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Effect of NaHCO3 on lactate kinetics in forearm muscles during leg exercise in man


Medicine & Science in Sports & Exercise: June 1996 - Volume 28 - Issue 6 - p 692-697
Basic Sciences/Regulatory Physiology: Original Investigations

We investigated NaHCO3 infusion effects on plasma lactate removal by forearm muscles and performance during intensive leg exercise. Seven subjects performed the force-velocity (FV) test with placebo and NaHCO3 (2 mEq·min-1) with a double-blind crossover protocol. Blood samples for arterial ([LA]A) and venous ([LA]V) lactate determinations were taken 1) at rest before infusion, and 2, 6, 10, 14, 18, and 22 min following its start; and 2) at the end of each exercise bout. The arteriovenous difference ([LA]A-V) was determined for each sampling. NaHCO3 significantly increased arterial bicarbonate concentration and pH during rest (P < 0.001; P < 0.001) and the FV test (P < 0.001; P < 0.05). During the test,[LA]A and [LA]V were significantly higher with NaHCO3(P < 0.05, P < 0.001). At test onset, [LA]A-V became positive and increased until the braking force of 6 kg, with NaHCO3 and placebo, with values significantly lower for NaHCO3(P < 0.001). Peak anaerobic power (Wanae, peak) and the corresponding braking force (Fmax) were also determined. Fmax was significantly increased with NaHCO3 (P < 0.001). In conclusion, the increasing rise in [LA]A and [LA]V induced by NaHCO3 may be partly explained by a decreased rate of lactate uptake by forearm skeletal muscles. NaHCO3 did not improve Wanae, peak, but improved Fmax, thus increasing FV duration.

Laboratoire de Physiologie des Interactions, Service d'Exploration de la Fonction Respiratoire, Hôpital Arnaud de Villeneuve, 34295 Montpellier Cedex 5, FRANCE

Submitted for publication October 1994.

Accepted for publication June 1995.

The authors thank Dr. Pierre Wintrebert for his technical assistance.

Address for correspondence: Pascale Granier, Ph.D., Laboratoire de Physiologie des Interactions, Service d'Exploration de la Fonction Respiratoire, Hôpital Arnaud de Villeneuve, 371 Avenue du Doyen Gaston Giraud, 34295 Montpellier Cedex 5, France.

Previous studies concerning the effects of alkalosis on skeletal muscle metabolism have shown that induced alkalosis causes a rise in blood lactate accumulation during incremental exercise beyond that observed at similar workloads under control conditions (13,22). Different mechanisms have been suggested to explain these higher blood lactate levels associated with metabolic alkalosis. Indeed, some studies(2,29) attributed these elevations of blood lactate to changes in muscle lactate production, and another (17) to the increased rate of lactate efflux from muscle.

Lactate tracer techniques and measurements of venoarterial lactate difference across specific tissue beds have revealed that skeletal muscle has an important role in the removal of lactate from blood during prolonged exercise (1,4,27). During an intermittent exercise test that strongly stimulates glycolytic metabolism, i.e., the force-velocity test (FV) (24,25), we found that lactate uptake by the forearm skeletal muscle significantly increased(9). Furthermore, the rate of lactate uptake was closely correlated with the increase in arterial plasma lactate concentration and power. It was thus of interest to determine whether removal of an arterial lactate load generated by the FV test would be modified during alkalosis, which induces an elevation of blood lactate concentration.

The purpose of the present study was to investigate the effect of a continuous intravenous infusion of NaHCO3 on plasma lactate removal by forearm skeletal muscles during bouts of incremental intensive leg exercise, such as the FV test. We also studied the effect of alkalinization on performance estimated by peak anaerobic power.

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Seven healthy male volunteers aged (mean ± SEM) 29 ± 2 yr with a height of 176 ± 3 cm and a weight of 70 ± 1 kg participated in this study. One week before the experiment, all underwent a physical examination, including a medical history and a resting electrocardiogram. None of these subjects was known to be suffering from any chronic disease and none was on any regular medication. A preliminary FV test on cycle ergometer was performed to familiarize the subjects with procedures, equipment, and laboratory environment. The nature and procedures of the study were explained to each subject and informed written consent was obtained before their participation.

