Acute Dietary Nitrate Supplementation Increases Maximal Cycling Power in Athletes

Abstract

Muscle shortening velocity and hence power has been shown to increase in the presence of nitric oxide (NO). NO availability increases after consuming nitrate (NO₃⁻). Ingestion of NO₃⁻-rich beetroot juice (BRJ) has increased muscle power in untrained adults.

PURPOSE

This study determined if NO₃⁻ supplementation could acutely enhance maximal power in trained athletes.

METHODS

In this double-blind, crossover study, 13 trained athletes performed maximal inertial-load cycling trials (3-4 s) immediately before (PRE) and after (POST) consuming either NO₃⁻-rich (NO3) or NO₃⁻-depleted (PLA) BRJ to assess acute changes (i.e., within the same day) in maximal power (P_MAX) and optimal pedaling rate (RPM_OPT). Participants also performed maximal isokinetic cycling (30 s) to assess performance differences after supplementation.

RESULTS

2×2 repeated measures ANOVA indicated a greater increase in P_MAX from PRE to POST NO3 (PRE: 1160±301 to POST: 1229±317 W) compared to PLA (PRE: 1191±298 to POST: 1213±300 W) (p=0.009; ή²=0.45). A paired t-test verified a greater relative change in P_MAX after NO3 (6.0±2.6%) compared to PLA (2.0±3.8%) (p=0.014; d=1.21). RPM_OPT remained unchanged from PRE (123±14) to POST PLA (122±14 rpm) but increased from PRE (120±14) to POST NO3 (127±13 rpm) (p=0.043; ή²=0.30). There was no relative change in RPM_OPT after PLA (−0.3±4.1%) but there was an increase after NO3 (6.5±11.4%) (p=0.049; d=0.79). No differences were observed between the 30 s isokinetic trials.

CONCLUSIONS

Acute NO₃⁻ supplementation can enhance maximal muscle power in trained athletes. These findings may particularly benefit power-sports athletes who perform brief explosive actions.

INTRODUCTION

Dietary nitrate (NO₃⁻) supplementation enhances aerobic exercise performance by increasing nitric oxide (NO) production via the exogenous NO₃⁻-nitrite (NO₂⁻)-NO pathway¹. The potential benefits and possible underlying mechanisms by which dietary NO₃⁻ supplementation affects endurance exercise performance have been recently reviewed². NO₃⁻ ingestion may also affect powerful exercise performance. In fact, chronic supplementation (7 d) of NO₃⁻-rich beetroot juice (BRJ) has augmented the rate of force production during electrically evoked isometric knee extension in untrained men³, and, increased total work achieved across multiple cycling sprints performed by recreational team-sport athletes.⁴

Aside from chronic supplementation, rodent studies^5,6,7,8 highlight potential mechanisms by which increased NO availability could acutely increase neuromuscular power (see DISCUSSION). Therefore, NO₃⁻ ingestion could acutely increase muscle power in humans. Indeed, Coggan and colleagues reported greater maximal voluntary isokinetic knee extension speed and power in healthy adults⁹ and even greater increases in heart failure patients¹⁰, after a single bolus of concentrated BRJ. Such effects^9,10 could potentially benefit athletic populations, but this has not been investigated. The primary purpose of this investigation was to determine if NO₃⁻-rich BRJ could acutely (i.e., within the same day) increase power and optimal pedaling rate during a short bout of maximal cycling (3-4 s) performed by trained athletes, compared to a NO₃⁻-depleted placebo. A secondary purpose was to determine if a potential NO₃⁻-mediated increase in maximal power could increase performance during a fatiguing maximal cycling task (30 s).

METHODS

Design

This randomized, double-blind, crossover, repeated-measures design compared 1) acute changes in maximum power and optimal pedaling rate during maximal cycling (3-4 s) performed immediately before and ~2.5 h after consuming concentrated BRJ either rich or depleted in NO₃⁻, and 2) differences in performance during a fatiguing isokinetic (120 rpm) cycling trial (30 s) performed only after BRJ supplementation, in trained athletes.

