Effect of sodium bicarbonate ingestion on measures of football performance - with reference to the impact of training status

Ávirkanin av natriumbikarbonat inntøku á mát fyri kropslig fótbóltsavrik við støði í árinunum av kropsligari venjingarstøðu

 

Magni Mohr

Faculty of Natural and Health Sciences, University of the Faroe Islands, Tórshavn, Faroe Islands.

 

DOI: http://dx.doi.org/10.18602/fsj.v62i0.30

 

Abstract

Purpose: To investigate effects of acute sodium bicarbonate (NaHCO3) ingestion on performance during a football-specific protocol, with reference to mediating effects of intermittent training status. Methods: Ten male university football players (age:21±1 yrs, height: 180±2 cm, mass: 78.8±2.8 kg) completed two six-a-side football matches after ingesting either 0.4 g·kg-1 NaHCO3 (staggered over 90-min) or no supplement (CON) in a randomised, counterbalanced order. Activity profiles, blood [lactate], HR and gastrointestinal distress determined throughout. Training status was evaluated using Yo-YoIR1, Yo-YoIR2 and repeated-sprint tests. Results: Players performed 70.3% more high-speed running (17-21 km·h-1) during 0-5min following NaHCO3 ingestion vs. CON (17.9±5.2 vs. 10.5±3.1 m, P<0.05). No other significant activity profile differences, including high-intensity running (HIR; >14km·hr-1), existed between conditions during any period (P>0.05). However, total HIR increased for 70% of participants following NaHCO3 vs. CON (P>0.05). Large-very large correlations (0.5<r<0.9) existed between training status measures and HIR improvement from CON to NaHCO3 during certain match periods (P<0.05). Conclusions: Acute NaHCO3 ingestion appears ergogenic for some, but not all, football performance measures. Furthermore, individual variability in HIR response suggests this ergogenic potential is not realised by everyone. Correlational analysis suggests higher intermittent training status may potentiate NaHCO3 efficacy.

 

Úrtak

Endamál: At kanna ávirkanina av natriumbikarbonat (NaHCO3) inntøku á kropslig avrik í fótbólti, umframt árinini av kropsligari venjingarstøðu. Mannagongd: Tíggju mannligir fótboltsspælarar (aldur:21±1 ár, hædd: 180±2 cm, vekt: 78,8±2,8 kg) spældu tveir fótbóltsdystir (6 ímóti 6) eftir inntøku av antin 0,4 g·kg-1 NaHCO3 (inntikið í tablettformi 90-60 min áðrenn dystirnar) ella uttan inntøku av NaHCO3 (CON). Inntøkan av NaHCO3 var skipað tilvildarliga í dysti 1 og 2. Rennimynstur, blóðmjólkasýra, pulsur og neilig árin á maga-tarm skipanina var mátað undir dystunum. Kropsliga venjingarstøðan var mett við Yo-Yo IR1, Yo-Yo IR2 og skjótleikatestum. Úrslit: Spælarar runnu 70,3% longri við høgari renniferð (17-21 km·t-1) í fyrstu 5 min av dystunum eftir NaHCO3 inntøku vs. CON (17,9±5,2 vs. 10,5±3,1 m, P<0,05). Eingin annar signifikantur munur var á skjótari renning (øll renning >14 km·t-1) ímillum NaHCO3 og CON (P>0,05), hóast samlaða nøgdin á skjótari renning øktist hjá 70% av leikarunum í NaHCO3 vs. CON (P>0,05). Stórar og sera-stórar korrelatiónir (0,5<r<0.9) vóru ímillum kropsliga venjingarstøðu og framgongd í skjótari renning frá CON til NaHCO3 í serstøkum dystartíðarbilum (P<0,05). Niðurstøða: Inntøka av NaHCO3 stimbrar nøkur mát, men ikki øll, fyri kropslig avrik í fótbóltsdystum. Stórir individuellir munir eru á, hvussu stór henda ávirkan er. Korrelatiónsanalysan vísti, at jú betri kropsliga venjingarstøðan er, betri er ávirkanin av NaHCO3 inntøku á kropsligu avrikini.

 

Keywords: activity profiles, alkalosis, fatigue, intermittent exercise, training status.

