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Basic Sciences: Original Investigations

Lactate distribution in the blood during steady-state exercise

SMITH, EDITH W.; SKELTON, MICHELE S.; KREMER, DUANN E.; PASCOE, DAVID D.; GLADDEN, L. BRUCE

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Medicine& Science in Sports & Exercise: September 1998 - Volume 30 - Issue 9 - p 1424-1429
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Abstract

During exercise there is an increased rate of lactic acid production by contracting muscles and an increase in the rate of lactate release from those muscles. This results in an increase in the rate of lactate entry into the plasma. Once in the plasma lactate can enter red blood cells (RBCs) via three parallel pathways (20): 1) an anionic exchange mechanism called the Band 3 system in which lactate is most likely exchanged for bicarbonate or chloride, 2) nonionic diffusion of free lactic acid, and 3) a specific monocarboxylate carrier that co-transports lactate and a proton. These transport pathways for lactate are important in equilibrating plasma and RBC lactate concentrations ([La])(7,8,10,20,21). Although some researchers(2,6) report that [La] is equal in the plasma and RBCs at rest, most (4,5,9,12,15,16,18,22) have found that at rest [La] in the plasma is approximately twice that found in RBCs. Accordingly, it is generally accepted that the resting RBC:plasma[La] ratio is about 0.5, and that the resting plasma-to-RBC [La] gradient (the difference between plasma [La] and RBC [La]) is approximately 0.5 mM. This unequal distribution of lactate between plasma and RBCs is probably the result of a Donnan equilibrium (3,13,15,17).

The[La] gradient from plasma to RBCs increases in response to intense exercise(15,18,19). In fact, Juel et al. (18) reported a decrease in the resting RBC:plasma [La] ratio from 0.5 at rest to values as low as 0.2 as a result of exhaustive knee extensor exercise that elevated arterial plasma [La] to 12 mM. Apparently, the rate of lactate release from the exercising muscles was greater than the rate of net inward lactate transport across the RBC membrane. There are at least two possible explanations for these results: 1) lactate could have equilibrated across the RBC membrane according to a new electrochemical equilibrium established by concurrent changes in RBC membrane potential and changes in the transmembrane concentrations of Cl, HCO3, K+, Na+, and/or other ions; or 2) lactate release from the exercising muscles could have exceeded the ability of the RBC lactate transport pathways to equilibrate the [La] across the RBC membrane.

There appears to be adequate equilibration of lactate across the RBC membrane during progressive incremental exercise even when the increment duration is only 1 min (22). This is evidenced by the fact that the RBC:plasma [La] ratio was never significantly different from the resting value during the exercise (22).

There seem to be no studies that have examined the distribution of lactate within the blood during submaximal steady-state exercise. Therefore, it is not known how the plasma to RBC [La] gradient or the RBC:plasma [La] ratio change with differing intensities of submaximal steady-state exercise. Submaximal steady-state exercise at an intensity above the lactate threshold (LT) will result in a greater increase in blood [La] than will a submaximal steady-state exercise intensity below LT (23). At the onset of exercise above LT, the work rate increase from rest would be large in comparison with the small work rate increases that occur during progressive incremental exercise. One can hypothesize that when submaximal steady-state exercise is performed at an intensity above LT, plasma [La] may increase at a rate greater than the increase in RBC [La] at the onset of the exercise when the rate of lactate release from muscles is expected to be greatest. The result could be an increase in the plasma to RBC [La] gradient and a decrease in the RBC:plasma [La] ratio. However, steady-state exercise below LT causes only a slight increase in blood [La] (23). Accordingly, [La] gradients and ratios during steady-state exercise at an intensity less than LT may not differ significantly from those found under resting conditions. Therefore, the purpose of this investigation was to examine the plasma to RBC [La] gradient and RBC:plasma [La] ratio during 30 min of steady-state cycle ergometer exercise at work rates below LT (≈40% of peak cycle ergometer O2 uptake {V˙O2peak}) and above LT (≈70% of V˙O2peak).

