Sodium citrate and anaerobic performance: implications of dosage

Summary The use of sodium bicarbonate to improve anaerobic performance is well known but other buffering agents have been used with some success. Sodium citrate is one such substance which has been used but without the normal gastro-intestinal discomfort usually associated with sodium bicarbonate ingestion. The effects of five doses of sodium citrate (0.1 g·kg^–1 body mass, 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass, 0.4 g·kg^–1 body mass and 0.5 g·kg^–1 body mass) on anaerobic performance were studied in order to determine the minimal and most productive dose required for performance enhancement. A maximal test was performed for 1^–1, min on a cycle ergometer. Total work and peak power were measured at the end of the exercise period. Blood was drawn 1.5 h prior to the test session and measured for pH, partial pressure of carbon dioxide and concentrations of bicarbonate, base excess and lactate. In all but the control and placebo trials subjects then ingested one of five doses of sodium citrate which was contained in 400 ml of flavoured drink. Blood was again taken 90 min later and this was repeated after the completion of the exercise test. The greatest amount of work was completed in the trial with citrate given at 0.5 g·kg^–1 body mass (44.63 kJ, SD 1.5) and this was also true for peak power (1306 W, SD 75). The post-exercise blood lactate concentration was also highest during this trial 15.9 mmol·1^–1, SD 1.1. Post-exercise pH decreased significantly in all trials (P<0.0001) while the administration of the sodium citrate in all doses above 0.1 g·kg^–1 body mass significantly increased resting pH values. Blood bicarbonate concentrations also increased with dose in an almost linear fashion with the administration of sodium citrate. Bicarbonate increases were all significant, P<0.05 (citrate 0.1 g·kg^–1 body mass), P<0.01 (citrate 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass and 0.4 g·kg^–1 body mass) and P<0.005 (citrate 0.5 g·kg^–1 body mass). The administration of sodium citrate also significantly increased base excess values (citrate 0.1 g·kg^–1 body mass,P<0.01; 0.2 g·kg^–1body mass, P<0.001; 0.3 g·kg^–1 body mass, P<0.001; 0.4 g·kg^–1 body mass, P<0.001; 0.5 g·kg^–1 body mass, P<0.0001) above control and placebo values. All post-exercise base excess values were significantly lower than basal or pre-exercise values (P<0.0001). It was concluded that sodium citrate was an effective ergogenic aid for anaerobic performance of approximately 60-s duration, with the most effective of those dosages tested being 0.5 g·kg^–1 body mass.     

The effects of buffer ingestion on metabolic factors related to distance running performance

We examined the effects of sodium bicarbonate (BIC) and sodium citrate (CIT) ingestion on distance running performance. Seven male runners [mean = 61.7 (SEM 1.7) ml · kg^–1 · min^–1] performed three 30-min treadmill runs at the lactate threshold (LT) each followed by a run to exhaustion at 110% of LT. The runs were double-blind and randomly assigned from BIC (0.3 g · kg body mass^–1), CIT (0.5 g · kg body mass^–1) and placebo (PLC, wheat flour, 0.5 g · kg body mass^–1). Venous blood samples were collected at 5, 15 and 25 min during the run and immediately post-exhaustion (POST-EX) and analysed for pH, and the concentrations of lactate ([1a^–]_b) and bicarbonate ([HCO₃ ^– ]). Performance was measured as running time to exhaustion at 110% of LT (TIME-EX). The pH was significantly higher (P 0.05) for the BIC and CIT trials during exercise, but not POST-EX compared to PLC. The [1a^–]_b was significantly higher (P 0.05) for the CIT trial compared to PLC during exercise, and for both CIT and BIC compared to PLC at POST-EX. Blood [HCO₃ ^–] was significantly higher (P 0.05) during exercise for BIC compared to PLC. TIME-EX was not significantly different among treatments: BIC 287 (SEM 47.4) s; CIT 172.8 (SEM 29.7) s; and PLC 222.3 (SEM 39.7) s. Despite the fact that buffer ingestion produced favourable metabolic conditions during 30 min of high intensity steady-state exercise, a significant improvement in the subsequent maximal exercise run to exhaustion did not occur.     