 

Abbreviations

ANOVA:

Analysis of variance 

ATP:

Adenosine-tri-phosphate

Ca2+:

Calcium ions

FSG:

Full-Sized Game

GI:

Gastro-Intestinal

GPS:

Global Positioning System

H+:

Hydrogen ions

HCO-3:

Bicarbonate

HIR:

High Intensity Running (>15 km·h-1)

HR:

Heart Rate

K+:

Potassium ions

KATP:

ATP sensitive potassium channels

LSD:

Least Significant Difference

Na+:

Sodium ions

NaHCO3:

Sodium bicarbonate

PFI:

Permanent Fatigue Index

PFK:

Phospho-fructo-kinase

RST:

Repeated-Sprint-Test

RPE:

Rate of Perceived Exertion

SEM:

Standard Error of the Mean

SSG:

Small-Sided-Games

TFI:

Temporary Fatigue Index

VAS:

Visual Analogue Scales

Yo-Yo IR:

Yo-Yo Intermittent Recovery test

 

Introduction

Football is characterised by prolonged high-intensity intermittent exercise (Bangsbo et al., 1991). The ability to repeatedly perform and recover from high-intensity activities is a key performance determinant; validly evaluated using high-intensity running (HIR) distance during match-play, which correlates with performance quality during full-(Mohr et al., 2003) and small-sided games(Dellal et al., 2011). However, this ability declines temporarily during, and towards the end of a game (Mohr et al., 2003). Metabolic perturbations resulting from extensive anaerobic energy turnover have been implicated in this match-related fatigue (Bangsbo et al., 2006)

Temporary fatigue, as demonstrated by ~50% reduction in HIR in the 5-min following the most intense 5-min period (Mohr et al., 2005), negatively affects tactical (Bradley et al., 2009), technical (Lyons et al., 2006), and repeated-sprint (Krustrup et al., 2006a) abilities. The aetiology of temporary fatigue is complex (Rampinini et al., 2008), but appears unrelated to muscle [phosphocreatine], [ATP], [glycogen] and [lactate] (Mohr et al., 2005). Instead, interstitial potassium (K+) accumulation, and concomitant muscle cell excitability disturbances appear heavily implicated (Clausen, 2003;Mohr et al., 2005). Furthermore, muscle pH transiently declines below 7.0 during match-play (Krustrup et al., 2006a). Although dismissed as a direct contributor to temporary fatigue development per se (Krustrup et al., 2006a), intra muscular hydrogen ion (H+) accumulation opens ATP-sensitive K+ (KATP) channels, thus potentiating the aforementioned exercise-induced rise in interstitial [K+], and reducing muscle function(Davies, 1990). Moreover, intramuscular acidosis is also associated with impaired Ca2+ release and binding during actomyosin cross-bridge formation, impaired glycolytic enzyme activity (e.g. PFK) and accelerated central fatigue development (Cairns, 2006); all of which are detrimental to high-intensity exercise performance. Accordingly, improving pH (and H+) regulation during match-play could attenuate these deleterious effects, including match-induced hyperkalaemia, and thus ameliorate temporary fatigue resistance to increase overall HIR, and ultimately improve performance. Sodium bicarbonate (NaHCO3), an alkalinizing agent, may be beneficial in this regard (Peart et al., 2013).

Permitted by the World Anti-Doping Agency and FIFA (Dvorak et al., 2006), NaHCO3 has several mechanisms that may attenuate temporary fatigue development during football match-play. Firstly, NaHCO3 ingestion elevates blood [bicarbonate] (HCO3-) ~2.6-7.3mmol.L-1 following 0.3-0.4 g·kg-1 body mass dose (Siegler et al., 2010; Krustrup et al., 2015). HCO3- provides the predominant extracellular buffering mechanism, sequestering excess H+(Bishop, 2010). Accordingly, NaHCO3 ingestion enhances extracellular, as opposed to intracellular, H+ buffer capacity (Hollidge-Horvat et al., 2000). Specifically, the increased [HCO3-] and concomitant reduced extracellular [H+] creates a large muscle-to-blood [H+] gradient (Street et al., 2005), which facilitates H+ efflux from exercising muscle, thus attenuating exercise-induced muscular pH. Therefore, NaHCO3 ingestion can attenuate aforementioned deleterious effects associated with intramuscular acidosis, which also is suggested by recent studies (Marriott et al., 2015; Krustrup et al., 2015). However, it is unknown, how NaHCO3 ingestion affects football match performance.

