (60% vs. 40% peak oxygen uptake). Moreover, TR subjects oxidize more fat than UNTR subjects when exercising at moderate to high intensities (>60% peak oxygen uptake).