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Am J Physiol Regul Integr Comp Physiol 276: R184-R188, 1999;
0363-6119/99 $5.00
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Vol. 276, Issue 1, R184-R188, January 1999

Potassium fluxes in contracting human skeletal muscle and red blood cells

C. Juel, Y. Hellsten, B. Saltin, and J. Bangsbo

Copenhagen Muscle Research Centre, August Krogh Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark

    ABSTRACT
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Abstract
Introduction
Methods
Results
Discussion
References

The present study examined K+ fluxes in red blood cells and muscle during muscle contractions. Seven subjects performed two-legged submaximal knee-extensor exercise for 30 min. After 10 min of leg exercise (L1), intense arm exercise was also performed for 10 min (L2+A). Plasma epinephrine and norepinephrine concentrations were higher (P < 0.05) in L2+A compared with L1. Arterial plasma K+ at the end of L2+A was higher than in L1 (5.6 vs. 4.4 mM, P < 0.05) and returned to the L1 level on cessation of arm exercise. A net K+ release of 0.16 mmol/min from the active legs during L1 was turned to a net K+ uptake of 0.79 mmol/min during L2+A. Both arterial and venous red blood cell K+-to-hemoglobin ratios were constant during exercise. The present data suggest that contracting muscle can take up K+ probably by a combination of K+ and hormone activation of the Na+-K+ pump. Furthermore, changes in red blood cell K+ concentrations during muscle activity appear to be due to water movements and not transmembrane fluxes of K+.

catecholamines; sodium-potassium pump; blood flow

    INTRODUCTION
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Abstract
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Methods
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Discussion
References

SKELETAL MUSCLE contractile activity is associated with a flux of K+ from muscle to blood, which is related to the frequency of action potentials (7). This outward-directed K+ flux across sarcolemma is mainly due to the activity of the voltage-dependent K+ channels associated with the action potentials, but ATP-dependent (9) and Ca2+-dependent K+ channels may also be involved. The main part of the K+ released is immediately taken up by the contracting fibers, but a minor fraction is lost to the blood. It is generally accepted that the net release from muscle to blood is due to an insufficient K+ reuptake mediated by the catecholamine-sensitive sarcolemmal Na+-K+-ATPase, which is either inadequately activated or the maximal capacity is reached (7). It is well known that inactive muscle take up K+ in periods of elevated blood K+ concentration; however, it is unclear whether exercising muscle can take up K+.

K+ released to the blood accumulates in plasma. There have been some conflicting reports regarding the magnitude of K+ uptake in red blood cells (RBCs). It was found that the arterial RBC K+ concentration (calculated from whole blood and plasma K+ as well as hematocrit) increased by 6-7 mmol/l at the end of two intense exercise bouts (16, 19). Based on the estimated increase in arterial RBC K+, it was concluded that RBC store a large fraction of the K+ released from active muscle (17, 19) and that no significant RBC volume changes took place (16, 20). In contrast, other studies have observed changes in RBC volume (25) and only minor changes in RBC K+ during muscle activity (15, 25). K+ uptake by RBC during muscle contractions could be mediated by the Na+-K+ pump or the Na+-K+-2Cl- cotransporter. The Na+-K+ pump in human RBCs is sensitive to the internal Na+ concentration (22), which may be affected by an increased activity of the Na+/H+ exchanger caused by the acidification during intense muscle contraction, and the possibility exists that the pump is stimulated by catecholamines. The Na+-K+-2Cl- cotransporter is sensitive to catecholamines, K+, osmolality, cellular Na+, and pH (5, 12). Thus K+ uptake in RBCs may be triggered by a combination of elevated K+, osmolality, catecholamines, and lowered pH. However, the role of such factors for the K+ balance in RBCs is unknown.

Thus the aim of the present study was to examine K+ exchange in exercising muscles and RBCs during leg exercise at different levels of arterial K+, epinephrine, norepinephrine, and acidification (created by additional arm exercise). Part of the results from the present study have been reported previously with a specific focus on muscle pH regulation (3).

