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joellemj · 5 years

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Training to the positive muscle failure point

Introduction Few concepts in the world of strength training have been more hotly debated than the need (or not) to reach muscle failure during your sets. Is it necessary for muscle growth? No. However, I feel it is necessary for optimal growth. Some argue that training to failure is either dangerous or can lead to CNS fatigue. Others argue that training to failure too often will cause too much muscle damage and can lead to localized overtraining. Some of these misconceptions stem from the fact that muscle failure is not well understood.

The biggest proponents of training to failure have defined it as “creating a maximum amount of inroads to the muscle on each set”. This is fine and well however am I the only one who doesn’t understand what they mean by that? It is important to correctly describe what muscle failure is and why it happens. This information will allow us to make an objective assessment of the need (or not) of training to failure.

What is the point of failure? Failure is easy to understand. It’s simply the incapacity to maintain the required amount of force output (Edwards 1981, Davis 1996). In other words, at some point during your set, completing more repetitions will become more and more arduous until you are unable to produce the required amount of force to complete a repetition. Failure isn’t the amount of “inroad” to the muscle; it’s nothing esoteric as we just saw.

The causes of failure If the concept of training to failure is actually quite easy to grasp, the causes underlying this occurrence are a bit more complex. There is no exclusive cause of training failure; rather there are quite a few of them.

1. Central/Neuromuscular factors: the nervous system is the boss! It’s the CNS that recruits the motor-units involved in the movement, set their firing rate and ensure proper intra and intermuscular coordination. Central fatigue can contribute to muscle failure, especially the depletion of the neurotransmitters dopamine and acetylcholine. A decrease in acetylcholine levels is associated with a decrease in the efficiency of the neuromuscular transmission. In other words, when acetylcholine levels are low, it’s harder for your CNS to recruit motor-units.

2. Psychological factors: The perception of exhaustion or exercise discomfort can lead to a premature ending of a set. This is especially true of beginners who are not accustomed to the pain of training intensely. Subconsciously (or not) the individual will decrease his force production as the set becomes uncomfortable. This is obviously not an “acceptable” cause of failure in the intermediate or advanced trainees, but beginners who are not used to intense training could slowly break into it by gradually increasing their pain tolerance.

3. Metabolic and mechanical factors: It is well known that an increase in blood acidity reduces the magnitude of the neural drive as well as the whole neuromuscular process. Lactic acid and lactate are sometimes thought to be the cause of this acidification of the blood, but this is actually not the case. The real culprit is hydrogen. Hydrogen ions can increase blood acidity, inhibits the PFK enzyme (reducing the capacity to produce energy from glucose), interferes with the formation of the actin-myosin cross bridges (necessary for muscle contraction to occur) and decrease the sensitivity of the troponin to calcium ions. Potassium ions can also play a role in muscle fatigue during a set. Sejersted (2000) has demonstrated that intense physical activity markedly increases extra-cellular levels of potassium ions. Potassium accumulation outside the muscle cell leads to a dramatic loss of force which obviously makes muscle action more difficult. Finally we can include phosphate molecules into the equation. Phosphate is a by-product of the breadown of ATP to produce energy. An accumulation of phosphate decreases the sensitivity of the sarcoplasmic reticulum to calcium ions. Without going into excessive detail, this desensitization reduces the capacity to produce a decent muscle contraction.

4. Energetic factors: Muscle contraction requires energy. Strength training relies first and foremost on the use of glucose/glucogen for fuel with the phophagen system (ATPCP) also playing a role. Intramuscular glycogen levels (glucose reserve in the muscle) is very limited and can become depleted as the training session progresses. The body can compensate by mobilizing glucose stored elsewhere in the body (but this amount is also finite), by transforming amino acids into glucose (which is a less powerful way of producing energy for intense muscle contractions), or turn to free fatty acids and ketone bodies. The last two solutions cannot provide energy as fast as intramuscular glycogen can. As a result, even though it will be possible to continue exercising with a depleted muscle, it is impossible to maintain the same level of intensity and force production.

