REVIEW
Swifter, higher, stronger:
What’s on the menu?
Louise M. Burke1,2
* and John A. Hawley2
The exploits of elite athletes delight, frustrate, and confound us as they strive to reach
their physiological, psychological, and biomechanical limits. We dissect nutritional
approaches to optimal performance, showcasing the contribution of modern sports
science to gold medals and world titles. Despite an enduring belief in a single, superior
“athletic diet,” diversity in sports nutrition practices among successful athletes arises
from the specificity of the metabolic demands of different sports and the periodization
of training and competition goals. Pragmatic implementation of nutrition strategies in
real-world scenarios and the prioritization of important strategies when nutrition themes
are in conflict add to this variation. Lastly, differences in athlete practices both promote
and reflect areas of controversy and disagreement among sports nutrition experts.
A
ncient Olympians manipulated their diets
according to prevailing beliefs, with Pythagoras
being credited (probably incorrectly)
for introducing athletes to meat and proteinrich
foods in place of traditional figs, cereals,
and cheese (1). Meanwhile, modern-day
athletes are bombarded with social media “warriors”
who evangelize vegan, Paleo, and low-carb
“keto” diets for peak performance. In contrast to
the battle over the perfect menu, contemporary
sports nutrition embraces diversity in dietary
practices, underpinning the demands of training
and competition with the philosophies of specificity,
periodization, and personalization (2).
The metabolic demands of elite sport are
complex, with events lasting from seconds (jumps,
throws, and lifts) to several weeks (Grand Tour
cycling races). Performance outcomes culminate
from deliberate, sport-specific training aimed at
maximizing adaptations toward the fulfilment
of individual genetic potential (3). Although some
elite athletes benefit from systematic, sciencedriven
advice on training adaptation and competition
performance, others use trial-and-error
approaches under the guidance of experienced
coaches, leaving scientists to explain post hoc
how diet might have contributed to their performance
peaks (3).
Solving the fuel crisis
Energy for competitive sports is provided by
transforming chemical energy (intramuscular
glycogen and lipids) into mechanical energy
(contraction), with adenosine triphosphate (ATP)
being the metabolic intermediary (4). Because
intramuscular ATP stores are small, exerciseassociated
increases in ATP turnover within
active myocytes (up to 100 times the resting
turnover rate) pose a major energetic challenge.
Metabolic pathways for resynthesizing ATP are
rapidly activated during short-term (<30-s)
sprints, primarily through substrate-level phosphorylation:
phosphocreatine (PCr) breakdown
and the conversion of muscle glycogen to lactate.
However, as ATP production becomes unable to
match rates of utilization, a range of metabolic
by-products accumulates. Some of these, such as
hydrogen ions, appear to exert negative feedback
on the pathways that produce them to prevent
further disruption to homeostasis, whereas others,
including adenosine monophosphate (AMP) and
organic phosphate, stimulate energy sensors, such
as the 5′-AMP–activated protein kinase, to maintain
cellular homeostasis by regulating anabolic
and catabolic pathways, thereby ensuring a balance
between energy supply and demand.
Sporting activities lasting several minutes to
several hours and performed either as a steady
state (e.g., marathon running) or with intermittent
high-intensity bursts (e.g., team sports) are
fueled principally by the oxidation of intramuscular
glycogen and, to a lesser extent, lipids,
whereas the mobilization of extramuscular substrates
[plasma glucose from the liver and gut
and free fatty acids (FFAs) released from adipocytes]
becomes more important as exercise duration
increases. Training enhances the metabolic
flexibility of the myocyte, enhancing the size
of substrate pools and the capacity to rapidly
switch between carbohydrate (CHO)– and fatbased
fuels to meet the demands of the working
muscles.
The location- or fiber-specific depletion of
muscle glycogen stores is often associated with
fatigue, and since the introduction of the percutaneous
needle biopsy technique to exercise
science in the 1960s (5), numerous investigations
have examined strategies to promote the
storage of glycogen before or between exercise
bouts. The key factor in the synthesis of this
macromolecule is the quantity of dietary CHO
consumed (6), but because maximal hourly synthesis
rates are equivalent to ~5% of the size of
normalized stores, athletes need to plan adequate
time as well as sufficient CHO intake to increase
Burke et al., Science 362, 781–787 (2018) 16 November 2018 1 of 7
1
Australian Institute of Sport, Belconnen ACT 2616, Australia.
2
Exercise and Nutrition Research Program, The Mary
MacKillop Institute for Health Research, Australian Catholic
University, Melbourne 3000, Australia.
*Corresponding author. Email: louise.burke@ausport.gov.au
Box 1. Move over, muscle: The brain’s the boss!
The brain and CNS are implicit in skilled tasks and events requiring concentration and
decision-making. Only recently, however, have we recognized their role in the performance
of even simple locomotor events, including strategies around pacing. A century ago, Bainbridge
wrote, “There appear, however, to be two types of fatigue, one arising entirely within the central
nervous system, the other in which fatigue of the muscles themselves is superadded to that of
the nervous system” (71). Despite this early insight, sports nutrition has evolved with a bias
toward studying peripheral mechanisms of fatigue and their role in performance, possibly
because of the opportunities provided by available research tools (72). Exceptions are noted;
hypoglycemia has long been recognized as a cause of fatigue during endurance sports (73),
and brain astrocytes are now known to have labile glycogen stores (74). Furthermore, we now
explain the ergogenic benefits of caffeine through central roles (reduced perception of effort
and increased neural recruitment of muscle fibers) rather than a metabolic origin (muscle
glycogen sparing because of increased availability and oxidation of plasma FFAs) (75).
An intriguing theme in modern sports nutrition involves the CNS and nutrients that can
enhance performance without even being absorbed (76). This interest emerged from the
recognition that exogenous CHO intake could improve ~1-hour cycling time trial performance,
even though muscle substrate (glycogen) availability is not rate limiting for this event (76).
The same performance benefits were detected when the mouth was simply rinsed with a
glucose or maltodextrin solution (77), exposing receptors in the oral cavity to CHO and
stimulating reward centers in the brain to increase pace or work output (78). The “oral sensing”
benefits of CHO have been shown to be robust and repeatable when undertaken throughout an
event, offering new performance nutrition strategies and a different range of targeted sports
(76). Although this science is still in its infancy, evidence shows benefits of oral sensing from
other tastants (e.g., fluid and caffeine), and effects have been reported for menthol (perception
of cooling), quinine [activation of the autonomic nervous system and/or corticomotor excitability
for brief events (79)], and capsaicin, acetic acid, cinnamaldehyde, and other plant chemicals that
are known transient receptor potential channel activators and may prevent exercise-associated
muscle cramps (80).