    METHODS
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Methods
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Subjects. Seven healthy male subjects ranging in age from 24 to 27 yr with an average height of 182 (range 178-188) cm and an average body mass of 72.4 (range 66.1-82.3) kg participated in the experiments. The subjects were fully informed of any risk and discomfort associated with the experiment before giving their oral consent to participate. The study was approved by the local ethics committee.

Procedure. The subjects performed two-legged knee-extensor exercise on an ergometer in the sitting position, which permitted the exercise to be confined to the quadriceps muscles. They also performed a period of arm cranking.

About 1 h before the experiment, catheters were placed in the femoral artery of the right leg under local anesthesia. The tip of the catheter was positioned about 1-2 cm proximal to the inguinal ligament. Another catheter was placed in the femoral vein of the right leg with the tip of the catheter positioned about 1-2 cm distal to the inguinal ligament. A thermistor for measurements of venous blood temperature was inserted through the catheter and was advanced 8-10 cm proximal to the tip.

The subjects performed two-legged knee-extensor exercise at an intensity of 10 W for 5 min as a warming up exercise. The kicking frequency was 1 Hz. This was immediately followed by a 10-min period (L1, Fig. 1) at an intensity of 36 ± 1.6 W (mean ± SE, each leg), and after that arm exercise was added to the leg exercise (L2+A). The arm cranking started without external load (1 Hz), and the power output was increased stepwise by 58 W each 0.5 min for 1.5-2.5 min; thereafter, the intensity of the arm exercise was maintained constant (167.1 ± 6.2 W) until the total duration of the arm exercise was 6 min. Next, the arm exercise was increased by an intensity of 29 W each minute until the subject was unable to maintain the frequency (~4 min). The final intensity was 240.4 ± 14.3 W. After the arm exercise, the subjects maintained the leg exercise for another 10 min, still at an intensity of 36.0 ± 1.3 W (L3; Fig. 1).


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  		Fig. 1.   Schematic representation of the experimental design. Two-legged knee-extensor exercise at a constant intensity (72 W) was performed in L1 (10 min of leg exercise), L2+A (L1 followed by intense arm exercise), and L3 (L2+A plus an additional 10 min of leg exercise). Arrows and numbers indicate blood sampling and flow measurements.

Leg blood flow was measured immediately before blood sampling. An occlusion cuff placed below the knee was inflated just before and during the blood flow measurements, which were carried out by the thermodilution technique (1). Briefly, ice-cold saline was infused at a constant rate in the femoral vein for 10-15 s to achieve a blood temperature decrease of 0.8-1.0°C.

Heparinized syringes were used to draw blood simultaneously from the femoral artery and vein at rest, after 7.5 and 9.5 min of L1, after 3.5, 5.5, and ~9.5 min of L2+A, and after 0.5, 7.5, and 9.5 min of L3. The blood samples were placed in ice-cold water.

A part of the blood sample was immediately (within 15 s of sampling) separated from RBCs by centrifugation (35 s, 20,000 g, high acceleration) at room temperature. Plasma was stored at -20°C for later analysis, and samples of packed RBCs were obtained from the pellet after removal of the "buffy coat" and the upper layers of cells. Packed RBCs (3 × 10 µl) were hemolyzed in 1,990 µl water containing Triton X and centrifuged. The K+ content in the supernatant and in plasma was measured in a flame photometer (FLM3, Radiometer; each sample was run in triplicate). Hemoglobin (Hb) in the hemolysate and in whole blood was measured spectrophotometrically after addition of CN- reagent (11).

Catecholamines were measured according to Christensen (6). Blood lactate was analyzed using a lactate analyzer (model 23; Yellow Springs Instruments).

Calculations. The RBC K+ concentration was measured in samples of packed RBC and was corrected for external RBC no-water space (5%) and for plasma K+ in this trapped volume. Muscle K+ uptake was calculated as (arterial plasma K+ - venous plasma K+) × (leg blood flow) × (1 - hematocrit).

Statistics. Two-way analysis of variance was used for comparison between each part of the experiments (L1, L2+A, and L3). Student's paired t-test was used to locate the differences if data passed a normality test, otherwise a Wilcoxon rank test was used (SigmaStat). A significance level of 0.05 was chosen.