METHODS

Subjects. The protocol for these experiments was reviewed and approved by the Auburn University Institutional Review Board for the Use of Human Subjects in Research. Eight male volunteers gave their informed consent to perform one progressive incremental exercise test to exhaustion and two submaximal, constant metabolic rate exercise tests on a Monark (Monark Crescent AB, Varberg, Sweden) cycle ergometer. Physical and physiological characteristics of the subjects (mean ± SE) were: age, 22.1 ± 0.7 yr; height, 174.0± 2.1 cm; weight, 79.6 ± 5.0 kg; V˙O2peak, 41.6 ± 1.6 mL·kg−1·min−1; LT, 57.9 ± 1.2% of V˙O2peak. Although each subject regularly engaged in some form of exercise, none was specifically trained in any type of physical activity.

Progressive incremental exercise test. The protocol began with unloaded pedaling at 60 rpm for 4 min. Thereafter the work rate was increased by 30 W every minute until volitional fatigue. Blood samples were drawn every minute for determination of [La]. LT was determined from plots of whole blood [La] versus time. The time at which the whole blood [La] reached 2 mM was chosen as the LT; this time was then entered into a regression equation relating V˙O2 to time to calculate the V˙O2 at the LT.

Inspired minute ventilation (V˙I), expired oxygen fraction (FEO2), and expired carbon dioxide fraction(FECO2) were measured continuously throughout the test and averaged over 30-s intervals. Subjects inspired room air through a Hans Rudolph (Kansas City, MO) valve that directed the expired air into a Plexiglass mixing chamber. V˙I was measured by a calibrated Parkinson-Cowan (Ventura, CA) gas meter that was fitted with a rotary potentiometer. Mixed expired air was continuously drawn from the mixing chamber through a small tube containing a drying agent (Aquasorb; Mallinckrodt, Paris, KY) and through gas analyzers that measured FEO2 (Ametek S-3A/I; Pittsburgh, PA) and FECO2 (Beckman Instruments LB-2; Fullerton, CA). The gas analyzers were calibrated with gases from tanks of known concentrations before each test. Output from the gas meter and analyzers was directed to an automated gas exchange system(Rayfield, Inc.; Waitsfield, VT) that calculated V˙O2, carbon dioxide output (V˙O2), and respiratory exchange ratio (R) over 30-s intervals using standard equations. V˙O2peak was verified by demonstration of at least three of the following criteria: 1) a plateau or decrease in V˙O2 with increasing work rate; 2) an R of > 1.15; 3) attainment of age predicted maximal heart rate; and 4) an immediate postexercise whole blood [La] of 8 mM or greater.

Submaximal constant metabolic rate exercise. Subjects performed submaximal steady-state exercise bouts of low intensity (≈40% V˙O2peak= <LT) and moderate intensity (≈70% V˙O2peak = >LT) in random order and at least 1 wk apart. The metabolic rate was maintained constant throughout each bout by adjusting the cycle ergometer resistance to maintain a constant V˙O2 corresponding to either 40% or 70% of V˙O2peak. The average V˙O2 for <LT was 41.1 ± 1.3% V˙O2peak, while the >LT mean was 71.1 ± 1.5% V˙O2peak. These work rates were below and above the lactate threshold (LT) of 57.9 ± 1.2% V˙O2peak, respectively.

Blood sampling and biochemical analyses. At the beginning of each testing session, a 19-gauge catheter (Baxter Healthcare Corp., Deerfield, IL) was inserted into a prominent forearm vein. Arterialization (blood PO2 ≥ 70 mm Hg) of blood samples drawn from this arm was achieved by warming the subject's hand in a heated box that circulated air with a temperature of ≈60°C and by wrapping the upper arm in a heating pad (medium setting). The catheter was flushed with a small amount of sterile saline solution containing 100 USP U·mL−1 of heparin to maintain patency among samples. A total of 6 mL of blood was drawn into two heparinized 3-mL syringes at rest and during the 30 s preceding minutes 2, 4, 6, 8, 10, 15, 20, 25, and 30 of each steady-state exercise bout. The first syringe of each pair was used for whole blood measurements. From this syringe approximately 1 mL of blood was placed in a spot plate from which 200 μL were immediately transferred to each of two test tubes containing 2 mL of cold perchloric acid. The perchloric acid extracts were frozen (−80°C) for subsequent analysis of lactate. Also from the first syringe approximately 0.5 mL of blood was placed in a test tube from which hematocrit (Hct) samples were drawn into microhematocrit capillary tubes. Hct was determined in duplicate by centrifugation of these capillary tubes for 5 min at 13,460g in a Micro-MB centrifuge (International Equipment Company; Needham Heights, MA). A 4% correction factor was applied for trapped plasma (3,5). The syringe, with the remaining blood sample, was capped and then placed in ice water for the short time before it was analyzed for blood gases and whole blood pH (IL 1304 blood gas, pH analyzer). Subsequently, water content was determined.