Few studies have investigated intermittent team-sport players (e.g. football (De Ste Croix & Pope, 2006)), however, their protocols fail to elicit activity profiles and metabolic responses specific to football match-play. Likewise, no study has used actual match-play as its protocol; problematic due to the task-specific nature of fatigue (Enoka & Stuart, 1992). Therefore, limited ecological validity of previous studies reduces practical applicability of results to football match-play, meaning any potential ergogenic effects of NaHCO3 for football match-play remain to be determined. Furthermore, to the author’s knowledge, no research has investigated the effect of intermittent training status on NaHCO­3 efficacy; highlighting two gaps in our current knowledge. Such research would allow individual recommendations regarding NaHCO3 efficacy to be made specifically for football players based on football-specific evidence; important because supplement use in football often lacks scientific backing (Taioli, 2007). Thus, the purpose of the current study was to investigate the potential ergogenic effects of acute NaHCO3 ingestion during a protocol specific to football match-play, with reference to the mediating effects of training status; research that is currently unavailable. Specifically, small-sided games (SSGs) were used to elicit match-specific metabolic responses to test the following experimental hypotheses: 1) NaHCO3 will affect distances covered in various activity categories; 2) NaHCO3 will increase match performance as measured by HIR; 3) NaHCO3 efficacy will be mediated by participant training status.     

 

Methods

Participants

Ten male university football players familiar with intense intermittent exercise participated in the study (age: 21±1 years, height: 180±2 cm, body mass: 79±3 kg). Players were fully informed of the experimental protocol, and risks (e.g. GI distress) and benefits associated with participation before freely providing written consent. The study was approved by the University of Exeter Research Ethics Committee.      

 

Experimental design

A fully repeated-measures design was used (condition x time). Participants completed a familiarisation trial, a Yo-Yo Intermittent Recovery test level 1 (Yo-Yo IR1) and level 2 (Yo-Yo IR2) and a repeated-sprint test (RST) separated by ≥48-h to determine intermittent training status. Participants subsequently completed two 6-a-side football matches under two conditions (NaHCO3 and control) in a randomised, counterbalanced, cross-over manner, separated by five days. Activity profile, blood [lactate], heart rate (HR), Gastro-Intestinal (GI) distress and Rate of Perceived Exertion (RPE) data collected throughout match-play. Artificial grass used throughout to ensure standardised surface conditions.

 

Preparation procedures

Players instructed to refrain from: caffeine (24-h before), strenuous activity (48-h before), alcohol (48-h before), other supplementation (throughout). Prior to all testing sessions, players were fitted with a Global Positioning System (GPS) unit (GPS Sports Systems, SPI Pro X, Australia) and HR chest belt (Polar heart rate monitor, Polar Electro, Finland) to collect activity patterns and HR data, respectively.    

Food and fluid intake (type, volume/mass) recorded prior to match one, and replicated prior to match two to prevent diet-induced changes in acid-base balance (Greenhaff et al., 1988). Participants reported to the football pitch 100-min prior to kick-off to complete supplementation. Both matches played at 1.30 pm; avoiding circadian variation (Reilly, 1986). The same GPS unit was worn by the individual player for both matches to minimise inter-device measurement error (Jennings et al., 2010)

 

Experimental protocol

Familiarisation.Before testing, participants completed a familiarisation of each performance test to increase test reproducibility (Bangsbo and Mohr, 2012). Body mass (Seca digital scale column SEC-170, Seca, Hamburg, Germany) and height (Seca stadiometer SEC-225, Seca, Hamburg, Germany) were also measured.    

Performance testing. The Yo-Yo IR1 and IR2 tests consist of repeated 2x20m shuttles interspersed by 10-s active recovery in 2m wide lanes at progressively increasing speed as controlled by audio cues as described by Krustrup et al. (2006b). Yo-Yo IR1 evaluates the ability to repeatedly perform high-intensity aerobic work, while Yo-Yo IR2 simultaneously stimulates aerobic and anaerobic energy turnover, warranting inclusion of both (Bangsbo et al., 2008). Test performance correlates with HIR distance (Krustrup et al., 2006b), thus providing a reproducible, sensitive and valid (external, discriminant) determination of football-specific training status (Ingebrigtsen et al., 2012). Peak HR achieved during Yo-Yo IR1 considered as participant’s HRmax(Bangsbo et al., 2008).