Subjects

After providing written, informed consent, 13 competitively trained athletes from various sports (Table 1) participated in this study, which was approved by the Institutional Review Board at the University of Utah, in the spirit of the Helsinki Declaration. All participants followed a year-round regimen intended to improve performance in their respective sports and they were free of injury. Participants did not use tobacco products, prescription medication, or dietary supplements intended to increase sports performance.

Table 1.

Athletic background and anthropometric data of participants.

Sport	n	Competitive Level	Age (yrs)	Height (cm)	Weight (kg)
Tennis	♂=5	NCAA Division I	20.7±1.2	180.8±3.3	72.2±5.0
Alpine Ski	♂=2	NCAA Division I	23.7±0.1	174.0±1.8	75.9±3.2
American Football	♂=1	NCAA Division I	24.1	175.3	78.2
Cycling	♀=2	USA Cycling Category 1	35.7±8.1	171.5±1.8	56.6±2.9
	♂=1	USA Cycling Category 4	41.0	182.9	89.1
Triathlon	♂=2	USAT Top 15 (Rocky Mtn)	25.9±5.6	192.4±8.1	79.1±8.3
TOTAL	♀ =2 ♂ =11		25.9±7.5	180.6±7.5	73.8±10.3

Values are mean±SD.

Note that ♀=female; ♂=male; NCAA=National Collegiate Athletic Association; USAT=USA Triathlon.

Methodology

Figure 1 illustrates the experimental protocol requiring 1 or 3 d of familiarization¹¹ and 2 d of experimentation. On the first visit, anthropometric data were collected and participants were fitted for seat height and cycling shoes, which were held constant during all remaining visits. On the final day of familiarization, participants were instructed to maintain their habitual nutritional and training regime until completion of the study. Each experimental day required at least one night’s rest from regular training activities, or three night’s rest from competition. To insure consistency, both experimental days were scheduled after similar schedules. Participants abstained from antibacterial mouthwash and chewing gum to avoid eradication of oral bacteria that contribute to the NO₃⁻-NO₂⁻-NO pathway¹², and they refrained from alcohol or caffeine ingestion for at least 24 and 6 h, respectively¹³.

Figure 1.

Trained athletes practiced maximal cycling sprints for 1 or 3 d. ^*Specifically, cyclists require 1 d of familiarization while untrained cyclists (i.e., athletes from other sports) require 3 d of familiarization to reliably produce maximal power on an inertial-load cycle ergometer¹¹. Participants warmed-up for 5 min at 90 rpm and at their self-elected intensity, and then rehearsed four maximal cycling trials (3-4 s). During the final day of familiarization, participants rehearsed a highly-fatiguing maximal cycling trial lasting 30 s on a separate isokinetic cycle ergometer. The beetroot juice (BRJ) supplementation trials occurred across two experimental days. Immediately prior to BRJ supplementation (PRE), participants warmed-up, and then performed four maximal cycling trials. They were then issued either nitrate-rich (NO3) or nitrate-depleted (PLA) BRJ. Participants rested without sleeping, exercising, or eating, but water was permitted, for ~2.5 h and then they repeated the morning protocol to assess acute changes in maximal cycling power after BRJ supplementation (POST), with the addition of a 30 s maximal cycling sprint. ^**The only difference between experimental days was ingestion of either NO3 or PLA.

