Mechanistic Insights into the Efficacy of Sodium Bicarbonate Supplementation to Improve Athletic Performance

From an energetic perspective, any physiological effects of NaHCO₃ supplementation that translate to an increase in performance should be observed in the rates and amounts of energy provision and/or the efficiency of energy transduction to power and work. However, very little research has investigated, or indeed attempted to quantify, anaerobic and aerobic energy yields, accumulated oxygen deficits or energetic efficiency during conditions of metabolic alkalosis. Beyond a handful of studies that have modelled whole-body VO₂ kinetics (e.g. VO₂ fast and slow components [50‐52]), most of the research on NaHCO₃ and metabolism has been conducted on single muscle or isolated muscle groups and their metabolic response to various task demands.

From studies conducted in the 1970s [32, 53‐55], a causal link between increased intramuscular lactate (La⁻) concentrations and La⁻ efflux, reduced proton (H⁺) accumulation and improved muscular performance had been posited to explain the performance improvements observed following NaHCO₃ supplementation [6]. To further clarify the influence of NaHCO₃ on intramuscular [La⁻] and La⁻ efflux during intense exercise, Spriet and colleagues minimised the limitations associated with in vivo contracting muscle measurement (e.g. varying work rates and metabolite accumulation) by applying continuous supramaximal stimulation (5 V at 0.5 Hz) for 20 min to a perfused gastrocnemius-plantaris-soleus (GPS) muscle group [56]. NaHCO₃ increased the rate of La⁻ efflux from the muscle group, but did not attenuate the decline in muscle tension as compared to control conditions [56]. Methodological limitations inherent to the perfusion and stimulation protocol only allowed the authors to speculate as to whether or not the increased La⁻ efflux was a result of increased rates of glycogenolysis and/or glycolysis, or due to an increased rate of La⁻ release from the muscle.

Nearly 15 years later, Hollidge-Horvat and colleagues used human muscle tissue samples obtained at different steady-state exercise intensities (i.e. 30, 60 and 75 % VO₂max) to investigate the mechanisms responsible for the increased La⁻ efflux by then commonly observed after NaHCO₃ ingestion [57]. These authors eloquently detailed a complex, intensity-dependent response in key metabolic enzymes and regulatory steps after NaHCO₃ ingestion as compared to control conditions. Briefly, the authors observed a similar increase in La⁻ efflux to that of previous studies after NaHCO₃ ingestion, but only at 75 % VO₂max [57]. The authors speculated that the increased [La⁻] observed in circulation may have been due to a decrease in La⁻ uptake by inactive tissue [58] or an altered H⁺ gradient on the transporters (later confirmed by others as an increase in monocarboxylate transporter (MCT) activity [59]). The authors also documented an increased degradation of muscle glycogen in the NaHCO₃ compared to the control trials [57]. As performance was not assessed in this study, whether or not this increased reliance on muscle glycogen stores in the NaHCO₃ trial would have influenced performance at the higher intensities remains unknown.

As the capacity to study exercising muscle metabolism in vivo improved beyond the limitations of the biopsy, others have subsequently expanded upon these findings to include exercise performance measures. Using phosphorus-31 magnetic resonance spectroscopy (³¹P-MRS) and a constant-rate progressive wrist-flexion exercise (1-s contraction/1-s relaxation) to volitional exhaustion, Raymer and colleagues reported an approximate 12 % increase in time to failure after NaHCO₃ supplementation and attributed the performance effect to a delayed onset of intracellular acidosis (evident at ~60 % peak power) in the alkalotic condition [60]. Furthermore, concomitant to the delayed intracellular acidosis was a delay in the slow-to-rapid increase in the [PCr]/[Pi] to power output relationship (repeatedly observed in subsequent studies by this same group [61, 62]). As metabolic perturbation caused by acidosis had been associated with the inhibition of glycolysis and glycogenolysis [63], increased phosphocreatine (PCr) degradation and inorganic phosphate (P_i) accumulation ([PCr]/[P_i]) within the myocyte [64], the authors speculated that the delayed accumulation of intracellular H⁺ induced by NaHCO₃ was the primary cause of the performance effect.

