Venous and capillary blood hematocrit at rest and following submaximal exercise.

The purpose of this study was to determine if finger tip capillary blood hematocrit is a valid estimate of anticubital venous blood hematocrit at rest and after submaximal exercise. Simultaneous samples of finger tip cpaillary and venous blood were drawn from thirty-one subjects (15 males, 16 females) before and after a 15 min submaximal exercise on a bicycle ergometer. Venous and capillary blood hcts. were 42.0% +/- 3.9 and 42.0% +/- 3.5 respectively before exercise and 43.3% +/- 3.5 and 42% +/- 3.8 after exercise (X +/- s). The regression equation for predicting venous hct. from finger tip capillary blood after exercise was: Hctv = 0.87 Hctc + 6.44 with r = 0.95 (P less than 0.05). The results indicate that the finger tip capillary microhematocrit method is a valid indicator of venous blood hct. following exercise.     

The effect of different blood sampling sites and analyses on the relationship~ between exercise intensity and 4.0 mmol ·1? blood lactate concentration

The aim of the study was to examine whether the difference in lactate concentration in different blood fractions is of practical importance when using blood lactate as a test variable of aerobic endurance capacity. Ten male firefighters performed submaximally graded exercise on a cycle ergometer for 20-25 min. Venous and capillary blood samples were taken every 5 min for determination of haematocrit and lactate concentrations in plasma, venous and capillary blood. At the same time, expired air was collected in Douglas bags for determination of the oxygen consumption. A lactate concentration of 4.0 mmol.l-1 was used as the reference value to compare the oxygen consumption and exercise intensity when different types of blood specimen and sampling sites were used for lactate analysis. At this concentration the exercise intensity was 17% lower (P less than 0.01) when plasma lactate was compared to venous blood lactate, and 12% lower (P less than 0.05) when capillary blood lactate was used. Similar discrepancies were seen in oxygen consumption. The results illustrated the importance of standardizing sampling and handling of blood specimens for lactate determination to enable direct comparisons to be made among results obtained in different studies.     

Exercise alters the distribution of ammonia and lactate in blood

Six subjects (3 males, 3 females) worked for 4 min on a cycle ergometer at 115% of peak O2 uptake (VO2). Venous samples drawn before, directly after, and 15 min after exercise were analyzed for ammonia (NH3) and lactate concentrations of plasma, whole blood, and erythrocytes (RBCs) to examine the effect of exercise on blood NH3 and lactate distribution. Exercise increased (P less than 0.05) the [NH3] of plasma and RBCs, with the larger (P less than 0.05) change in plasma (1.8- vs. 0.7-fold). This reduced (P less than 0.05) the RBC-to-plasma [NH3] ratio of 2.4 at rest to 1.3. The plasma-to-RBC [lactate] gradient (P less than 0.05) at rest (0.5 mmol/l) increased (P less than 0.05) 16-fold immediately after exercise (8.7 mmol/l), reflecting the greater increase (P less than 0.05) in plasma than RBCs [lactate] (15.5 vs. 7.5 mmol/l). [Lactate] and [NH3] did not decrease (P greater than 0.05) immediately after to 15 min after exercise. Plasma and whole blood [NH3] or [lactate] were correlated (r greater than 0.93, P less than 0.01) at all sample times, but the slopes of the relations for [NH3] (immediately after vs. 15 min after exercise) or for [lactate] (before and immediately after vs. 15 min after exercise) differed (P less than 0.05). The results indicate that supramaximal exercise alters the distribution of NH3 and lactate between plasma and RBC, thus changing the relations between plasma and whole-blood concentrations of these metabolites. The alteration of NH3 distribution may reflect changes in the pH gradient between plasma and RBCs.     