Experimental visits were separated by 3-7 d. A minimum washout of 3 d was chosen because elevations in plasma [NO₃⁻] and [NO₂⁻] after concentrated BRJ approach baseline levels after ~1 d¹³. On both experimental mornings, participants arrived at approximately the same time (~07:00 h) in a near-fasted state, that is, ~25 min after eating only one large apple. According to previous reports, apples have very low NO₃⁻ content (i.e., <20 mg NO₃⁻/kg)¹⁴. Upon arrival, participants verified compliance with the above-described instructions, then warmed-up and performed four trials of maximal cycling (3-4 s) on an inertial-load cycle ergometer, with a 2 min static recovery between trials. The inertial-load cycling protocol, which has been described previously¹⁵, measures maximal cycling power across a range of pedaling rates (e.g., 60–180 rpm) in a single brief trial (Figure 2). Maximal power in each trial was identified as the apex of the power-pedaling rate relationship and has been shown to be highly reliable¹⁵—the intra-session coefficient of variation (CV) in this study was 2.1±0.2%. To control for minor fluctuation in the power-pedaling rate relationship, quadratic regression was performed¹⁶. The greatest power measured across the four sprints (P_MAX) and optimal pedaling rate (RPM_OPT; the pedaling rate at which P_MAX was achieved)¹⁵ was recorded before BRJ consumption (PRE) and used for subsequent analysis.

Figure 2.

The inertial-load method measures power (W) across a variety of pedal rates (rpm) in a single maximal cycling effort. Curves drawn with closed and open circles illustrate changes in the power-pedal rate relationships achieved by competitive athletes (n=13) immediately before (PRE) and ~2.5 h after (POST) consuming beetroot juice (BRJ), respectively. Individual data points represent power and corresponding pedal rates of single pedal revolutions occurring immediately before and after the revolution eliciting peak power and optimal pedal rate (enlarged circles) at the apex of each curve. Panels A and B illustrate acute changes in power and pedal rate from PRE to POST after consuming nitrate-depleted (PLA) and nitrate-rich (NO3) BRJ, respectively. Both panels display an upward shift in the power-pedal rate curve from PRE to POST, indicating an acute increase in maximal power after both PLA and NO3 (^*p<0.001; ή²=0.83), but NO3 induced a greater rising power (^†p=0.009; ή²=0.45). The rightward shift in the power-pedal rate curve in panel B indicates that there was an acute increase in optimal pedal rate from PRE to POST NO3 (^‡p=0.043; ή²=0.30). Note: Values are represented as means. SD error bars were removed for clarity.

Immediately after the PRE trials, participants ingested two, 70 mL doses (separated by 30 min) of BRJ (Beet It Sport, James White Drinks Ltd., Ipswich, UK) either with (NO3) or without (PLA) NO₃⁻. NO3 contained ~11.2 mmol NO₃⁻, and PLA was created by passing NO3 through an ion exchange resin, rendering a drink depleted in NO₃⁻ (~0.004 mmol) that was similar in appearance, odor, and taste¹⁷. A neutral administrator coded the NO3 and PLA bottles so that neither the investigators nor the participants knew their identities. This strategy allowed random assignment on each experimental day by letting participants choose either pair on the first experimental day, with the other pair used on the second experimental day. The two doses of BRJ were separated by 30 min to help insure that the post-drink cycling sprints (POST) occurred within the 2-3 h window when plasma [NO₂⁻] peaks after dietary NO₃⁻ supplementation¹³.

After drinking the first dose of BRJ, participants left the lab for ~2.5 h with instructions to consume the second dose of BRJ 30 min after the first dose, and to abstain from sleep, exercise, food, or drink. Water was allowed ad libitum. Participants were instructed to eat another large apple 25 min before returning, upon which time they verified compliance with the aforementioned instructions. They warmed-up and then initiated the follow-up (i.e., POST) inertial-load sprints153±10 min and 123±10 min (mean±SD) after consuming the first and second doses of BRJ, respectively. P_MAX and RPM_OPT were recorded for POST, and relative changes in P_MAX and RPM_OPT from PRE to POST BRJ within the same day were calculated and expressed as percentages:

$$\%\Delta {\mathrm{P}}_{\mathrm{MAX}}=\left(\text{POST}{\mathrm{P}}_{\mathrm{MAX}}-\text{PRE}{\mathrm{P}}_{\mathrm{MAX}}\right)∕\text{PRE}{\mathrm{P}}_{\mathrm{MAX}}\mathrm{x}100$$ (Eq1)

$$\%\Delta {\text{RPM}}_{\text{OPT}}=\left({\text{POST RPM}}_{\text{OPT}}-{\text{PRE RPM}}_{\text{OPT}}\right)∕{\text{PRE RPM}}_{\text{OPT}}\mathrm{x}100$$ (Eq2)