To briefly summarise, much of the research in this area has been centred around muscle metabolism, from the earlier observations on intramuscular [La⁻] and La⁻ efflux to the more recent focus on glycolytic intermediates and high-energy phosphate kinetics (e.g. PCr). NaHCO₃ appears to effect the [PCr]/[Pi]-power relationship, glycolytic intermediates and the intra- and extracellular distribution of metabolites and other strong ions (Fig. 2) [56, 57, 60, 65, 66]. Not surprisingly, this effect is more pronounced during periods of prolonged, intense contractile activity where a larger proportion of energy provision is derived from classically defined anaerobic pathways. Contextually, this effect may also partially explain the ergogenic findings of many performance-based studies on athletes that have imposed a high demand on these pathways either with single or repeated bouts of intense exercise [39, 67‐70].

Inducing a state of alkalosis also affects the intra- and extracellular balance of other strong ions such as Na⁺, K⁺ and Cl⁻ [60], all of which contribute to the maintenance of skeletal muscle contractile function [13]. In general, and irrespective of acid-base balance, fatiguing exercise induces ion concentration changes between the intracellular, interstitial and extracellular compartments. Although ultimately dependent upon the level of contractile activity, as well as diffusion and perfusion limitations, muscle K⁺ will tend to decrease whereas muscle Na⁺, Cl⁻ and Ca²⁺ will tend to increase with intense exercise (H⁺ will increase in both intra- and extracellular compartments) [13]. Collectively, changes in these ionic concentrations have been demonstrated to decrease resting membrane potential and impair sarcolemmal excitability [13]. The effect of NaHCO₃ specifically on the distribution of these ions between compartments, in particular the NaHCO₃ ⁻-induced reduction in K⁺ efflux from the muscle, has been the focus of other studies investigating the effect of alkalosis on the interstitial and plasma concentrations of strong ions and skeletal muscle fatigue [65, 66, 71].

In terms of exercise performance, however, only Sostaric and colleagues have demonstrated an improvement after NaHCO₃ supplementation [65]. By incorporating a small muscle mass, and therefore inducing a larger reduction in muscle K⁺ than commonly observed during whole-body exercise [72], the authors hypothesised that NaHCO₃ would attenuate the augmented K⁺ efflux from the small muscle mass and therefore better preserve muscle function [65]. Subsequently, they observed an increase in total exercise time of greater than 2 min (~25 % improvement) compared to a placebo during a constant rate, progressive concentric forearm flexion exercise task to volitional exhaustion [65]. NaHCO₃ also improved the regulation of circulating K⁺ and handling of Cl⁻ (but not Na⁺), which the authors proposed to have better preserved membrane excitability and therefore contributed to the performance improvement [65].

NaHCO₃ appears to delay the rise in muscle interstitial K⁺ that occurs during intense contractile activity and, via this effect, may attenuate the decline in muscle membrane excitability and the extent of K⁺-induced inactivation of myocytes during such activity [11, 66]. As previously stated, this effect may have contributed to not only the performance improvement observed by Sostaric and colleagues but also the earlier findings of Raymer as both used a similar exercise performance task [60, 65]. However, these studies also illustrate the relevance of muscle mass and task demand when determining the efficacy of NaHCO₃ as an ergogenic supplement. Issues such as agonist/antagonist muscle actions, synergistic contraction of larger muscle groups and recruitment order (e.g. Hennemen’s size principle) [73] during whole-body exercise may mitigate the performance effects observed in smaller, isolated muscles. As an example, the trend of NaHCO₃ improving incremental exercise to volitional exhaustion in smaller muscle groups [60, 65] is less consistent when large muscle groups (e.g. cycling) or whole-body exercise is incorporated within a similar task [32, 33, 35, 74, 75] (Table 2).

