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Effect of Astaxanthin on Cycling Time Trial Performance

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We examined the effect of Astaxanthin (AST) on substrate metabolism and cycling time trial (TT) performance by randomly assigning 21 competitive cyclists to 28 d of encapsulated AST (4 mg/d) or placebo (PLA) supplementation. Testing included a VO2max test and on a separate day a 2 h constant intensity pre-exhaustion ride, after a 10 h fast, at 5% below VO2max stimulated onset of 4 mmol/L lactic acid followed 5 min later by a 20 km TT. Analysis included ANOVA and post-hoc testing. Data are Mean (SD) and (95% CI) when expressed as change (pre vs. post). Fourteen participants successfully completed the trial. Overall, we observed significant improvements in 20 km TT performance in the AST group (n=7; -121 s; 95% CI, -185, -53), but not the PLA (n=7; -19 s; 95% CI, -84, 45). The AST group was significantly different vs. PLA (P<0.05). The AST group significantly increased power output (20 W; 95% CI, 1, 38), while the PLA group did not (1.6 W; 95% CI, -17, 20). The mechanism of action for these improvements remains unclear, as we observed no treatment effects for carbohydrate and fat oxidation, or blood indices indicative of fuel mobilization. While AST significantly improved TT performance the mechanism of action explaining this effect remains obscure.
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882 Nutrition
Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
accepted after revision
May 16 , 2011
Bibliography
DOI http://dx.doi.org/
10.1055/s-0031-1280779
Published online:
October 7, 2011
Int J Sports Med 2011; 32:
882–888 © Georg Thieme
Verlag KG Stuttgart · New York
ISSN 0172-4622
Correspondence
Dr. Conrad. P. Earnest, PhD
Pennington Biomedical
Research Center
Exercise Biology Laboratory
Perkins Road
70808 Baton Rouge
United States 6400
Tel.: +1/225/763 2632
Fax: +1/225/763 2632
Conrad.Earnest@pbrc.edu
Key words
cycling
nutrition
ergogenic aid
performance
supplement
E ect of Astaxanthin on Cycling Time Trial
Performance
However, if enhanced lipid metabolism is a pro-
posed bene t of AST supplementation, it seems
more intuitive to examine exercise bouts of
longer duration. Accordingly we are unaware of
any published studies examining the e ect of
AST supplementation for prolonged periods of
exercise endurance performance in humans. The
primary aim of our current study was to examine
whether 28 days of AST supplementation would
improve exercise following a 2 h pre-exhaustion
ride designed to minimize carbohydrate contri-
bution during exercise performance. Our second-
ary aim was to determine whether 28 days of AST
supplementation modulates indices of carbohy-
drate and lipid metabolism.
Material and Methods
Participants
We recruited amateur endurance-trained males
from 18 to 39 years of age who had a VO2 max
50 ml/kg/min, were actively participating in
competitive cycling activities such as competi-
tive road cycling or triathlons, and were accumu-
Introduction
Astaxanthin (AST) is a carotenoid belonging to a
larger class of phytochemicals known as terpenes
that can be found in microalgae, yeast, salmon,
trout, krill, shrimp, cray sh, crustaceans, and the
feathers of some birds [ 5 , 7 , 9 , 10 , 16 ] . Currently,
the FDA permits the use of AST as a food coloring,
as well as an additive for animal and sh foods.
Perhaps AST’s most notable use is as a feed addi-
tive for farm raised salmon, giving the salmon its
reddish tissue color. While AST is a natural nutri-
tional component found in food it can also be
purchased over-the-counter as a dietary supple-
ment. Astaxanthin has recently received atten-
tion due to its ability to scavenge free radicals,
decrease in ammation, improve indices of lipid
metabolism and attenuate lipid accretion, and
increase exercise time to exhaustion in mice
[ 1 , 2 , 7 , 12 , 15 ] .
To date, only one study has examined the e cacy
of AST supplementation on endurance exercise
performance in humans, whereby 4 weeks of AST
supplementation was shown to reduced lactic
acid build up following 1 200 m of running [ 14 ] .
Authors C. P. Earnest
1 , M. Lupo
1 , K. M. White
2 , T. S. Church
3
A liations
1 Pennington Biomedical Research Center , Exercise Biology Laboratory , Baton Rouge , United States
2 Gatorade, Sports Science Institute , Barrington , United States
3 Pennington Biomedical Research Center , Preventive Medicine , Baton Rouge , United States
Abstract
We examined the e ect of Astaxanthin (AST) on
substrate metabolism and cycling time trial (TT)
performance by randomly assigning 21 competi-
tive cyclists to 28d of encapsulated AST (4 mg/d)
or placebo (PLA) supplementation. Testing
included a VO
2max test and on a separate day a
2 h constant intensity pre-exhaustion ride, after
a 10 h fast, at 5 % below VO
2max stimulated onset
of 4 mmol/L lactic acid followed 5 min later by a
20 km TT. Analysis included ANOVA and post-
hoc testing. Data are Mean (SD) and (95 % CI)
when expressed as change (pre vs. post). Four-
teen participants successfully completed the
trial. Overall, we observed signi cant improve-
ments in 20 km TT performance in the AST group
(n = 7; 121 s; 95 %CI, 185, 53), but not the
PLA (n = 7; 19 s; 95 %CI, 84, 45). The AST group
was signi cantly di erent vs. PLA (P < 0.05). The
AST group signi cantly increased power output
(20 W; 95 %CI, 1, 38), while the PLA group did
not (1.6 W; 95 %CI, 17, 20). The mechanism of
action for these improvements remains unclear,
as we observed no treatment e ects for carbohy-
drate and fat oxidation, or blood indices indica-
tive of fuel mobilization. While AST signi cantly
improved TT performance the mechanism of
action explaining this e ect remains obscure.