Participants rested for 5 min after the POST sprints, and then performed a maximal cycling trial for 30 s on an isokinetic cycle ergometer, which has been described previously¹⁸. Power during the 30 s trial was recorded at 2 Hz using an SRM power meter (Schoberer Rad Messtechnik, Jülich, Germany), which has been shown to provide valid and reliable measures¹⁹. Pedaling rate was set to 120 rpm, the approximate RPM_OPT achieved at P_MAX during pilot testing. To minimize pacing during the 30 s trial, participants were highly encouraged to achieve their within-session P_MAX at the onset of the trial, then to continue pedaling maximally for the entire duration in an effort to produce a linear decrease in power over time. Peak power during the 30 s trial was defined as the highest power recorded during any 0.5 s interval (one crank revolution)¹⁸. Total work was calculated by summing the incremental work values sampled at each 0.5 s data point (incremental work = sampled power × 1/f)¹⁸. Rate of fatigue was expressed as the average percent drop in power per second.

Statistical Analysis

All values are expressed as mean±SD, and analyses were performed using SPSS 22.0 (SPSS, Inc., Chicago, IL, USA). Because this study was concerned with acute changes in performance from PRE to POST BRJ supplementation during the same day, a 2×2 repeated measures ANOVA was used to assess main effects of time (PRE vs. POST) and treatment (PLA vs. NO3) and their interaction on P_MAX and RPM_OPT. A paired t-test was used to compare relative changes (%ΔP_MAX and %ΔRPM_OPT) between PLA and NO3. Paired t-tests also compared peak power, total work, and rate of fatigue during the 30 s trials, which were only performed after PLA and NO3. Partial eta squared (ή²) and effect size (Cohen’s d) was used to determine the magnitude of the effect for significant outcomes (α=0.05) in the ANOVA and t-tests, respectively.

RESULTS

PRE BRJ P_MAX was 1191±298 W and 1160±301 W in the PLA and NO3 treatments, respectively. POST BRJ P_MAX was 1213±300 W for PLA and 1229±317 W for NO3. The repeated measures ANOVA revealed a main effect for time (PRE vs. POST) (F_(1,12)=56.40, p<0.001; ή²=0.83; 1-β=1.0) indicating that P_MAX acutely increased from PRE to POST on both experimental days. There was no main effect for treatment (PLA vs. NO3) (F_(1,12)=0.34, p=0.571), but there was a significant interaction between time and treatment on P_MAX (F_(1,12)=9.70, p=0.009; ή²=0.45; 1-β=0.82). Specifically, there was a greater increase in P_MAX from PRE to POST NO3 compared to PLA (Figure 2). This observation was verified by the paired t-test, which revealed a greater %ΔP_MAX after NO3 (6.0±2.6%) compared to PLA (2.0±3.8%) (p=0.014; d=1.21; 1-β=0.91) (Figure 3).

Figure 3.

Acute relative changes in maximal power (%ΔP_MAX) after consuming concentrated beetroot juice (BRJ) that was either depleted (PLA; open bar) or rich (NO3; closed bar) in dietary nitrate. %ΔP_MAX was significantly greater after NO3 compared to PLA (*p=0.014; d=1.21). Note: Values represent mean±SD.

PRE PLA RPM_OPT was 123±14 rpm and POST PLA RPM_OPT was 122±14 rpm, and PRE and POST NO3 RPM_OPT were 120±14 rpm and 127±13, respectively. There was no main effect for time (F_(1,12)=2.60, p=0.13) or treatment (F_(1,12)=0.22, p=0.651), but there was a significant interaction between time and treatment (F_(1,12)=5.13, p=0.043; ή²=0.30; 1-β=0.55). Specifically, RPM_OPT did not change from PRE to POST PLA but increased from PRE to POST NO3 (Figure 2), which is consistent with the t-test results for %ΔRPM_OPT (PLA: −0.3±4.1% vs. NO3: 6.5±11.4%; p=0.049; d=0.79; 1-β=0.74).