Sodium citrate ingestion and muscle performance in acute hypobaric hypoxia

Eight subjects were studied on four occasions following ingestion of a 300-ml solution containing either sodium citrate (C, 0.4g · kg^–1 body mass) or placebo (P, sodium chloride 0.045 g · kg^–1 body mass), at local barometric pressure (N, P _B approximately 740 mmHg, 98.7 kPa) or hypobaric hypoxia (HH, P _B = 463 mmHg, 61.7 kPa). At 2 h after ingestion of the solution, the subjects performed prolonged isometric knee-extension at 35% of the maximal voluntary contraction (MVC) measured either in N or HH. Results showed that ingestion of C led to an improvement in muscle endurance (P < 0.01). However, this increase in endurance time for knee extensor muscles was only significant in N ( +22%, P < 0.05, compared to + 15%, NS, at N and HH, respectively). Following ingestion of sodium citrate, pre-exercise bicarbonate concentrations and pH levels were significantly higher than those measured after P ingestion. A significant treatment effect was observed for blood lactate concentrations with values higher for C than for P after 4, 6 and 10 min of recovery (P < 0.05). Electromyographic signals (EMG) were obtained from the vastus lateralis muscle during the prolonged isometric contraction at 35% MVC. The mean power frequency (MPF) significantly decreased in time under both N-P and N-C conditions. In HH, no significant decrease in MPF was observed with time. The results suggest that C ingestion was an ergogenic aid enhancing endurance during a sustained isometric contraction. In addition, it is suggested that fatigue during prolonged isometric contraction in HH was not directly related to factors determining the EMG signs of fatigue.     

Sodium bicarbonate ingestion improves performance in interval swimming

Summary In an effort to determine the effects of bicarbonate (NaHCO₃) ingestion on exercise performance, ten male college swimmers were studied during five different trials. Each trial consisted of five 91.4m (100-yd) front crawl swims with a two-minute rest interval between each bout. The trials consisted of two NaHCO₃ treatments, two placebo trials and one test with no-drink. One hour before the onset of swimming, the subjects were given 300 ml of citric acid flavored solution containing either 17 mmol of NaCl (placebo) or 2.9 mmol of NaHCO₃ · kg^–1 body weight (experimental), or received no drink (no-drink). Performance times for each 91.4 m swim were recorded. Blood samples were obtained before and one hr after treatment, two min after warmup, and two min after the final 91.4 m sprint. Blood pH, lactate, standard bicarbonate (SBC) and base excess (BE) were measured. No differences were found for performance or the blood measurements between the placebo and no-drink trials. Bicarbonate feedings, on the other hand, produced a significant (P<0.05) improvement in performance on the fourth and fifth swimming sprints. Blood lactate, pH, SBC and BE were significantly higher (P<0.05) at post-exercise in NaHCO₃ treatments. These data are in agreement with previous findings that during repeated bouts of exercise pre-exercise administration of NaHCO₃ improves performance, possibly by facilitating the efflux of hydrogen ions from working muscles and thereby delaying the onset of fatigue.     

The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise

Summary The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate (C) or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg⁻¹ body weight. Pre-exercise blood pH was 7.44±0.06, 7.42±0.05, 7.41±0.05 and 7.38±0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p<0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO₃ ⁻], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.     

Post-exercise rehydration in man: effects of electrolyte addition to ingested fluids