    RESULTS
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Abstract
Introduction
Methods
Results
Discussion
References

Leg blood flow, blood lactate, and pH. Leg blood flow before exercise of 0.46 ± 0.03 l/min increased (P < 0.05) to 4.84 ± 0.28 l/min during L1 and remained constant throughout the exercise periods (3). The arterial blood lactate concentration was 1.6 mmol/l at the end of L1, increased (P < 0.05) to 8.3 mmol/l during L2+A, and decreased (P < 0.05) to 6.6 mmol/l during L3. Arterial blood pH was 7.40 at rest, 7.38 at the end of L1, and reduced (P < 0.05) to 7.29 at the end of L2+A, whereas it was 7.32 at the end of L3.

Catecholamines. The plasma epinephrine and norepinephrine concentrations in L1 were not different from the values at rest (Table 1). Both plasma epinephrine and norepinephrine concentrations in L2+A were higher (P < 0.05) than in L1 and at the end of L3 (Table 1).

                              
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  		Table 1.   Arterial epinephrine and norepinephrine concentrations during submaximal knee-extensor exercise for 30 min

RBC K+ concentration and volume changes. The RBC K+ concentration in L1, L2+A, and L3 was ~2 mmol/l higher (P < 0.05) in arterial than femoral venous blood (Fig. 2A). The RBC K+ concentrations in neither arterial nor venous blood changed with time during exercise.


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  		Fig. 2.   A: red blood cell (RBC) K+ concentration during L1, L2+A, and L3. K+ content was measured in a fixed volume of sedimented (packed) cells, and the concentration was calculated per liter of cellular water. Values are means ± SE. Arterial RBC K+ content is higher (P < 0.05) than the venous RBC K+ content if all data are tested together; however, the single data pairs are not different. B: RBC hemoglobin (Hb) content during L1, L2+A, and L3. Hb content was measured in a fixed volume of packed cells. Values are means ± SE. Large SE values are due to interindividual variations. Arterial Hb content is higher (P < 0.05) than the venous Hb content if all data are tested together; however, the single data pairs are not different. C: ratio of RBC K+ to Hb content during L1, L2+A, and L3. Values are mean ± SE. Inset symbolizes the experimental procedure explained in legend to Fig. 1.

The Hb content of RBC measured in packed (sedimented) cells was ~0.5 mmol/l higher (P < 0.05) in arterial than venous blood (Fig. 2B). Changes in RBC Hb content indicate that volume changes took place through passage of the thigh muscle. To correct the measured RBC K+ concentration for these volume changes, the ratio of RBC K+ to Hb content was calculated. This ratio was not affected by exercise in neither arterial nor venous blood (Fig. 2C).

Plasma K+ and leg K+ exchange. Arterial plasma K+ increased (P < 0.05) from 3.98 mmol/l at rest to 4.38 mmol/l during L1 and to 5.56 mmol/l during L2+A and was reduced (P < 0.05) to 4.33 mmol/l during L3 (Fig. 3). Venous plasma K+ increased from 4.02 to 4.47 mmol/l during L1 and to 5.21 mmol/l during L2+A, after which it decreased to 4.43 mmol/l during L3. Thus leg plasma K+ arteriovenous (a-v) concentration difference was negative (P < 0.05) at the end of L1 (-0.09 ± 0.05 mmol/l), positive at the end of L2+A (0.35 ± 0.07 mmol/l), and negative at the end of L3 (-0.10 ± 0.04 mmol/l).


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  		Fig. 3.   Arterial and venous plasma K+ concentration during L1, L2+A, and L3. Inset symbolizes the experimental procedure explained in legend to Fig. 1. Values represent means ± SE. * Significant difference between arterial and venous plasma K+.

Leg K+ release (based on plasma values, as no fluxes of K+ between RBC and plasma occurred, see RBC K+ concentration and volume changes) at the end of L1 was 0.16 mmol/min. In L2+A, the uptake in the active leg was 0.79, 0.37, and 0.59 mmol/min after 3.5, 5.5, and 9.5 min, respectively, whereas the K+ release at the end of L3 was 0.24 mmol/min (Fig. 4).