So as you can see, it is impossible to attribute muscle failure to a single phenomenon. Rather, it’s a mix of several factors that cause muscle failure. Contrary to popular beliefs, reaching muscle failure in one set doesn’t ensure the complete fatigue and stimulation of all the muscle fibers in a muscle. Far from it! Failure can occur way before full contractile fatigue has been reached. This means that the “one set per exercise to failure” method is not ideal for maximal growth. As a part of a more complex training system it can be beneficial from time to time, but not as a discrete training system. Where to buy steroids online will be the concern of most, however concentrating of this list of tips will greatly improve your performance until you reach the point where you will require anabolics.

At some point it becomes necessary to increase training volume to fully stimulate a larger pool of muscle fibers. Remember that simply recruiting a motor-unit doesn’t mean that it’s been stimulated. To be stimulated a muscle fiber must be recruited and fatigued (Zatsiorsky 1996).

If training to failure doesn’t ensure full motor-unit stimulation within a muscle, not taking a set to positive muscle failure (the point where a technically correct full repetition cannot be completed) is even less effective since it will not fatigue the HTMUs as much and remember that a muscle fiber that isn’t fatigued isn’t fully stimulated! In other words training to failure doesn’t guarantee maximal motor-unit stimulation but not taking a set to failure drastically reduces the efficacy of a set. This indicates that high volume of work without going to failure isn’t ideal for maximal muscle growth (but it’s okay for strength and power oriented training). But the other end of the spectrum: low-volume training taken to failure isn’t ideal either. Failure and volume are both needed for maximal motorunit stimulation. That’s not to say that you should use a huge volume of work, but a moderate volume of sets taken to failure is necessary for maximal muscle growth.

And what about the so-called CNS drain that can occur when you take your sets to failure? While I do agree that for continuous improvements to occur one should avoid CNS burnout/overtraining (also called the Central Fatigue Syndrome). I understand the theory behind avoiding going to failure: going to failure increases the implication of the nervous system because as fatigue sets in (accumulation of metabolites and energetic depletion) it must work harder to recruit the last HTMUs. The argument is that we should minimize training that has a high demand on the nervous system. However, most people who espouse the “don’t go to failure” theory are generally proponents of heavy lifting and/or explosive lifting. Both of which are just as demanding (if not more) on the nervous system as training to failure.

Why are they against one neural intensive method but for another one? The fact is that the nervous system is an adaptive system just like the rest of our body and it can become more efficient at stimulating muscle contraction when it’s trained properly. And while the CFS is a real problem, its occurrence in bodybuilders or individual training for muscle mass gains is minimal, close to nil. Sure, we can suffer from CNS fatigue after a training session (just like our muscles are fatigued too), but the body can recover from that. Neurotransmitter depletion might be a concern, but rarely is a real problem. Using a supplement like Biotest’s Power Drive can help in that regard by boosting acetylcholine and dopamine levels.

Key points

1, Muscle failure isn’t an indication that every muscle fiber within a muscle has been fully stimulated.

2. Muscle failure can occur because of neural, psychological, metabolic or energetic factors.

3. A moderate amount of work to failure is required for full motor-unit stimulation within a muscle.

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juniperpublishersjcmah · 5 years

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Effects of Sodium Bicarbonate Supplementation on Repeated-sprint Ability in Professional vs. Amateur Soccer Players