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Exercise testing. The FV test was conducted on a Monark cycle ergometer (864, Monark-Crescent AB; Varberg, Sweden). Each FV test consisted of repetitive maximal sprints against increasing braking forces (F) with a 5-min between-sprint recovery period (31). Duration of each sprint was fixed at 6 s, the maximum time it took for the motivated subject to attain his maximal velocity (V) after the starting signal. Each FV test was performed with the subject in a sitting position. Subjects started the test against an F of 2 kg, and then recovered for 5 min before repeating the same bout of intensive exercise against an F increased by 2 kg. At the end of the test, F was increased by 1 kg in order not to underestimate Wanae, peak. Indeed, we assumed that the subject attained the braking force(Fmax) corresponding to his highest power value (Wanae, peak) if an additional braking force induced a power decrease (Wanae, peak+1). The first two bouts of exercise against 2 kg (E2) and 4 kg (E4) were considered as warm-up. The braking force-velocity relationships were calculated by an automatic system (24) that allowed the determination of V from the measurement of pedal frequency, and, for each F, the power corresponding to the product: FV.

NaHCO3 and placebo administration. NaHCO3(alkalosis) and isotonic NaCl (control) were intravenously infused. The placebo was indistinguishable from NaHCO3 because they were identically packaged. Indeed, NaHCO3 1.4% (Aguettant; Lyon, France) and NaCl 0.9%(Aguettant; Lyon, France) were supplied in the same 250-ml bottle and infused at a constant rate by a dropper into a superficial forearm vein. To determine the dose of NaHCO3 inducing alkalosis, a preliminary resting kinetic study was performed with four subjects with a 2-wk interval between the NaHCO3 and placebo kinetics. The dose of 2 mEq·min-1 of NaHCO3 resulted in a significant increase in arterial pH (F = 98.11,P < 0.001) and HCO3 - concentration (F = 346.62,P < 0.001). This significant increase appeared 2 min after the beginning of NaHCO3 infusion and continued to rise throughout the 22-min resting kinetic period. Indeed, the arterial pH had a basal value of 7.40 that reached 7.44 after 2 min and 7.47 after 22 min of continuous NaHCO3 infusion; concomitantly, the HCO3 - concentration basal value of 24.20 mmol·l-1 increased to 26.60 mmol·l-1 after 2 min up to 29.57 mmol·l-1 after 22 min of NaHCO3 infusion.

Blood samples and analysis. Arterial blood samples were obtained from a plastic Cathlon IV 20G catheter inserted under local anesthesia in the radial artery at the wrist of the nondominant arm. Venous blood samples were drawn from a Teflon 32-mm Cathlon IV 4426 catheter placed in a superficial forearm vein of the other arm (5). Prior to each sampling, the catheter dead space was cleared. In order to minimize the number of catheters, one catheter only was inserted in the vein. Infusion of drug or placebo and venous blood sampling were thus done with the same venous catheter by a three-way tap. The preliminary resting kinetic study on four subjects allowed us to verify that there was no significant difference between venous plasma lactate concentrations with infusion of drug or placebo and those without infusion. For blood gas analysis, 2 ml of arterial blood were drawn anaerobically into heparinized syringes and immediately analyzed for PaO2, PaCO2, and pH at 37°C using the appropriate electrodes(IL Meter 1306; Milan, Italy). Plasma bicarbonate (HCO3 -) was calculated. For lactate analysis, 2 ml of arterial blood and 2 ml of venous blood were collected in Vacutainer tubes (Becton Dickinson, NJ) containing fluoride/ethylenediaminetetraacetic acid, and placed immediately on ice. Plasma was obtained via centrifugation (5 min at 3000 rpm at 4°C) in a model CR 4-12 refrigerated centrifuge (Jouan; Paris, France). The decanted plasma was then separated and frozen at -15°C until assayed. As for previous studies (24,25), all arterial([LA]A) and venous ([LA]V) plasma lactate concentrations were determined within 48 h by a fully enzymatic method (Boehringer kit). The different readings were taken by a centrifugal analyzer (Cobas Bio; Roche, France).