This study examined the effects on water balance of adding electrolytes to fluids ingested after exercise-induced dehydration. Eight healthy male volunteers were dehydrated by approximately 2% of body mass by intermittent cycle exercise. Over a 30-min period after exercise, subjects ingested one of the four test drinks of a volume equivalent to their body mass loss. Drink A was a 90 mmol·l^–1 glucose solution; drink B contained 60 mmol·l^–1 sodium chloride; drink C contained 25 mmol·l^–1 potassium chloride; drink D contained 90 mmol·l^–1 glucose, 60 mmol·l^–1 sodium chloride and 25 mmol·l^–1 potassium chloride. Treatment order was randomised. Blood and urine samples were obtained at intervals throughout the study; subjects remained fasted throughout. Plasma volume increased to the same extent after the rehydration period on all treatments. Serum electrolyte (Na⁺, K⁺ and Cl^–) concentrations fell initially after rehydration before returning to their pre-exercise levels. Cumulative urine output was greater after ingestion of drink A than after ingestion of any of the other drinks. On the morning following the trial, subjects were in greater net negative fluid balance [mean (SEM);P<0.02] on trial A [745 (130) ml] than on trials B [405 (51) ml], C [467 (87) ml] or D [407 (34) ml]. There were no differences at any time between the three electrolyte-containing solutions in urine output or net fluid balance. One hour after the end of the rehydration period, urine osmolality had fallen, with a significant treatment effect (P=0.016); urine osmolality was lowest after ingestion of drink A. On the morning after the test, subjects were in greater net negative sodium balance (P<0.001) after trials A and C than after trials B and D. Negative potassium balance was greater (P<0.001) after trials A and B than after C and D. Chloride balance was positive after drink D and a smaller negative balance (P<0.001) was observed after drink B than after A and C. These results suggest that although the measured blood parameters were similar for all trials, better whole body water and electrolyte balance resulted from the ingestion of electrolyte-containing drinks. There appeared, however, to be no additive effect of including both sodium and potassium under the conditions of this experiment.     

Comparison of the effects of pre-exercise feeding of glucose,glycerol and placebo on endurance and fuel homeostasis in man

Summary Six men were studied during exercise to exhaustion on a cycle ergometer at 73% of following ingestion of glycerol, glucose or placebo. Five of the subjects exercised for longer on the glucose trial compared to the placebo trial (p<0.1; 108.8 vs 95.9 min). Exercise time to exhaustion on the glucose trial was longer (p<0.01) than on the glycerol trial (86.0 min). No difference in performance was found between the glycerol and placebo trials. The ingestion of glucose (lg · kg^–1 body weight) 45 min before exercise produced a 50% rise in blood glucose and a 3-fold rise in plasma insulin at zero min of exercise. Total carbohydrate oxidation was increased by 26% compared to placebo and none of the subjects exhibited a fall in blood glucose below 4 mmol · l^–1 during the exercise. The ingestion of glycerol (lg · kg^–1 body weight) 45 min before exercise produced a 340-fold increase in blood glycerol concentration at zero min of exercise, but did not affect resting blood glucose or plasma insulin levels; blood glucose levels were up to 14% higher (p<0.05) in the later stages of exercise and at exhaustion compared to the placebo or glucose trials. Both glycerol and glucose feedings lowered the magnitude of the rise in plasma FFA during exercise compared to placebo. Levels of blood lactate and alanine during exercise were not different on the 3 dietary treatments. These data contrast with previous reports that have indicated glucose feeding pre-exercise produces hypoglycaemia during strenuous submaximal exercise and reduces endurance performance. It appears that man cannot use glycerol as a gluconeogenic substrate rapidly enough to serve as a major energy source during this type of exercise.     

The effects of induced alkalosis on the metabolic response to prolonged exercise in humans

To examine the effects of alkalosis on the metabolic response to prolonged exercise, seven healthy males cycled for 1 h at approximately 70% of maximum oxygen uptake on two occasions, 1-week apart. Starting 3 h prior to exercise, subjects consumed either CaCO₃ (placebo) or NaHCO₃ (0.3 g · kg^–1 body mass) over a 2-h period. Arterialised-venous blood samples were drawn before and during exercise for the determination of acid-base status and blood metabolites (lactate, glucose, glycerol and plasma free fatty acids). Expired gas was collected during exercise for determination of oxygen uptake and respiratory exchange ratio to estimate fuel oxidation rates. Ratings of perceived exertion (RPE) and heart rates were also recorded. A significant (P < 0.01) alkalosis was observed at all times following bicarbonate ingestion. Blood lactate was significantly (P < 0.05) higher at all sample times throughout exercise following bicarbonate ingestion. Blood lactate concentration [mean (SEM)] reached peak values of 2.90 (0.16) and 4.24 (0.45) mmol · l^–1 following 20 min of exercise following placebo and bicarbonate, respectively. No differences between treatments were noted at any time for the other metabolites. and RPE were significantly higher (P < 0.01) with the bicarbonate trial. At a constant power output increases in are generally associated with increases in fat oxidation, however, no evidence for an altered fuel oxidation was obtained in the present study. The differences in blood lactate indicate that induced alkalosis increased lactate efflux from muscle, but it cannot be confirmed whether this represents an increased rate of glycolysis within the muscle.     

