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The effects of an oral glucose load on plasma K+ and electrolyte homeostasis at rest, during high intensity intermittent exercise and recovery and on skeletal muscle Na+,K+-ATPase isoform abundance

C.H. Steward,1 R. Smith,1,2 N.K. Stepto,1 M. Brown,3 I. Ng4 and M.J. McKenna,1 1Institute of Sport, Exercise and Active Living (ISEAL), Victoria University, Melbourne, VIC 8001, Australia, 2Western Hospital, Footscray, VIC 3011, Australia, 3Department of Pharmacology, University of Melbourne, Parkville, VIC 3052, Australia and 4Royal Melbourne Hospital, Melbourne, VIC 3000, Australia.

The regulation of K+ and Na+,K+-ATPase (NKA) are of major physiologic importance, including during exercise where muscle K+ disturbances have been linked to fatigue (McKenna et al., 2008). The effects of acute oral glucose supplementation on carbohydrate metabolism are well established, however the effects on muscle NKA and K+ homeostasis are not well known. Insulin infusion reduced plasma [K+], with K+ uptake in the splanchnic region and skeletal muscle due to NKA stimulation (DeFronzo et al., 1980). This study therefore investigated the effects of glucose supplementation on endogenous insulin, arterial plasma electrolyte and acid-base homeostasis before, during and after high-intensity intermittent cycling exercise; in addition the effects on skeletal muscle NKA isoform protein abundance were examined. Participants performed two trials in a randomised cross over design, ingesting either 75 g glucose (CHO) or a placebo (CON); sixty min later participants commenced exercise, which comprised three cycling exercise bouts (EB) for 45 s at 130% V̇O2peak, followed by a fourth bout at 130% V̇O2peak continued until fatigue. Radial arterial (a) and antecubital venous (v) blood samples taken simultaneously throughout the rest, exercise and recovery phases were analysed for plasma K+, Na+, H+, glucose and Lac concentrations ([ion]), and their arterio-venous [ion] differences calculated. A vastus lateralis muscle biopsy was taken prior to glucose/placebo ingestion, immediately prior to exercise and at fatigue, and analysed for muscle NKA α1-3 and β1-3 isoform protein abundance (western blotting).

The [glucose]a was greater during CHO than CON (main effect; P<0.001). The [glucose]a during CHO was greater than CON from 10 min after ingestion through until EB3 (P<0.001); a similar temporal pattern was observed for [glucose]v (P<0.001). Arterial plasma [insulin] was increased at each time point measured (P<0.001) and was greater during CHO than CON (P<0.001). The [K+]a increased during exercise for both conditions, however [K+]v only increased during CON whereas a decrease compared to rest was found for CHO. During CHO, both [K+]a and [K+]v were lower after glucose ingestion compared to CON, with the effect most prominent during exercise and early recovery (P<0.05). The [K+]a-v across the forearm increased during exercise and was more positive in CHO (p<0.05), indicating a greater net uptake of K+ into the relatively inactive forearm muscles during exercise. During exercise the change in [K+]v from rest was positive for CON and remained negative following CHO, indicating an increase in in vivo NKA activity. Arterial [Na+] was higher in CHO (P<0.05) increasing throughout the exercise period, with [Na+]a-v more positive in CHO than CON (P<0.05) during exercise and early recovery. There was no difference in time to fatigue during the final bout between trials. There were no significant main effects for time, treatment or time–by-treatment interactions for any of the NKA α, β1 or β2 isoforms following glucose ingestion or for exercise. The muscle NKA β3 protein abundance was however increased following exercise (P<0.05) during CON only. Thus glucose ingestion attenuated the exercise-induced rise in plasma [K+] during exercise, likely consequent to increased [insulin]. These systemic K+-lowering effects probably indicate increased NKA activity consistent with the greater [K+]a-v. This increased activity was not due to increased NKA isoform protein abundance and therefore would reflect greater in vivo NKA activation.

DeFronzo RA, Felig P, Ferrannini E, Wahren J. (1980) American Journal of Physiology, 238: E421-427.

McKenna MJ, Bangsbo J, Renaud JM. (2008) Journal of Applied Physiology, 104: 288-95.