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  		Fig. 4.   K+ uptake by the thigh of the exercising leg based on the individual plasma K+ concentrations and plasma flow. Values are means ± SE. Inset symbolizes the experimental procedure explained in legend to Fig. 1. * Significantly different from 0.

    DISCUSSION
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Abstract
Introduction
Methods
Results
Discussion
References

The main findings in the present study are that contracting skeletal muscle can take up K+ when arterial K+ and catecholamines are elevated and that the changes in K+ concentration in RBCs of arterial and venous blood during exercise are due to water shifts and not due to fluxes of K+ between RBCs and plasma.

K+ uptake in active muscles. Although the legs continued to exercise at the same intensity, the net K+ release turned to an uptake when arm exercise was added. The net rate of K+ uptake in the L2+A period even exceeded the net rate of K+ release in the L1 and L3 periods.

Part of the K+ uptake in the exercising leg may have occurred in inactive tissue. Bangsbo et al. (4) measured K+ uptake in a resting leg during contralateral one-legged (65 W) exercise supplemented with arm exercise. In that study, at arterial plasma K+ and catecholamine concentrations similar to the values at the end of L2+A of the present study, the K+ uptake in the thigh of the resting leg was 0.4 mmol/min. On the basis of these data, the inactive muscles of the active leg can be assumed to take up ~0.2 mmol/min. The exercise intensity of 36 W of each leg is expected to make up ~15% of the peak power output. Therefore, not all fibers and especially not all type II fibers were recruited. Because a fraction of the fibers are active during exercise, the K+ uptake in the resting fibers of the quadriceps muscles is expected to be lower than 0.2 mmol/min. With a total K+ uptake in the active leg in L2+A of 0.37-0.79 mmol/min, it is therefore likely that part of the K+ uptake took place in the active fibers. However, it is not possible from the present results to discriminate between uptake in passive and active fibers.

The theoretical maximal Na+-K+ pump capacity of a muscle is ~5 mmol · kg-1 · min-1 (7). The difference in K+ extrusion in the active leg between L1 (net K+ release) and L2+A (net K+ uptake) was maximally 0.95 mmol/min, which is equivalent to ~0.4 mmol · min-1 · kg-1 of muscle. Thus the reversal from net release to net K+ uptake from L1 to L2+A demands an increase in Na+-K+ pump activity of <10% of the maximal pump capacity. Therefore, the increase in K+ uptake is of a magnitude that can be handled by a moderate further activation of the pump. The question is what may have activated the pumps.

The Na+-K+ pump is mainly sensitive to cellular Na+ (22), whereas extracellular K+ is of minor importance. It has been reported that 20 and 50 mM of extracellular K+ increase the pump activity in rat skeletal muscle by only 16 and 28%, respectively (13). Thus the K+ increase (to 5.5 mM) during L2+A is likely to have only a minor effect on the pump, and the K+ increase alone can hardly explain the uptake in L2+A.

Although the pumps in contracting muscle are already active and the sensitivity to catecholamines is reduced compared with the sensitivity of resting muscles (14, 21, 24), the increased level of blood catecholamines during L2+A may induce a further activation of the pump (8), but other factors may also be important. It has been shown in rat muscle that excitation leads to a rapid and pronounced (up to 15-fold) stimulation of the pump (13). This stimulation is independent of an increase in bulk intracellular Na+ but may be induced by Na+ accumulated locally, close to the membrane. Of special interest for the present study is that K+ has been shown to release the calcitonin gene-related peptide (CGRP) from sensory and motor nerve terminals in skeletal muscle (23) and that CGRP is known to stimulate the Na+-K+ pump in skeletal muscle (2). Such a local stimulation of the Na+-K+ pump could contribute to the net K+ uptake in active leg in periods of elevated arterial K+.

Skeletal muscles could possess other transport systems mediating K+ fluxes. However, volume control in muscle is reported to be dependent on NaCl cotransport rather than Na+-K+-2Cl- cotransport known from other tissues (10); therefore, it is unlikely that K+ balance is influenced by such cotransporters.

In summary, the most likely explanation for the induction of the switch from leg K+ release to K+ uptake in the period in which arm exercise was added is probably a combination of increased arterial K+ and catecholamine concentrations.