Soccer is described within the research as a high-speed and high-intensity intermittent sport exposing players across many levels to a continued physical, physiological, technical, tactical and psychological demands. This variance of stressors encountered during actual training and competitive match-play have shown fatigue to become a prevalent issue, especially following periods of high intensity bouts. As a result this investigation has been developed in order to compare the effects of sodium bicarbonate ingestion (NaHCO3) on professional and amateur soccer player’s RSA (7 x professional players: mean±SD: age 21.7±2.1yrs; weight 79.7±9.5kg; and 7 x amateur players: mean±SD: age 22.8±1.2yrs; weight 79.3±4.9kg). Each player ingested 0.3g.kg-1 NaHCO3 or placebo microcrystalline cellulose (MC) in a randomized, double-blind, crossover order, 90-minutes before the repeated-sprint ability (RSA) test (5 x 6-seconds maximal-effort sprints). No differences were found in La- concentrations among professional or amateur players in MC or NaHCO3 conditions pre-exercise (P>0.05). The NaHCO3 trial revealed significantly higher post-exercise La-concentrations in professional (9.57±1.09vs. 10.77±0.90mmol/L-1) vs. amateur players (10.06±1.45 vs. 10.87±1.25 mmol/L-1). NaHCO3 resulted in significant improvements in mean power output in sprints 2 (512.3±199.4 vs. 547.6±185.3W) and 3 (468.6±209.4 vs. 491.6±199.0W) in amateurs, but no effect in professionals. Therefore, it may be suggested that amateur participants in soccer may benefit from NaHCO3 ingestion more than professional players as a result of their reduced physical conditioning level when compared to professional level players.

Keywords: Sodium bicarbonate; Repeated sprint; Soccer

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Introduction

Soccer is characterized by its unique, unpredictable, intermittency profile in both training and competitive games [1]. Previous research has suggested that during match play, high intensity efforts last for anything between 3.7-4.4 seconds in duration [2,3]. Furthermore, elite level players complete significantly more sprints than their amateur counterparts (1.4±0.1 vs. 0.9±0.1%, p<0.05) [4]. Recent research has revealed a strong correlation between repeated-sprint ability and elite soccer performance [3]. Energy produced during repeated sprints predominantly derives from anaerobic glycolysis [5], a metabolic pathway limited by the progressive increase in acidity through the accumulation of lactate (La) and hydrogen ions (H+) in muscle and blood [6]. Fatigue during high-intensity exercise remains contentious, with further uncertainty surrounding fatigue in soccer [7]. While the mechanism of H+ accumulation is well documented, other mechanisms are largely involved in the RSA fatigue. Earlier research in this area suggestH+accumulation could result in alterations in enzyme activity, perceived effort, ion regulation; or inhibition of essential glycolytic rate limiting enzymes phosphofructokinase and lactic dehydrogenase [8]. Various intracellular buffering mechanisms become active with increased repeated-sprints in an attempt to neutralize the increased H+ in the blood, including the monocarboxylate transporters 1 and 4, although it is believed bicarbonate (HCO3- ) is the most active [9]. The body’s natural stores of HCO3- are limited; therefore, when the body’s buffering capacity is exceeded through increased H+ production acidosis occurs, resulting in fatigue [6]. Elevated H+ concentrations as a result may increase pyruvate dehydrogenase activity, thus enhancing aerobic participation. Evidence indicates La- and H+ accumulation, and the resultant acidosis are not the sole cause of fatigue [2].

The ingestion of sodium bicarbonate (NaHCO3) prior to exercise is suggested to enhance high-intensity sport performance particularly in sports which involve rapid motorunit activity and large muscle-mass recruitment such as soccer [10]. Induced alkalosis following NaHCO3 ingestion is thought to increase the body’s extracellular buffering capacity, delaying the onset of fatigue, and pH decrease, increasing muscle contractile capacity, through enhanced muscle glycolytic ATP production, and increased muscle La- efflux [11]. Evidence suggests NaHCO3 ingestion~120-minutes pre-exercise in a dosage of 0.3g. kg-1. BM may improve high-intensity sport performance by~2% [12]. However, conflicting reports exist during repeated-sprint protocols with performance enhancement in some [2] but not others [13].