DIET AND HEALTH
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
glycogentolevelscommensuratewith the demands
of the upcoming session (6). Factors reducing
the efficiency of glycogen synthesis from a given
CHO intake include muscle damage and inadequate
energy intake, whereas other factors
(training status, the severity of glycogen depletion,
intake within the hours following strenuous
exercise, and co-ingestion of protein) can increase
synthesis rates or absolute stores (6). The resting
glycogen concentrations in endurance-trained
muscle are higher than those in sedentary individuals;
furthermore, glycogen supercompensation
(“CHO loading”) can be achieved in trained
muscle with as little as 24 to 48 hours of reduced
activity and high intakes of CHO [10 to 12 g per
kilogram of body mass (BM) per 24 hours] (6).
For at least 50 years, such techniques have been
used by athletes to enhance their performance
in endurance events in which glycogen depletion
would otherwise occur (7).
Of course, the fuel demands of many sports
exceed muscle glycogen storage capacity or the
athlete’s opportunity to replete endogenous stores
between events. Exogenous CHO (CHO consumed
in the hours before and/or throughout exercise)
maintains euglycemia by “sparing” hepatic glucose
production (8), with blood glucose making
an increasing contribution to rates of muscle CHO
oxidation as glycogen stores become depleted
(9). Strong evidence suggests that performance
in a range of sports and exercise scenarios is
enhanced by consuming CHO during exercise,
with intakes targeted to the muscle’s need to
supplement its diminishing glycogen reserves
[30 to 60 g/hour in endurance events of up to
2 to 3 hours duration and 60 to 90 g/hour in
ultra-endurance events lasting 8 to 10 hours
(10)]. Intestinal CHO absorption is likely the
rate-limiting step in the oxidation of ingested
CHO (11). However, to some extent this can be
overcome by “training the gut”: increasing CHO
intake in the diet and during exercise to increase
tolerance and the activity of sodiumdependent
glucose transporter SGLT-1 (12, 13).
The use of glucose-fructose mixtures that utilize
different gut transporters can also increase total
intestinal absorption and rates of muscle oxidation
of ingested CHO (14).
The relatively large lipid stores in even the
leanest of athletes have, understandably, intrigued
sports scientists as a potential source of fuel for
prolonged aerobic exercise. However, whereas
CHO oxidation is closely geared to the energetic
demands of the working muscles, no mechanisms
exist for closely regulating the availability
and metabolism of FFAs to the prevailing energy
expenditure. Short-term strategies [overnight fasting
or low-CHO, high-fat (LCHF) eating] have
proven unsuccessful in enhancing performance,
despite increasing FFA availability: The small
increase in FFA oxidation is insufficient to replace
the contribution of CHO after near depletion
of liver and muscle CHO stores (15). An
alternative strategy (16) to potentially boost the
use of both substrate pools involves exposure
(5 days) to LCHF (60 to 70% fat) diets to promote
muscle retooling to enhance FFA transport
and utilization, followed with restoration of
endogenous and exogenous CHO availability
(24 hours of high-CHO diet and CHO intake
before and during exercise). Despite substantial
increases in rates of fat oxidation after such
protocols, benefits to endurance performance
have been, at best, limited to specific scenarios
or individuals (17).
More notably, the observed reduction in the
utilization of CHO during submaximal exercise
(“glycogen sparing”), initially thought to be advantageous
in preserving this fuel for later oxidation,
was discovered to be impaired CHO
oxidation, caused by reduced muscle glycogenolysis
and the down-regulation of flux through
the citric acid cycle secondary to reduced pyruvate
dehydrogenase activity (18). In sports where
success is determined by high-intensity aerobic
exercise, either throughout the event (such as in
a cycling time trial or 10,000-m run) or at critical
stages [within team sports or the “breakaways”
and finishes in marathons, Ironman
triathlons (19), and longer cycle races (20)], the
highest sustainable rates of muscle energy turnover
require the better economy of ATP production
from CHO oxidation. Short-term fat
adaptation strategies, or even long-term adaptation
to ketogenic LCHF diets (80% fat, <50 g
of CHO/day), which can increase normal rates
of fat oxidation by two or three times (21, 22),
are limited in application to a small range of
sporting events in which utilization is low
enough for muscle energy to be provided by
fat oxidation (21, 23). To date, it appears that
protocols that substantially increase fat oxidation
also decrease metabolic flexibility by reducing
CHO substrate pools and/or the ability to
rapidly oxidize them. The bottom line is that
when elite athletes train for and compete in
most sporting events, CHO fuels are the predominant
and critical substrate for the working
muscles, and the availability of CHO (22, 24),
rather than fat, wins gold medals. We propose
that the increased rates of fat oxidation observed
after endurance training and “train-low”
strategies (see When less is more) are a proxy for
an increase in mitochondrial density; for competition
success, this machinery is best utilized
by harnessing it to enhance the oxidation of CHObased
fuels.
Burke et al., Science 362, 781–787 (2018) 16 November 2018 2 of 7
AMPK
Mitochondria
Nucleus
FFAPPAR
p38 MAPK
Replete muscle
glycogen stores
(500 mmol/kg
dry muscle)
Lowered muscle
glycogen stores
(<250 mmol/kg
dry muscle)
High Intensity
training (PM)
“Train High”
Fasted, prolonged,
low-intensity training (AM)
“Train Low”
Low CHO meal
“Sleep Low”
p53
PGC-1α
Mitochondrial biogenesis
COX subunits,
PGC-1α,Tfam,
Drp1, Mfn2, CPT-1,
CD36, PDK4
COX subunits
Fig. 1. Periodized nutrition: Evolution of a nutritional practice. Commencing endurance
training with lowered muscle glycogen stores (training low) results in greater transcriptional
activation of enzymes involved in CHO and fat oxidation, as well as greater mitochondrial
biogenesis, than undertaking exercise with a normal or elevated glycogen content
(29, 30). Restricting CHO availability during the early (1 to 5 hours) postexercise recovery
period also acutely up-regulates various markers of substrate metabolism and endurance
training adaptation in skeletal muscle (45). Against this background, we formulated a
novel approach in which we can undertake high-quality, high-intensity training and then
prolong the duration of low CHO availability during recovery and subsequent aerobic exercise,
thereby potentially extending the time course of transcriptional activation of metabolic
genes and their target proteins. We have termed this practice “train high, sleep low” (45, 46).
PPAR, peroxisome proliferator–activated receptor; AMPK, 5′-AMP–activated protein kinase;
MAPK, mitogen-activated protein kinase; COX, cyclooxygenase.
ILLUSTRATION:V.FALCONIERIBASEDONL.M.BURKEANDJ.A.HAWLEY
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
Training nutrition: A balancing act
A reductionist view of training identifies a range
of interdependent adaptations that permit athletes
to sustain the highest rate and yield of
energy production, optimize economy of motion,
defend cellular homeostasis, and delay the onset
of fatigue while simultaneously attaining the
optimal physique and technical skills specific
to their events (3, 25). To achieve these ends,
elite athletes and their coaches integrate a series
of workouts that individually target important
competition performance traits into a periodized
training program composed of (weekly) microcycles
and (3- to 6-week) mesocycles, culminating
in targeted competition peaks within the
(annual) macrocycle. The long-term adaptations
to exercise training, such as those observed in
elite athletes, result from the cumulative effect
of the many transient increases in mRNA transcripts
encoding various proteins after each acute
exercise session (26, 27). These repeated bursts in
mRNA expression appear to be essential to drive
the chronic intracellular adaptive response to
exercise training (27).