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One week before the experiment, all subjects received standardized instructions as to the testing procedure. Clinical examinations with a resting 12-lead ECG tracing were conducted. A preliminary FV test was performed on the cycle ergometer to allow subjects to familiarize themselves with the procedure, equipment, and laboratory environment.

In a double-blind randomized crossover design, each subject performed two FV tests, once with placebo and once with NaHCO3, separated by a 2-wk interval. On the experimental days, subjects reported to the laboratory in the morning after an overnight fast. Twenty minutes after arrival at the laboratory, one catheter was inserted in the artery, the other in the vein. Subjects were then allowed a 30-min rest period. NaHCO3 and NaCl were continuously infused throughout the rest period, as well as during the testing period. Based on the results of the resting kinetics, which indicated that the increase in arterial pH and HCO3 - concentrations was significant from 2-4 min up to 22 min after the beginning of NaHCO3 infusion, the test was started 22 min after the beginning of drug or placebo injection. Arterial and venous blood samples were taken concomitantly before (To) and 2, 6, 10, 14, 18, and 22 min following the beginning of the infusion(T2, T6, T10, T14, T18, T22). To minimize arm movements, the subjects kept their hands on the handlebar of the bicycle throughout the rest and exercise periods. Blood samples were drawn for each F when the subject stopped pedaling A three-lead ECG [DII, V2, V5] (Quinton Q3000; Seattle, WA) was monitored continuously during the rest period preceding the exercise test, from the beginning to the end of testing, and during the 15 min of recovery.

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At rest and during the FV test, the arteriovenous difference for lactate([LA]A-V) was determined from arterial and venous plasma concentrations measured from the concomitant arterial and venous blood samples.

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Statistical Analyses

Values are reported as mean ± SEM. After verification of a normal distribution, values of Wanae, peak and Fmax with placebo and NaHCO3 were compared using a t-paired test. A two-way analysis of variance for repeated measures (two-way ANOVA) was applied to each set of placebo versus NaHCO3 measurements at rest and during the FV test at the following braking forces: the three common loads for all subjects(E2, E4, E6), the load corresponding to the Wanae, peak, and the following load Wanae, peak+1. When the ANOVAF-ratio was significant, a post-hoc Newman-Keuls test was performed to compare placebo and NaHCO3 measurements at each time and braking force. The limit for statistical significance was always set atP < 0.05.

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Bicarbonate, pH, and Plasma Lactate Concentrations

Intravenous infusion of NaHCO3, as seen in Figure 1 (upper panel), significantly elevated arterial blood bicarbonate concentration compared to NaCl (placebo) during the rest period, from a To value of 24.13 ± 0.56 mmol·l-1 to a final T22 value of 28.66 ± 0.42 mmol·l-1. This increase appeared 2 min after the beginning of drug administration and remained significant throughout the 22-min rest period (F = 16.36, P < 0.001), as well as throughout the entire FV test (F = 23.51, P < 0.001). As a consequence of the NaHCO3 infusion, arterial blood pH(Fig. 1, lower panel) was significantly higher during the pretest resting period, from T2 to T22 (F = 180.91, P< 0.001) and throughout the FV test (F = 3.59, P < 0.05).

The time courses of [LA]A and [LA]V measured at rest and during the FV test with and without NaHCO3 are shown inFigure 2. During the 22-min pretest period, they did not significantly differ between NaHCO3 and placebo. During the FV test, the plasma lactate concentration was higher with NaHCO3 in the arterial(F = 5.23, P < 0.05) and venous (F = 15.09, P < 0.001) samples, especially for the high forces, i.e., forces corresponding to Wanae, peak (P < 0.05, P < 0.01) and Wanae, peak+1 (P < 0.05, P < 0.05).

The time course of [LA]A-V following each exercise bout is illustrated in Figure 3: patterns were similar, with an increase from the beginning of the test up to E6, where a slight decrease appeared. However, [LA]A-V values with NaHCO3 were significantly lower than placebo values (F = 6.32, P < 0.001), especially at the end of the test for the force corresponding to Wanae, peak (P < 0.05) and Wanae, peak+1 (P < 0.05).

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Wanae, peak and Fmax

The individual and mean values of Wanae, peak and Fmax obtained during the placebo and NaHCO3 trials are shown inTable 1. The mean value of Fmax was significantly greater with NaHCO3 (P < 0.001).

