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213
ORIGINAL RESEARCH
International Journal of Sport Nutrition and Exercise Metabolism, 2017, 27, 213 -219
https://doi.org/10.1123/ijsnem.2016-0186
© 2017 Human Kinetics, Inc.
The authors are with the Dept. of Nutrition and Foods, School
of Family and Consumer Sciences, Texas State University,
San Marcos, TX. Address author correspondence to Krystle E.
Zuniga at k_z17@txstate.edu.
Influence of Dietary Acid Load on Exercise Performance
Catherine Applegate, Mackenzie Mueller, and Krystle E. Zuniga
Diet composition can affect systemic pH and acid-base regulation, which may in turn inuence exercise
performance. An acidic environment in the muscle impairs performance and contributes to fatigue; therefore,
current trends in sports nutrition place importance on maximizing the alkalinity of the body with ergogenic
aids and dietary strategies. This review examines the evidence on the effects of dietary manipulations on
acid load and exercise performance. Ten studies that investigated the effect of high versus low dietary acid
loads on athletic performance generally identied that low dietary acid loads increased plasma pH, but did
not consistently improve exercise performance at maximal or submaximal exercise intensities. In addition,
the few studies conducted have several limitations including lack of female subjects and use of exercise tests
exclusive to cycling or treadmill running. Although the research does not strongly support a performance
benet from low dietary acid loads, a more alkaline dietary pattern may be benecial for overall health, as
dietary induced acidosis has been associated with greater risk of cardiovascular disease and bone disease. The
review includes dietary recommendations for athletes to reduce dietary acid load while still meeting sports
nutrition recommendations.
Keywords: alkaline diet, renal acid load, acid-base balance, aerobic performance, anaerobic performance
High dietary acid loads can contribute to a chronic
low-grade acidosis that has been associated with a greater
risk for cardiovascular, kidney, and bone disease (Cordain
et al., 2005). Diet composition can be modied to reduce
acid loads and improve acid-base balance (Hietavala et
al., 2012), and new diets and supplements to combat aci-
dosis have emerged (Cordain et al., 2005, Adeva & Souto,
2011). Alkaline diets have gained popularity and are mar-
keted in books, diets, and products such as alkaline water
and ergogenic aids (Fenton & Huang, 2015). Changes in
acid-base balance contribute to the onset of fatigue; thus,
athletes may be interested in utilizing dietary strategies
or ergogenic aids to enhance the buffering capacity of the
muscle for performance benets. Early sports nutrition
research identied a relationship between low carbohy-
drate diets and acute acidosis that resulted in reduced high
intensity exercise and endurance performance (Greenhaff
et al., 1987, 1988a, 1996; Ball, Greenhaff et al., 1996).
Current investigations question how alkaline diets low in
protein and fat and high in carbohydrate, could improve
performance and reduce acidosis before, during, and after
exercise. This review will examine the evidence on the
impact of dietary modications on acid-base balance and
subsequent exercise performance.
Physiological Systems Regulating
Acid-Base Balance
Maintenance of a stable intracellular and extracellular
pH in the body is essential for normal physiological
function (Goel & Calvert, 2012) and involves complex
biological processes. As thoroughly reviewed by Goel
and Calvert (2012), the systems that regulate acid-base
balance include extracellular and intracellular buffers, the
respiratory system, and the renal system. The changes of
the acid-base balance by cellular metabolism is highly
inuenced by dietary composition, as the metabolism of
lipids, carbohydrates, and proteins all impact pH in the
body and generate approximately 2–3 mEq/kg/day of H+
ions (Goel & Calvert, 2012).
Extracellular buffering relies on the use of bicarbon-
ate (HCO3-) in the extracellular uid, which can bind to
H+ ions to release carbon dioxide (CO2) and water (H2O)
(Yucha, 2004). The intracellular buffer system is domi-
nated by a nonbicarbonate system which utilizes proteins
and organic phosphates for acid-base regulation (Goel &
Calvert, 2012). Buffering systems are only short-term
solutions for alkalaemia or acidaemia; thus, compensa-
tory mechanisms exist to regulate extracellular pH such as
the respiratory and renal systems. The respiratory system
can increase respiration to expel weakly acidic CO2 when
extracellular H+ ion concentration is sensed (Goel &
Calvert, 2012). Conversely, a decrease in H+ ion con-
centration stimulates chemoreceptors in the brain to slow
respiration and retain CO2 (Clancy & Mcvicar, 2007).