With regard to the training diet, early nutrition
guidelines promoted a singular and somewhat
static approach, focusing predominantly
on CHO-based fuels as the major energy source
for muscle. However, contemporary guidelines
acknowledge differences in the requirements and
goals of different sessions or phases of training,
leading to a periodization of the athlete’s diet
(2, 28). In principle, nutrient support is organized
around each training session to maximize physiological
outcomes within a framework that addresses
larger nutrition goals. Recommendations
target total energy and fuel availability, with a
focus on protein and CHO intakes and their
distribution throughout the day (2). For highintensity
or high-quality training sessions, high
endogenous and exogenous CHO availability is
recommended, with the timing and intake of
CHO matching or exceeding the muscle fuel requirements
to support training quality (2, 28, 29).
Some training sessions should develop competition
fluid and CHO intake plans, incorporating
practice of event-specific behaviors as well as
training the gut function needed to tolerate and
deliver these nutrients into the bloodstream.
CHO intake can be reduced for lighter training
loads (2, 29); furthermore, adaptations to endurance
training may be enhanced by deliberately
commencing some sessions under conditions of
low exogenous and endogenous CHO availability
(28–30) (see When less is more and Fig. 1).
As a result, daily CHO intakes typically vary from
2 to 12 g per kilogram of BM among athletes and
across training cycles (31).
New perspectives on protein intake target the
daily consumption of useful amounts (~0.3 g
per kilogram of BM) of high-quality sources at
four to six meals or snacks, particularly during
the 1- to 3-hour window after key training sessions
(32, 33) and, perhaps, a double dose before
sleep (34). This approach extends previous recognition
that athletes have total daily protein
requirements in excess of the standard Recommended
Dietary Allowances to optimize the
sustained (~24-hour) increase in contractionstimulated
synthesis of muscle protein that
occurs after strength or endurance exercise by
supplying leucine to further up-regulate the mammalian
target of rapamycin complex 1 (mTORC1)
pathway (32, 33). Attention to nutrients for which
athletes have increased requirements [such as
water, electrolytes, and iron (35)] or risks of
deficiency [such as vitamin D (36)] is also important
in maximizing training adaptation, especially
during training blocks undertaken in
the heat or at high altitude (3).
Elite athletes straddle a thin line between
maximizing overall training stimulus to promote
sport-specific adaptation and remaining free of
illness or injury. Within the framework of any
periodized training program, each acute exercise
session is an integral part of a long-term goal,
with the training impulse (the sum of the intensity,
duration, and frequency of sessions) being
finely balanced to underpin optimal adaptation
for a specific competition peak. The integration
of nutrition goals for a specific training session
or phase within the larger nutrition plan often
creates tension between opposing themes. Athletes,
both males and females, can develop relative
energy deficiency in sport (RED-S), with a
mismatch between energy intake and the energy
expended in exercise leading to impairments
in metabolic rate, bone health, protein synthesis,
production of reproductive hormones, and performance
gains (37). Yet, RED-S can occur secondarily
to the body fat manipulation and very
high training volumes that typically underpin
success (38); this necessitates careful implementation
and scheduling of such phases into the
annual plan (39). Other strategies that need to
be balanced or strategically managed include
training with low CHO availability, which increases
the inflammatory (interleukin-6) response
to exercise, with acute disturbances to the immune
system (40) and bone metabolism (41) that
appear to persist with long-term exposure (42).
Similarly, the use of antioxidant supplements
acutely reduces free oxygen radical damage to
muscle fibers but potentially dampens the training
response by interfering with redox-sensitive
signaling pathways; this has also been seen to
translate into a reduction in performance (43).
When less is more
The application of molecular biology techniques
to exercise science has identified the complexity
and breadth of intracellular signaling networks
by which different exercise modes drive adaptive
changes that underpin the athletic phenotype
(3, 25). Altering nutrient availability, particularly
endogenous CHO stores, selectively modulates
gene expression and intracellular signaling within
the muscle; mechanisms include alterations in
cell osmolality and increased activity of molecules
within the regulatory CHO-binding domain
of the AMP-activated protein kinase, as
well as perturbations to circulating FFAs and
hormones in concert with plasma glucose and
Burke et al., Science 362, 781–787 (2018) 16 November 2018 3 of 7
Box 2. Performance in a bottle.
Sports products represent a lucrative portion of the worldwide explosion in the manufacture
and marketing of supplements; according to one report, sports supplements generated global
revenue of $9 billion in 2017, with a doubling of this value forecasted by 2025 (81). Surveys
confirm the high prevalence of sports food and supplement use among athletes, including
greater use at higher levels of competition (82). Despite earlier reluctance, many expert groups,
including the International Olympic Committee (83), now pragmatically accept the use of
supplements passing a risk-benefit analysis as being safe, effective, legal, and appropriate to
an athlete’s age and maturation in their sport. Supplements used by athletes fall into different
categories (83): nutrient supplements for the treatment or prevention of deficiencies (e.g., iron
and vitamin D); sports foods providing energy or nutrients when it is impractical to consume
everyday foods (e.g., sports drinks and protein supplements); performance supplements that
directly enhance exercise capacity; and supplements that provide indirect benefits through
recovery, body composition management, and other goals. Despite enthusiastic marketing, from
the latter two groups, only a few products enjoy robust evidence of efficacy [e.g., caffeine,
creatine monohydrate, bicarbonate, b-alanine, and nitrate (84)] (Fig. 2).
Any benefits associated with supplement use must be balanced against the expense, the
potential for adverse outcomes due to poor protocols for use (e.g., excessive doses or interactions
with other supplements), and the dangers inherent with products whose manufacture
and marketing are less regulated than those of foods or pharmaceutical goods. There are safety
issues around dietary supplements in general, which accounted for ~23,000 notifiable emergency
department visits in the United States in 2015 (85). Elite athletes also need to consider
that supplements have been found to contain contaminants or undeclared ingredients that are
prohibited by the antidoping codes (86) under which they compete; these include stimulants,
anabolic agents, selective androgen receptor modulators, diuretics, anorectics, and b2 agonists
(87). Strict liability codes mean that a positive urine test can trigger an Adverse Doping Rule
Violation with potentially serious effects on the athlete’s career, livelihood, and reputation,
despite unintentional intake or minute (ineffective) doses. Third-party auditing of products can
help elite athletes make informed choices about supplement use but cannot provide an absolute
guarantee of product safety (83).
