Regulation of muscle potassium: exercise performance, fatigue and health implications

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

“…This muscle K + uptake acts to restrict the rise in plasma [K + ] to prevent potentially life‐threatening effects of hyperkalemia on the myocardium, but also to conserve muscle intracellular K + stores, which are essential K + donors during periods of fasting, to preserve plasma [K + ] and prevent deleterious effects of hypokalemia (McDonough & Youn, 2017). Post‐exercise hypokalemia has been identified as increasing the risk of arrhythmias (Lindinger & Cairns, 2021) and was recently shown to be correlated with QT hysteresis, indicating impaired cardiac repolarization and increased risk of arrhythmias (Atanasovska et al., 2018).…”

“…During the first hour of an insulin clamp conducted under resting conditions, around 30% of K + uptake was attributable to peripheral tissues including skeletal muscles, with the splanchnic bed responsible for the remaining 70% (Andres et al., 1962). While the contracting musculature is responsible for the large rise in circulating [K + ] during exercise (Lindinger & Cairns, 2021; Sejersted & Sjøgaard, 2000), inactive muscle also plays a key modulatory role on [K + ]; the relatively inactive forearm muscles extract circulating K + during leg cycling exercise, (Kowalchuk et al., 1988; Lindinger et al., 1990) thus attenuating the rise in plasma [K + ] (Lindinger, 1995). The wide [K + ] a‐v across the forearm found here during HIIC is consistent with this role for the relatively inactive forearm muscles during leg cycling exercise.…”

“…Ongoing K + regulation is vital to preserve excitability and contractile function in skeletal, as well as cardiac muscle (Lindinger & Cairns, 2021; Sejersted & Sjøgaard, 2000). In contracting skeletal muscle, 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). 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).…”

“…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 therefore, that the Na + ,K + ‐ATPase (NKA), which plays a central role in acutely regulating K + homeostasis in all tissues (Lindinger & Cairns, 2021), is also rapidly activated in contracting skeletal muscle, transporting K + back into the intracellular compartment. Even brief muscle contractions activate the muscle NKA, which attenuates the excitation‐induced decline in intracellular [K + ] and rise in intracellular [Na + ], and exerts an electrogenic effect on the membrane potential (Clausen, 2008).…”

“…Insulin is also an important regulator of skeletal muscle NKA and thus also of K + homeostasis. Early reports indicated that insulin lowered plasma [K + ] in humans (Alvestrand et al., 1984; Andres et al., 1962; DeFronzo, 1988; DeFronzo et al., 1980; Ferrannini et al., 1988; Zierler & Rabinowitz, 1964), reflecting K + uptake into skeletal muscle (Clausen, 1998; Clausen & Flatman, 1987; Ewart & Klip, 1995; Lindinger & Cairns, 2021). Insulin stimulates NKA in isolated muscles and membrane extracts (Clausen & Kohn, 1977; Erlij & Grinstein, 1976; Gavryck et al., 1975; McKenna et al., 2003; Moore, 1973), independently of increased muscle glucose transport (Clausen, 1986).…”