The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95% of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8)% protein (Pro), 37.5 (2.2)% fat (Fat) and 47.5 (2.1)% carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3)% Pro, 64.4 (1.5)% Fat and 2.2 (0.4)% CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO₃ or CaCO₃ (3.6 and 3.0 mmol · kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO₃. Blood pH, bicarbonate (HCO₃ ^– ) and base excess (BE) were higher following NaHCO₃ ingestion after the normal diet than all of the other experimental conditions (P < 0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P < 0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO₃ ^– and BE were higher following the ingestion of NaHCO₃ irrespective of the pre-exercise diet (P < 0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO₃ when compared to the low-CHO diets with either NaHCO₃ or placebo (P < 0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.     

The influence of metabolic alkalosis upon exercise metabolism in the thoroughbred horse

Summary Six thoroughbred horses exercised on a motorised treadmill on two separate occasions at a speed of 11 or 12 m· s^–1 for up to 2 min. 4 h prior to exercise each horse was given a 21 test solution of sodium bicarbonate (NaHC0₃; 0.6 g·kg^–1 body mass) or a control solution of water by nasogastric intubation, the order of administration of the two solutions was randomised. Blood samples (n=15) were obtained before and during the 4 h after intubation, during exercise and for 30 min after exercise. (NaHC0₃; ingestion resulted in changes in pre-exercise acid-base status. The changes in blood lactate and base excess with exercise were greater after (NaHC0₃; administration; after 1 min of exercise in the case of lactate (P<0.05) and immediately after exercise in the case of base excess (P<0.05). Plasma ammonia levels were lower during (P<0.05) and immediately after (P<0.05) exercise following (NaHC0₃; ingestion. The peak change in plasma ammonia with exercise was also lower after (NaHC0₃; ingestion (P<0.05). Following exercise after (NaHC0₃; ingestion, five horses demonstrated lower muscle adenosine 5-triphosphate loss (P<0.05) and inosine 5-monophosphate formation (P=0.05) and higher glycerol 3-phosphate formation (P<0.05). There is evidence to suggest that metabolic alkalosis may delay the onset of fatigue by decreasing the extent of adenine nucleotide loss during high-intensity exercise.     

Induced metabolic alkalosis and its effects on 400-m racing time

Summary Six trained male athletes who competed regularly in 400 metre races, were studied under control, alkalotic (NaHCO₃) and placebo (CaCO₃) conditions to study the effect of induced metabolic alkalosis on 400 m racing time. Pre and post exercise blood samples in the three conditions were analysed for pH, bicarbonate and base excess. Following ingestion of NaHCO₃, pre-exercise pH, bicarbonate and base excess levels were significantly higher than either control or placebo conditions. In the alkalotic condition the subjects ran significantly (p<0.005) faster (1.52 s) than either the control of placebo conditions. The post-exercise pH, bicarbonate and base excess levels were all lower in the alkalotic condition than in the others. The results suggest that NaHCO₃ can be used as an effective ergogenic aid and support the speculation that the increased extracellular buffering afforded by NaHCO₃ ingestion facilitated efflux of H⁺ from the working tissues, thus decreasing intracellular pH and hence offsetting fatigue.     