To minimize transport of lactate between the plasma and RBCs, the second 3-mL syringe of each sample pair was immediately capped and submerged in a dry ice-ethanol slurry for 10 s and then placed in ice water. Although equilibration of lactate across the RBC membrane occurs quickly at 37°C (5,17,18), equilibration is greatly slowed at 0°C, taking as long as 100 h (17). Our own preliminary experiments showed that 10 s in the dry ice-ethanol slurry was sufficient to drop the temperature to 4°C without hemolysis. At completion of each exercise test, syringes were centrifuged(2000g, 15 min, 4°C) with plungers down. This allowed easy separation of the plasma from RBCs. Two hundred microliters of the separated plasma were placed in each of two test tubes containing cold perchloric acid for later lactate analysis. The separated plasma was also analyzed for water content. After removal of the plasma from the second syringe, the remaining packed RBCs were lysed by freezing three times in a dry ice-ethanol slurry; each freeze was interrupted by 10-15 min of thawing. Syringes of lysed RBCs were then centrifuged (2000g, 15 min, 4°C). The pH of the supernatant was considered to represent RBC pH (1,3,13). Water content of whole blood and plasma was determined by drying samples weighing approximately 200-400 mg at 100°C for 24 h.

Whole blood and plasma [La] were determined by a spectrophotometric modification of the enzymatic technique described by Gutmann and Wahlefeld (14). All lactate concentrations were reported as concentration per liter of water. RBC[La] was calculated from whole blood and plasma lactate concentrations as follows (2,5,6,12,15): (Equation 1) where Cc is the [La] in cell water, Cb is [La] in whole blood water, Cp is the [La] in plasma water, and Hct is the corrected hematocrit.

Statistical analysis. Repeated measures ANOVA (work intensity × time) comparisons of means were used to determine significant differences. Pairwise post-hoc contrasts were used to determine where significant differences occurred. The 0.05 level was used for statistical significance. The analyses were done with SuperANOVA (Abacus Concepts, Inc.; Berkeley, CA), a statistical package for the MacIntosh computer. All data are presented as mean ± SE.

RESULTS

At rest, no significant differences were observed between <LT and >LT for whole blood, plasma, or RBC [La]. Similarly, the [La] gradient from plasma to RBCs at rest before <LT (0.68 ± 0.10 mM) did not differ significantly from the gradient observed before >LT (0.78 ± 0.11 mM). The RBC:plasma[La] ratio at rest also was not different between <LT and >LT (0.56± 0.07 vs 0.52 ± 0.05).

During <LT whole blood, plasma, and RBC lactate concentrations increased significantly above resting values by minute 2 and reached peak values by min 6 (1.96 ± 0.25 mM, 2.38 ± 0.30 mM, and 1.38 ± 0.21 mM, respectively). These responses are illustrated in Figure 1. After 20 min of <LT, whole blood, plasma, and RBC lactate concentrations had declined at similar rates to levels that were not significantly different from the rest. As shown in Figure 2, the plasma to RBC [La] gradient during <LT rose significantly above the resting gradient and reached a peak after 4 min. The gradient declined but still remained significantly elevated over resting values until 15 min of <LT were completed. From 20 to 30 min, the gradient was not significantly different from its resting level. The RBC:plasma[La] ratio was never different from the resting value at any time during the 30 min of <LT.

Figure 1
Figure 1:
Whole blood [La](a), and plasma and RBC [La] (b) during 30 min of steady-state exercise at <LT and >LT. * represents a significant increase above the rest value (zero time point) within each measurement (P < 0.05). All [La] values were significantly different between <LT and >LT for each measurement type (i.e., whole blood, plasma, and RBC [La]) throughout the 30 min of exercise (P < 0.05). Lactate concentration values at rest were not significantly different between <LT and >LT.
Figure 2
Figure 2:
Plasma to RBC [La] gradient during 30 min of <LT and >LT. * represents a significant increase above the rest value (zero time point) within each exercise intensity (P < 0.05). † represents a significant difference between values for <LT vs >LT (P < 0.05).

