Sodium citrate ingestion and its effects on maximal anaerobic exercise of different durations

Summary The effects of an alkalising agent were studied in ten subjects who participated in anaerobic testing on a cycle ergometer to determine the effectiveness of sodium citrate (0.5 g·kg^–1 body mass) as an ergogenic aid during exercise of 10-s, 30-s, 120-s and 240-s duration. Blood was collected prior to, after ingestion of sodium citrate (NaHCO₃), and postexercise, from a heated (43–46°C) fingertip and analysed immediately postcollection for pH, partial pressure of oxygen and carbon dioxide, base excess and blood bicarbonate. Total work undertaken (kJ) and peak power (W) achieved during the tests was also obtained via a work monitor unit. The results indicated that a dose of 0.5 g sdkg^–1 body mass sodium citrate had no ergogenic benefit for exercise of either 10-s or 30-s duration. Blood bicarbonate concentrations, however, were significantly increased (P<0.05) following ingestion of the citrate during these trials. Exercise periods of 120 s and 240 s were significantly increased (P<0.05) above the control and placebo conditions following sodium citrate ingestion. Blood bicarbonate concentrations were again increased above control and placebo conditions and blood lactate concentrations were also increased following the citrate trials. The pH decreased significantly (P<0.05) in all trials below the control and placebo conditions. On the basis of the exercise undertaken in this study we would suggest that a dose of 0.5 g·kg^–1 body mass of sodium citrate could improve anaerobic exercise performance of 120-s and 240-s duration.     

The effect of citrate loading on exercise performance,acid-base balance and metabolism

Summary Nine subjects ( 65±2 ml·kg⁻¹·min⁻¹, mean±SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g·kg⁻¹ body mass) or a sodium chloride placebo (P, 0.045 g·kg⁻¹ body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% , followed by exercise to exhaustion at 95% . Pre-exercise arterialized-venous [H⁺] was lower in C (36.2±0.5 nmol·l⁻¹; pH 7.44) than P (39.4±0.4 nmol·l⁻¹; pH 7.40); the plasma [H⁺] remained lower and [HCO ₃ ⁻ ] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% was similar in C (310±69 s) and P (313±74 s). Cardiorespiratory variables (ventilation, , , heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195±19 μmol·l⁻¹; P, 81±7 μmol·l⁻¹) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% . Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate

The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg^?1 body mass of sodium bicarbonate (NaHCO₃) (BICARB), or a placebo of 0.045 g kg^?1 body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO₃ is unlikely to be due to a decreased oxidative stress.     

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.     

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.     

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.     

Effect of sodium citrate on performance and metabolism of human skeletal muscle during supramaximal cycling exercise

The aim of this study was to examine whether the alkalosis-induced improvement in supramaximal performance could be explained by a less-altered muscle metabolic status. Eight subjects first performed exhausting exercise at 120% peak oxygen uptake after ingesting either a placebo (PLC) or sodium citrate (CIT) at a dose of 0.5 g · kg^?1 body mass to determine exhaustion time (t _exh). They then, performed exercise (Lim-EX) at the same relative intensity lasting PLCt _exh minus 20 s in both treatments. Samples were taken from vastus lateralis muscle at rest (90-min after the ingestion) and at the end of Lim-EX. Arterial blood samples were obtained at rest (immediately prior to and 90 min after ingesting the drug) and during the 20-min post-exercise recovery. The t _exh was significantly increased by CIT [PLC 258 (SD 29) s, CIT 297 (SD 45) s]. The CIT raised the rest [citrate] in blood [PLC 0.11 (SD 0.01) mmol · l^?1, CIT 0.34 (SD 0.07) mmol · l^?1] and in muscle [PLC 0.78 (SD 0.23) mmol · kg^?1 dry mass, CIT 1.00 (SD 0.21) mmol · kg^?1 dry mass]. Resting muscle pH and buffering capacity were unchanged by CIT. The same fall in muscle pH was observed during Lim-EX in the two conditions. This was associated with similar variations in both the cardio-respiratory response and muscle energy and metabolism status in spite of a better blood acid-base status after CIT. Thus, CIT would not seem to allow the alkalinization of the muscle cytosolic compartment. Though sodium citrate works in a similar way to NaHCO₃ on plasma alkalinization and exercise performance, the exact nature of the mechanisms involved in the delay of exhaustion could be different and remains to be elucidated.     