Some suggest physical characteristics have a significant impact upon participant’s responses to NaHCO3 supplementation [14]. Anaerobically trained, elite participants are likely to fatigue as a result of mechanisms other than acidosis during highintensity exercise [15] as they possess higher muscle buffer capacities which blunt the ergogenic effects of exogenous buffers [16]. This may have specific implications on soccer performance, where amateur or youth players, or players returning from injury who display significantly lower anaerobic capacities [17]. A recent meta-analysis [18] concluded that the ergogenic effects of NaHCO3 are diminished among amateur or untrained athletes. Additionally, this is the first study to examine the impact of training status upon the ergogenic effects of NaHCO3 supplementation during repeated-sprint ability exercise. As a result, the purpose of this investigation is to compare the effects of NaHCO3 ingestion on the repeated-sprint performance in amateur and professional soccer players.

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Methods

Experimental approach to the problem

Upon commencement of the investigation, participants completed 3-separate sessions composed of one familiarization session (e.g. laboratory introduction, testing requirements, introduction to testing equipment, practice sprints and anthropometrics) and two testing sessions. Although a familiarization session was performed, the players involved within the study were fully aware of the tests used due to their ongoing club seasonal sport science testing battery [19]. To begin the investigation, players were placed in a randomized placebocontrolled, double-blind crossover design method. Following the ingestion of either 0.3g.kg-1.bm (body mass) of NaHCO3 or 0.3g. kg.bm of microcrystalline cellulose (MC-Placebo) in identical capsules, the players completed 5 x 6-second cycle bursts with 24-seconds passive rest between maximal efforts. Following a 7-day separation crossover trial period, both sets of repeatedsprints were conducted at the same time of day (10:00hrs to 11:30hrs) to control for diurnal effects. Capillary blood was taken from the fingertip before capsule ingestion (baseline), 100-minutes post-ingestion (pre-exercise), and immediately after repeated-sprint (post-exercise). Participants were informed to maintain normal dietary patterns and training throughout the study. Participants were also asked to refrain from consuming food and beverages (other than water) 2-hours before testing, they were also asked to avoid alcohol or any vigorous exercise 24-hours before testing. The experimental design is shown in Figure 1, with the overview of the experimental protocol presented in Figure 2. The experimental protocol has previously been described used in accordance with recent research [2]. This research was approved by the ethics board and research committee within the nominated University and participants were informed of the research requirements, benefits and risks before giving written consent.

Subjects

Fourteen soccer players were tested as part of this investigation (7 x professional players: mean±SD: age 24.7±2.8yrs; weight 79.7±9.5kg; and 7 x amateur players: mean±SD: age 19.9±1.2yrs; weight 79.3±4.9kg). All participants had been involved in soccer for over 5 years at various levels ranging from amateur participation to professional and the testing took place in the mid-season phase as to ensure stable physical player profiles. Participants were excluded from the study if they were taking medication known to affect pH balance, suffering from chronic disease, recently suffered an episode of fatigue/ flu or were currently taking performance enhancing supplements.

Training Status

Participants were assigned to one of two groups based on their training status; characteristics of each group are presented (Table 1). Professional soccer players were assumed to be well trained, whereas amateur soccer players were assumed to be untrained. These assumptions were confirmed by the results of a non-exercise model questionnaire [20], and a high-intensity training questionnaire. Participants were deemed to be well trained if they had a MET of <13 and took part in at least 3 highintensity training sessions each week, for at least 5 consecutive weeks.

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Procedures

Substance ingestion

Participants ingested either 0.3 g.kg-1 NaHCO3 or 0.3g.kg-1 MC in 18-24 gelatin capsules, 120-minutes prior to performing the repeated-sprint test. Capsules were closely matched for weight, sight and size, and were assigned in a randomized, double-blind, crossover manner.