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Continuous infusion of NaHCO3 resulted in an increase in plasma lactate concentration and attenuated the arteriovenous difference for lactate following repeated bouts of intensive exercise during the FV test. These modifications were associated with an increase in Fmax.

In this study we chose the FV test as a model of intensive intermittent exercise. Indeed, it has been shown that, during heavy exercise, anaerobic glycolysis in muscle is associated with a metabolic acidosis in blood and a drop in muscle pH (16). Moreover, Hermansen and Osnes(10) showed that intermittent work induces a more acidic environment than is achieved during continuous work. Thus the FV test, because it is both intensive and intermittent, seems an excellent model for inducing alterations in acid-base status and for investigating the effects of bicarbonate loading. To do this, we continuously infused the drug or placebo in a superficial forearm vein throughout the 22-min rest period and the entire exercise testing period. To our knowledge, only Wijnen et al.(33) used this kind of administration. But in their study, the 30-min infusion was stopped 60 min before the beginning of exercise. In most studies, bicarbonate has been administered orally, in solution or in capsule form, at differing dose rates. Moreover, the time of administration before the beginning of exercise has varied considerably. Gastrointestinal problems have often been associated with the use of increasing doses of bicarbonate employed per os, thus probably limiting any attempt to improve performance by this method(23). Also, the time between administration and start of test seems to influence the results. In order to avoid these problems, a continuous infusion was chosen for our study. Concerning the posology of sodium bicarbonate, a dose rate of 0.3 g·kg-1 body weightper os has generally been employed to induce alkalosis. Such a dose rate results in an increase of 4-5 mmol·l-1 of bicarbonate concentration and 0.03-0.06 units pH in venous plasma 2-3 h after administration (23). In our study the dose rate of 2 mEq·l-1 induced an increase of 4.53 mmol·l-1 of bicarbonate at the end of the 22-min rest period, corresponding to a rise of 0.06 units pH in the arterial plasma, a much more precise measure than the venous pH.

The NaHCO3 infusion, continued throughout the FV test, was associated with higher arterial and venous plasma lactate levels. The concentrations observed at the end of exercise with NaHCO3 infusion can be explained by a higher rate of lactate efflux and/or an increased contribution of glycolysis to energy production. Indeed, several investigators have reported that the rate of lactate efflux from muscle is influenced by the pH and bicarbonate concentration in the extracellular fluid or perfusing medium (11,18-21). Three possible mechanisms may explain lactate efflux from muscle: diffusion of the undissociated acid, ionic diffusion of lactate, or transport via a proton-linked carrier (22). The most probable mechanism seems to be the existence of a carrier symport lactate/hydrogen ion(14,15,17). These increased plasma lactate concentrations with metabolic alkalosis may also be consecutive to increased lactate production by maintenance of a high rate of glycolysis flux. Indeed, it has been shown that a decreased extracellular pH inhibits glycolysis due to an effect on the activity of phosphofructokinase(7,30). Moreover, Sutton et al.(29) showed from a variety of animal preparations that the rate at which H+ ions leave muscle is influenced by the bicarbonate concentration of the fluid-perfusing preparation. Based on these findings and on the small degree of acidosis occurring in our study, it seems reasonable to conclude that a small part of the variation in lactate concentration may be attributed to differences in glycolytic rate secondary to changes in blood pH. This was confirmed by the Bouissou et al. study (2), which indicated, from human muscle biopsies, that alkalosis increases muscle lactate accumulation during exhaustive exercise. However, according to McCartney et al. (17), blood acid-base alterations have only a small effect on the change in glycolytic flux, but a substantial effect on the rate of lactate efflux from muscle.