Bicarbonate ingestion has no ergogenic effect on consecutive all out sprint tests in BMX elite cyclists

The aim of the present study was to examine the effect of sodium bicarbonate ingestion on consecutive "all out" sprint tests, analyzing the acid-base status and its influence on performance and perceived effort. Ten elite bicycle motocross (BMX) riders (20.7 ± 1.4 years, training experience 8-12 years) participated in this study which consisted of two trials. Each trial consisted of three consecutive Wingate tests (WTs) separated by 15 min recovery. Ninety minutes prior to exercise subjects ingested either NaHCO(3) (-) (0.3 g kg(-1) body weight) or placebo. Blood samples were collected for the assessment of blood acid-base status: bicarbonate concentration ([HCO(3) (-)]), pH, base excess (BE) and blood lactate concentration ([La(-)]). Performance variables of peak power (PP), mean power (MP), time to peak power and fatigue index were calculated for each sprint. Significant differences (p < 0.05) were observed in acid-base variables [pH before WT1: 7.47 ± 0.05 vs. 7.41 ± 0.03; [HCO(3) (-)] before WT1: 29.08 ± 2.27 vs. 22.85 ± 0.24 mmol L(-1) (bicarbonate vs. placebo conditions, respectively)], but there were not significant differences in performance variables between trials [PP WT1: 1,610 ± 373 vs. 1,599 ± 370 W; PP WT2: 1,548 ± 460 vs. 1,570 ± 428 W; PP WT3: 1,463 ± 361 vs. 1,519 ± 364 W. MP WT1: 809 ± 113 vs. 812 ± 108 W; MP WT2: 799 ± 135 vs. 799 ± 124 W; MP WT3: 762 ± 165 vs. 782 ± 118 W (bicarbonate vs. placebo conditions, respectively)]. Rating of perceived effort (RPE) was not influenced nor ratings of perceived readiness. Sodium bicarbonate ingestion modified significantly the blood acid-base balance, although the induced alkalosis did not improve the Wingate test performance, RPE and perceived readiness across three consecutive WTs in elite BMX cyclists.     

The influence of acetaminophen on repeated sprint cycling performance

Introduction

The aim of this study was to investigate the effect of acetaminophen on repeated sprint cycling performance.

Methods

Nine recreationally active male participants completed a graded exercise test, a familiarisation set of Wingate Anaerobic Tests (WAnTs) and two experimental sets of WAnTs (8 × 30 s sprints, 2 min active rest intervals). In the experimental WAnTs, participants ingested either 1.5 g acetaminophen or a placebo in a double-blind, randomised, crossover design. During the WAnT trials, participants provided ratings of perceived pain 20 s into each sprint. Mean and peak power output and heart rate were recorded immediately following each sprint, and percentage decrement in mean power output was subsequently calculated.

Results

Participants cycled at a significantly greater mean power output over the course of 8 WAnTs (p < 0.05) following the ingestion of acetaminophen (391 ± 74 vs. 372 ± 90 W), due to a significantly greater mean power output during sprints 6, 7 and 8 (p < 0.05). Percentage decrements in mean power output were also significantly reduced (p < 0.05) following acetaminophen ingestion (17 ± 14 vs. 24 ± 17 %). No significant differences in peak power output, perceived pain or heart rate were observed between conditions.

Conclusion

Acetaminophen may have improved performance through the reduction of pain for a given work rate, thereby enabling participants to exercise closer to a true physiological limit. These results suggest that exercise may be regulated by pain perception, and that an increased pain tolerance can improve exercise performance.     

Arterio‐venous differences of blood acid–base status and plasma sodium caused by intense bicycling

After intense exercise muscle may give off hydrogen ions independently of lactate, perhaps by a mechanism involving sodium ions. To examine this possibility further five healthy young men cycled for 2 min to exhaustion. Blood was drawn from catheters in the femoral artery and vein during exercise and at 1‐h intervals after exercise. The blood samples were analysed for pH, blood gases, lactate, haemoglobin, and plasma proteins and electrolytes. Base deficit was calculated directly without using common approximations. The leg blood flow was also measured, thus allowing calculations of the leg’s exchange of metabolites. The arterial blood lactate concentration rose to 14.2 ± 1.0 mmol L^–1, the plasma pH fell to 7.18 ± 0.02, and the base deficit rose 22% more than the blood lactate concentration did. The femoral‐venous minus arterial differences peaked at 1.8 ± 0.2 mmol L^–1 (lactate), –0.24 ± 0.01 (pH), and 4.5 ± 0.4 mmol L^–1 (base deficit), and –2.5 ± 0.7 mmol L^–1 (plasma sodium concentration corrected for volume changes). Thus, near the end of the exercise and for the first 10 min of the recovery period the leg gave off more hydrogen ions than lactate ions to the blood, and sodium left plasma in proportion to the extra hydrogen ions appearing. The leg’s integrated excess release of hydrogen ions of 0.88 ± 0.45 mmol kg^–1 body mass was 67% of the integrated lactate release. Base deficit calculated by the traditional approximate equations underestimated the true value, but the error was less than 10%. We conclude that intense exercise and lactic acidosis may lead to a muscle release of hydrogen ions independent of lactate release, possibly by a Na⁺,H⁺ exchange. Hydrogen ions were largely buffered in the red blood cells.     