Participants completed a 5x30m RST interspersed with 25-s active recovery (jog back to start) (Krustrup et al., 2006a). Tests commenced 5-min after a 10-min standardised warm-up consisting running at increasing intensity, including 2x20m sprints. Starting position was standardised. A 5-s countdown provided for each sprint. Sprint times recorded using wireless timing gates with an accuracy of 0.01-s (Brower TC Timing System, Draper, Utah, USA) adjusted to participant hip height. Fastest sprint time, mean sprint time and fatigue index () were derived from the RST (Bangsbo and Mohr, 2012).

Experimental model.Players completed two 6-a-side matches (one following NaHCO3, one following control) on a half-sized out-door artificial pitch lasting 90-min (2x45-min) after a standardised warm-up. During the first game five players representing both teams received NaHCO3 and during the second game the remaining five players received NaHCO3. Mimicking full-sized game (FSG) match-play was vital to fulfil study aims. SSGs simulate overall activity patterns and closely replicate physiological and technical aspects of FSGs (Dellal et al., 2012), maximising ecological validity and justifying the protocol. A goalkeeper was each team’s sixth player, but was not a participant of the study. Blood [lactate] was measured at rest, half-time and full-time via fingertip capillary blood sampling (Lactate Pro, Blood lactate test meter, Arkray Inc, Kyoto, Japan). HR was collected throughout at 5-s intervals, and recorded as absolute (bpm) and relative (%HRmax) values.

GPS analysis used as it provides a time-effective, sensitive and detailed analysis of activity patterns with minimal error (TEM=5.5%) (Aughey, 2010), allowing valid evaluation of fatigue development and supplement efficacy (Randers et al., 2010). The locomotor categories used were modified from Mohr et al. (2003): standing (0-1.99km·h-1); walking (2-6.99km·h-1); low-speed running (7-13.99km·h-1); moderate-speed running (14-16.99km·h-1); high-speed running (17-20.99km·h-1); very high-speed running (21-23.99km·h-1); sprinting (>24km·h-1). HIR (considered the most valid physical performance measure) categorised as the sum of moderate-speed running, high-speed running, very high-speed running and sprinting (Mohr et al., 2003). Distance of each recorded at 5-Hz frequency for pre-determined 5-, 15-, 45- and 90-min periods. Total distance (TD) calculated as the sum of all distances. Peak and mean distance covered in HIR in a single 5-min period determined. Sprint frequency and speed data (average and peak) also determined. Two permanent fatigue indexes (PFI1 and PFI2) and one temporary fatigue index (TFI) were calculated in accordance with Mohr et al. (2012)

Eleven 100mm visual analogue scales (VAS) validly quantified acute GI distress (Cameron et al., 2010) and ratings of perceived exertion (RPE) (Rebelo et al., 2012) at baseline, half-time and full-time. Participants placed a dash on each VAS to rate; effort, demand, nausea, flatulence, stomach cramping, belching, stomach ache, bowel urgency, diarrhoea, vomiting and stomach bloating. Length of line left of the dash used as the result (0-100mm). Examples below (figure 1).

Figure 1. Example VAS scales. 

 

Supplementation protocol

Prior to the two matches, participants ingested either NaHCO3or no supplement (control) in a randomised, counterbalanced, cross-over manner. NaHCO3 dosing protocol selected in accordance with Marriott et al. (2015). Specifically, participants ingested 0.4g·kg-1 body mass NaHCO3 prior to one match; selected because ≥0.3g·kg-1 is required to induce alkalosis (McNaughton, 1992), but ≥0.5g·kg-1 likely induces significant GI distress (Requena et al., 2005). Indeed, Bishop and Claudius (2005) reported performance enhancement using 0.4g·kg-1. Doses administered orally via 20-25 gelatine capsules are minimising GI distress risk vs. solution (Peart et al., 2012). Four-five capsules ingested with water ad libitum at 90-, 80-, 70-, 60- and 50-min before kick-off as staggered dosing gains maximal alkalosis and minimises GI distress (Siegler et al., 2012)

 

Statistics

Data analysed using SPSS v19.0 for Windows (SPSS Inc., Chicago, IL, USA). Results presented as mean±SEM. Assumptions of normality verified using Kolmogorov-Smirnov test. Sphericity tested using Mauchley’s test, with violations corrected using Greenhouse-Geisser (GG) correction (controlling type I error rate). Within-within differences in activity profiles, HR, blood [lactate] and VAS data between conditions evaluated using two-way (condition x time) analysis of variance (ANOVA) for repeated-measures. Least significant difference (LSD) post-hoc tests located any significant differences. Many time points (up to 18) made Bonferroni inappropriate as type II error risk would be extremely high (Field, 2005); justifying use of LSD. Differences in whole game data between conditions determined using Student’s paired t-tests. Relationships between delta increase in HIR distance from control to NaHCO3 and each performance test, as well as between PFI1, PFI2 and TFI with each performance test determined using Pearson’s product-moment correlation coefficient. Correlation strengths determined in accordance with Hopkins (2000). Significance accepted at P<0.05.     