Plasma [H+] regulation and whole blood [CO2] in exercising ponies

The major objective was to determine in ponies whether factors in addition to changes in blood PCO2 contribute to changes in plasma [H+] during submaximal exercise. Measurements were made to establish in vivo plasma [H+] at rest and during submaximal exercise, and CO2 titration of blood was completed for both in vitro and acute in vivo conditions. In 19 ponies arterial plasma [H+] was decreased from rest 4.5 neq/l (P less than 0.05) during the 7th min of treadmill running at 6 mph, 5% grade (P less than 0.5). A 5.6-Torr exercise hypocapnia accounted for approximately 2.9 neq/l of this reduced [H+]. The non-PCO2 component of this alkalosis was approximately neq/l, and it was due presumably to a 1.7-meq/l increase from rest in the plasma strong ion difference (SID). Despite the arterial hypocapnia, mixed venous PCO2 was 2.7 Torr above rest during steady-state exercise. Nevertheless, mixed venous plasma [H+] was 1.2 neq/l above rest during exercise, which was presumably due to the increase in SID. Also studied was the effect of submaximal exercise on whole blood CO2 content (CCO2). In vitro, at a given PCO2 there was minimal difference in CCO2 between rest and exercise blood, but plasma [HCO3-] was greater for exercise blood than for rest blood. In vivo, during steady-state exercise, arterial plasma blood. In vivo, during steady-state exercise, arterial plasma [HCO3-] was unchanged or slightly elevated from rest, but CaCO2 was 4 vol% below rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peak blood ammonia and lactate after submaximal, maximal and supramaximal exercise in sprinters and long-distance runners

The purpose of this study was to elucidate the difference in peak blood ammonia concentration between sprinters and long-distance runners in submaximal, maximal and supramaximal exercise. Five sprinters and six long-distance runners performed cycle ergometer exercise at 50% maximal, 75% maximal, maximal and supramaximal heart rates. Blood ammonia and lactate were measured at 2.5, 5, 7.5, 10 and 12.5 min after each exercise. Peak blood ammonia concentration at an exercise intensity producing 50% maximal heart rate was found to be significantly higher compared to the basal level in sprinters (P less than 0.01) and in long-distance runners (P less than 0.01). The peak blood ammonia concentration of sprinters was greater in supra-maximal exercise than in maximal exercise (P less than 0.05), while there was no significant difference in long-distance runners. The peak blood ammonia content after supramaximal exercise was higher in sprinters compared with long-distance runners (P less than 0.01). There was a significant relationship between peak blood ammonia and lactate after exercise in sprinters and in long-distance runners. These results suggest that peak blood ammonia concentration after supramaximal exercise may be increased by the recruitment of fast-twitch muscle fibres and/or by anaerobic training, and that the processes of blood ammonia and lactate production during exercise may be strongly linked in sprinters and long-distance runners.     

Determinants of endurance in well-trained cyclists

Fourteen competitive cyclists who possessed a similar maximum O2 consumption (VO2 max; range, 4.6-5.0 l/min) were compared regarding blood lactate responses, glycogen usage, and endurance during submaximal exercise. Seven subjects reached their blood lactate threshold (LT) during exercise of a relatively low intensity (group L) (i.e., 65.8 +/- 1.7% VO2 max), whereas exercise of a relatively high intensity was required to elicit LT in the other seven men (group H) (i.e., 81.5 +/- 1.8% VO2 max; P less than 0.001). Time to fatigue during exercise at 88% of VO2 max was more than twofold longer in group H compared with group L (60.8 +/- 3.1 vs. 29.1 +/- 5.0 min; P less than 0.001). Over 92% of the variance in performance was related to the % VO2 max at LT and muscle capillary density. The vastus lateralis muscle of group L was stressed more than that of group H during submaximal cycling (i.e., 79% VO2 max), as reflected by more than a twofold greater (P less than 0.001) rate of glycogen utilization and blood lactate concentration. The quality of the vastus lateralis in groups H and L was similar regarding mitochondrial enzyme activity, whereas group H possessed a greater percentage of type I muscle fibers (66.7 +/- 5.2 vs. 46.9 +/- 3.8; P less than 0.01). The differing metabolic responses to submaximal exercise observed between the two groups appeared to be specific to the leg extension phase of cycling, since the blood lactate responses of the two groups were comparable during uphill running. These data indicate that endurance can vary greatly among individuals with an equal VO2 max.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epinephrine-induced changes in muscle carbohydrate metabolism during exercise in male subjects