DIET AND HEALTH
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
insulin concentrations (3, 29). Within their repertoire
of training nutrition strategies, athletes
can now include practices that augment adaptive
processes in skeletal muscle; these include
commencing training with low exogenous CHO
availability (fasting overnight and/or withholding
CHO during a session) or the more potent trainlow
strategy of deliberately commencing selected
training sessions with lowered muscle glycogen
stores (e.g., using a first session to deplete glycogen
and then training for a second time after
withholding CHO to prevent glycogen restoration)
(29, 30).
Although studies consistently report augmented
cellular responses as a result of trainlow
strategies, the translation to performance
enhancement has been less clear (29, 30). Early
investigations failed to detect superior performance
outcomes; this was attributed to the overemphasis
of such sessions within the training
program and their resultant impairment
of training intensity (44). These sessions
need to be appropriately placed into a
periodized program to complement highquality
training (7). A recent, clever sequencing
of practices (Fig. 1) integrates
a performance-promoting session and an
adaptation-focused session while adding
the benefits of a prolonged increase in
exercise-stimulated cellular signaling and
posttranscriptional regulation during
glycogen-depleted recovery and exercise
(45). In subelite populations at least, better
integration of train-low and train-high sessions
into the training sequence (Fig. 1) has
been associated with superior performance compared
with the same training undertaken with
normal CHO availability (46). So far, however,
this does not seem to be the case in studies
involving elite populations (22, 47), although
it is often incorporated into real-world training
sessions (48). Although further studies are
needed, part of the challenge in advancing this
area of research is the lack of agreement with
regard to the terminology and implementation
of the practices involved; we have tried to address
this in a separate commentary (7).
Fighting fatigue: Eating to win
Each sport has distinct features, but characteristics
shared by all competitors are a desire to
pace their performance to achieve the highest
sustainable outputs or speeds and maintain
technical proficiency, with the likelihood of a
reduction in some performance metrics intermittently,
toward the end of the event, or both.
“Fatigue” is defined operationally as a periodic
or sustained decline in the athlete’s ability to
optimally perform the tasks required of their
sport. Although fatigue is often characterized as
muscular (decreased force or power production)
or mental (increased ratings of perceived exertion
or loss of skill and cognitive abilities),
there is interplay between these phenomena.
Muscular fatigue has both peripheral (related
to the exercising muscle) and central [related to
the ability of the central nervous system (CNS)
to enervate the muscle fibers] input. Although
some events require maximum performance to
break world records or personal bests, others
reward a superior performance relative to those
of other competitors. The factors underpinning
fatigue or performance power or speed are specific
to the event, the environment in which it is
undertaken, and the individual athlete.
Figure 2 provides a simplified summary of
the most common fatigue factors in competitive
sport to which evidence-based nutrition
strategies can be applied to reduce or delay the
onset. Such strategies can involve chronic protocols
that work synergistically with training to
make the body more resilient to these factors.
For example, in team sports involving repetition
of short (e.g., 6-s) high-intensity sprints, a
progressive decay in speed related to the failure
to fully recover PCr stores in the intervening
recovery periods (>30 to 120 s) can be addressed
by supplementation with creatine monohydrate
to increase the size of the muscle PCr pool (49).
This may not only directly enhance match performance
by altering the sprint decay profile (50)
but also allow the athlete to train harder (i.e.,
complete more sprints during training sessions)
to increase adaptations in other physiological
systems. Acute pre-event strategies such as CHO
loading (24 to 48 hours of preparation) to increase
the muscle glycogen stores or glycerolassisted
hyperhydration (2 hours of preparation)
to increase body water storage can enhance performance
in specific events if they can increase
the time of optimal output before the body
reaches a critical level of glycogen depletion (51)
or fluid deficit (52), respectively. Intake of CHO
(10) or fluid (53) during the event can also address
these peripherally limiting factors but,
intriguingly, may provide a benefit though a
CNS effect associated with the oral sensing of
these nutrients (Boxes 1 and 2).
Lastly, for real-world events, the development
of a competition nutrition plan is challenged by
the complexity of addressing a multitude and
overlay of these fatigue factors, the practical
constraints imposed by the event or the nature of
the exercise, and the beliefs and tolerance of the
athlete. This is covered in Box 3 and illustrated by
recent activities around the marathon (42.2 km).
In 2017, in a carefully orchestrated attempt to
break the 2-hour barrier (54) and after much
scientific banter (55), Kenyan Eliud Kipchoge
came within 25 s of a sub-2-hour performance.
Kipchoge already had two of the three “success
factors” for prolonged endurance events: high
aerobic power and the ability to run at a very high
proportion of his aerobic capacity for prolonged
periods without losing metabolic control (56).
His attempt, albeit outside the International
Association of Athletics Federations rules, targeted
mainly the third factor: running economy
(achieving the highest speed for the lowest oxygen
cost). Strategies to improve economy included
running on a flat motor racing track
without sharp corners to preserve speed, running
in aerodynamic formation behind other
runners, using a car-mounted time clock to provide
a windshield as well as pacing assistance,
and wearing shoes developed to return 4% extra
energy via carbon-fiber inserts (57).
Nutritional strategies were also used to enhance
economy, and future improvements are
likely. The beneficial effects of beetroot juice,
a popular performance aid providing a supplemental
source of inorganic nitrate, are
mediated through the enhancement of
exercise economy: A secondary nitric
oxide (NO)–generating pathway (nitratenitrite-NO)
is believed to enhance NOmediated
increases in capillary O2 delivery
to the muscle and reduce mitochondrial
proton leakage (58). Furthermore, despite
current claims that ketogenic LCHF diets
provide unlimited substrate for prolonged
exercise (21), both century-old empirical
data (59) and recent interventions involving
world-class race walkers (22) remind
us that the oxidation of CHO yields ~5% more
ATP per unit of O2 than fat. Future nutrition
strategies for the marathon may focus on increasing
CHO availability and oxidation by shifting
away from the use of fat from the mitochondrial
furnace. Tactics include achieving maximally supercompensated
glycogen stores, increasing the
opportunities for aggressive in-race feedings, and
training the gut to use multiple CHO sources to
increase overall intestinal absorption of CHO (12).