 

Results

Activity profiles

Significant main effect of time (P<0.05), but not condition (P>0.05), on distances covered in all activity profile categories (including HIR) during 5-, 15- and 45-min periods, except no main effect of time on very high-speed running and sprinting during 45-min periods (P>0.05).

No significant condition x time interaction effects on distances standing, walking, low-speed running, moderate-speed running, very high-speed running, sprinting or HIR (all P>0.05), but there was on distance high-speed running (F (17, 153) =1.764, P<0.05). Specifically, post hoc LSD revealed players covered 70.3% more distance high-speed running following NaHCO3 (18±5 m) compared to control condition (11±3 m) during 0-5 min (P<0.05; Figure 2).

Figure 2. High speed running distance in 5-min intervals. for control and NaHCO3 (mean±SEM). *Denotes significant difference compared to control (P<0.05).

 

No significant difference existed between conditions for peak HIR (NaHCO3:79±7 vs. CON: 69±6 m) or mean 5-min HIR (NaHCO3:31±4 vs. CON: 30±4 m) HIR distance (P>0.05).  However, HIR distance during the 5-min interval after peak the 5-min period tended to be higher in NaHCO3 (34±5 m) than in CON (24±4 m) (t (9) =2.169, P=0.058; Figure 3). Finally, HIR tended (P=0.06) to be lower than mean HIR in this period in CON only.

Figure 3. Peak 5-min, following 5-min and average 5-min HIR distance for control and NaHCO(mean±SEM)

 

No significant condition x time interaction on distances standing, walking, moderate-speed running, fast-speed running, very fast-speed running, sprinting and HIR (all P>0.05). However, players covered greater low-speed running distance in control (467±36 m) compared to NaHCO3 (370±34 m) during 30-45min (F (5, 45)=2.417, P<0.05).

No significant condition x time interaction effect on distances standing, walking, low-speed running, moderate-speed running, fast-speed running, very fast-speed running, sprinting, HIR or TD (Figure 4B) (all P>0.05). HIR increased from control to NaHCO3 in 60% and 70% of participants in each half and whole game, respectively (Figure 4A).

Figure 4. Mean and individual scores for HIR (A) and mean±SEM for TD (B) in each half and overall for control and NaHCO.

 

No significant differences existed between conditions in total distance covered in all activity profile data (including HIR, TD, >17km·h-1, >21km·h-1), PFI1, PFI2 and TFI across the whole match (all P>0.05; Table 1).

No significant main or interaction effects on average and peak speed during any match-play period (P>0.05).   

 

Table 1. Whole match activity profile, fatigue indexes and HR data (n=10).

 

0-90 min

 

NaHCO3

Control

Activity profile distance (m)

 

 

Standing

195±7

195±9

Walking

4086±116

4096±98

Low-speed running

2572±103

2626±152

Moderate-speed running

413±45

388±41

High-speed running

168±24

159±24

Very high-speed running

18±4

23±5

Sprinting

0.3±0.1

1.3±1

Cumulative distances (m)

 

 

HIR

600±70

572±65

TD

7453±193

7489±236

>17km·h-1

187±27

184±27

>21km·h-1

19±4

25±5

Fatigue index (%)

 

 

PFI1

-3.4±20.7

29.1±14.9

PFI2

-13.3±17.8

24.2±9.0

TFI

54.4±8.0

63.8±5.5

Absolute HR (bpm)

 

 

Average

151±5

152±5

Peak

186±4

186±5

Relative HR (%HRmax)

 

 

Average

78.0±2.5

78.6±2.5

Peak

96.3±2.0

96.0±2.4

Game variable and heart rate during a game in NaHCO3 and control condition. Values are mean±SEM.. *Significant difference between conditions (P<0.05).