Epinephrine increases glycogenolysis in resting skeletal muscle, but less is known about the effects of epinephrine on exercising muscle. To study this, epinephrine was given intraarterially to one leg during two-legged cycle exercise in nine healthy males. The epinephrine-stimulated (EPI) and non-stimulated (C) legs were compared with regard to glycogen, glucose, glucose 6-phosphate (G6P), alpha-glycerophosphate (alpha-GP), and lactate contents in muscle biopsies taken before and after the 45-min submaximal exercise, as well as brachial arterial-femoral venous (a-fv) differences for epinephrine, norepinephrine, lactate, glucose, and O2 during exercise. During exercise the arterial plasma epinephrine concentration was 4.8 +/- 0.8 nmol/l and the femoral venous epinephrine concentrations were 10.3 +/- 2.1 and 3.9 +/- 0.6 nmol/l, respectively, in the EPI and C leg. During exercise the a-fv difference for lactate was greater (-0.41 +/- 0.14 vs. -0.21 +/- 0.14 mmol/l; P less than 0.001), and the a-fv difference for glucose was smaller (0.07 +/- 0.12 vs. 0.24 +/- 0.12 mmol/l; P less than 0.01) in the EPI than in the C leg, but the a-fv differences for O2 were similar. Muscle glycogen depletion (137 +/- 63 vs. 99 +/- 43 mmol/kg dry muscle; P less than 0.1) and the muscle concentrations of glucose (P less than 0.05), alpha-GP (P less than 0.1), G6P (P greater than 0.1), and lactate (P greater than 0.1) tended to be higher in the EPI than the C leg after exercise. These findings suggest that physiological concentrations of epinephrine may enhance muscle glycogenolysis during submaximal exercise in male subjects.     

Effects of supramaximal exercise on blood glucose levels during a subsequent exercise

The purpose of the present investigation was to examine the effects of hyperglycemia induced by supramaximal exercise on blood glucose homeostasis during submaximal exercise following immediately after. Six men were subjected to three experimental situations; in two of these situations, 3 min of high-intensity exercise (corresponding to 112, SD 1% VO2max) was immediately followed by either a 60-min period of submaximal exercise (68, SD 2% VO2max) or a 60-min resting period. In the third situation, subjects performed a 63-min period of submaximal exercise only. There were no significant differences between the heart rates, oxygen uptakes, and respiratory exchange ratios during the two submaximal exercise bouts (greater than 15 min) whether or not preceded by supramaximal exercise. The supramaximal exercise was associated within 10 min of the start increases (P less than 0.05) in blood glucose, insulin, and lactate concentrations. This hyperglycemia was more pronounced when subjects continued to exercise submaximally than when they rested (at 7.5 min; P less than 0.05). There was a more rapid return to normal exercise blood glucose and insulin values during submaximal exercise compared with rest. The data show that the hyperinsulinemia following supramaximal exercise is corrected in between 10-30 min during submaximal exercise following immediately, suggesting that this exercise combination does not lead to premature hypoglycemia.     

Differences between lactate concentration of samples from ear lobe and the finger tip

Blood lactate concentrations in capillary samples obtained from the ear lobe or from the finger tip are used indistinctly, since they are considered equivalents. The aim of the study reported in this paper was to verify whether that assumption is valid due to the practical implications which any possible differences between these two sampling sites would have in the planning and assessing of an athletic training program. Twenty six healthy male athletes competing in different sports at the national level (9 rowers, 7 cyclists and 10 runners) were studied during the performance of a graded exercise test up to the point of exhaustion, on specific ergometers. In each group, capillary blood samples were obtained simultaneously from both the ear lobe and the finger tip at three different times during the test: 1) in resting conditions; 2) when exercising at a submaximal work load and 3) seven minutes after the point of exhaustion. Significant differences were found between the blood lactate concentrations of samples obtained from the ear lobe and from the finger tip (p < 0.001). The method error of repeated measurements for lactate concentrations from paired samples obtained in resting conditions was 27%, when exercising at a submaximal work load, 16% and at maximal work load, 3%. Capillary blood samples collected from the finger tip consistently showed higher values in lactate concentration than those obtained, at the same time, from the ear lobe.     

Skeletal muscle metabolism during exercise is influenced by heat acclimation

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.     