Fluid replacement drinks during high intensity exercise effects on minimizing exercise-induced disturbances in homeostasis

Summary The purpose of these experiments was to examine the influence of various fluid replacement drinks on exercise-induced disturbances in homeostasis during heavy exercise. Nine trained cyclists performed constant load exercise on a cycle ergometer to fatigue on three occasions with 1-week separating experiments. The work rate was set initially at 85% of (range 82–88%) with fatigue being defined as a 10% decline in power output below the initial value. During each experiment subjects consumed one of the following three beverages prior to and every 15 min during exercise: (1) non-electrolyte placebo (NEP; 31 mosmol · kg^–1); (2) glucose polymer drink containing electrolytes (GP; 7% CHO, 231 mosmol · kg^–1), and (3) electrolyte placebo drink without carbohydrate (EP; 48 mosmol · kg^–1). Both the GP and EP beverage contained sodium citrate/citric acid (C) as a flavoring agent while C was not contained in the NEP drink. Although seven of nine subjects worked longer during the GP and EP treatment when compared with the NEP trial, the difference was not significant (P>0.05). No differences (P>0.05) existed between the GP and EP treatments in performance time. Exercise changes in rectal temperature, heart rate, % plasma volume and plasma concentrations of total protein, free fatty acids, glucose, lactate, potassium, chloride, calcium, and sodium did not differ (P>0.05) between trials. In contrast, blood hydrogen ion concentration [H⁺] was significantly lower (P<0.05) at 30 min of exercise during the GP and EP treatment when compared with the NEP run. These data provide evidence that electrolyte drinks do not minimize exercise-induced disturbances in blood-electrolyte concentrations during heavy execrcise when compared with nonelectrolyte drinks; however, these results suggest that fluid replacement beverages containing buffers (i.e. C) and/or electrolytes may minimize blood alterations in [H⁺] during intense exercise. Additional research is required to determine if the buffering influence of these beverages has an ergogenic benefit during heavy exercise.     

Exercise induces pentane production and neutrophil activation in humans. Effect of propranolol

Summary The effect of -adrenergic receptor blockade on exercise-induced lipid peroxidation in man has been examined by measuring the production of pentane in expired air. For this purpose, five healthy male subjects were subjected to dynamic exercise of graded intensity on a cycle ergometer (10 min at 45%, 5 min at 60% and 75% maximal oxygen uptake 1 h after ingestion of either a placebo or 40-mg propranolol. At rest, mean pentane concentration ([pent]) with placebo was 4.13 pmol · l^–1, SD 2.14. After exercise, this value significantly increased by 310% (17.1 pmol · l^–1, SD 7.73, P < 0.01). Oral administration of 40-mg propranolol significantly lowered the mean resting [pent] to 1.75 pmol · l^–1, SD 0.77, P < 0.05. After exercise, the increase of [pent] was much smaller (240%) and was less significant (P < 0.2) than with the placebo. The mechanism of this inhibitory effect of propranolol remains to be elucidated. However, as indicated by the measurement of plasma myeloperoxidase concentration, it can be concluded that the antioxidant property of propranolol cannot be attributed to the inhibition of neutrophil activation, a possible source of free radicals during exercise.     

Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise

Summary Nine bodybuilders performed heavy-resistance exercise activating the quadriceps femoris muscle. Intermittent 30-s exhaustive exercise bouts comprising 6–12 repetitions were interspersed with 60-s periods for 30 min. Venous blood samples were taken repeatedly during and after exercise for analyses of plasma free fatty acid (FFA) and glycerol concentration. Muscle biopsies were obtained from the vastus lateralis muscle before and after exercise and assayed for glycogen, glycerol-3-phosphate, lactate and triglyceride (TG) content. The activities of citrate synthase (CS), lactate dehydrogenase, hexokinase (HK), myokinase, creatine kinase and 3-hydroxyacyl-CoA dehydrogenase (HAD), were analysed. Histochemical staining procedures were used to assess fibre type composition, fibre area and capillary density. TG content before and after exercise averaged (SD) 23.9 (13.3) and 16.7 (6.4) mmol kg^–1 dry wt. The basal triglyceride content varied sixfold among individuals and the higher the levels the greater was the change during exercise. The glycogen content decreased (P<0.001) from 690 (82) to 495 (95) mmol kg^–1 dry wt. and lactate and glycerol-3-phosphate increased (P<0.001) to 79.5 (5.5) and 14.5 (7.3) mmol kg^–1 dry wt., respectively, after exercise. The HK and HAD/CS content respectively correlated with glycogen or TG content at rest and with changes in these metabolites during exercise. FFA and glycerol concentrations increased slightly (P<0.001) during exercise. Lipolysis may, therefore, provide energy during heavy-resistance exercise of relatively short duration. Also, storage and utilization of intramuscular substrates appear to be influenced by the metabolic profile of muscle.     