 

Cardiovascular loading and blood lactate

Average HR values were higher (P<0.05) in the first vs. second half for absolute (157±4 vs. 146±4 bpm, respectively) and relative HR (81.1±1.9 vs. 75.4±1.8 %HRmax, respectively­) HR. No condition x time interaction on all HR measures (P>0.05). No significant differences in all HR measures between conditions over whole match (P>0.05; Table 1).

Blood [lactate] was significantly higher at half-time (4.7±0.6 mmol.L-1) and full-time (4.3±0.8 mmol.L-1) vs. baseline (1.8±0.2 mmol.L-1) (P<0.05), with no significant differences between halves (P>0.05). No condition x time interaction effect existed for blood [lactate] (P>0.05; Table 2).

 

Table 2. Blood [lactate] data (n=10).

 

Baseline

Half-time

Full-time

 

NaHCO3

Control

NaHCO3

Control

NaHCO3

Control

Blood [lactate]

1.9±0.2

 

1.6±0.3

 

4.5±0.7

 

4.8±1.2

 

3.6±1.0

 

5.0±1.1

 

Data are in mmol·l-1. Values are mean±SEM.

 

VAS ratings

There were no condition x time interactions on perceived effort, perceived demand, nausea, stomach ache, bowel urgency, diarrhoea and vomiting (all P>0.05), but there was on flatulence (FGG(1.299, 11.690)=4.471, P<0.05), stomach cramping (F(2, 18)=10.214, P<0.05), belching (FGG(1.184, 10.654)=6.048, P<0.05) and stomach bloating (FGG(1.108, 9.970)=8.889, P<0.05). Post hoc LSD located these differences (Figure 5). No significant VAS differences between conditions at kick-off (P>0.05).

Figure 5. VAS rating in first- (A) and second-half (B) for control and NaHCO(mean±SEM). *Significantly higher in NaHCO3 (P<0.05).

 

Correlations

Delta HIR increase (m) from control to NaHCO3 represents NaHCO3 HIR-control HIR (positive=NaHCO3>control; negative=NaHCO3<control). Training status data presented below (Table 3).

 

Table 3. Participant training status data (n=10).

Performance measure

Test result/score

Yo-YoIR1 (m)

1324±122

Yo-YoIR2 (m)

524±52

RST fastest sprint (s)

4.64±0.07

RST mean sprint (s)

4.77±0.09

RST fatigue index (%)

5.2±1.0

Values are mean±SEM.  

 

Significant correlations between Yo-Yo IR1 (Figure 6A), Yo-Yo IR2 (Figure 6B and 6C) and RST measures (Table 4) with delta HIR increase during different match-play periods presented below. PFI1 (r= -0.58) and PFI2 (r= -0.76) significantly correlated with Yo-Yo IR2 performance in control condition only (P<0.05). TFI was not significantly correlated with any performance test in either condition (P>0.05). 

Figure 6. Relationships between: Yo-YoIR1 performance with delta HIR increase during 0-5min (A: r= 0.75; P<0.05) and Yo-YoIR2 performance with delta HIR increase during 0-5min (B: r= 0.67; P<0.05) and 50-55min (C: r= 0.59; P<0.05). 

 

Yo-Yo IR1 was not correlated with total HIR in either condition (P>0.05). Yo-Yo IR2 correlated with total HIR during 0-45, 45-90 and 0-90 min in both NaHCO3 (r= 0.65, 0.57 and 0.65 respectively; P<0.05) and control (r= 0.57, 0.58 and 0.61 respectively; P<0.05).

 

Table 4. Relationship between delta HIR increase and RST performance data

Performance measure

Time period

 

15-20 min

0-45 min

60-75 min

0-90 min

RST fastest sprint (s)

 

r= -0.75*

 

r= -0.63*

RST mean sprint (s)

 

r= -0.74*

r= -0.58*

r= -0.69*

RST FI (%)

r= -0.57*

 

r= -0.59*

r= -0.67*

*Statistical significance (P<0.05).

 

Discussion

The current study is the first to use football match-play to investigate the ergogentic effects of oral NaHCO3 supplementation. Major findings shows that players covered greater high-speed running (17-21 km·h-1) distance during 0-5 min of match-play in the NaHCO3 vs. control condition. However, all other activity profiles, including HIR, were unchanged by NaHCO3 during all match-play periods. Furthermore, NaHCO3 efficacy was extremely individual, potentially mediated by training status. Therefore, results support experimental hypotheses one and three, but not two. 