Elite athletes are different
Scrutiny of the evidence base for current sports
nutrition guidelines reveals that the individuals
who contribute blood, sweat, and tears to scientific
investigations are at best well trained,
often male, and almost always subelite. Interventions
with world-class athletes are rare: By
definition, such athletes are few in number, and
they are generally disinclined to interrupt successful
training or nutrition programs or submit
to invasive experimental techniques for the sake
of science. It is reasonable to ask, therefore,
whether the results of studies on nonelite populations
apply to their elite counterparts. Issues
include application of the intervention to the
specific scenarios in which elite athletes train or
compete, the inability of underpowered studies
to detect small but worthwhile differences or
changes in performance that could alter the
outcomes of elite sport, and the translation of
putative mechanisms to athletes who undertake
substantially larger volumes of specialized training
and potentially possess favorable genetic
Burke et al., Science 362, 781–787 (2018) 16 November 2018 4 of 7
“…the decisive day of this race,…over
a challenging mountainous terrain,
was achieved with a nutrition plan
providing 6663 kcal and 18.9 g of
CHO per kilogram (a total of 1.3 kg,
equivalent to ~85 slices of bread)…”
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
traits (60). In relation to some nutrition interventions,
evidence suggests a diminished response
in elite competitors. For example, beetroot
juice supplementation appears to be less effective
in achieving economy or performance improvements
in elite athletes (61); explanations
for nonresponsiveness to this supplement in
higher-caliber athletes include their different
muscle fiber composition and the legacy of
physiological adaptations attained through extensive
training, such as greater activity of the primary
arginine-NO pathway (62, 63). Nevertheless,
because this pathway is oxygen dependent, scenarios
can be identified in which elite athletes
could benefit from activity from the alternative
(oxygen- and pH-independent) nitrate-derived
NO production, justifying beetroot juice supplementation;
these include training or competing
at high altitude and competing in sports
involving small muscle groups, such as the arms,
in which lower blood flow increases the likelihood
of local hypoxia and acidosis (62, 63).
The challenge remains to determine whether
elite athletes are successful because, or in spite,
of their nutrition practices. There are few studies
of such groups or individuals, although elite East
African athletes who have dominated middledistance
and distance running for the past decades
have received scientific inquiry (64, 65).
Their dietary patterns include consistencies with
current athlete guidelines [high CHO intakes
(~60 to 80% of energy) but regular use of training
in a fasted state to achieve train-low sessions],
Burke et al., Science 362, 781–787 (2018) 16 November 2018 5 of 7
H+
H+
PCr
PCr
Fatigue Factors
Key Nutrition Strategies to Combat Fatigue Factors
Gold Medal Performance
Muscle Acidosis
Muscle Soreness HypoglycemiaMuscle Cramp
Gut Disturbances Hyponatremia Muscle Damage Muscle CHO
Depletion
Muscle PCr
Depletion
Suboptimal CNS
Activity
Hypohydration/
Hyperthermia
Decreased cellular
pH due to high
rates of anaerobic
glycolysis
Discomfort and
disruption of
planned event
nutrition
Decreased plasma
[sodium] primarily
due to
overhydration
(hypervolemic
hyponatremia).
Can be fatal
(cerebral oedema)
Fluid deficit > 2%
BM. Increased RPE
and physiological
strain, especially in
hot conditions.
Cramp etiology is
complex
Decreased PCr due
to inadequate
recovery between
sprints
Contraction-induced
loss of muscle force
and pain
Impairment of
afferent and
efferent neural
function Increased
RPE
Inadequate
endogenous and/or
exogenous CHO
availability for
muscle demands
Acute bicarbonate
loading
(extra-cellular
buffering)
Chronic B-alanine
supplementation
Gut training
Bespoke event
fluid and CHO
intake plan
Avoidance of
excessive fluid
intake pre and
during event (e.g.
intake > net
losses)
Hypovolemic
hyponatremia
(large Na and fluid
losses):
replacement of Na
in event fluid plan
Pre-event
euhydration
Between event
rehydration
Caffeine
pre/during event
Pre-event
hyperhydration
using osmotic
agent (e.g. glycerol,
Na)
Pre/during event
intake of ice slurry
Bespoke event
fluid/Na plan
Mouth sensing with
Trp channel
activating
phytochemicals
Legend: BM = body mass, CHO = carbohydrate, PCr = phosphocreatine, RPE = rating of perceived exertion, LCHF = low carbohydrate high fat; NAC = n-acetyl cysteine,TrP =
transient receptor potential, Na = sodium; Bold text reflects evidence-based strategies to combat these factors while regular text reflects strategies that are proposed but
require further proof of efficacy. Multiple icons denote an increased magnitude or level of risk of this factor.
Post-exercise
protein
Chronic
supplementation
with phenolic
phytochemicals
(e.g. cherries,
berries)
Chronic
supplementation
with anti-oxidants
(e.g.Vit C, E, NAC)
Caffeine
pre/during event
CHO mouth
sensing to reduce
decreased RPE and
increase central
drive
Mouth sensing of
menthol or cold
fluid in heat
Mouth sensing of
quinine in brief
events
LCHF diet or ketone
supplements for
alternative brain
fuel
During event CHO
intake
CHO intake during
24 h pre-event to
meet event
glycogen needs
Pre-event
CHO-rich meal
During event CHO
intake (30-60 g/h)
Between event
refueling
48h pre-event CHO
loading to
supercompensate
glycogen
During event CHO
intake (60-90 g/h)
Adaptation to LCHF
diet to promote
fat/ketone fuel use
Ketone supplement
for alternative fuel
Creatine
supplementation
Fig. 2. Nutrition can beat competition fatigue. Many factors that commonly cause fatigue (a periodic or sustained decline in the athlete’s ability to
optimally perform) in sporting events can be addressed by nutritional strategies that reduce the effects of these factors or delay their onset.
DIET AND HEALTH
ILLUSTRATION:V.FALCONIERIBASEDONL.M.BURKEANDJ.A.HAWLEY
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
as well as inconsistencies with either the guidelines
or typical practices of other elite athletes
[reliance on vegetable (80 to 90% of diet) rather
than animal food sources, very limited food variety,
distribution of energy to a small number
of meals in the day, and chronic periods of low
energy availability]. Case histories of scientistdevised
approaches to performance for elite
competitors, such as “weight making” for a
professional boxer (66) or a complex nutrition
plan followed by the winner of the 3-week Giro
d’Italia cycling race, do not necessarily allow
firm and reproducible conclusions about the
benefits of these strategies but show how practices
can be achieved within the complexities
of the sporting environment (see Box 3 and
Fig. 3). In the latter case, the competition plan
manipulated BM (by slight energy restriction
and the use of a low-residue diet to reduce gastrointestinal
contents) according to the benefits
of being lighter on hilly sections and fluctuated
daily energy and CHO intakes according to the
estimated metabolic cost of each stage (67). Notably,
the decisive day of this race, involving a
solo ride over a challenging mountainous terrain,
was achieved with a nutrition plan providing
6663 kcal and 18.9 g of CHO per kilogram
Burke et al., Science 362, 781–787 (2018) 16 November 2018 6 of 7
Box 3. Specificity and practicality require bespoke solutions.
The practical implementation of nutrition strategies by athletes in
real-world settings confounds the establishment of an evidence base
by traditional research methods and the development of generalizable
(and uncontroversial) guidelines. In most sports, performance is limited
by a number of interdependent factors, typically addressed by a coordinated
plan. We often consider several independently valuable nutrition
strategies in combination, despite the potential for redundancy,
amplification, attenuation, and competition between effects. The individual
benefits of fluid and CHO replacement for performance in the
heat are additive (88), caffeine is less effective when CHO intake is
also used to attenuate the performance decline during prolonged
exercise (89), and combining caffeine and bicarbonate supplementation
impairs the benefits of the former because of gastrointestinal
disturbances (90). However, because it is impractical to investigate
the many permutations and combinations of evidence-based nutrition
strategies (90), the overall effects on performance are unknown.