Endogenous opioids may modulate catecholamine secretion during high intensity exercise

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake ( O_2max)], nine fit men [mean (SE) ( O_2max, 63.9 (1.7) ml · kg^–1 · min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol · l^–1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol · l^–1 and 24 (2.2) versus 20 (1.7) nmol · · l^–1 respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol · l^–1 and 6.9 (1.1) versus 5.3 (0.9) mmol · l^–1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.     

The effect of acute branched-chain amino acid supplementation on prolonged exercise capacity in a warm environment

Eight males were recruited to examine the effect of branched-chain amino acid (BCAA) supplementation on exercise capacity in a glycogen-depleted state in a warm environment. Following a exercise and dietary regimen designed to reduce glycogen availability, subjects returned to the laboratory the following morning and remained seated for 2 h, before cycling to volitional exhaustion at 50% O₂ peak in a warm environment [30.0 (0.2)°C; mean (SD)]. Four 250 ml aliquots of a 12 g l^–1 BCAA solution or placebo were ingested at 30 min intervals prior to exercise, with an additional 150 ml consumed every 15 min throughout exercise. BCAA ingestion had no effect on exercise capacity [placebo 103.9 (26.9) min; BCAA 111.0 (29.2) min; P=0.129). No difference in heart rate (P=0.345), core temperature (P=0.628), or weighted mean skin temperature (P=0.114) was apparent between trials. Ingestion of the BCAA solution produced a marked increase in plasma BCAA immediately prior to exercise [+1126 (158) mol l^–1; P<0.001) with this difference maintained throughout. Consequently, a significant reduction in the plasma concentration ratio of free tryptophan to BCAA was observed during the BCAA trial when compared to the placebo (P<0.001). Plasma ammonia concentration was significantly elevated during exercise throughout the BCAA trial (P<0.001), with no change from rest apparent during the placebo trial (P=0.608). Blood glucose (P=0.114) and lactate (P=0.836) concentrations were not different between trials. Ingestion of a BCAA solution prior to, and during, prolonged exercise in glycogen-depleted subjects did not influence exercise capacity in a warm environment.     

Availability of glucose ingested during muscle exercise performed under acipimox-induced lipolysis blockade

This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [¹³C]glucose was used to follow the conversion of the ingested glucose to expired-air CO₂. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g · 3 h^–1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g · 3 h^–1]. Exogenous glucose oxidation during exercise G, calculated by the changes in¹³C:¹²C ratio of expired air CO₂, averaged 66 (SEM 5) g · 3 h^–1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g · 3 h^–1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.In conclusion, we found glucose ingestion during 3-h exercise with lipolysis blockade could provide metabolic substrate permitting a significant sparing of endogenous carbohydrate and consequently an improvement in performance.     

Ubiquinone supplementation and exercise capacity in trained young and older men

It has been suggested that ubiquinone improves exercise performance and antioxidant capacity. We studied the effects of ubiquinone supplementation (120 mg · day^–1 for 6 weeks) on aerobic capacity and lipid peroxidation during exercise in 11 young (aged 22–38 years) and 8 older (aged 60–74 years), trained men. The cross-over study was double-blind and placebo-controlled. Serum ubiquinone concentration increased after supplementation (P < 0.0001 for treatment) in both age groups. The maximal oxygen uptake ( ) was measured using a direct incremental ergometer test. In the young subjects, the after placebo and ubiquinone treatment was 58.5 (95% confidence interval: 53.0–64.0) and 59.0 ml · min^–1 · kg^–1 (52.2–66.8), respectively. The corresponding results in the older subjects were: 37.2 (31.7–42.7) and 33.7 ml · min^–1 · kg^–1 (26.2–41.7) (P < 0.0001 for age group,P > 0.05 for treatment). In a prolonged test (60-min submaximal, then incremental load until exhaustion) time to exhaustion was longer after the placebo [young men: 85.7 (82.4–89.0), older men: 82.9 min (75.8–89.9)] than after ubiquinone [young men: 82.1 (78.5–85.8), older men: 77.2 min (70.1–83.7);P = 0.0003 for treatment]. Neither ubiquinone supplementation nor exercise affected serum malondialdehyde concentration. Oral ubiquinone was ineffective as an ergogenic aid in both the young and older, trained men.     