Our study demonstrated that the arteriovenous differences for lactate following repeated bouts of exercise were higher with placebo than bicarbonate. It may be asked whether arm movement could explain this difference. Indeed, in spite of the precautions taken to minimize arm movement, it is not negligible in this type of pedaling exercise. However, given that subjects were tested according to the same methodology, these arteriovenous plasma lactate differences between placebo and NaHCO3 treatments cannot be the consequence of differences in arm movement during the test. Thus, our results indicate that lactate uptake is altered under an alkalizing condition. One explanation could be that lactate, independently of pH, affects the forearm blood flow and thus lactate uptake, because of the significant correlation observed by Rowell et al. (28) between mean arterial pressure and lactate. Another explanation could be that the metabolic alkalosis induced by NaHCO3 infusion decreased the lactate concentration gradient from muscle to blood plasma because of the increased muscle lactate production. In consequence, the sarcolemmal membrane would form a rate-limiting barrier for the lactate uptake(15). Similar observations of decreased utilization of lactate by nonexercising and exercising muscle have been reported during the recovery from exercise (1,27). Poortmans et al.(27) also suggested that, during the recovery period, since the arterial concentration is no longer rising, there is no net lactate uptake because of a reduced muscle/blood gradient. The higher plasma lactate levels associated with NaHCO3 treatment at the end of the FV test may therefore be indicative not only of a higher rate of lactate efflux and/or increased contribution of anaerobic glycolysis to energy production, but also of a striking reduction in the rate of lactate uptake by the nonexercising muscles.

Our study also showed that Wanae, peak did not increase significantly with NaHCO3 versus placebo. Concerning the influence of NaHCO3 treatment on exercise performance, conflicting results have been reported in the literature. Indeed, some studies have shown enhanced performance during exercise after bicarbonate administration(2,6,8,29); on the contrary, in other studies the performance was not improved by metabolic alkalosis(12,17,26,32,33). However, in all studies describing beneficial effects of bicarbonate, the performance has been assessed by the duration of the exercise or endurance time but never in terms of power. The interest of the FV test lies in the fact that it allows determination of both Wanae, peak and Fmax. Indeed, we demonstrated that NaHCO3 treatment had no beneficial effect on peak power, although it significantly increased the number of exercise bouts, since Fmax was higher in NaHCO3 than NaCl. This higher number of bouts may be due, as suggested by several authors(6,23,29), to an increased buffer capacity. This increase, by lessening the metabolic acidosis, would delay the onset of fatigue and enhance time to exhaustion. The greater number of bouts may also be explained by the higher plasma lactate concentrations induced by the NaHCO3 infusion. Indeed, because lactate is a major fuel source as well as a gluconeogenic precursor (3), the increase in available blood lactate may represent a saving factor for muscular glycogen, thus improving exercise duration via the number of bouts performed.

In conclusion, the increased plasma lactate concentration during the repeated bouts of exercise of the FV test, induced by a continuous NaHCO3 infusion, can be partly explained by a reduction in the rate of lactate uptake by the forearm muscles. Moreover, this induced metabolic alkalosis did not improve the Wanae, peak but it did improve Fmax, thus increasing the duration of the FV test, i.e., the number of exercise bouts performed.

Figure 1-A) The time courses of arterial blood bicarbonate concentrations during the 22-min pretest period and the FV test with (•) and without (○) NaHCO3 treatment. B) The time courses of arterial blood pH during the 22-min pretest period and the FV test with (•) and without (○) NaHCO3 treatment. *

Figure 1-A) The time courses of arterial blood bicarbonate concentrations during the 22-min pretest period and the FV test with (•) and without (○) NaHCO3 treatment. B) The time courses of arterial blood pH during the 22-min pretest period and the FV test with (•) and without (○) NaHCO3 treatment. *

Figure 2-The time courses of arterial plasma lactate concentrations with (▾) and without (▿) NaHCO3 treatment and venous plasma lactate concentrations with (•) and without (○) NaHCO3 treatment measured at rest during the 22-min pretest period and throughout the FV test. *

Figure 2-The time courses of arterial plasma lactate concentrations with (▾) and without (▿) NaHCO3 treatment and venous plasma lactate concentrations with (•) and without (○) NaHCO3 treatment measured at rest during the 22-min pretest period and throughout the FV test. *

Figure 3-The time courses for the arteriovenous plasma lactate differences with (•) and without (○) NaHCO3 treatment measured during the 22-min rest period and throughout the FV test.*

Figure 3-The time courses for the arteriovenous plasma lactate differences with (•) and without (○) NaHCO3 treatment measured during the 22-min rest period and throughout the FV test.*

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