Sodium bicarbonate can be used as an ergogenic aid in high-intensity, competitive cycle ergometry of 1 h duration

The aim of this study was to determine whether a dose of 300-mg?·?kg^?1 body mass of sodium bicarbonate would effect a high-intensity, 1-?h maximal cycle ergometer effort. Ten male, well-trained [maximum oxygen consumption 67.3 (3.3)?ml?·?kg^?1?·?min^?1, mean (SD)] volunteer cyclists acted as subjects. Each undertook either a control (C), placebo (P), or experimental (E) ride in a random, double-blind fashion on a modified, air-braked cycle ergometer, attached to a personal computer to which the work and power data was downloaded at 10?Hz. Fingertip blood was sampled at 10-min intervals throughout the exercise. Blood was also sampled at 1, 3, 5, and 10?min post-exercise. Blood was analysed for lactate, partial pressure of Carbon dioxide and oxygen, pH and plasma bicarbonate (HCO^? ₃) concentration. Randomly chosen pairs of subjects were asked to complete as much work as possible during the 60-min exercise periods in an openly competitive situation. The sodium bicarbonate had the desired effect of increasing blood HCO^? ₃ prior to the start of the test. The subjects in E completed 950.9 (81.1)?kJ of work, which was significantly more (F_(2,27)?=?5.28, P?相似文献   

Effect of alkalosis on plasma epinephrine responses to high intensity cycle exercise in humans

The purpose of this study was to determine the effects of alkalosis on epinephrine concentrations in response to a 90 s maximal exercise test. A group of ten healthy men ingested either a bicarbonate (BS) supplement (0.3 g·kg^–1 of body mass of sodium bicarbonate) or placebo mixture (P) prior to performing a 90 s maximal cycle ergometer test. An indwelling Teflon cannula was placed in the antecubital vein and blood samples were drawn at three times at rest separated by 10 min, immediately following the protocol, and at 2.5, 5, and 10 min post exercise to determine plasma epinephrine concentrations. Sodium bicarbonate ingestion significantly (P<0.05) induced alkalosis both at rest [mean (SD) pH=7.42 (0.02) BS, 7.38 (0.02) P] and after the exercise protocol [pH=7.16 (0.02) BS, 7.12 (0.02) P]. Plasma epinephrine concentrations were not significantly different immediately post exercise between the two conditions [4.2 (0.6) compared to 4.2 (0.7) pmol·ml^–1 in BS and P, respectively]. Work performed and power output attained were not significantly different between the two treatment conditions [mean power=258.7 (35.1) W BS, 260.3 (35.4) W P; peak power=534.7 (61.6) W BS, 535.7 (54.4) W P]. The primary finding of this investigation was that orally-induced alkalosis does not significantly affect plasma epinephrine concentrations or performance following 90 s of maximal cycle exercise in untrained men. Electronic Publication     

Fractional use of anaerobic capacity during a 30- and a 45-s Wingate test

This study examined the suitability of the Wingate test as a means of assessing the maximal oxygen deficit (MOD), and the influence of the anaerobic capacity on the fraction of the MOD used during a 30- and a 45-s Wingate test in 19 male subjects. The MOD incurred in constant-intensity supramaximal exercise was higher (P < 0.01) than that for the 45-s and 30-s Wingate tests [68.6 (3.4) vs 60.9 (2.2) and 53.7 (1.6) ml · kg⁻¹, respectively], corresponding to a 10% higher value for the 45-s compared to that for the 30-s test (P < 0.001). A close correlation was found to occur between MOD and the oxygen deficit incurred during the 30- and 45-s Wingate tests, as well as between both all-out tests (r = 0.86–0.90; P < 0.001). The oxygen deficit accumulated during the first 30 s of the 45-s Wingate test was similar to that accumulated during the 30-s Wingate test. The intraclass correlation coefficient for the oxygen deficit after 30 s of all-out exercise (two treatments) was 0.96. The higher the MOD the lower was its fractional recruitment during the 30-s (r = −0.88, P < 0.001) and during the 45-s (r = −0.74, P < 0.01) Wingate tests. In conclusion, 80–90% as an assessment of the oxygen deficit incurred during a Wingate test is valid as an estimate of the anaerobic capacity. The fraction of the anaerobic capacity used in a 30- and 45-s all-out test in inversely related to the anaerobic capacity. Accepted: 15 April 1997     