Repeated sprint protocol

Participants performed a pre-test warm up 90-minutes following capsule ingestion consisting of 5-minutes cycling at 80W. This was followed by 3 practice starts, where participants were required to pedal at near maximal speed for 2-3 seconds interspersed with 20-seconds slow pedaling followed by a 90-second rest. Participants then performed a 6-second maximal assessment sprint test on the cycle ergometer (Monark Ergomedic 828e, Sweden). The power output completed in the first sprint was used as the criterion score during the subsequent 5 x 6-second cycle test. The subjects were allowed 5-minute off bike rest following the assessment sprint. The 5 x 6-second cycle test consisted of five, 6-second maximal sprints commencing every 30-seconds, with mean power output recorded for each individual sprint. Participants were required to achieve at least 95% of the criterion score for the first sprint, as a check of pacing. Participants that failed to achieve the 95% criterion score were allowed further 5-minutes rest and recommenced the 5 x 6-second cycle test. The 24-seconds between sprints consisted of active recovery, with participants instructed to maintain a cycling speed of 80 RPM with no load and counted in from 5-seconds before commencing the next sprint. All maximal tests were undertaken using the standard Wingate anaerobic test load (7.5g.kg-1.BW) and procedures [21]. Standardized verbal encouragement was provided to each subject during all sprints, with all sprints performed in the seated position. A similar repeated-sprint has been used previously [2] and has been reported to be a valid and reliable test of repeated-sprint ability [22].

Blood sampling and analysis

Whole-blood La- was taken from finger-prick blood samples and assessed for physiological responses to both NaHCO3 and MC. Participants fingers were prepared for sampling using an alcoholic wipe, dried with a tissue then punctured with a disposable lancet (Owen, Mumford, Oxford, UK). The initial droplet of blood was removed with a tissue; subsequent droplets of volume 5μl were collected on the La strip of the La Pro LT- 1710 (Arkray, Kyoto, Japan). Blood samples were taken on arrival~100-minutes post-capsule ingestion, and immediately post-exercise. The La Pro is considered a viable measuring tool for the analysis of blood La owing to its proven reliability [23].

Gastrointestinal tolerability assessment

Acute GI discomfort questionnaires were completed at rest, pre-exercise and post-exercise. The questionnaire has been used in previous literature [24] and participants were required to report the intensity of sickness and stomachache by selfselecting a number along the scale provided. The scales showed integers from 0 to 10, with descriptors at 0, 3, 6, 9, and 10. The descriptors along the sickness scale included: not at all, slightly, quite, very, and sickness, and along the stomach ache scale: none at all, dull ache on and off, moderate continuous, severe continuous and severe doubled up

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Statistical analyses

All values are reported as mean±standard deviation. Within group difference in blood La, mean power output and GI-tolerability was analyzed using a paired t-test. Independent t-test was used to analyze the percentage change between groups for mean power outputs from placebo to NaHCO3, and absolute difference for La concentrations and GI-tolerability from placebo to NaHCO3. Statistical significance was accepted at P<0.05. Between trial differences were also assessed using Cohen’s effect size with modified descriptors (Hopkins, 2002), using the following criteria:<0.2= trivial, 0.2-0.6 = small, >0.6- 1.2 = moderate, >1.2–2.0=large, and >2.0=very large. Precision of the estimate of observed effects was indicated with confidence limits (±95% CL).

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Results

Power output

All participants achieved at least 95% of the criterion score on first attempt. NaHCO3 improved power output in sprint 2 (P=0.011) and sprint 3 (P=0.021) in amateur participants. NaHCO3 had no effect on the power output of professional participants in any of the repeated sprints (P>0.05) (Figure 3). From sprint 1, mean power output was reduced in all subsequent sprints in both placebo and NaHCO3 in amateur (P<0.001) (Figure 4). No reduction in power output occurred in subsequent sprints from sprint 1 in professional participants (P>0.05) (Figure 3). Absolute difference between trials in professional and amateur was trivial (effect size = <0.01). Percentage difference in mean power output was greater amongst amateur players in sprint 2 (P=0.013; d=-0.183) and sprint 3 (P=0.025; d=-0.113) when compared to professional players