Environmental conditions and competition schedules add further
practical challenges. Premiere championships can be hosted under
“hostile” conditions (such as high altitude in the 1968 Mexico City
Olympic Games or heat in the 2019 Doha Athletics World Championships)
or with unusual timetables (such as late-night swimming at the
2016 Rio Olympic Games to coincide with primetime television in the
United States). Thus, athletes often need bespoke strategies for different
iterations of the same event. Lastly, sport involves rules, logistical
considerations, and cultures that dictate opportunities for nutrient intake
before, during, and between events (91). Some provide adequate opportunities
for beneficial intake (e.g., basketball players drink during substitutions
and time-outs). However, conditions in other events, such as
weight-division sports, encourage substantial pre-event dehydration and
energy restriction to “make weight” (92). Soccer prohibits breaks or access
to fluids during each half, and the practical challenge of drinking while
running at ~21 km/hour in a marathon limits the volumes ingested (68).
It is important to consider whether the traditional conduct and evaluation
of scientific research adequately inform elite athletes. In many areas of
our lives, we are content with generalizable truths (strategy X is good)
and guidelines (we should all implement strategy X by doing Y). Figure 3
illustrates a hierarchy of types of scientific evidence.The types of studies
that provide the strongest or highest-quality evidence (such as randomized
controlled trials) are extremely hard to achieve with high-caliber competitors
or may provide generic information inappropriate for a specific task. Lack of
appreciation of these concepts has caused angst within the sports science
community and an unfair dismissal of the integrity of its outputs.
Sports science was criticized in an assessment by epidemiologically trained
scientists (93, 94). Although valid methodological issues were raised, the
analysis failed to appreciate that sports scientists working in elite sport
typically seek highly context-specific information (Fig. 3). Evidence-based but
bespoke solutions for small numbers of individuals require special designs and
research tools; thevalidity, reliability, and sensitivityof measurements are critical.
We must consider repeatability in studydesign orcase history approaches to
account forsmall sample sizes. Even individual responsiveness to interventions
may vary. New or refined statistical approaches may be required (60, 90).
Controversy regarding guidelines for fluid intake during sport exemplifies
a lack of appreciation for context. Critics of current guidelines
for an individualized approach (95) who argue that athletes should be
told to drink only when thirsty during events (96) fail to recognize that
opportunities for fluid intake are often beyond the athlete’s control and
unrelated to need. Therefore, it is reasonable to develop a bespoke plan
for specific events that optimizes opportunities to consume fluid and
CHO before and throughout the event to integrate gut comfort, fuel
needs, a tolerable fluid deficit, and thirst management.
Generalizable truth: Community interest
(e.g. Does Strategy X work? How does it work? What is the best protocol? What type of events
might it best work for?)
Specific questions: Sub-elite athlete
(e.g.Will Strategy X protocol improve performance in 400 m swimming race? Will it improve
marathon performance?)
Bespoke questions: Elite athlete
(e.g.Will Strategy X allow me to run faster than other marathon competitors in hot and humid
Doha World Championship conditions, at midnight race time, when I am also taking caffeine?
Can I repeat the use of Supplement X for both the morning heats and evening finals of my 400
m swim when I am also bicarbonate loading?
Preliminary ideas/hypotheses
(e.g.What is Strategy/Supplement X? How can it be used to alter performance? How might
this be useful to a sporting competition or training program? Is there any basis for thinking it
might work?
Strength/qualityofevidence
Meta-analyses and
systematic reviews
Controlled trial
Case Control studies
Case reports, Case studies
Cross sectional studies
Ideas, ‘expert’ opinion, editorials, anecdote
Cohort Studies
Used less frequently
to provide evidence
of benefits from
performance
strategies
Fig. 3. Perspectives on the evidence base for elite athlete practices. Developing an evidence base for the nutritional practices of elite athletes
requires acknowledgment that specific answers to research questions and interpretations of guidelines are needed. [Adapted from (60)]
ILLUSTRATION:V.FALCONIERIBASEDONL.M.BURKEANDJ.A.HAWLEY
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
(a total of 1.3 kg, equivalent to ~85 slices of bread),
with race supplies being provided by domestique
teammates and a support crew at planned intervals
to avoid the need for the cyclist to carry
the weight burden (67). We can never know how
much this plan contributed to the rider’s eventual
success. Equally, we need to intellectualize
that athletic success can be achieved in the face
of apparently suboptimal practice. For example,
that the winner of an elite marathon incurred a
loss of 10% of BM over the race (68) fails to disprove
that hypohydration impairs performance;
rather, it demonstrates that this athlete was faster
than other competitors on that day and potentially
was best able to tolerate the conditions.
Although elite athletes can learn from sports
science, many lessons have also flowed in the
opposite direction. Sports nutrition recommendations
have often been updated when practices
observed among elite athletes were found
to be beneficial. For example, caffeine guidelines
for sport changed when the flat cola beverages
consumed by elite cyclists toward the end of
prolonged races (~1 to 2 mg of caffeine per
kilogram at the onset of fatigue) were found to
be as effective as the “scientifically proven”
protocols (6 to 9 mg/kg taken 1 hour pre-event)
(69). Ammunition to update guidelines for CHO
intake during prolonged (>2.5 hours) events
came from observations that the intakes of many
elite cyclists and triathletes (~90 g/hour) were
higher than the earlier recommendations (30
to 60 g/hour) and correlated with success (70).
Clearly, future outcomes will be best achieved
with a two-way interaction between sports scientists
and elite athletes and their coaches.
In the final analyses, modern sports nutrition
offers a feast of opportunities to assist elite
athletes to train hard, optimize adaptation, stay
healthy and injury free, achieve their desired
physique, and fight against fatigue factors that
limit success. Although there will be challenges
and changes to sports nutrition guidelines as
they evolve beyond the frontiers of current knowledge
and practice, we can be excited to know that
sports science in many guises contributes to the
outcomes that delight and amaze us from our
sofas and the grandstand.
REFERENCES AND NOTES
1. L. E. Grivetti, E. A. Applegate, J. Nutr. 127 (Suppl), 860S–868S
(1997).
2. D. T. Thomas, K. A. Erdman, L. M. Burke, Med. Sci. Sports
Exerc. 48, 543–568 (2016).
3. J. A. Hawley, C. Lundby, J. D. Cotter, L. M. Burke, Cell Metab.
27, 962–976 (2018).
4. B. Egan, J. A. Hawley, J. R. Zierath, Cell Metab. 24, 342–342.e1
(2016).
5. J. Bergström, E. Hultman, Nature 210, 309–310 (1966).
6. L. M. Burke, L. J. C. van Loon, J. A. Hawley, J. Appl. Physiol.
122, 1055–1067 (2017).