Greater than LT resulted in elevations in whole blood, plasma, and RBC lactate concentrations that were significantly greater than those occurring during <LT; these responses are shown in Figure 1. Whole blood [La] after 2 min of >LT (3.1 ± 0.5 mM) was significantly greater than the resting concentration(1.3 ± 0.2 mM). Whole blood [La] continued to rise and reached its highest value after 10 min of >LT (7.1 ± 0.91 mM). As the moderate intensity exercise continued, whole blood [La] declined slightly over the remainder of the exercise session to 5.39 ± 0.35 mM after the entire 30 min of exercise. As shown in Figure 1, plasma and RBC lactate concentrations rose to peak values after 8-10 min of >LT (plasma = 8.75 ± 1.07 mM and RBC = 4.81 ± 0.68 mM). These values were approximately five times greater than the concentrations observed under resting conditions (1.66 ± 0.20 mM and 0.88 ± 0.14 mM for plasma and RBCs, respectively). Thus, the plasma to RBC [La] gradient likewise increased approximately 5-fold from 0.78 ± 0.11 mM to 4.0 ± 0.45 mM during >LT as shown in Figure 2. However, since the increases in plasma and RBC lactate concentrations occurred at the same relative rate, there was no significant change in the RBC:plasma ratio during the 30 min of >LT.

Figure 3 shows the plasma and RBC [H+] responses to both <LT and >LT. No significant difference was observed in either the plasma [H+] or RBC [H+] between treatment groups before steady-state exercise. At rest the mean plasma [H+] was 40.0 ± 0.4 nM (pH = 7.398 ± 0.005) and mean RBC [H+] was 65.7 ± 0.8 nM (pH = 7.183 ± 0.005). Plasma [H+] and RBC [H+] during steady-state exercise sessions differed significantly between <LT and >LT as soon as 2 min into the sessions and remained different throughout the entire 30-min duration. Above LT, steady-state exercise resulted in significantly larger increases in both plasma and RBC [H+] than did <LT. During <LT, plasma [H+] was significantly greater than rest at 2 min (41.0 ± 0.6 nM; pH = 7.387 ± 0.006) and RBC [H+] was significantly above rest at 4 min (67.2 ± 1.2 nM; pH = 7.173 ± 0.008). After plasma [H+] reached its peak of 42.8 ± 0.8 nM (pH = 7.368 ± 0.008) at 6 min and RBC pH reached a high point of 67.7 ± 1.3 nM (pH = 7.170 ± 0.008) at 6 min, both plasma and RBC [H+] gradually decreased toward resting levels. After only 8 min of <LT, RBC [H+] was back to pre-exercise levels; however, plasma [H+] did not return to pre-exercise levels even after 30 min (40.7 ± 0.4 nM) of <LT. However, despite the significant differences that were found, the absolute magnitude of [H+] change observed in <LT was small.

Figure 3
Figure 3:
Plasma and RBC [H+] during 30 min of <LT and >LT. * represents a significant increase above the rest value (zero time point) within each exercise intensity (P < 0.05). † represents a significant difference between values for <LT vs >LT (P < 0.05).

During>LT, plasma [H+] and RBC [H+] increased significantly from resting levels after only 2 min and then increased further to peaks of 47.6± 1.1 nM (pH = 7.323 ± 0.007) at 10 min for plasma [H+] and 75.4 ± 1.9 nM (pH = 7.123 ± 0.011) at 8 min for RBC [H+]. Thereafter, both plasma and RBC [H+] gradually decreased toward resting values. Although RBC [H+] was no longer significantly higher than resting levels after 25 min, plasma [H+] was still significantly higher than resting values after 30 min (42.7 ± 0.6 nM, pH = 7.370 ± 0.006).

Despite changing [H+] in the plasma and RBC during<LT and >LT, the distribution of H+ within the blood was not affected by either steady-state intensity. The plasma [H+]:RBC [H+] ratio did not change significantly from rest during either <LT or >LT, remaining near 0.63.