Effects of feeding on muscle blood flow during prolonged exercise in miniature swine

Eight exercise-trained miniature swine were studied during prolonged treadmill runs (100 min) under fasting and preexercise feeding conditions. Each animal ran at identical external work loads that corresponded to 65% of the heart rate reserve (210-220 beats/min) for the two exercise bouts. Cardiac outputs and stroke volumes were higher and heart rates lower for fed than for fasting runs (P less than 0.05). Preexercise feeding did not alter oxygen consumption, core temperature, mean arterial pressure, and arterial-mixed venous oxygen difference during prolonged exercise; however, mixed venous lactate concentration was lower at end exercise than during fasting conditions (1.2 vs. 2.6 mM, P less than 0.05). Microsphere measurements of regional blood flow revealed significantly higher total gastrointestinal flow (23%) for fed than for fasting conditions. Throughout the exercise bout, blood flow to the biceps femoris, semitendinosus, and tibialis anterior muscles was lower in fed than in fasted animals (P less than 0.05). Combined hindlimb muscle blood flow averaged 15 ml.min-1.100 g-1 (18%, P less than 0.05) lower under feeding than fasting run conditions. These findings provide further evidence that cardiovascular reflexes originate in the gut after feeding to increase cardiac output and redistribute a portion of the blood flow away from active muscle to the gastrointestinal tract during prolonged exercise.     

Hyperammoniemia during prolonged exercise: an effect of glycogen depletion?

Eight healthy men exercised to exhaustion on a cycle ergometer at a work load of 176 +/- 9 (SE) W corresponding to 67% (range 63-69%) of their maximal O2 uptake (exercise I). Exercise of the same work load was repeated after 75 min of recovery (exercise II). Exercise duration (range) was 65 (50-90) and 21 (14-30) min for exercise I and II, respectively. Femoral venous blood samples were obtained before and during exercise and analyzed for NH3 and lactate. Plasma NH3 was 12 +/- 2 and 19 +/- 6 mumol/l before exercise I and II, respectively and increased during exercise to exhaustion to peak values of 195 +/- 29 (exercise I) and 250 +/- 30 (exercise II) mumol/l, respectively. Plasma NH3 increased faster during exercise II compared with exercise I and at the end of exercise II was threefold higher than the value for the corresponding time of exercise I (P less than 0.001). Blood lactate increased during exercise I and after 20 min of exercise was 3.7 +/- 0.4 mmol/l and remained unchanged until exhaustion. During exercise II blood lactate increased less than during exercise I. It is concluded that long-term exercise to exhaustion results in large increases in plasma NH3 despite relatively low levels of blood lactate. It is suggested that the faster increase in plasma NH3 during exercise II (vs. exercise I) reflects an increased formation in the working muscle that may be caused by low glycogen levels and impairment of the ATP resynthesis.     

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

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 less than 0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p greater than 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 less than 0.01). Although plasma lactate values during alkalosis were consistently elevated above control there was no significant difference in the linear trend (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

Time course of muscular blood metabolites during forearm rhythmic exercise in hypoxia

O2 concentration, PO2, PCO2, pH, osmolarity, lactate (LA), and hemoglobin (Hb) concentrations in deep forearm venous blood were repeatedly measured during submaximal exercise of forearm muscles. Concentrations of arterial blood gases were determined at rest and during exercise. Experiments were conducted under normoxia and hypobaric hypoxia (PB = 465 Torr). In arterial blood, data obtained during exercise were the same as those obtained during rest under either normoxia or hypoxia. In venous muscular blood, PO2 and O2 concentration were lower at rest and during exercise in hypoxia. The muscular arteriovenous O2 difference during exercise in hypoxia was increased by no more than 10% compared with normoxia, which implied that muscular blood flow during exercise also increased by the same percentage, if we assume that exercise O2 consumption was not affected by hypoxia. Despite increased [LA], the magnitude of changes in PCO2 and pH in hypoxia were smaller than in normoxia during exercise and recovery; this finding is probably due to the increased blood buffer value induced by the greater amount of reduced Hb in hypoxia. Hence all the changes occurring in hypoxia showed that local metabolism was less affected than we expected from the decrease in arterial PO2. The rise in [Hb] that occurred during exercise was lower in hypoxia. Possible underlying mechanisms of the [Hb] rise during exercise are discussed.     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man.

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects (VO2max = 53.0 +/- 2.0 mL.kg-1.min-1, mean +/- SE) for 10-12 days with each exercise session lasting for 2 h at an average intensity of 59% of VO2max. This training protocol resulted in reductions (p less than 0.05) in blood lactate concentration (mM) at 15 min (2.96 +/- 0.46 vs. 1.73 +/- 0.23), 30 min (2.92 +/- 0.46 vs. 1.70 +/- 0.22), 60 min (2.96 +/- 0.53 vs. 1.72 +/- 0.29), and 90 min (2.58 +/- 1.3 vs. 1.62 +/- 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p less than 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p less than 0.05) were observed for blood beta-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p less than 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p less than 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.     