The response of the respiratory system is relatively quick,
214 Applegate et al.
IJSNEM Vol. 27, No. 3, 2017
changing pH concentrations within minutes to hours. The
renal system is much more complex and slow, changing
hydrogen ion concentrations within hours or days (Clancy
& Mcvicar, 2007). During the renal response, excess H+
ions and ammonium (NH4+) are excreted in the urine.
Ammonia (NH3), produced in renal tubule cells, diffuses
into the intraluminal space to combine with H+ ions and
facilitate their irreversible excretion during periods of
acidosis. In addition, potassium ions (K+), calcium ions
(Ca2+), and urinary phosphate (H2PO4) are excreted in
the urine during acute and chronic acidosis (Adeva &
Souto, 2011; Poupin et al., 2012). Plasma bicarbonate is
preserved for its function as a buffer and is reabsorbed
by the renal system and released back into plasma. Cel-
lular metabolism is responsible for the constant ux in
the acid-base balance, which is then corrected through
one or more of these compensatory processes.
Influence of Diet on Acid-Base
Balance
During normal physiological conditions, the net endog-
enous acid production is primarily modied by diet
(Poupin et al., 2012). Dietary choices provide acidic or
alkaline substrates for the body to respond to or use as
buffering agents. The major source of H+ ion production
is the reversible hydrolysis of ATP and the production of
carbonic acid (H2CO3) that occurs during the metabo-
lism of lipids, carbohydrates, and proteins (Poupin et
al., 2012). The catabolic and anabolic reactions during
macronutrient metabolism generate and consume equal
amounts of H+ ions to maintain acid-base homeostasis.
Not only do macronutrients inuence the acid-base bal-
ance, but the dietary consumption of organic and inor-
ganic acids can also mediate changes. The consumption
of organic acids ingested in the form of salts such as
citrate, malate, and lactate lead to the production of
bicarbonate (Poupin et al., 2012). The potassium salts
of the organic acid anions such as citrate and malate are
present in fruits and vegetables (Adeva & Souto, 2011).
Other nonmetabolisable organic acids such as uric, oxalic,
tartrate, and hippuric acids are directly excreted in the
urine without producing bicarbonate and result in H+
retention (Poupin et al., 2012).
A direct relationship exists between the composi-
tion of the diet and urinary pH (Aerenhouts et al., 2011).
The Western diet, which is low in fruits and vegetables
and high in animal products and sodium chloride, is
considered to be an acidic diet (Adeva & Souto, 2011).
Animal proteins and cereal grains are abundant in sulfur-
containing amino acids such as methionine, homocysteine
and cysteine, and oxidation of these amino acids gener-
ates sulfate, a nonmetabolisable anion that is a major
contributor to daily acid production (Adeva & Souto,
2011). Proteins are generally considered to be buffers
due to their negative charge and H+ ion-consuming amine
and carboxylic acid groups that can bind to excess H+
ions and release H+ ions (Poupin et al., 2012). It has been
suggested that the Western diet induces a chronic state of
metabolic acidosis, which increases the renal glomerular
ltration rate to excrete acids in the urine (Adeva & Souto,
2011). Compared with individuals with a plant-based
diet, the Western diet results in more acidic urine and an
increased rate of kidney hypertrophy (Adeva & Souto,
2011). In a more balanced diet, additional alkali loads,
such as those consumed from foods containing sodium
citrate, can increase the alkali reserve in the plasma to
raise urinary pH and compensate for the protein-related
increase in acid production (Remer, 2001).