The 30 s isokinetic trials were performed only after BRJ consumption on both days. Maximal effort by the participants was verified by peak powers that were 97.5±4.8% of their within-session P_MAX in addition to a linear decrease in power with time (r =-0.99). After BRJ, there was no significant difference in peak power (PLA: 1185±249 W vs. NO3: 1173±255 W; p=0.44), total work (PLA: 23.0±4.4 kJ vs. NO3: 22.8±4.8 kJ; p>0.53), or rate of fatigue (PLA: −2.2±0.4%/s vs. NO3: −2.0±0.2%/s; p=0.22) between days.

DISCUSSION

The main finding of this study was that dietary NO₃⁻ acutely increased P_MAX and RPM_OPT. To our knowledge, this is the first study demonstrating that NO₃⁻ ingestion can acutely increase muscle power in trained athletes performing maximal voluntary multi-joint actions. Our findings add to recent reports that dietary NO₃⁻ can enhance explosive exercise performance in animal²⁰ and human muscle^3,4,9,10. Chronic (7 d) NO₃⁻ supplementation has increased rate of muscular force production in mice²⁰ and healthy men³, as well as total cumulative work across several brief cycling sprints performed by recreational athletes⁴. Hernández and colleagues²⁰ attributed their findings in mice to improved calcium handling, while Haider & Folland³ postulated that their results in men were possibly due to similar mechanisms. According to observations in mice²¹, Thompson and colleagues⁴ speculated that their findings were possibly due to an NO-induced increase in O₂ delivery to fast-twitch muscle. Adaptations to chronic NO₃⁻ supplementation may not apply to the current investigation, however, because changes in P_MAX were assessed acutely, from PRE to POST BRJ supplementation in the same day. Therefore, our findings are more consistent with those from Coggan and colleagues, who reported increases in maximal voluntary isokinetic knee extension power in healthy adults⁹ and heart failure patients¹⁰ after consuming a single bolus of NO₃⁻.

The exact mechanisms responsible for the acute effect of NO₃⁻ ingestion on human muscle power are unknown. Assuming that the observed effects are due to increased NO availability through the exogenous NO₃⁻-NO₂⁻-NO pathway¹, animal studies^5,6,7,8 suggest possible mechanisms by which NO may enhance neuromuscular power in people. NO₃⁻ ingestion appears to increase blood flow and vascular conductance to fast-twitch rat muscle to a greater extent than slow-twitch muscle²¹. Increasing blood flow to fast-twitch muscle could increase delivery of circulating NO precursors to the neuromuscular region. There, NO has directly increased the action of acetylcholine in the neuromuscular junction of fast-twitch rat muscle, resulting in greater motor endplate electrical currents⁵. Indirectly, increased NO availability may acutely enhance neuromuscular power by activating soluble guanylate cyclase, and thus increasing cyclic guanosine monophosphate (_CGMP). An NO/_CGMP-dependent mechanism has been shown to augment excitability of trigeminal motorneurons (responsible for actions of the jaw) in guinea pigs⁶, and to increase maximal shortening velocity and hence maximal power of fast-twitch rodent muscle^7,8. To date, no research has investigated the neural or contractile mechanisms by which dietary NO₃⁻ supplementation may acutely enhance neuromuscular power in humans. Based on the aforementioned animal studies^5,6,7,8,21, it is possible that there is increased action of NO in fast-twitch muscle. If this were true in humans, then individuals with more fast-twitch muscle (i.e., power-sports athletes) may particularly benefit from NO₃⁻ ingestion. Interestingly, elite power-sports athletes appear to be more genetically endowed to produce endogenous NO than elite endurance athletes²². This hypothesis must be considered with extreme caution because no research has tested it, and because post-hoc analysis revealed no apparent differences in %ΔP_MAX (p=0.53) or %ΔRPM_OPT (p=0.54) between the endurance and power-sports athletes in this study.