DISCUSSION

The new information provided by the present study consists of the lactate concentrations of the plasma versus RBC fractions of the blood during submaximal steady-state exercise. We hypothesized that exercise above LT might result in a greater rate of increase in plasma [La] as compared with RBC [La] and therefore an increase in the plasma to RBC [La] gradient and a decrease in the RBC:plasma [La] ratio. This was not the case. There was an increase in the plasma to RBC [La] gradient at both exercise intensities; the increased gradient was larger and more prolonged during>LT steady-state exercise as compared with <LT exercise. However, the relative increases in both the plasma and RBC lactate concentrations were similar such that even for >LT exercise, there was no change in the RBC:plasma [La] ratio. This ratio averaged about 0.58 for all measurements, a value that is within the range reported by others (4-6,12,15,16,18).

These data for steady-state submaximal exercise are generally similar to data previously reported by Foxdal et al. (12) and Smith et al. (22) from our laboratory. Both these investigations studied the lactate distribution in blood during progressive incremental exercise; Foxdal et al. (12) used a work rate increment duration of 5 min, whereas we (22) employed two protocols, one with an increment duration of 4 min and a second with an increment duration of 1 min. In both studies (12,22), the plasma to RBC [La] gradient increased with increasing work rate above the LT (i.e., when whole blood [La] increased above resting levels). However, equilibration of plasma and RBC lactate concentrations was suggested by the fact that the RBC:plasma [La] ratio was never significantly different from the resting value in either of the studies. Overall, these observations suggest that there is adequate time for exchange of lactate between plasma and RBCs in either progressive incremental exercise or at the onset of submaximal constant work rate exercise, regardless of whether the intensity is above or below the LT. These results are also consistent with the notion of lactate distribution according to Donnan equilibrium(3,11,13,15,17). This is further reinforced by the finding of a constant plasma:RBC [H+] ratio throughout both steady-state exercise protocols as well.

Our finding of a larger and more prolonged change in [H+] during the moderate intensity steady state was not surprising since the rate of lactic acid production and entry into the blood during >LT exercise is greater than with <LT exercise. We proposed that lactate transport across the RBC membrane might limit the entry rate of lactate into RBCs. If this occurred, then [La] in the plasma would increase out of proportion to the increase in RBC [La], resulting in a decrease in the RBC:plasma[La] ratio. Under such conditions, lactate might be considered an impermeant anion that would influence the Donnan equilibrium and possibly alter the distribution of small cations such as H+ across the RBC membrane. However, since the lactate distribution ratio did not change from rest during either <LT or >LT exercise, we also did not observe a change in the H+ distribution in the blood.

In interpreting lactate distribution in the blood, two practical experimental issues should be emphasized. First, immediately upon collection of blood samples, exchange of lactate between plasma and RBCs must be minimized. Arrest of lactate exchange can be accomplished by immediate, rapid centrifugation (18) or by rapid cooling followed by centrifugation as in the current study. In practical terms, blood sampling as typically performed allows time for considerable exchange of lactate between plasma and RBCs. A second important consideration is the fact that blood was sampled from a forearm vein during leg exercise in the present study. During circulation of the blood from the legs to the forearm vein, lactate can be taken up from the plasma into RBCs, allowing partial, if not complete, equilibration of lactate across the RBC membrane according to Donnan equilibrium.

In summary, lactate is unequally distributed between the plasma and RBCs at rest. During constant metabolic rate exercise, the [La] gradient from plasma to RBCs increases, particularly at work rates above the LT. Despite this increase in the plasma to RBC[La] gradient, unchanging ratios of RBC:plasma [La] and plasma:RBC[H+] suggest that lactate is equilibrated between the plasma and RBCs. During leg exercise, some time elapses before blood draining those exercising muscles affects metabolite concentrations at a distant blood collection site such as a forearm vein. During this circulation time, the lactate transport pathways across the RBC membrane are apparently able to distribute lactate between the plasma and RBCs according to the Donnan equilibrium. Under this equilibrium, the majority of the increase in blood [La] is carried in the plasma, whereas a greater amount of the [H+] increase is sequestered inside the RBCs.

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Keywords:

LACTATE THRESHOLD; LACTATE TRANSPORT; RED BLOOD CELLS

©1998The American College of Sports Medicine