Potential Renal Acid Load (PRAL)
PRAL is an estimate of the acidic potential of foods
expressed in mEq of H+ ions per 100 g of a particular
food (Aerenhouts et al., 2011). A positive PRAL food
(PRAL > 0) increases the renal acid load by producing
H+ ions. Conversely, a negative PRAL food (PRAL
< 0) is considered to decrease the renal acid load and
thus increase the buffering capacity of the body. Fruits
and vegetables have a negative PRAL while grains and
animal products rich in protein, phosphorous, potassium,
calcium, and magnesium such as eggs, meat, and cheese
have a positive PRAL (Aerenhouts et al., 2011). The diet-
dependent net acid production can be calculated as the
sum of organic acids produced from basal metabolism
and the PRAL of all consumed food items (Aerenhouts et
al., 2011). It has been suggested that long-term net acid
excretion should not exceed 100–120 mEq/day because
it can result in long-term increased renal acid load and a
lower availability of plasma bicarbonate (Aerenhouts et
al., 2011). To compensate for this long-term metabolic
acidosis, some studies have suggested that the bone may
release large quantities of alkalinizing minerals, such as
calcium, to buffer the increased acid load (Aerenhouts
et al., 2011). Indeed, higher rates of urinary calcium
excretion have been identied in omnivores compared
with vegetarians, which is likely a result of higher protein
intake that increased renal acids (Ball & Maughan, 1997).
In the European Prospective Investigation into Cancer and
Nutrition (EPIC)-Norfolk Population study, increased
vegetable and fruit and decreased meat consumption
was positively associated with alkaline urine pH and an
alkaline PRAL diet. (Welch et al., 2008).
Athletes need to consume larger amounts of car-
bohydrates and protein to compensate for the increased
metabolic breakdown of these macronutrients during
training periods, and are thus at risk for consuming
perpetually positive PRAL diets. To achieve the recom-
mended 5–10 g carbohydrates/kg body weight and 1–2
g protein/kg body weight (Thomas et al., 2016), athletes
may consume diets rich in grains such as bread, pasta,
and rice, and animal proteins which are positive PRAL
foods. Aerenhouts et al. (2011) calculated the acid load of
adolescent sprinters’ usual diets. Sixty adolescents aged
12–18 years old were followed for 3 years, during which,
7-day dietary intakes were recorded every 6 months and
used to estimate the net endogenous acid production. All
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Dietary Acid Load and Exercise Performance 215
IJSNEM Vol. 27, No. 3, 2017
individuals consumed consistently positive PRAL diets
throughout the duration of the study. Those with lower
PRAL diets reported consuming more fruits and fruit
juices than those with higher PRAL diets. Adherence to
sports nutrition recommendations may result in a positive
PRAL diet; however, lowering the PRAL of diets can be
achieved through increasing consumption of fruits and
vegetables, rather than limiting the consumption of pro-
tein from moderate PRAL sources like legumes and beans
or high PRAL sources such as meat, poultry, and sh.
Influence of Exercise on the Acid-
Base Balance
While diet composition continuously inuences the acid-
base balance of the body through changes incurred by
the metabolism of individual dietary components, other
physiological factors such as exercise can acutely affect
pH levels. Exercising muscles can generate lactate and
H+ ions that contribute to minor or moderate states of
muscle acidosis in the short-term, until compensatory
mechanisms respond to the decrease in pH to neutralize
the excess acid (Cairns, 2006; Lindinger et al., 1985).
During prolonged submaximal exercise, muscle pH
is minimally affected, whereas the largest pH change
can be observed during maximal continuous exercise
of 1–10 min in duration (Cairns, 2006). Muscle pH is
subsequently restored to its resting level after 10 min of
recovery (Bangsbo et al., 1993). During low-intensity
exercise, muscles are adequately supplied with oxygen
to enable aerobic respiration. Small amounts of lactate
are produced anaerobically through substrate level
phosphorylation; however, the levels remain low as the
lactate is continually produced and removed from the
blood by aerobic tissues (Blair et al., 1996). As exer-
cise intensity increases, the rate of ATP produced by
nonaerobic systems generates H+ ions, promoting an
acidic environment. This acidosis results in a decrease in
muscle contractile force and potentially amplies muscle
fatigue during additional exercise events (Cairns, 2006).