Potassium kinetics and its relationship with ventilation during repeated bouts of exercise in women

The purpose of this study was to determine the electrolyte concentration changes in arterial plasma from high-intensity repeated bouts of cycling exercise in well-trained females and to determine the relationships between arterial plasma lactate, potassium (K⁺), bicarbonate (HCO₃⁻), and pH with minute ventilation. Fourteen female subjects (mean age = 27 ± 4 years; mean height = 170 ± 7 cm; mean weight = 62 ± 7 kg; maximal oxygen uptake = 50 ± 6 ml/kg/min) were recruited to perform 3 × 5 min bouts of exercise at 236 ± 27 W with 10 min recovery between each set. Minute ventilation, arterial plasma lactate, potassium, calcium, chloride, and sodium ion concentrations were measured a minute 0, 1, 2, 3, 4, 5 of each set and midway through recovery (21 sampling points total per subject). The results showed that the strongest relationship was between arterial plasma K⁺ concentration and minute ventilation (r ² = 0.91), and, that arterial plasma lactate mirrored both arterial plasma HCO₃⁻ and pH. In conclusion, this study demonstrates that women exhibit similar electrolyte responses as reported elsewhere in men, and support the idea that K⁺ may partly contribute to controlling ventilation during high-intensity exercise and recovery.     

Influence of ingested fluid volume on physiological responses during prolonged exercise

The effect of different rates of fluid ingestion on heart rate, rectal temperature, plasma electrolytes, hormones and performance was examined during prolonged strenuous exercise conducted at 21 °C. Seven well-trained males (24 ± 1 yr; 68.6 ± 2.9 kg; Vo ₂ peak = 4.69 ± 0.17 L min^?1; mean ± SEM) cycled for 2 h at 69 ± 1% Vo ₂ peak while receiving either no fluid replacement (NF), a volume of water estimated to prevent body weight loss (FR-100 = 2.32 ± 0.10 L 2 h^?1) or 50% of this volume (FR-50 = 1.16 ± 0.05 L 2 h^?1). The 2-h exercise bout was followed by a ride to exhaustion at a workload estimated to be 90% Vo ₂ peak. After 2 h of exercise, NF was associated with a 3.2 ± 0.1% weight loss, while FR-50 and FR-100 resulted in losses of 1.8 ± 0.1 and 0.1 ± 0.1%, respectively. Compared with FR-100, heart rate and rectal temperature were elevated (P < 0.05) during the second hour of exercise in NF, with FR-50 intermediate. Reductions in plasma volume during exercise were greater in NF and FR-50, compared with FR-100 and plasma sodium concentration was elevated in NF, decreased slightly in FR-100, with FR-50 intermediate. Plasma renin activity, aldosterone and atrial natriuretic peptide increased to similar extents in the three trials. Plasma vasopressin remained unchanged for FR-100, increased for NF, with intermediate values for FR-50. Exercise time to exhaustion at 90% Vo ₂ peak was longer in FR-100 (328 ± 93 s) than NF (171 ± 75 s) with FR-50 (248 ± 107 s) not significantly different from either FR-100 or NF. In conclusion, the responses of heart rate, rectal temperature, plasma sodium, and vasopressin during, and performance following, prolonged cycling exercise conducted at 21 °C are related to the amount of fluid ingested (i.e. the degree of dehydration).     

Cardiac output but not stroke volume is similar in a Wingate and \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} test in young men

Wingate test (WT) training programmes lasting 2?C3?weeks lead to improved peak oxygen consumption. If a single 30?s WT was capable of significantly increasing stroke volume and cardiac output, the increase in peak oxygen consumption could possibly be explained by improved oxygen delivery. Thus, we investigated whether a single WT increases stroke volume and cardiac output to similar levels than those obtained at peak exercise during a graded cycling exercise test (GXT) to exhaustion. Fifteen healthy young men (peak oxygen consumption 45.0?±?5.3?ml?kg^?1?min^?1) performed one WT and one GXT on separate days in randomised order. During the tests, we estimated cardiac output using inert gas rebreathing (nitrous oxide and sulphur hexafluoride) and subsequently calculated stroke volume. We found that cardiac output was similar (18.2?±?3.3 vs. 17.9?±?2.6?l?min^?1; P?=?0.744), stroke volume was higher (127?±?37 vs. 94?±?15?ml; P?<?0.001), and heart rate was lower (149?±?26 vs. 190?±?12 beats?min^?1; P?<?0.001) at the end (27?±?2?s) of a WT as compared to peak exercise during a GXT. Our results suggest that a single WT produces a haemodynamic response which is characterised by similar cardiac output, higher stroke volume and lower heart rate as compared to peak exercise during a GXT.     