Blood lactate

Blood La concentrations for the placebo and NaHCO3 trials are summarized in Table 2. Blood La concentrations were similar in both trials at rest in professional (P=0.893; d=- 0.107) and amateur (P=0.080; d=0.045), although increased in both conditions pre-exercise but still remained similar in professional (P=0.176; d=-0.87) and amateur (P=0.849; d=- 0.09). Post-exercise blood La concentration was significantly greater in professional participants during NaHCO3 trial than placebo trial (P=0.011; d=-1.19) although no difference in the two conditions in amateur (P=0.093; d=-0.59). Additionally, the absolute difference from placebo to NaHCO3 was similar in both professional and amateur at rest (P=0.497), pre-exercise (0.250) and post-exercise (0.491).

Gastrointestinal discomfort

Stomachache and sickness feelings in both trials did not differ at rest in professional (P=0.317), amateur (P=0.317) or pre-exercise in professional (P=0.157) or amateur (P=0.083). Post-exercise gastrointestinal discomfort increased from rest in NaHCO3 trial in both professional and amateur participants (P=0.002), but not in placebo trial (P>0.05). The absolute difference in feelings of gastrointestinal discomfort between professional and amateur were no different when compared to rest (P=1.00), pre-exercise (P=0.298) or post-exercise (P=0.268) values.

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Discussion

The primary aim of this investigation was to compare the effects of sodium bicarbonate ingestion (NaHCO3) on anaerobic performance of professional and amateur soccer players during repeated-sprint bouts. Results have revealed that despite an improved mean power output of amateur participants in the mid-section of the repeated bouts (sprint 2 and 3 out of 5) in the test, NaHCO3 had no greater effect on amateur than professional participants throughout the testing protocol. Additionally, secondary findings from the study highlighted the failure of NaHCO3 to affect post-exercise blood La concentrations of amateur participants, whereas NaHCO3 increased the postexercise blood La concentrations of professional participants

As seen within the study, the mean power output of professional participants was not altered by NaHCO3 ingestion. The higher endogenous muscle buffer capacity of the professional participants within this study may provide a possible explanation to this observation. Indeed, muscle buffer capacity may be increased by 25% following five consecutive weeks of high-intensity interval training (3-sessions/week) [25]. Furthermore, elite athletes are known to possess greater muscle buffer capacities when compared to their amateur counterparts [25,26]. In accordance with the findings of this specific study, previous research also suggests a greater endogenous muscle buffer capacity of professional participants is more than likely responsible for the maintenance of mean power output throughout both NaHCO3 and placebo trials. Subsequently, it should be noted that this would not explain the conflicting reports of Bishop et al. [2] who, using a similar experimental protocol, reported an 8.5% reduction from sprint 1 to 5.

The lack of any ergogenic effect of NaHCO3 among professional participants suggests their greater endogenous buffering capacity blunted any performance enhancing effects of the NaHCO3 supplementation [16]. The improved performance amongst the amateur participants following the NaHCO3 supplementation highlights the positive buffering effect of acute supplementation on less trained individuals. Such findings are in agreement with previous data associating NaHCO3 with no performance effect in anaerobically trained professional athletes when compared to amateurs [2,13,14]. From a practical perspective, professional players who are recently returning to training (e.g. injured) may benefit from a NaHCO3 supplementation to maintain increased training intensity

Recent research has suggested that NaHCO3 is effective in its role of decreasing post-exercise La- [2,27]. Consistent with previous research [2,28] NaHCO3 failed to improve mean peak power output of both professional and amateur participants during the first sprint. It was suggested that a single 6-second sprint maybe too brief for the buffering mechanisms of NaHCO3 to be effective, however, repeated 6-second sprints may benefit through greater facilitation of H+ efflux from the muscle [28]. Similarly, it has been suggested that single short sprints with brief recovery (~17-seconds) may not allow adequate translocation of metabolites from the myoplasm [5]. Again, consistent with previous research [28] and supportive of recent suggestions that NaHCO3 is effective during longer exercise of ~1-minute for instance [12].