As previously reviewed (Cairns, 2006; Green, 1997),
other factors such as the increase in ADP and AMP, the
accumulation of inorganic phosphate, changes in calcium
cycling, and imbalances of the sodium/potassium pump
contribute to fatigue during high intensity exercise. Intra-
cellular and extracellular changes in pH affect the buffer-
ing capacity of the muscle and contribute to the onset of
fatigue, thus strategies to enhance the buffering capacity
of the muscle such as ergogenic aids, training, or dietary
conditions are promoted to enhance performance and
delay the onset of fatigue (Sahlin, 2014). Sodium citrate
and sodium bicarbonate are well-studied ergogenic aids
that enhance performance during both anaerobic activity
and prolonged exercise (McNaughton et al., 2008; Peart
et al., 2012; Sahlin, 2014). These results are attributed to
the alkalinizing effect of these supplements, increasing
lactate efux and neutralizing lactic acidosis (Schubert
& Astorino, 2013).
Influence of Diet on Acid Load and
Performance During Exercise
Diet type and exercise strongly inuence the acid-base
homeostasis of the body by their own mechanisms;
however, they may also interact, inuencing exercise
performance. It has been hypothesized that creating a
more alkaline systemic environment through reducing
dietary acid load can enhance the clearance of protons and
inhibitory molecules that affect working muscles during
exercise-induced acidosis, thus, improving aerobic and
anaerobic exercise performance.
Greenhaff, Gleeson, and Maughan (1988a) proposed
that diets low in carbohydrate and high in fat and protein
would lead to a resting state of metabolic acidosis. Since
enzyme activity is highly dependent on intracellular pH
values, Greenhaff and colleagues suggested that meta-
bolic acidosis would reduce muscle buffering capacity
and decrease the rate of muscle glycolysis and H+ ion
efux during high intensity exercise. To test the effect of
diet on muscle pH and glycolytic activity, Greenhaff and
colleagues completed a randomized, cross-over design,
in which six healthy young men consumed a diet high
in carbohydrates (73% of energy), low in fat, and low in
protein (low acid load), a diet low in carbohydrate (3% of
energy), high in fat, and high in protein (high acid load),
or a normal carbohydrate (47% of energy), low in fat, and
high in protein diet for 4 days. In a high-intensity cycling
test at 100% VO2max for 3 min, the low carbohydrate,
high protein diet resulted in a lower plasma pH, partial
pressure of CO2, and bicarbonate levels before exercise
compared with both the normal and high carbohydrate
diet. However, there were no differences in postexercise
measures of plasma pH or blood base excess between
dietary treatments. Similar results were found in another
investigation by Greenhaff, Gleeson, and Maughan
(1988b) in which ve subjects cycled for three minutes
at 100% VO2max on either a low carbohydrate or high
carbohydrate diet. Preexercise measures showed a lower
plasma pH, partial pressure of CO2, plasma bicarbonate,
and blood base excess from the low carbohydrate diet.
Muscle biopsies indicated that the low carbohydrate diet
(high acid load) resulted in a pH decline during exercise
that was 104% greater than the high carbohydrate diet.
Intramuscular lactate concentrations were not different
between treatments, and similarities between postexercise
measures among the treatments suggest that lactate efux
was not the cause of fatigue. Greenhaff, Gleeson, and
Maughan (1987) found that subjects consuming a low
protein and high carbohydrate diet for 4 days presented
with increased plasma pH values and a greater time to
exhaustion in a cycling test compared with individuals on
a high protein and low carbohydrate diet. Together these
early studies by Greenhaff et al. (1987, 1988a, 1988b)
suggest that variation in the levels of dietary carbohydrate
and protein changes the acid-base status of plasma and
skeletal muscle, before and during exercise, perhaps
affecting performance. Thus, it was hypothesized that
a high carbohydrate diet would improve performance
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216 Applegate et al.