7. L. M. Burke et al., Int. J. Sport Nutr. Exerc. Metab. 28, 451–463
(2018).
8. A. N. Bosch, S. C. Dennis, T. D. Noakes, J. Appl. Physiol. 76,
2364–2372 (1994).
9. E. F. Coyle, A. R. Coggan, M. K. Hemmert, J. L. Ivy, J. Appl.
Physiol. 61, 165–172 (1986).
10. T. Stellingwerff, G. R. Cox, Appl. Physiol. Nutr. Metab. 39,
998–1011 (2014).
11. J. A. Hawley, A. N. Bosch, S. M. Weltan, S. C. Dennis,
T. D. Noakes, Pfluegers Arch. 426, 378–386 (1994).
12. A. E. Jeukendrup, Sports Med. 47 (suppl. 1), 101–110 (2017).
13. R. J. S. Costa et al., Appl. Physiol. Nutr. Metab. 42, 547–557
(2017).
14. A. E. Jeukendrup, Curr. Opin. Clin. Nutr. Metab. Care 13,
452–457 (2010).
15. L. M. Burke, J. A. Hawley, Med. Sci. Sports Exerc. 34,
1492–1498 (2002).
16. L. M. Burke et al., Med. Sci. Sports Exerc. 34, 83–91 (2002).
17. L. M. Burke, Sports Med. 45 (suppl. 1), 33–49 (2015).
18. T. Stellingwerff et al., Am. J. Physiol. Endocrinol. Metab. 290,
E380–E388 (2006).
19. E. Maunder, A. E. Kilding, D. J. Plews, Sports Med. 48,
2219–2226 (2018).
20. L. Havemann et al., J. Appl. Physiol. 100, 194–202 (2006).
21. J. S. Volek et al., Metabolism 65, 100–110 (2016).
22. L. M. Burke et al., J. Physiol. (London) 595, 2785–2807 (2017).
23. S. D. Phinney, B. R. Bistrian, W. J. Evans, E. Gervino,
G. L. Blackburn, Metabolism 32, 769–776 (1983).
24. J. A. Hawley, J. J. Leckey, Sports Med. 45, S5–S12 (2015).
25. J. A. Hawley, M. Hargreaves, M. J. Joyner, J. R. Zierath, Cell
159, 738–749 (2014).
26. V. G. Coffey, J. A. Hawley, Sports Med. 37, 737–763 (2007).
27. C. G. Perry et al., J. Physiol. (London) 588, 4795–4810 (2010).
28. A. E. Jeukendrup, Sports Med. 47 (suppl. 1), 51–63 (2017).
29. S. G. Impey et al., Sports Med. 48, 1031–1048 (2018).
30. J. D. Bartlett, J. A. Hawley, J. P. Morton, Eur. J. Sport Sci. 15,
3–12 (2015).
31. L. M. Burke, G. R. Cox, N. K. Culmmings, B. Desbrow, Sports
Med. 31, 267–299 (2001).
32. T. Stokes, A. J. Hector, R. W. Morton, C. McGlory, S. M. Phillips,
Nutrients 10, 180 (2018).
33. D. R. Moore, D. M. Camera, J. L. Areta, J. A. Hawley, Appl.
Physiol. Nutr. Metab. 39, 987–997 (2014).
34. P. T. Res et al., Med. Sci. Sports Exerc. 44, 1560–1569
(2012).
35. G. Clénin et al., Swiss Med. Wkly. 145, w14196 (2015).
36. D. J. Owens, R. Allison, G. L. Close, Sports Med. 48 (suppl. 1),
3–16 (2018).
37. M. Mountjoy et al., Int. J. Sport Nutr. Exerc. Metab. 28, 316–331
(2018).
38. L. M. Burke, B. Lundy, I. L. Fahrenholtz, A. K. Melin, Int. J. Sport
Nutr. Exerc. Metab. 28, 350–363 (2018).
39. T. Stellingwerff, Int. J. Sport Nutr. Exerc. Metab. 28, 428–433
(2018).
40. S. Bermon et al., Exerc. Immunol. Rev. 23, 8–50 (2017).
41. C. Sale et al., J. Appl. Physiol. 119, 824–830 (2015).
42. A. K. A. McKay et al., Med. Sci. Sports Exerc. 10.1249/
MSS.0000000000001816 (2018).
43. T. L. Merry, M. Ristow, J. Physiol. (London) 594, 5135–5147 (2016).
44. W. K. Yeo et al., J. Appl. Physiol. 105, 1462–1470 (2008).
45. S. C. Lane et al., J. Appl. Physiol. 119, 643–655 (2015).
46. L. A. Marquet et al., Med. Sci. Sports Exerc. 48, 663–672 (2016).
47. K. D. Gejl et al., Med. Sci. Sports Exerc. 49, 2486–2497
(2017).
48. T. Stellingwerf, Int. J. Sport Nutr. Exerc. Metab. 22, 392–400
(2012).
49. D. Bishop, Sports Med. 40, 995–1017 (2010).
50. G. Cox, I. Mujika, D. Tumilty, L. Burke, Int. J. Sport Nutr. Exerc.
Metab. 12, 33–46 (2002).
51. J. A. Hawley, E. J. Schabort, T. D. Noakes, S. C. Dennis, Sports
Med. 24, 73–81 (1997).
52. E. D. B. Goulet, M. Aubertin-Leheudre, G. E. Plante, I. J. Dionne,
Int. J. Sport Nutr. Exerc. Metab. 17, 391–410 (2007).
53. R. W. Kenefick, Sports Med. 48 (suppl. 1), 31–37 (2018).
54. M. Z. Donahue, “Runner comes excruciatingly close to breaking
two-hour marathon banner,” 6 May 2017; https://news.
nationalgeographic.com/2017/05/extreme-running-marathon-
nike-science/.
55. M. J. Joyner, J. R. Ruiz, A. Lucia, J. Appl. Physiol. 110, 275–277
(2011).
56. M. J. Joyner, E. F. Coyle, J. Physiol. (London) 586, 35–44
(2008).
57. W. Hoogkamer et al., Sports Med. 48, 1009–1019 (2018).
58. A. M. Jones, Appl. Physiol. Nutr. Metab. 39, 1019–1028 (2014).
59. A. Krogh, J. Lindhard, Biochem. J. 14, 290–363 (1920).
60. L. M. Burke, P. Peeling, Int. J. Sport Nutr. Exerc. Metab. 28,
159–169 (2018).
61. R. K. Boorsma, J. Whitfield, L. L. Spriet, Med. Sci. Sports Exerc.
46, 2326–2334 (2014).
62. K. L. Jonvik, J. Nyakayiru, L. J. van Loon, L. B. Verdijk, J. Appl.
Physiol. 119, 759–761 (2015).