Effect of dichloroacetate on lactate concentration in exercising humans

The precise mechanism responsible for the increase in plasma lactate concentration during exercise in humans is not known. We have used dichloroacetate to test the hypothesis that a limitation in pyruvate dehydrogenase activity is responsible for the rise in plasma lactate. Dichloroacetate stimulates the activity of pyruvate dehydrogenase, which is normally the regulatory enzyme in the oxidation of glucose when tissue oxygenation is adequate. Six subjects were studied twice according to a randomized, crossover protocol, involving one test with saline infusion and another with dichloroacetate infusion. Exercise load on a bicycle ergometer was increased progressively until exhaustion. Blood samples were drawn each minute throughout exercise and periodically throughout 120 min of recovery. Dichloroacetate significantly lowered the lactate concentration during exercise performed at less than 80% of the average maximal O2 consumption. The peak concentration of lactate at exhaustion was not affected by dichloroacetate treatment, but dichloroacetate did lower lactate concentration throughout recovery. These results suggest that a limitation in pyruvate dehydrogenase activity contributes to the increase in plasma lactate during submaximal exercise and recovery.     

Contribution of erythrocytes to the control of the electrolyte changes of exercise

Five healthy males performed four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Arterial and femoral venous blood was sampled during and for 90 min following exercise. During exercise, arterial erythrocyte [K+] increased from 117.0 +/- 6.6 mequiv./L at rest to 124.2 +/- 5.9 mequiv./L after the second exercise bout. Arterial erythrocyte [K+] returned to the resting values during the first 5 min of recovery. No significant change was observed in femoral venous erythrocyte [K+]. Arterial erythrocyte lactate concentration ([Lac-]) increased during exercise from 0.2 +/- 0.1 mequiv./L peaking at 9.5 +/- 1.5 mequiv./L at 5 min of recovery, after which the values returned to control. Femoral venous erythrocyte [Lac-] changed in a similar fashion. Arterial erythrocyte [Cl-] rose during exercise to 76 +/- 3 mequiv./L and returned to resting values (70 +/- 2 mequiv./L) by 25 min recovery. During exercise there was a net flux of Cl- into the erythrocyte. We conclude that erythrocytes are a sink for K+ ions leaving working muscles. Furthermore, erythrocytes function to transport Lac- from working muscle and reduce plasma acidosis by uptake of Cl-. The erythrocyte uptake of K+, Lac-, and Cl- helps to maintain a concentration difference between plasma and muscle, facilitating diffusion of Lac- and K+ from the interstitial space into femoral venous plasma.     

Erythrocyte ion regulation across inactive muscle during leg exercise.

Ion concentration changes in whole blood, plasma, and erythrocytes across inactive muscle were examined in eight healthy males performing four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Blood was sampled from the arm brachial artery and deep antecubital vein during the intermittent exercise period and for 90 min of recovery. Arterial and venous erythrocyte lactate concentration ([Lac-]) increased from 0.3 +/- 0.1 to 12.5 +/- 1.3 (p < 0.01) and 1.1 +/- 0.4 to 8.5 +/- 1.5 mmol/L (p < 0.01), respectively, returning to control values during recovery. Arterial and venous plasma [Lac-] increased from 1.5 +/- 0.2 to 27.7 +/- 1.8 and from 1.3 +/- 0.4 to 25.7 +/- 3.5 mmol/L, respectively, and was greater than erythrocyte [Lac-] throughout exercise and recovery. Arterial and venous [K+] increased in erythrocytes from 119.5 +/- 5.1 to 125.4 +/- 4.6 (p < 0.01) and from 113.6 +/- 1.7 to 120.6 +/- 7.1 mmol/L, respectively, decreasing to control during recovery. In arterial and venous plasma, [K+] increased from 4.3 +/- 0.1 to 6.1 +/- 0.2 (p < 0.01) and from 4.5 +/- 0.2 to 5.3 +/- 0.2 mmol/L (p < 0.01), respectively, decreasing to control during recovery. The efflux of Lac- out of erythrocytes against an electrochemical concentration gradient suggests the presence of an active transport system. Efflux of K+ from erythrocytes as blood passes across inactive muscle affords an important adaptation to the K+ release from muscle activated in heavy exercise.