A single oral glucose load decreases arterial plasma [K+ ] during exercise and recovery.

Collene H Steward,Robert Smith,Irene Ng,Malcolm Brown,Nigel K Stepto,Michael J Mckenna

doi:10.14814/phy2.14889

Abstract

AimWe investigated whether acute carbohydrate ingestion reduced arterial potassium concentration ([K+]) during and after intense exercise and delayed fatigue.MethodsIn a randomized, double‐blind crossover design, eight males ingested 300 ml water containing 75 g glucose (CHO) or placebo (CON); rested for 60 min, then performed high‐intensity intermittent cycling (HIIC) at 130% V˙O2peak, comprising three 45‐s exercise bouts (EB), then a fourth EB until fatigue. Radial arterial (a) and antecubital venous (v) blood was sampled at rest, before, during and after HIIC and analyzed for plasma ions and metabolites, with forearm arteriovenous differences (a‐v diff) calculated to assess inactive forearm muscle effects.ResultsGlucose ingestion elevated [glucose]a and [insulin]a above CON (p = .001), being, respectively, ~2‐ and ~5‐fold higher during CHO at 60 min after ingestion (p = .001). Plasma [K+]a rose during and declined following each exercise bout in HIIC (p = .001), falling below baseline at 5 min post‐exercise (p = .007). Both [K+]a and [K+]v were lower during CHO (p = .036, p = .001, respectively, treatment main effect). The [K+]a‐v diff across the forearm widened during exercise (p = .001), returned to baseline during recovery, and was greater in CHO than CON during EB1, EB2 (p = .001) and EB3 (p = .005). Time to fatigue did not differ between trials.ConclusionAcute oral glucose ingestion, as used in a glucose tolerance test, induced a small, systemic K+‐lowering effect before, during, and after HIIC, that was detectable in both arterial and venous plasma. This likely reflects insulin‐mediated, increased Na+,K+‐ATPase induced K+ uptake into non‐contracting muscles. However, glucose ingestion did not delay fatigue.

Highlights

Ongoing K+ regulation is vital to preserve excitability and contractile function in skeletal, as well as cardiac muscle (Lindinger & Cairns, 2021; Sejersted & Sjøgaard, 2000)
The depolarization phase of action potentials is linked with cellular K+ efflux, resulting in increased interstitial [K+], decreased intracellular [K+] and membrane depolarization; these changes are proposed as one factor in muscular fatigue (Lindinger & Cairns, 2021; McKenna et al, 2008)
The key finding of this study was that an acute oral glucose load routinely undertaken clinically via an oral glucose tolerance test and under physiological conditions, affected systemic, and skeletal muscle K+ homeostasis during high-intensity intermittent cycling (HIIC) exercise and recovery

Summary

Introduction

Ongoing K+ regulation is vital to preserve excitability and contractile function in skeletal, as well as cardiac muscle (Lindinger & Cairns, 2021; Sejersted & Sjøgaard, 2000). Experiments utilizing in vitro isolated muscle preparations demonstrate that high extracellular [K+] strongly depresses maximal force (Cairns et al, 1997; de Paoli et al, 2007). It is fundamentally important that the Na+,K+-ATPase (NKA), which plays a central role in acutely regulating K+ homeostasis in all tissues (Lindinger & Cairns, 2021), is rapidly activated in contracting skeletal muscle, transporting K+ back into the intracellular compartment. Upon cessation of exercise, plasma [K+] rapidly falls to rest or below resting concentrations within the first minutes of recovery, due to rapid re-uptake of K+ by previously active muscle (Atanasovska et al, 2014; Lindinger & Cairns, 2021; Lindinger et al, 1992)

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