Acute resistance exercise does not change the hormonal response to sublingual androstenediol intake

Sublingual intake of 21.4 mg androstenediol increases serum testosterone concentrations whereas swallowing 200 mg androstenediol does not. The duration of increase in serum testosterone following sublingual androstenediol (SL-DIOL) is unknown. Resistance exercise (EX) following SL-DIOL may cause larger increases in serum estradiol concentrations than while at rest. This project evaluated the duration of change in, and the effects of acute EX on, the hormonal response to SL-DIOL. Six young resistance trained males consumed either placebo (PL) or SL-DIOL before a single session of EX or no exercise (Rest) in a random, double blind, crossover manner (for a total of four trials). Blood samples were collected before supplementation, and at 60, 120, 180, 240, 480, and 720 min post-supplementation, with the exercise occurring between 60 and 120 min. The serum [total testosterone] increased (P < 0.05) at 60 min similarly in SL-DIOL-EX and SL-DIOL-Rest by ∼115%, and at 120 min by ∼107% with no differences due to exercise. The serum [estradiol] increased (P < 0.05) similarly in SL-DIOL-EX and SL-DIOL-Rest by ∼33% at 60 min and ∼45% at 120 min, with no differences due to exercise. Serum [testosterone] returned to baseline by 240 min and serum [estradiol] returned to baseline by 720 min post-intake. These findings indicate that SL-DIOL acutely elevates serum testosterone and estradiol concentrations, that EX does not alter the endocrine response to SL-DIOL, and that the increases in serum estradiol last between 480 and 720 min while the increases in serum testosterone last <240 min following acute SL-DIOL intake.     

Dose-related elevations in venous pH with citrate ingestion do not alter 40-km cycling time-trial performance

The purpose of the current investigation was to determine whether sodium citrate enhances endurance cycling performance and, if so, what dosage(s) produces this effect. Eight trained [peak power output: 362 (48) W; power:weight: 5.1 (0.4) W · kg⁻¹, mean (SD)] male cyclists were requested to complete four, 40-km time-trials, each separated by 3–7 days, on their own bicycles, mounted on a Kingcycle ergometer. To mimic the stochastic nature of cycle road races, the time-trials included four 500-m, four 1-km and two 2-km sprints. The experimental conditions involved the ingestion of three dosages of sodium citrate dissolved in 400 ml water: 0.2 g · kg⁻¹, 0.4 g · kg⁻¹ and 0.6 g · kg⁻¹ body mass (b.m.) and a placebo (calcium carbonate, 0.1 g · kg⁻¹ b.m.). Subjects were asked to complete both the sprints and total distance in the fastest time possible. Venous blood samples were collected before, as well as at 10-km intervals during the trials for the analysis of plasma lactate and glucose concentrations and for the measurement of blood pH and PCO₂ levels. Immediately before, as well as during exercise, pH was significantly higher in the group ingesting the highest citrate dose (range 7.36–7.45) compared to the placebo (range 7.31–7.39) and the two lower citrate dosages. Despite this, no significant differences in power output (P=0.886) or time taken to complete the 40 km (P=0.754) were measured between the four trials. The average performance times (in min:s, with SD in parentheses) and average power output (in W) for the 40-km time-trials were: 58:46 (5:06) [265 (62) W], 60:24 (6:07) [251 (59) W], 61:47 (5:07) [243 (44) W] and 60:02 (5.05) [255 (55) W] for the 0.2, 0.4, 0.6 g · kg⁻¹ b.m. sodium citrate and placebo trials, respectively. There were also no significant differences measured between treatments in terms of time, power output, speed or heart rate during the 500-m, 1-km and 2-km sprints. The ingestion of increasing sodium citrate dosages before exercise produced dose-dependent changes in pH, base excess and HCO⁻ ₃ concentrations before and during the 40-km time-trial. However, these changes influenced neither the time-trial time nor the sprinting performance times. Accepted: 7 June 2000