The notion that NO can acutely increase muscle shortening velocity through a NO/_CGMP-dependent mechanism^7,8 is consistent with the 6.5% increase in RPM_OPT observed in this study. Pedal speed (crank angular velocity × crank length) has been shown to highly correlate with joint angular velocity at the knee and hip and thus likely provides a surrogate measure for shortening velocity of mono-articular muscles spanning those joints^23,24. Additionally, pedaling rate (cycle frequency) influences maximal power by limiting the time for muscle excitation and relaxation²⁴. Increases in muscle shortening velocity directly affect muscular power because by definition, power is the product of force and velocity. As such, the observed increase in RPM_OPT after NO3 could explain most, if not all, of the observed increase in P_MAX, suggesting why maximal force (measured by cycling torque) remained unchanged (post-hoc analysis: p=0.40).

Both P_MAX and RPM_OPT acutely increased after NO3. Interestingly, there was a 2% increase in P_MAX after PLA. This increase was possibly due to an expected diurnal rhythm in maximal power, which correlates closely with the circadian variation in core body temperature. In particular, Lericollais and colleagues reported an 8.2% increase in peak power of highly trained competitive cyclists from 06:00 h to 18:00 h, an average increase of ~0.7%/h²⁵. At this rate, we might expect an increase in power of ~1.8% in the current study from PRE (~07:00 h) to POST (~09:30 h). This may explain, in part, the 2% increase in power we observed after PLA, in addition to contributing to the 6% increase in P_MAX after NO3.

Accounting for the plausibility of a diurnal rhythm contributing up to a 2% increase in P_MAX after both PLA and NO3, the acute 6% increase in P_MAX after NO3 may not be as large as observed (i.e., up to ~4.0%). Further, the acute 6% increase in P_MAX observed in this study is likely not as large as the ~6% and ~13% increases in isokinetic (6.28 rad/s) knee extension power observed in healthy adults⁹ and heart failure patients¹⁰, respectively. Coggan and colleagues^9,10, however, might have observed even larger effects if testing occurred immediately before and then after NO₃⁻ supplementation. The current study assessed acute changes in maximal power from PRE to POST NO₃⁻ ingestion in the same day. Thus, by using a highly reproducible method (CV=2.1±0.2% in the current study) and by accounting for day-to-day variations in power via a within-day control trial (i.e., PRE), we were able to detect statistically significant changes in maximal power that otherwise might have been overlooked. This interpretation is supported by the fact that post-hoc analysis revealed no difference in P_MAX between POST PLA and POST NO3 (p=0.31). Although trained athletes may not experience similar increases in power from dietary NO₃⁻ as untrained healthy adults⁹ or disease patients¹⁰, the large effect sizes for %ΔP_MAX (d=1.21) and %ΔRPM_OPT (d=0.79) indicate that the current findings may have practical significance. The current findings may particularly benefit power-sports athletes, especially those who depend on brief (i.e., ≤4 s) explosive actions (e.g., accelerating, jumping, throwing, etc.).

It is important to note that our primary finding, that NO availability augments neuromuscular power, diverges from previous studies that investigated the effects of acute dietary NO₃⁻ supplementation on the energetics and fatigue resistance of “sprint-type” exercise. One study²⁶ assessed if a single dose of dietary NO₃⁻ could improve performance across repeated kayak sprints (5 × 10 s, w/50 s rest between each sprint). In that study, trained kayakers performed a 15 min aerobic exercise trial immediately prior to performing repeated sprints, which may have prevented achievement of maximal power due to residual fatigue. In fact, the highest reported powers achieved by the participants did not occur until the final 10 s sprints²⁶, which further suggests residual fatigue during the sprints—when repeated sprint protocols are initiated without fatigue, the first sprint is usually the one eliciting maximal power²⁷. Another study²⁸ assessed the acute effect of NO₃⁻ ingestion on performance during repeated 8 s cycling sprints. Team sport athletes commenced the repeated sprint protocol in a non-fatigued state, but the authors did not report sprint-by-sprint peak or average powers because they were interested in how NO₃⁻ supplementation affected performance and fatigue across all sprints²⁸. In contrast, the present study focused on the acute effect of NO₃⁻ ingestion on maximal power in a non-fatigued state. The effects of acute and chronic NO₃⁻ supplementation on fatiguing high-intensity exercise performance have been well documented², but more research is needed to further assess how NO₃⁻ ingestion affects brief, maximal exercise without fatigue.