63. M. Hultström et al., J. Appl. Physiol. 119, 762–769 (2015).
64. L. Y. Beis et al., J. Int. Soc. Sports Nutr. 8, 7 (2011).
65. V. O. Onywera, F. K. Kiplamai, P. J. Tuitoek, M. K. Boit,
Y. P. Pitsiladis, Int. J. Sport Nutr. Exerc. Metab. 14, 709–719 (2004).
66. J. P. Morton, C. Robertson, L. Sutton, D. P. MacLaren,
Int. J. Sport Nutr. Exerc. Metab. 20, 80–85 (2010).
67. T. Fordyce, “Chris Froome: Team Sky’s unprecedented release
of data reveals how British rider won Giro d’Italia,” 4 July 2018;
https://www.bbc.com/sport/cycling/44694122.
68. L. Y. Beis, M. Wright-Whyte, B. Fudge, T. Noakes,
Y. P. Pitsiladis, Clin. J. Sport Med. 22, 254–261 (2012).
69. G. R. Cox et al., J. Appl. Physiol. 93, 990–999 (2002).
70. A. Jeukendrup, Sports Med. 44 (suppl. 1), S25–S33 (2014).
71. F. A. Bainbridge, The Physiology of Muscular Exercise
(Longmans, Green & Co., 1919).
72. J. A. Hawley, R. J. Maughan, M. Hargreaves, Cell Metab. 22,
12–17 (2015).
73. S. A. Levine, B. Gordon, C. L. Derick, JAMA 82, 1778–1779
(1924).
74. T. Matsui et al., J. Physiol. (London) 590, 607–616 (2012).
75. L. L. Spriet, Sports Med. 44 (suppl. 2), S175–S184 (2014).
76. L. M. Burke, R. J. Maughan, Eur. J. Sport Sci. 15, 29–40 (2015).
77. J. M. Carter, A. E. Jeukendrup, D. A. Jones, Med. Sci. Sports
Exerc. 36, 2107–2111 (2004).
78. E. S. Chambers, M. W. Bridge, D. A. Jones, J. Physiol. (London)
587, 1779–1794 (2009).
79. S. Gam, K. J. Guelfi, P. A. Fournier, Sports Med. 46, 1385–1390
(2016).
80. D. H. Craighead et al., Muscle Nerve 56, 379–385 (2017).
81. Persistence Market Research, “Global market study on sports
supplements: Non-protein products to witness substantial
growth during 2017 – 2025” (Rep. PMRREP3034, Persistence
Market Research, January 2018); https://www.
persistencemarketresearch.com/market-research/sports-
supplements-market.asp.
82. I. Garthe, R. J. Maughan, Int. J. Sport Nutr. Exerc. Metab. 28,
126–138 (2018).
83. R. J. Maughan et al., Int. J. Sport Nutr. Exerc. Metab. 28,
104–125 (2018).
84. P. Peeling, M. J. Binnie, P. S. R. Goods, M. Sim, L. M. Burke, Int.
J. Sport Nutr. Exerc. Metab. 28, 178–187 (2018).
85. A. I. Geller et al., N. Engl. J. Med. 373, 1531–1540 (2015).
86. World Anti-Doping Agency, The Code; https://www.wada-ama.
org/en/what-we-do/the-code.
87. J. M. Martínez-Sanz et al., Nutrients 9, 1093 (2017).
88. P. R. Below, R. Mora-Rodríguez, J. González-Alonso, E. F. Coyle,
Med. Sci. Sports Exerc. 27, 200–210 (1995).
89. S. A. Conger, G. L. Warren, M. A. Hardy,
M. L. Millard-Stafford, Int. J. Sport Nutr. Exerc. Metab. 21,
71–84 (2011).
90. L. M. Burke, Sports Med. 47 (suppl. 1), 79–100 (2017).
91. A. K. Garth, L. M. Burke, Sports Med. 43, 539–564 (2013).
92. R. Reale, G. Slater, L. M. Burke, Int. J. Sports Physiol. Perform.
13, 459–466 (2018).
93. C. Heneghan, R. Perera, D. Nunan, K. Mahtani, P. Gill, BMJ 345,
e4797 (2012).
94. C. Heneghan et al., BMJ 345, e4848 (2012).
95. M. N. Sawka et al., Med. Sci. Sports Exerc. 39, 377–390 (2007).
96. D. Cohen, BMJ 345, e4737 (2012).
ACKNOWLEDGMENTS
Competing interests: L.M.B. is a director of the International
Olympic Committee Diploma in Sports Nutrition program and has
been funded by the Australian Institute of Sport High Performance
Research Funds, Australian Catholic University, and the Australian
Research Council, as well as industry partners including the
Alliance for Potato Research and Education (APRE), South African
Potato Producers Organisation, Dairy Health and Nutrition Research
Consortium, Dairy Australia, Nestle Research Centre, Nestle Australia,
Kellogg’s Australia, Mars Australia, and Gatorade Australia. L.M.B. was
a member of the Gatorade Sports Science Expert Panel from 2014
to 2015, for which her workplace received an honorarium. J.A.H. has
received funding for studies in nutritional metabolism from APRE;
the Novo Nordisk Foundation; the Australian Sports Commission; Dairy
Health and Nutrition Research Consortium, Australia; the Australian
Research Council; Nestec, Switzerland; the National Heart Foundation
of Australia; the Diabetes Australia Research Trust; Uncle Ben’s of
Australia, a division of EFFEM Foods; Polar Electro, Finland; SmithKline
Beecham Consumer Healthcare (Nutrition), United Kingdom; the
South African Potato Board; Bromor Foods, South Africa; the Sugar
Association of South Africa; and Wander Research and Development,
Switzerland. J.A.H. was a member of the Gatorade Sports Science
Expert Panel from 2014 to 2015.
10.1126/science.aau2093
Burke et al., Science 362, 781–787 (2018) 16 November 2018 7 of 7
DIET AND HEALTH
onMarch19,2019http://science.sciencemag.org/Downloadedfrom
Swifter, higher, stronger: What's on the menu?
Louise M. Burke and John A. Hawley
DOI: 10.1126/science.aau2093
(6416), 781-787.362Science
ARTICLE TOOLS http://science.sciencemag.org/content/362/6416/781
CONTENT
RELATED
http://science.sciencemag.org/content/sci/362/6416/776.full
http://science.sciencemag.org/content/sci/362/6416/770.full
http://science.sciencemag.org/content/sci/362/6416/764.full
http://science.sciencemag.org/content/sci/362/6416/762.full
REFERENCES
http://science.sciencemag.org/content/362/6416/781#BIBL
This article cites 90 articles, 5 of which you can access for free
PERMISSIONS http://www.sciencemag.org/help/reprints-and-permissions
Terms of ServiceUse of this article is subject to the
is a registered trademark of AAAS.Science
licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. The title
Science, 1200 New York Avenue NW, Washington, DC 20005. 2017 © The Authors, some rights reserved; exclusive
(print ISSN 0036-8075; online ISSN 1095-9203) is published by the American Association for the Advancement ofScience
onMarch19,2019http://science.sciencemag.org/Downloadedfrom