The effects of elevated levels of sodium bicarbonate (NaHCO3) on the acute power output and time to fatigue of maximally stimulated mouse soleus and EDL muscles

Abstract This study examined the effects of elevated buffer capacity [~32 mM HCO3(-)] through administration of sodium bicarbonate (NaHCO3) on maximally stimulated isolated mouse soleus (SOL) and extensor digitorum longus(EDL) muscles undergoing cyclical length changes at 37 C. The elevated buffering capacity was of an equivalent level to that achieved in humans with acute oral supplementation. We evaluated the acute effects of elevated [HCO3 (-)] on (1) maximal acute power output (PO) and (2) time to fatigue to 60 % of maximum control PO (TLIM60), the level of decline in muscle PO observed in humans undertaking similar exercise, using the work loop technique. Acute PO was on average 7.0 ± 4.8 % greater for NaHCO3-treated EDL muscles (P<0.001; ES = 2.0) and 3.6 ± 1.8 % greater for NaHCO3 treated SOL muscles (P<0.001; ES = 2.3) compared to CON. Increases in PO were likely due to greater force production throughout shortening. The acute effects of NaHCO3 on EDL were significantly greater (P<0.001; ES = 0.9) than on SOL. Treatment of EDL (P = 0.22; ES = 0.6) and SOL(P = 0.19; ES = 0.9) with NaHCO3 did not alter the pattern of fatigue. Although significant differences were not observed in whole group data, the fatigability of muscle performance was variable, suggesting that there might be inter-individual differences in response to NaHCO3 supplementation. These results present the best indication to date that NaHCO3 has direct peripheral effects on mammalian skeletal muscle resulting in increased acute power output

Do multiple ionic interactions contribute to skeletal muscle fatigue?

During intense exercise or electrical stimulation of skeletal muscle the concentrations of several ions change simultaneously in interstitial, transverse tubular and intracellular compartments. Consequently the functional effects of multiple ionic changes need to be considered together. A diminished transsarcolemmal K+ gradient per se can reduce maximal force in non-fatigued muscle suggesting that K+ causes fatigue. However, this effect requires extremely large, although physiological, K+ shifts. In contrast, moderate elevations of extracellular [K+] ([K+]o) potentiate submaximal contractions, enhance local blood flow and influence afferent feedback to assist exercise performance. Changed transsarcolemmal Na+, Ca2+, Cl− and H+ gradients are insufficient by themselves to cause much fatigue but each ion can interact with K+ effects. Lowered Na+, Ca2+ and Cl− gradients further impair force by modulating the peak tetanic force–[K+]o and peak tetanic force–resting membrane potential relationships. In contrast, raised [Ca2+]o, acidosis and reduced Cl− conductance during late fatigue provide resistance against K+-induced force depression. The detrimental effects of K+ are exacerbated by metabolic changes such as lowered [ATP]i, depleted carbohydrate, and possibly reactive oxygen species. We hypothesize that during high-intensity exercise a rundown of the transsarcolemmal K+ gradient is the dominant cellular process around which interactions with other ions and metabolites occur, thereby contributing to fatigue