IJSNEM Vol. 27, No. 3, 2017
similar to sodium citrate supplementation (Ball &
Maughan, 1997). However, Ball and Maughan (1997)
showed that in six untrained, young men, sodium citrate
in combination with an alkalinizing high carbohydrate
diet did not improve cycling performance (as measured
by TTE) when compared with placebo + high carbo-
hydrate diet or placebo + low carbohydrate diet. While
both Greenhaff et al. (1988a) and Ball and Maughan
(1997) demonstrated that high carbohydrate diets do
create a more alkaline environment before exercise when
compared with high protein and low carbohydrate diets,
this difference alone did not result in improvements in
cycling performance in small groups of active men. Con-
versely, a study involving both men and women indicated
improvements in performance by a reduced dietary acid
load. Rios Enriquez et al. (2010) instructed 13 active men
and women to consume either a positive PRAL (acidic
diet) or negative PRAL diet (alkaline diet) for 2.5 days
with a crossover after a 7-day washout. The alkaline diet
resulted in an 83% higher urinary pH than the acidic diet,
and TTE on a cycling test was longer in 58% of subjects
consuming the alkaline diet. The PRAL of the diet may
aid in creating a less acidic environment during exercise,
but the evidence does not suggest a consistent benet in
exercise performance as measured by TTE.
To determine if diet related acidosis contributes to the
onset of fatigue during high intensity exercise, Ball et al.
(1996) conducted a study in which subjects consumed a
normal or low carbohydrate dietary regimen in addition to
supplementation with alkalizing agents: sodium bicarbon-
ate or sodium citrate. The low carbohydrate diet resulted
in metabolic acidosis before exercise, but the addition of
sodium bicarbonate acutely returned blood pH, HCO3,
and base excess to match values obtained from the normal
diet supplemented with sodium citrate. Subjects cycled
to voluntary exhaustion at 95% VO2max, and endur-
ance time was lower after the low carbohydrate diet,
irrespective of sodium bicarbonate supplementation. The
ingestion of sodium bicarbonate during low carbohydrate
dietary regimens was effective in reversing acidosis but
not at correcting the reduced performance, highlighting
that factors other than acidosis inuence fatigue (Ball et
al., 1996). A study involving nine recreationally active
young men found no acid-base status alterations or per-
formance enhancements from consuming a low protein
vegetarian diet (Hietavala et al., 2012). Participants
consumed their normal diet for 4 days before completing
submaximal and maximal aerobic cycling timed trials.
After a 10–16 day washout period, the subjects crossed
over to a low protein vegetarian (LPV) diet for 4 days
before completing the same exercise tests. The LPV
diet consisted mainly of fruits and vegetables to keep
the PRAL value of every food consumed below zero,
and subjects were not allowed to consume meat, cheese,
eggs, or bread. Measurements collected at rest and during
exercise indicated similar venous pH, total concentration
of weak acids and partial pressure of CO2 and HCO3
between both diets. Strong ion difference, a measure of
acid-base disturbances, increased 3.1% during the LPV
diet, reecting a trend toward alkalosis. Although VO2
was signicantly higher in the LPV diet group during
submaximal aerobic cycling, no differences were noted
in TTE or VO2max during the VO2max testing indicating
the alkaline diet did not improve submaximal or maximal
aerobic performance.
Due to age related declines in kidney function,
increased age is related to impaired ability to maintain
acid-base equilibrium (Pizzorno et al., 2010). To examine
the acid-base response and performance effects of diet
among three age groups, Hietavala et al. (2015) tested
recreationally active adolescents (ages 12–15 years),
young adults (ages 25–35 years), and elderly adults (ages
60–75 years) at rest and during exercise. Participants
were randomized to consume a normal protein diet
with high fruits and vegetables (HV) for 7 days, with a
crossover to a 7-day high protein diet with no fruits and
vegetables (HP) after a 2–4 week washout period. Lower
amounts of protein, higher amounts of carbohydrates,
and less calories were consumed in the HV diet than the
HP diet. The HV diet pattern exhibited negative PRAL
values (-47.1, -68.1, -61.8 mEq/day in the adolescent,
young adult, and elderly adults, respectively), and the
HP group consumed diets with positive PRAL values
(22.8, 53.3, 53.5 mEq/day in the adolescent, young adult,
and elderly adults, respectively). At the end of each diet
period, participants underwent three, 10-min cycling trials
at 35, 55, and 75% of their VO2max. Young adults and
elderly adults both exhibited higher plasma and urinary
pH values at rest and during exercise while consuming
the HV diet when compared with consumption of the HP
diet. There were no differences in plasma or urinary pH
values among adolescents at rest or during high intensity
cycling regardless of diet type, suggesting age is a predic-
tor of the ability of buffering systems to compensate for
dietary acid load changes.