Players performed 70% more high-speed running following NaHCO3 vs. control during the initial 5-min of the first half, which on average wass the most intense 5-min interval of both game-trials (Figure 2). The first part of a game is usually the period with most high intensity running (Mohr et al., 2003) and may therefore be the period challenging the acid-base homeostasis to the highest degree. Thus, the potential effect of NaHCO3 supplementation may be greatest in the initial phase of a game. No previous study has used game activity pattern as dependent variable, making direct comparisons impossible. However, corroboratory evidence has been reported during repeated-sprint (Bishop et al., 2004) and intense intermittent exercise (Krustrup et al., 2015; Marriott et al., 2015); exercise protocols relevant to football match-play. Additionally, HIR during the 5-min interval following the peak 5-min period was lowered below mean (tendency; P=0.06) for control, as also shown by others (Mohr et al., 2003), but not in the NaHCO3-trial (non-significant), and HIR in this period tended (P=0.058) to be higher (~41%) in NaHCO3 than control; possibly representing attenuated temporary fatigue development following NaHCO3 intake. These performance enhancements are valuable and may result from reduced efflux and increased reuptake of K+ in the exercising muscles via the Na+-K+ ATPase, and resultant attenuated exercise-induced rise in muscle interstitial [K+] associated with alkalosis(Street et al., 2005); important given the likely role of interstitial K+accumulation in temporary fatigue development (Mohr et al., 2005). Indeed, reducing interstitial [K+] has been associated with improved intermittent exercise performance (Mohr et al., 2011). However, high-intensity repeated/intermittent-sprint performance is not always improved after NaHCO3 intake despite inducing alkalosis (De Ste Croix & Pope, 2006; Price & Simons, 2010; Tan et al., 2010), thus contradicting current findings. The different doses used in these studies and the use of solution (increases GI distress risk vs. capsules; Peart et al., 2012) may contribute to the lack of performance improvements in these studies. Furthermore, staggering ingestion as in the present study has been associated with improved performance (Bishop & Claudius, 2005; Marriott et al., 2015; Krustrup et al., 2015), whereas single bolus was not (e.g. Tan et al., 2010). Varying exercise modality, physiological demands, circadian variation and participant training status may also contribute to aforementioned discrepancies (Douroudos et al., 2006).   

Paradoxically, all other activity data, including HIR, were unaffected by NaHCO3 throughout. Lack of performance effect supports some (e.g. Tan et al., 2010), but not all (Bishop et al., 2004) previous investigations. Peak speed was also unaffected by NaHCO3, agreeing with Zinner et al. (2011). Furthermore, non-significant tendency for less high-speed running following NaHC­O3 during 25-30 and 55-60 min could suggest an ergolytic effect. Frequent lower-intensity periods during match-play would be expected to be conducive to NaHCO3 efficacy(Siegler et al., 2008). However, no significant TFI improvement suggests temporary fatigue was not attenuated with NaHCO3, possibly contributing to lack of HIR change. Lack of HIR increase could also be ascribed to failure of supplementation to induce the increases in pH (0.05-0.1unit) and [HCO3-] (~5.0mmol.L-1) generally required for improved repeated/intermittent-sprint performance (Bishop, 2010), as this would nullify aforementioned ergogenic mechanisms associated with NaHCO3. However, these targets are usually exceeded following staggered 0.4 g·kg-1 NaHCO3 ingestion (Bishop & Claudius, 2005). Therefore, factors other than H+accumulation, such as interstitial [K+] (temporary fatigue) and glycogen depletion in individual muscle fibres (‘permanent’ fatigue), may have limited performance (Krustrup et al., 2006a), meaning additional extracellular buffer capacity afforded by NaHCO3 would provide limited performance benefits. This may contribute to the lack of performance improvement, and further dismiss H+ accumulation as a major contributor to football-specific fatigue. Indeed, alkalosis can occur without concomitant performance enhancements (Tan et al., 2010).  