K+ uptake in RBCs. The Hb content in a volume of packed RBC was found to be higher in arterial than venous samples (Fig. 3B) throughout the experiments. This indicates that the RBC volume is (approx 2%) lower in arterial than venous samples, as the Hb content per RBC is assumed to be constant through the time period investigated. The cause of this volume change is probably an osmotically induced water uptake due to bicarbonate accumulation in venous blood. This is in line with the observation of a 5- to 6-mmol/l higher bicarbonate concentration in venous compared with arterial blood in all phases of exercise (3) and is also in line with the observation that the bicarbonate a-v concentration difference was almost constant in periods with large concentration changes. The RBC K+ content was ~2 mmol/l higher (~2%) in arterial compared with venous blood, which is in agreement with the RBC volume increase during the passage of the muscle. Thus the positive RBC a-v K+ concentration difference is due to water fluxes rather than to a transmembrane K+ flux.

The observation that the RBC K+-to-Hb ratio is similar in venous and arterial blood throughout the 30 min of leg exercise (Fig. 2C) supports the conclusion that the RBC K+ concentration changes are due to water movements. In contrast, Lindinger et al. (16) and McKelvie et al. (19) reported a significant RBC K+ increase in arterial blood during exercise as well as an a-v K+ concentration difference. The main methodological difference is that the RBC K+ concentration in the present study was obtained from direct measurements of K+ content in a fixed volume of sedimented (packed) cells, whereas in their studies RBC K+ concentration was calculated from whole blood and plasma K+ content as well as Hct. Because Hct is influenced both by water movements from blood to tissue and by the RBC volume, this method can not be used to discriminate between concentration fluctuations due to volume changes and those due to transmembrane K+ fluxes. A resent paper by Maassen et al. (18) confirmed that RBC do not take up K+ in association with intense arm exercise.

The most likely explanation for the induction of the switch from leg K+ release to K+ uptake in a period when arm exercise is added is probably a combination of increased arterial K+ and catecholamine concentrations.

Changes in RBC K+ concentration during exercise are due to water fluxes rather than a transmembrane K+ flux.

Hypokalemia and hyperkalemia in association with pathophysiological states and exercise may interfere with excitability and contractile performance. Thus the processes influencing K+ distribution are of clinical importance. Skeletal muscles contain the largest single pool of K+ in the body and are therefore of major importance for the whole body K+ homeostasis. The present study illustrates that the K+ distribution between a given muscle and blood is influenced by the K+ balance of other muscles and that the delicate K+ homeostasis is controlled by several regulatory mechanisms.

    ACKNOWLEDGEMENTS

We thank Annelise Honig for excellent technical assistance.

    FOOTNOTES

The study was supported by The Danish National Research Foundation.

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests: C. Juel, Copenhagen Muscle Research Centre, August Krogh Institute, Universitetsparken 13, DK-2100 Copenhagen, Denmark.

Received 16 June 1998; accepted in final form 1 September 1998.

    REFERENCES
Top
Abstract
Introduction
Methods
Results
Discussion
References

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2.   Andersen, S. L. V., and T. Clausen. Calcitonin gene-related peptide stimulates active Na+-K+ transport in rat soleus muscle. Am. J. Physiol. 264 (Cell Physiol. 33): C419-C429, 1993[Abstract/Free Full Text].

3.   Bangsbo, J., C. Juel, Y. Hellsten, and B. Saltin. Dissociation between lactate and proton exchange in muscle during intense exercise in man. J. Physiol. (Lond.) 504: 489-499, 1997.

4.   Bangsbo, J., B. Kiens, and E. A. Richter. Ammonia uptake in inactive muscles during exercise in humans. Am. J. Physiol. 270 (Endocrinol. Metab. 33): E101-E106, 1996[Abstract/Free Full Text].

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6.   Christensen, N. J. Plasma noradrenaline and adrenaline in patients with thyrotoxicosis and myxoedema. Clin. Sci. Mol. Med. 45: 163-171, 1973.