Although earlier work had illustrated a relationship between muscle pH and skeletal muscle force and/or muscle shortening velocity [76‐78], the first to show an independent effect of acidosis on fast- and slow-twitch fibres appears to be Metzger and Moss in 1987 [79]. Using single fibres of rat soleus (SOL) and vastus lateralis (VL) muscles, previously characterised as predominately type I (SOL) or IIa and b (VL), respectively [80, 81], maximal isometric tension and maximum shortening velocity was assessed as a function of pH. Although initial declines in pH induced a concomitant reduction in tension and shortening velocity in both SOL and VL, as pH decreased below 6.2, the relative loss in tension was greater in VL [79]. The first to study the effect of NaHCO₃ on fibre-specific force production was Lindinger and colleagues in 1990 [82]. These authors examined the effects of NaHCO₃ on SOL and white gastrocnemius (WG) muscle tension at rest and during 5 min of intense stimulation [82]. Although NaHCO₃ differentially altered the ionic composition (specifically K⁺, Cl⁻ and Mg²⁺) and the rate of La⁻ efflux from the muscle fibres, it had no effect on muscle tension in either muscle [82].

In 2007, Broch-Lips and colleagues stimulated the SOL and extensor digitorum longus (EDL), another muscle characterised as predominately type IIa, under normal or alkalotic conditions. In addition to the isometric force measurement, the authors also estimated rate of force development (RFD) as the maximal numerical slope value of the force development during contraction [71]. Although NaHCO₃ induced increases in pH from 7.4 to 7.6, neither maximum force nor RFD was affected in either muscle [71]. However, more recent evidence using a fatiguing, mechanically controlled stretch-shortening work cycle model has shown that NaHCO₃ administration may improve RFD [83]. Avoiding the limited degree of shortening that occurs during isometric contractions [71], Higgins and colleagues subjected both SOL and EDL mouse muscles to repeated length changes matched to the expected stride frequency of the mice during normal locomotion (10 % strain with a cycle frequency for EDL of 8 Hz and SOL of 5 Hz) and demonstrated an approximate 7 % improvement in force production during shortening in the EDL compared to a 3 % improvement in the SOL after NaHCO₃ incubation.

To date, the fibre-type dependent findings related to contractile properties have not been replicated in the exercising human given the methodological constraints addressed earlier of isolating fibre-type contributions to whole-body locomotion [84], quantifying properties of diffusion and other factors associated with intramuscular blood supply [85, 86]. However, collectively, this body of research suggests that NaHCO₃ may affect the metabolic properties associated with contractile shortening velocity and that this effect appears more pronounced in fast-twitch fibres (Fig. 2). The effect on rates of contractile shortening but not maximal force may also explain the limited efficacy of NaHCO₃ observed in performance-based studies only measuring maximal voluntary force [87, 88].

Interestingly, although shortening velocity of slow-twitch fibres after acute NaHCO₃ administration does not appear to be improved when compared to fast-twitch fibres, chronic ingestion coupled with high-intensity training may improve the oxidative capacity of these fibres [89‐91]. After 8 weeks (three times per week) of chronic NaHCO₃ ingestion coupled with high-intensity (between 140 and 170 % lactate threshold (LT)) intermittent training, Edge and colleagues reported a significant improvement in both LT (~11 %) and performance (~25 %) (time to failure) in moderately trained females when compared to a control group matched for total work (kJ). The authors speculated that as H⁺ accumulation has been shown to impair oxidative capacity and various components of cellular respiration [57], training in an alkalotic state may have attenuated the impairment and allowed for prolonged cellular respiration to occur during training [89].