Alternatively, average match intensity (~80% HRmax) may not have provided sufficient metabolic stress (including [H+]) to benefit from additional extracellular buffer capacity afforded by NaHCO3, further contributing to lack of HIR improvement. Additionally, consensus suggests NaHCO3 is ergogenic during exercise of 1-15 min (Bellinger et al., 2012), possibly explaining why high-speed running only improved during the first 5-min interval of the game, and why HIR over 90-min was not improved. Nevertheless, HIR was non-significantly higher during the first-half (1.9%), second-half (8.9%) and whole match (4.9%) following NaHCO3 and may have failed to reach statistical significant due to the small sample size. However, such improvements may have practical significance.

Perceived effort and demand were not significantly affected by NaHCO3, agreeing with some (Zabala et al., 2011), but not others who report reduced RPE following NaHCO3; discrepancies partly attributable to varying protocol metabolic requirements (Marriott et al., 2015; Krustrup et al., 2015).This lack of effect may further contribute to lack of HIR improvement. Furthermore, NaHCO3 significantly increased rating of flatulence, stomach cramping, belching and stomach bloating, possibly attributable to increased small intestine [Na+] (Heigenhauser, 1991). GI distress is frequently reported, and may have negated potential ergogenic effects of NaHCO3, possibly contributing to lack of HIR increase.

NaHCO3 had no significant effect on blood [lactate], contrasting increased concentrations reported previously (Hollidge-Horvat et al., 2000). This result suggests glycolytic turnover and/or lactate efflux were not enhanced following NaHCO3,possibly further explaining the lack of HIR increase (Juel, 1998). However, it is likely that the blood lactate levels have been higher early in the first half, where the effects of the NaHCO3 are likely to peak, which also is indicated by the great amount of high intensity running during the first 5 min of the game (Figure 2).

HIR increased from control to NaHCO3 in 60% and 70% of participants in each half and whole game, respectively (figure 4A), reiterating the low vs. high-responder effect frequently reported following drug manipulations(Price & Simons, 2010). This large individual variability may have prevented statistical significance for HIR. Interestingly, large-very large significant correlations (0.5<r<0.9) exist between training status and improvement in HIR from control to NaHCO3; suggesting fitness level may mediate this inter-individual variability. Specifically, higher Yo-Yo IR1 and IR2 performances were related to greater HIR increases following NaHCO3 vs. control during 0-5 and 50-55min (Yo-Yo IR2 only). Additionally, lower values for RST FI, fastest and mean sprint time (greater training status) related to greater HIR gains during 0-45 (fastest and mean), 0-90 (all), 15-20 (FI) and 60-75min (mean and FI). Collectively, these results suggest higher training status (high Yo-Yo IR values, low RST values) may potentiate NaHCO3 efficacy, at least within this specific sample of sub-elite footballers. In support of this notion greater performance gains with higher training status have been reported previously (Carr et al., 2012); apparently particularly true during repeated-sprint exercise (weighted effect size: trained=0.18 vs. untrained=0.05) (Peart et al., 2012), as observed during football.

Inherent match-to-match variation in activity patterns (Gregson et al., 2010) and relatively small sample size possibly reduced statistical power (increasing type II error risk), thus preventing statistical significance. Furthermore, considerably lower training status of current sub-elite participants vs. elite players (Mohr & Krustrup, 2013), may make direct extrapolation of results to elite players erroneous. To overcome these limitations, future research could investigate NaHCO3 efficacy using a large sample of preferably elite players during the Copenhagen Soccer Test; a controlled, reproducible protocol that closely relates to match-play and effectively evaluates technical ability (not assessed in the current study but contributes to overall performance and nutritional interventions (Bendiksen et al., 2012). Additionally, components of an optimal dosing strategy using 0.4g·kg-1(e.g. timings, capsules vs. solution) should be identified; research that is lacking for this dose. Further improvements to the current study include use of a double-blind, placebo-controlled design, and analysis of blood samples for pH, [H+] and [K+] to allow a more mechanistic explanation of results to be provided.

In conclusion, despite no significant effect on total match HIR, the significant increase in high-speed running in the first 5-min vs. control suggests NaHCO3 may be an effective ergogenic aid for football players, with no significant ergolytic effect observed in any activity profile. Furthermore, results suggest individuals with higher training status may gain greater ergogenic benefits from NaHCO3 ingestion. Finally, individual variability in response reiterates the importance of evaluating performance changes on an individual basis before making recommendations regarding NaHCO­­3 intake.         

 

Acknowledgements

The author thanks the football players, coaches and club for their committed participation. The assistance of Nikolai B. Nordsborg, Steven Carter and Sarah Jackman are greatly appreciated.        

 

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