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

Abstract

Aim We investigated whether acute carbohydrate ingestion reduced arterial potassium concentration ([K+]) during and after intense exercise and delayed fatigue. Methods In 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% trueV˙normalO2peak, 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. Results Glucose 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. Conclusion Acute 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.

The Role of Muscle Glycogen Content and Localization in High-Intensity Exercise Performance: A Placebo-Controlled Trial

“…The carbohydrate intake, on the other hand, altered serum insulin and plasma FFA levels with higher and lower values in the carbohydrate-supplemented condition, respectively, which could alter the muscle metabolism and oxygen kinetics (40). Moreover, insulin is a known stimulator of Na + -K + -ATPase activity, and glucose ingestion has recently been demonstrated to alter potassium accumulation during high-intensity exercise, although with no impact on exercise tolerance and with the effects likely being minor compared with the large contraction-induced Na + -K + -ATPase activation (41,42). Finally, direct stimulatory effects of carbohydrate ingestion on reward centers in the brain could also have been present, yet the ingestion of carbohydrates was terminated more than an hour before the last test procedures (43).…”

A century of exercise physiology: effects of muscle contraction and exercise on skeletal muscle Na+,K+-ATPase, Na+ and K+ ions, and on plasma K+ concentration—historical developments

“…Insulin infusion was later found not to affect [K + ] a , to lower [K + ] acv and widen the [K + ] a-acv diff to ~ 0.35 mM, demonstrating K + uptake by forearm muscle (Andres et al 1962 ), with similar muscle K + uptake evident at ninefold lower insulin infusion (Zierler and Rabinowitz 1964 ). A standard oral glucose tolerance test elevated insulin, lowered both [K + ] a and [K + ] acv and increased the [K + ] a-acv diff during and after intense intermittent cycling exercise (Steward et al 2021 ). This K + -lowering with leg exercise was probably due to insulin increasing muscle NKA activity and thus also K + uptake in inactive forearm muscles.…”