Continuing this line of investigation, two subsequent studies by the same group used relatively similar NaHCO₃ dosing and high-intensity training protocols on rats to explore fibre-type dependent protein expression associated with H⁺ removal during rest and exercise [90, 91]. In the first study, the authors observed a differential effect of alkalosis on MCT-4 expression in the SOL but not EDL when compared to placebo and control conditions [90]. Additionally, citrate synthase concentration was higher in the alkalotic condition (23 vs. 16 %) after training in the SOL but not EDL. These findings led the authors to conclude that chronic NaHCO₃ ingestion was influencing protein expression associated with slow but not fast-twitch fibres. The final study in the series appeared to further confirm this observation, with the authors reporting an increase in mitochondrial respiration in the SOL as compared to the EDL after training in an induced alkalotic state [91].

The evidence that chronic use of NaHCO₃ coupled with appropriate training may lead to aerobic adaptations associated with improved mitochondrial efficiency in slow-twitch fibres is intriguing [91], and future work may clarify whether this is indeed a viable option for improving aerobic efficiency. Additionally, we are unaware of any studies that have investigated the efficacy of introducing chronic NaHCO₃ supplementation on mechanisms associated with muscle force production or rapid force-generating capacity. Given the preliminary evidence that NaHCO₃ may exhibit independent effects on fibre-specific mechanisms associated with improved contractile function both acutely and chronically, future study in this area is warranted.

Appropriately identifying whether NaHCO₃ ingestion may influence the underlying mechanisms associated with whole-body metabolism, muscle physiology and/or motor pathways within the context of a particular athletic endeavour or training stimulus is an important initial step when considering the use of this supplement. For example, in the context of athletic performance, delayed onset of H⁺ accumulation may be relevant to certain time frames within an event that demand rapid transitions between steady-state and higher intensity efforts (e.g. beginning a ‘long-finish’ earlier in a 1500-m race). In this scenario, NaHCO₃ supplementation may be appropriate based on the evidence indicating an attenuation of H⁺ accumulation during exercise intensities transitioning between aerobic and anaerobic pathways [60, 65, 89]. Another example, and specifically related to the evidence surrounding RFD and fast-twitch fibres [83, 97], would be to improve the propulsive force at the start of an explosive movement (e.g. the initiation of a pedal stroke). Considerations for the potential benefit of NaHCO₃ in these unique situations would require extensive consultation within an athlete’s support network, as well as a systematic integration of the supplement to accurately determine any efficacious response. Although often difficult to rigorously assess in the elite environment, any marginal improvement in performance gained by using NaHCO₃ for these specific purposes in competition may provide alternative uses for this supplement that extend beyond current recommendations [1, 5].

Although there have been few studies investigating the efficacy of implementing a chronic NaHCO₃ supplementation strategy on training outcomes [89, 119], given the recent evidence in animal models exhibiting enhanced oxidative/mitochondrial adaptations in slow-twitch fibres after chronic supplementation [90, 91], further work in this area may establish whether incorporating NaHCO₃ into an aerobic training paradigm is warranted. Furthermore, with research also supporting a potential ergogenic effect on RFD [97], particularly in fast-twitch fibres [83], applying a loading strategy during specific training and adaptation blocks (e.g. explosive power) may also have merit. In practice, however, incorporating a training strategy inclusive of a regular 0.3 g·kg⁻¹ NaHCO₃ load would require a systematic administration and monitored approach. Although we are unaware of any documented long-term adverse effects of chronic loading in either sporting [89, 120, 121] or clinical contexts [122‐124], given the relatively high sodium content (e.g. a 70-kg athlete would consume ~6 g), continually monitoring both blood acid-base and strong ions (e.g. Na⁺) would allow any irregularities from the ingestion regimen to be detected and ultimately corrected for the safety of the athlete(s). Additionally, and similar to other contemporary debates such as training in a low glycogen state [125], without further study potentially elucidating any maladaptation from consecutive training blocks after NaHCO₃ ingestion, it would be prudent to consider intermittently incorporating this strategy and only when certain training outcomes are desired (e.g. maximising the number of repeated efforts at top speed or high rates of force output).