7.   Clausen, T., and M. E. Everts. Regulation of the Na,K-pump in skeletal muscle. Kidney Int. 35: 1-13, 1989[Medline].

8.   Clausen, T., and J. A. Flatman. Effects of insulin and epinephrine on Na+-K+ and glucose transport in soleus muscles. Am. J. Physiol. 252 (Endocrinol. Metab. 15): E492-E499, 1987[Abstract/Free Full Text].

9.   Davies, N. W. Modulation of ATP-sensitive K+ channels in skeletal muscle by intracellular protons. Nature 343: 375-377, 1990[Medline].

10.   Dørup, I., and T. Clausen. Characterization of bumetanide-sensitive Na+ and K+ transport in rat skeletal muscle. Acta Physiol. Scand. 158: 119-127, 1996[Medline].

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13.   Everts, M. E., and T. Clausen. Excitation-induced activation of the Na+-K+ pump in rat skeletal muscle. Am. J. Physiol. 266 (Cell Physiol. 35): C925-C934, 1994[Abstract/Free Full Text].

14.   Hallén, J., L. Gullestad, and O. M. Sejersted. K+ shifts of skeletal muscle during stepwise bicycle exercise with and without beta -adrenoceptor blockade. J. Physiol. (Lond.) 477: 149-159, 1994[Medline].

15.   Juel, C., J. Bangsbo, T. Graham, and B. Saltin. Lactate and potassium fluxes from human skeletal muscle during and after intense, dynamic, knee extensor exercise. Acta Physiol. Scand. 140: 147-159, 1990[Medline].

16.   Lindinger, M. I., G. J. F. Heigenhauser, R. S. McKelvie, and N. L. Jones. Blood ion regulation during repeated maximal exercise and recovery in humans. Am. J. Physiol. 262 (Regulatory Integrative Comp. Physiol. 31): R126-R136, 1992[Abstract/Free Full Text].

17.   Lindinger, M. I., R. S. McKelvie, and G. J. F. Heigenhauser. K+ and Lac- distribution in humans during and after high-intensity exercise: role in muscle fatigue attenuation? J. Appl. Physiol. 78: 765-777, 1995[Abstract/Free Full Text].

18.   Maassen, N., M. Foerster, and H. Mairbäurl. Red blood cells do not contribute to removal of K+ released from exhaustively working forearm muscle. J. Appl. Physiol. 85: 326-332, 1998[Abstract/Free Full Text].

19.   McKelvie, R. S., M. L. Lindinger, G. J. F. Heigenhauser, and N. L. Jones. Contribution of erythrocytes to the control of the electrolyte changes of exercise. Can. J. Physiol. Pharmacol. 69: 984-993, 1991[Medline].

20.   McKelvie, R. S., M. I. Lindinger, N. L. Jones, and G. J. F. Heigenhauser. Erythrocyte ion regulation across inactive muscle during leg exercise. Can. J. Physiol. Pharmacol. 70: 1625-1633, 1992[Medline].

21.   Rolett, E. L., S. Strange, G. Sjøgaard, B. Kiens, and B. Saltin. beta 2-Adrenergic stimulation does not prevent potassium loss from exercising quadriceps muscle. Am. J. Physiol. 258 (Regulatory Integrative Comp. Physiol. 27): R1192-R1200, 1990[Abstract/Free Full Text].

22.   Sachs, J. R. Sodium movements in human red blood cell. J. Gen. Physiol. 56: 322-341, 1970[Abstract/Free Full Text].

23.   Sakaguchi, M., Y. Inaishi, Y. Kashihara, and M. Kuno. Release of calcitonin gene-related peptide from nerve terminals in rat skeletal muscle. J. Physiol. (Lond.) 434: 257-270, 1991[Abstract/Free Full Text].

24.   Savard, G., S. Strange, B. Kiens, E. A. Richter, N. J. Christensen, and B. Saltin. Noradrenaline spillover during exercise in active versus resting skeletal muscle of man. Acta Physiol. Scand. 131: 507-515, 1987[Medline].

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Am J Physiol Regul Integr Compar Physiol 276(1):R184-R188
0002-9513/99 $5.00 Copyright © 1999 the American Physiological Society


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