To determine whether a true VO2max has been
achieved, a respiratory exchange ratio (RER) of ³1.10 is
often required. The RER is inuenced by the CO2 pro-
duced during respiratory compensatory buffering. Caciano
and colleagues (2015) investigated the effects of a short-
term (4–9 days) low-PRAL or high-PRAL diet on the RER
during maximal and submaximal exercise. Ten participants
completed a crossover trial in which they consumed a low-
PRAL (<1.5 mEQ/d) or high-PRAL diet (>15 mEQ/d), and
completed a graded treadmill exercise test to exhaustion
and a high-intensity running TTE treadmill test after each
dietary intervention. Carbohydrate intakes during the low-
PRAL and high-PRAL diets met minimum sport nutrition
recommendations (5 g/kg/day) (Rodriguez et al., 2009),
and consideration was taken during the dietary phases to
ensure that total energy, carbohydrate, and fat intake did
not differ between the trials. Protein content of the inter-
vention diets were signicantly different, with low-PRAL
diets containing less protein (~60 g/day) than high-PRAL
diets (~110 g/day). The maximal RER achieved at 100%
VO2max was greater after adherence to the high-PRAL
diet compared with the low-PRAL trial (1.20 ± 0.05,
1.10 ± 0.02). TTE was 21% greater in the low-PRAL
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Dietary Acid Load and Exercise Performance 217
IJSNEM Vol. 27, No. 3, 2017
trial compared with the high-PRAL trial during the high-
intensity treadmill running. Niekamp et al. (2013) had
similar ndings from evaluating the relationship between
a habitually alkaline diet and RER during VO2max testing.
Seven-day food diaries of 57 sedentary men and women
(ages 47–63 years) were collected to determine habitual
intake, and diets were scored as low-PRAL (-10.8 mEq/
day on average), mid-PRAL (8.2 mEq/day on average), or
high-PRAL (27.1 mEq/day on average). Low-PRAL diets
correlated with a lower intake of protein and phosphorous
in the diet. Individuals consuming lower PRAL diets dem-
onstrated a higher RER (≥ 1.10) when tested to VO2max
on a treadmill than those consuming mid or higher PRAL
diets. It is interesting to note that these differences were
only seen at maximal RER, and that at submaximal exer-
cise, RER values were not associated with the PRAL of
the diet. Therefore, habitual dietary intake, either acidic
or alkaline, may affect variability in maximal RER, with
higher values attained during maximal exercise after low
acid loads. However, it is important to note that Niekamp
et al. did not report the macronutrient content of the differ-
ent diets. The relative substrate utilization of carbohydrate
and fat during exercise is dependent on several factors
including diet composition (Jeukendrup, 2003). Thus, it is
unknown if higher RER in the low-PRAL diet was due to
a lower dietary acid load or a higher rate of carbohydrate
oxidation due to greater availability of carbohydrates.
Future studies should examine the specic mechanisms
for the relationship between alkaline diets, VO2max, and
RER by measuring multiple metabolic parameters and
substrate utilization.