During intense exercise, obese women rely more than lean women on aerobic energy

 A series of untrained, healthy, obese women (body mass index 32.5 ± 0.9 kg·m^–2) were subjected to a protocol of intense exercise on a cycloergometer and compared with lean controls (body mass index 20.9 ± 0.5 kg·m^–2). Physiological parameters, blood lactate, bicarbonate, plasma metabolites, oxygen consumption and CO₂ production were measured. Impedance-derived extracellular water and plasma changes in lactate and bicarbonate were used to determine changes in bicarbonate pools and lactate-displaced CO₂. From these and respiratory gases, the respiratory quotient was calculated and thence overall fuel consumption. Anaerobic energy during exercise accounted for about 1.8% of all energy consumed in the lean but only 0.7% in the obese. Obese women fatigued at lower workloads and energy expenditure levels than did the lean, and their lactate buildup was similar when compared on the basis of fat-free mass. The data support the postulation of fatigue being triggered by a combination of factors: stretched cardiovascular work would be the main factor for obese women, in part limiting lactate production. For lean women, the triggering factor for fatigue could be the loss of buffering capacity; but it is the combination of stretching cardiovascular capacity, exhaustion of glycogen and available glucose and increase in lactate/loss of bicarbonate buffer that determines the onset of fatigue. Received: 10 December 1996 / Received after revision: 26 May 1997 / Accepted: 20 October 1997     

The effect of induced alkalosis and acidosis on plasma lactate and work output in elite oarsmen

Summary In order to test the effect of artificially induced alkalosis and acidosis on the appearance of plasma lactate and work production, six well-trained oarsmen (age=23.8±2.5 years; mass=82.0±7.5 kg) were tested on three separate occasions after ingestion of 0.3 g·kg⁻¹. NH₄Cl (acidotic), NaHCO₃ (alkalotic) or a placebo (control). Blood was taken from a forearm vein immediately prior to exercise for determination of pH and bicarbonate. One hour following the ingestion period, subjects rowed on a stationary ergometer at a pre-determined sub-maximal rate for 4 min, then underwent an immediate transition to a maximal effort for 2 min. Blood samples from an indwelling catheter placed in the cephalic vein were taken at rest and every 30 s during the 6 min exercise period as well as at 1, 3, 6, 9, 12, 15, 18, 21, 25 and 30 min during the passive recovery period. Pre-exercise blood values demonstrated significant differences (p<0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p>0.05), although a trend toward decreased production was evident in the acidotic condition. Analysis of exercise blood samples using ANOVA with repeated measures revealed that the linear increase in plasma lactate concentration during control was significantly greater than acidosis (p<0.01). Although plasma lactate values during alkalosis were consistantly elevated above control there was no significant difference in the linear trend (p>0.05). During recovery, there was no significant difference in the rate of lactate disappearance amongst the three conditions. It is concluded that under this protocol artificial manipulation of the acid-base status of the blood does not significantly influence work production despite significantly reduced plasma lactate concentrations during acidosis. The inability of these pH changes to alter exercise performance emphasizes the relative importance of the intracellular and the extracellular buffer systems in well trained athletes.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

Effects of chronic bicarbonate ingestion on the performance of high-intensity work

We have evaluated whether sodium bicarbonate, taken chronically (0.5?g?·?kg^?1 body mass) for a period of 5 days would improve the performance of eight subjects during 60?s of high-intensity exercise on an electrically braked cycle ergometer. The first test was performed prior to chronic supplementation (pre-ingestion) while the post-ingestion test took place 6 days later. A control test took place approximately 1 month after the cessation of all testing. Acid-base and metabolite data (n?=?7) were measured from arterialised blood both pre- and post-exercise, as well as daily throughout the exercise period. The work completed by the subjects in the control and pre-ingestion test [21.1 (0.9) and 21.1 (0.9) MJ, respectively] was less than (P?F _(2,21)?=?3.4, P?P?F _(5,36)?=?12.5, P?P??1 after 24?h of ingestion. In conclusion, the addition of sodium bicarbonate to a normal diet proved to be of ergogenic benefit in the performance of short-term, high-intensity work.