Equally important to the performance and training strategies, however, may be the ingestion protocol used to systematically introduce NaHCO₃. Research is only now highlighting what practitioners, coaches and athletes have been aware of for some time, and that is the inherent variability in individual responsiveness to this supplement [126‐130]. In part, the variability in many papers may eventuate from the wide range of exercise tasks and methodological applications, as well as heterogeneity between participant phenotypes. However, it may also result from the widespread assumption that applying mean data on time-to-peak buffering response rates after NaHCO₃ ingestion prior to commencing exercise is not influencing the outcome of many performance tasks [128, 129]. Amongst others [131, 132], we have profiled the ingestion time course of various doses of NaHCO₃ at rest in order to determine peak response rates (Fig. 1) [3]. Collectively, and variation in ingestion protocols notwithstanding (e.g. capsules, bolus loads or dispersed over time), these studies illustrate around 40 min of variation between subjects’ peak in blood buffering capacity [3, 131, 132]. Indeed, the large degree of inter-individual variability profiled in Fig. 1 has been recently observed again but under greater temporal resolution and in a larger study cohort [129]. Although we have shown that this variation may not be important for recreationally trained individuals [133], we are unaware of any studies that have documented the variability in elite athlete populations.

Finally, the origin of the 0.2 to 0.3 g·kg⁻¹ doses in the sport performance field is somewhat ambiguous. Although oral ingestion of between 25 to 40 g of NaHCO₃ has been documented as early as the 1920s and early 1930s in the clinical literature [124, 134, 135], this range is believed to have come from the work of Poulus and colleagues, who in 1974 published the first exercise performance paper using a physiochemical rationale for NaHCO₃ dose selection [74]. Citing earlier clinical work [122, 136], these authors determined the amount of NaHCO₃ to be administered intravenously using the following formula:where base deficit (BD) represented the excess of fixed acid in the blood measured after an incremental cycling test on a previous visit to the lab and compared to a standard (pH of 7.4 and a PCO₂ of 40 mmHg) [74]. The 0.3 represented a mean weighting factor derived from the equilibrating time course of NaHCO₃ throughout blood and the extravascular spaces [122, 123]. Of note, no subsequent studies have included BD in the equation for determining dose. This, coupled with the variation in individual weighting factors reported in the original study (0.25 to 0.38) [122], warrants further work to determine whether or not individualising dose concentrations is necessary, and whether issues related to HCO₃ ⁻ and [H⁺] rates of increase and clearance are impacting upon the efficacy of NaHCO₃ as a supplement [130].

The dosing papers most frequently cited in the sport performance literature date back to the late 1980s and early 1990s. These studies looked at a range of NaHCO₃ doses (0.1 to 0.5 g·kg⁻¹) and the relationship between performance and gastrointestinal (GI) disturbance, respectively [137, 138]. Collectively, these studies showed that performance could be improved when the acute dose ingested ranged between 0.2 and 0.3 g·kg⁻¹, but anything greater was not beneficial and only induced severe side effects. For the past 30 years, this dose range has been widely accepted as best practice. Yet, the small subject numbers (n < 9) coupled with their non-elite training status (e.g. ‘participating in athletic events’) of the original research should warrant further inquiry [138]. This, of course, also assumes that 0.2 or 0.3 g·kg⁻¹ are the optimal physiologic doses for maximising blood buffering capacity [130].

In light of the practical issues identified in this section, we recommend monitoring at an individual level the time-to-peak rise (and decay [130]) in [HCO₃ ⁻] at doses between 0.2 and 0.3 g·kg⁻¹ and to tailor the commencement of exercise accordingly [128]. An individualised loading strategy will also require systematically incorporating dose distribution and other planned nutritional interventions, documenting subjective feedback from the athlete (e.g. gastrointestinal distress [139]) and monitoring any physiological changes (e.g. acute weight gain from plasma volume expansion [21]) observed after ingestion.