In contrast to the acute increases in P_MAX and RPM_OPT discussed above, however, we did not observe any differences in performance between NO3 and PLA during the fatiguing 30 s trials. Therefore, our findings are consistent with both of the aforementioned studies^26,28 and others^9,29 who have reported no performance changes in maximal effort, highly-fatiguing exercise performed on separate days after acute NO₃⁻ ingestion. It is possible that we did not see any differences in performance during the 30 s cycling effort after NO3 because a baseline test was not performed before supplementation. If P_MAX improved by ~6% from PRE to POST, a similar improvement in peak power at the onset of the 30 s trial might have contributed to greater acute change in work, and thus greater performance across the trial, particularly if the rate of fatigue remained unchanged. Further research is suggested to test this hypothesis. Another possible explanation may be that the 30 s sprint was performed on an isokinetic ergometer. In other words, if NO availability increases muscle shortening velocity^7,8 without affecting maximal force production^3,29,30, then increases in power may not have been possible because the constant pedal speed (i.e., 120 rpm) would have also maintained a constant muscle shortening velocity^23,24.

An important limitation of this study was that baseline P_MAX before NO3 was ~2.6% less than before PLA. Although a post-hoc dependent t-test revealed that this difference was not significant (p=0.07; d=-0.10), a coincidental difference is not impossible. Day-to-day fluctuations in maximal power using inertial-load cycling³¹ and other methods of power assessment³² are expected among actively training and competing athletes. Our repeated measures design accounted for these individual fluctuations by having each subject serve as his or her own control, while the double-blind crossover procedures insured that neither the researchers nor participants knew which doses (i.e., PLA or NO3) were consumed on either day. Therefore, we are confident in our findings and conclude that dietary NO₃⁻ supplementation can acutely increase maximal power of competitively trained athletes. Finally, we did not assess changes in plasma [NO₃⁻], [NO₂⁻], or other NO biomarkers (e.g., breath NO or muscle [_CGMP]) before or after NO3 and PLA. Doing so would have allowed us to determine if there was a relationship between changes in NO biomarkers and changes in performance⁹. Despite this limitation, previous work has indicated significant increases in [NO³⁻], [NO₃⁻], and in breath NO within 2-4 h of consuming the same BRJ product as in the current study^9,10,13.

PRACTICAL APPLICATIONS AND CONCLUSIONS

Dietary NO₃⁻ supplementation using concentrated BRJ can acutely increase maximal power and contractile speed of trained athletes performing multi-joint concentric actions. Replication of this study should consider the diurnal rhythm in muscle power while exploring the neuromuscular mechanisms that could explain the current and previous^9,10 findings. One promising aspect of this study was that the observed effects occurred within the context of our participants’ usual environment, that is, they did not modify their habitual diets, training, or competition schedules. As such, measuring performance immediately before supplementation is a promising strategy for future research investigating how NO₃⁻ acutely affects performance among athletes, a population in whom benefits have not always been observed. Use of a within-day control would also aid future efforts to determine if acute NO₃⁻-induced increases in power may transfer to brief explosive actions such as sprinting, jumping, agility, throwing, kicking, and striking. Because this study used a “motley crew” of athletes, future research could also explore how dietary NO₃⁻ can increase power in athletes from different types of sports (i.e., endurance-sports vs. power-sports), age-ranges, or with different muscle fiber distributions (i.e., slow-twitch vs. fast-twitch muscle). Nevertheless, trained power-sports athletes may particularly benefit by ingesting NO₃⁻ ~2-3 h before training, practice, or competition.