Conclusion
Theoretically, the maintenance of high alkalinity in the
extracellular uid should enable a faster H+ ion removal
from the muscle cell, delaying the muscle fatigue due
to a lower muscle pH. Although alkalinizing ergogenic
aids such as sodium bicarbonate and sodium citrate have
shown to enhance buffering capacity and improve per-
formance, alkalinizing diets do not demonstrate the same
effect. Ingesting large amounts of sodium bicarbonate and
sodium citrate can result in large increases in pH, whereas
alkalinizing diets only serve to maintain a slightly more
alkaline environment. Side effects of sodium bicarbonate
such as gastrointestinal distress, low tolerability, and high
sodium content promote the use of alternative dietary
strategies to buffer excess H+ ions; however, the alkaline
environment achieved from the consumption of low or
negative PRAL diets is not sufcient to signicantly
enhance the neutralization or clearance of acids from the
muscle during exercise to improve performance (Caciano
et al., 2015). However, the current research has several
limitations which should be considered. The majority of
studies used short-term dietary interventions with young,
male subjects, and primarily assessed performance using
cycling tests to exhaustion. In addition, there was no
consistency in the level of dietary acid or alkaline load
tested among different studies. Future research should
include more diverse samples, longer dietary intervention
protocols, and examine different exercise intensities and
measures of performance.
Although the present review does not clearly estab-
lish and exercise performance benet of reduced dietary
acid load, current investigations support benefits of
reduced dietary acid loads to prevent disease and improve
health (Fenton & Huang, 2015). Reducing diet-dependent
acid loads in young and otherwise healthy athletes can
reduce cardio-metabolic risk factors (Murakami et al.,
2008) and risk of developing hepatic steatosis (Krupp et
al., 2012). Alkaline diets also promote bone health and
can reduce uric acid kidney stone formation (Sellmeyer
et al., 2001; Breslau et al., 1988; Niekamp et al., 2013).
Athletes may be more likely to consume positive PRAL
starches due to increased energy and carbohydrate
requirements, but the incorporation of fruits, vegetables,
and negative PRAL proteins in the diet may reduce the
risk of metabolic acidosis before, during, and after exer-
cise. A diet abundant in negative PRAL carbohydrates
that is low fat and low protein permits an alkaline state
and has the potential to increase muscle pH (Hietavala
et al., 2012; Greenhaff, Gleeson, & Maughan, 1988b).
It is important for athletes to adhere to sports nutrition
guidelines to maintain health and maximize performance
potential. Proper nutritional guidance should promote
adequate carbohydrate intakes (minimum 5 g/kg/day) to
maintain glycogen stores, even among athletes adhering
to low-PRAL diets (Caciano et al., 2015). This guidance
can also empower athletes to choose high nutritional qual-
ity carbohydrate sources such as fruits and vegetables to
meet nutritional needs, provide vitamins and minerals,
and maintain a more alkaline environment. Studies that
used dietary treatments with only modest differences
in protein content between acidic and alkaline diets did
not identify differences in exercise performance (Ball &
Maughan, 1997). Optimizing an athlete’s intake of fruits
and vegetables can also help to offset protein-induced
acidosis, which may occur from increased protein needs
(Adeva & Souto, 2011). In summary, it is practical to
recommend that athletes of all ages focus on consuming
ample amounts of fruits and vegetables to promote alka-
linity, attenuate protein-induced acidosis, and maintain
long-term health.
Novelty Statement
Research suggests that dietary acid load has little to no
inuence on submaximal exercise, and minor inuence
on exercise that requires maximal effort. Dietary modi-
cations such as increasing fruit and vegetable intake to
reduce the dietary acid load is relevant for athletes of all
ages to maintain long-term health and possibly impact
exercise performance at maximal intensities.
Practical Application
Nutritional guidance on consuming energy dense low-
PRAL foods like potatoes, dried fruits, and plant sources
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218 Applegate et al.
IJSNEM Vol. 27, No. 3, 2017
of fat in addition to nutrient rich fruits and vegetables
will promote energy intake and the alkaline status of the
individual, which has health benets beyond exercise
performance (Caciano et al., 2015). To improve per-
formance and prevent acid accumulation in muscle and
plasma, athletes should focus on training to attenuate
performance-inhibiting drops in pH during high-intensity
and long duration exercise.
Authorship
CA designed the review; literature review was conducted and
interpreted by CA, MM; data interpretation and manuscript
preparation were undertaken by CA, MM, and KZ. All authors
approved the nal version of the paper. The authors have no
conicts of interest to declare.
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