In contrast to previous findings [2] NaHCO3 failed to improve the performance of professional or amateur participants in sprints 4 or 5. Early research suggested the ergogenic effects of NaHCO3 are associated with large decrements in resting H+ [27] suggested maximal decrease in H+ occurs 60-90-minutes postingestion of 0.3g-1.kg-1 NaHCO3 however, NaHCO3 administered 60-minutes pre-exercise resulted in a 42% performance enhancement [28]. Latterly, recent research has suggested peak blood alkalosis can be expected ~120-150-minutes postingestion of 0.3g-1.kg-1 NaHCO3 [12].

It is possible the amateur participants began the exercise with suboptimal PCr stores following an intensive warm up (3 practice sprints and 10-second sprint) and only 5-minutes recovery; with PCr resynthesis reported to reach only 85.5±3.5% of resting levels during 6-minutes recovery following a 30-second sprint in amateur participants [29]. With strong correlations between percentage PCr resynthesis and percentage recovery of power output and maintenance of muscle power output [29] Professional athletes were better able to maintain power output during the repeated sprint than amateur, presumably because the rate of PCr resynthesis is known to be more rapid in professional athletes [30].

Interestingly, pre-exercise blood La concentrations were increased from rest in both professional and amateur participants, suggesting high rates of glycolysis during the warmup. Early studies suggested that La accumulation was the cause of fatigue during high-intensity exercise [31] meaning both professional and amateur participants began the exercise in an acutely relative fatigued state. Although recent reports reject this relationship, with new evidence suggesting reduced rates of PCr resynthesis is the main cause of reduced exercise performance during repeated sprints and not the acidosis resulting from La production [31].

Strong correlations exist between aerobic power and the maintenance of repeated-sprint performance [13]. The increased contribution of aerobic metabolism and reduced contribution of anaerobic glycolysis through repeated sprint repetition as reported by Gaitanos et al. [13] provides sufficient explanation of the current results; where the contribution of anaerobic glycolysis probably fell during sprints 4 and 5, offsetting the potential for performance enhancement by NaHCO3. Further, the probable lower aerobic power of the amateur participants meant they were unable to meet the increased contribution of aerobic metabolism in the latter sprints meaning they were unable to maintain mean power output.

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Perspective

Results within this investigation have revealed that despite an improved mean power output of amateur participants in the mid-section of the repeated bouts (sprint 2 and 3) test, NaHCO3 had no greater effect on amateur than professional participants throughout the testing protocol. This is in contrast to previous research who failed to show any performance improvement of professional or amateur players following NaHCO3 supplementation [2]. Furthermore, within this study professional players were better able to maintain power output during the repeated-sprint protocol than amateurs, presumably because the rate of PCr resynthesis is known to be more rapid in professional athletes [30]. From a practical perspective, the current investigation although unique in its concept suggests that amateur participants in soccer may benefit from NaHCO3 ingestion more than professional players

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Conclusion

It can be concluded from this particular investigation that despite no significant differences were found concerning the ergogenic effects of NaHCO3 among professional players, there was however a positive effect amongst the amateur soccer participants. Findings revealed how NaHCO3 may be used to create a positive buffering capacity during initial stages of repeated-sprint exercise bouts when supplemented amongst amateur participants or individuals with a less trained physical profile (e.g. recently injured, post-cessation of training). In addition, it was found that the increased levels of alkalosis failed to improve the mean power output of professional participants. Therefore, in conclusion, it may be suggested that amateur participants in soccer may benefit from NaHCO3 ingestion more than professional players.

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Acknowledgement

This manuscript is original and not previously published, nor is it being considered elsewhere until a decision is made as to its acceptability by the Editorial Review Board. There are no funding sources and are no conflicts of interest surrounding this scientific investigation

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Conflict of Interest

There are no conflicts of interest concerning this paper

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