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
Nutrition
lating a weekly cycling volume of 160 km per week. Initially, we
considered using a mixed cohort of men and women, however,
decided against it for 2 primary reasons. First, it has been pur-
ported that carbohydrate and fat metabolism di er between
genders with respect to prolonged exercise [ 18 ] . Thus, a mixed
cohort would add variance to our study that we would not be
able to account for using a relatively small sample size. Second,
we, and others in our community (Baton Rouge, LA, USA), have
found it di cult to recruit women for more strenuous exercise
protocols such as the one undertaken for this study. Hence, we
focused our current recruitment e orts on men, whose cardio-
respiratory tness measures are presented in
Table 1 . The
ethical review committee at Pennington Biomedical Research
Center approved our study and informed consent was obtained
from all participants before entering the trial. All study proce-
dures conformed to the Declaration of Helsinki and ethical
standards of IJSM [ 8 ] . We have provided a CONSORT schematic
outlining the overall study timeline in
Fig. 1 .
Recruitment and baseline testing
We initiated our recruitment e orts by contacting local cycling
clubs via email, who therein posted our study details on various
online forums and discussion boards. Upon expressing interest
in the study, we contacted potential candidates via phone and
email. Following a successful screening procedure we invited
study candidates to come to the Pennington Biomedical Research
Center Exercise Biology Laboratory Testing Core where they
were further screened to participate in our study protocol. The
entire length of the study for each participant ranged from 35 to
40 days. Brie y, participants attended a baseline run-in period,
inclusive of exercise testing to determine maximal cardio-
respiratory capacity (details below), 20 km TT rehearsals, and a
fasted 2 h pre-exhaustion ride that was followed immediately by
a 20 km TT (details below) on their own bike using a Compu-
trainer ergometer (Seattle, WA). Before each Computrainer test
the ergometer was turned on and allowed to warm-up for
30 min. Immediately before each TT we also performed an indi-
vidualized calibration procedure that accounts for rolling resis-
tance. We have presented a schematic of all testing procedures
in
Fig. 2a .
Maximal cardiorespiratory exercise
We instructed each subject to prepare for his VO
2max test as if
preparing for a race and to abstain from exercise for 24 h before
the test. This preparation included not changing their training
parameters or dietary patterns for the week preceding each test.
We asked participants to record what they ate in a food log 3
days before testing and to duplicate the same food intake on the
penultimate day before testing during the follow-up visit. Par-
ticipants were also instructed to eat a light snack ~3 h before
their tests and to abstain from ingesting any medications that
would in uence heart rate on the day of each test. The one
exception was ca eine, which we asked participants not to con-
sume for at least 5 h before testing.
We performed all VO
2max exercise tests on a Lode Excalibur Sport
Ergometer (Groningen, The Netherlands) and analyzed the riders
for various cardiorespiratory parameters using a Parvomedics
TrueMax Metabolic System (Salt Lake City, UT). Each cycling test
began with a warm-up at 50 W (10 min) and then progressed to
75 W (2 min). After the warm-up, the test began by increasing the
power output (PO) to 100 W. Once PO was set at 100 W, each stage
inclusive of the 100-W stage lasted 3 min and progressed 35 W
every 3 min until the rider reached exhaustion or could no longer
maintain a pedal cadence of 50 rpm. We allowed each rider to
choose their preferred cadence within a range of 70–90 rpm.
We collected gas exchange data continuously using an automated
computerized breath-by-breath Parvomedics TrueMax Metabolic
System. The TrueMax system uses a pneumotachometer, a para-
magnetic O
2 analyzer, and an infrared CO
2 analyzer to analyze
respiratory O
2 and CO
2 , respectively. Before each test, we followed
a standard calibration procedure for each metabolic cart including
a ow calibration using a 3-L calibration syringe and calibration
against standardized gases (16 % O
2 , 4 % CO
2 , and balanced nitro-
gen) obtained from the manufacturer of the metabolic system.
We averaged all gas exchange data in 60 s intervals and only the
last minute of each stage was used in our analyses. Blood samples
(25 uL) for the measurement of blood lactate (Lactate Pro, Ques-
nel, BC, Canada) were taken from the riders ngertips at rest and
during the last 30 s of each stage starting at 75 W. From these lac-
Fig. 1 CONSORT diagram of study enrollment.
Email Response
(N=79)
Eligible for Baseline
(N=26)
Exclusion
N=53, Failed to meet
inclusion criteria
Exclusion
N=3, Insufficient VO2max
N=2 Failure to complete
2 hr ride
Successfully Completed
Baseline (N=21)
Randomized to
Treatment (N=21)
Treatment
(N=11)
Completed
(N=7)
Completed
(N=7)
Placebo
(N=10)
Withdrawn
N=1, Illness
N=1, Computer
Failure
N=1, Unable to
Complete Protocol
N=1, Invalid
pretest
Withdrawn
N=2, Unable to
Complete Protocol
N=1, Invalid
pretest
All (N=14) Astaxanthin (n=7) Placebo (n=7)
V O 2max (L/min) 3.88 (0.4) 3.98 (0.3) 3.79 (0.4)
V O 2max (ml/kg/min) 52.84 (3.5) 54.14 (4.1) 51.53 (2.4)
Maximal PO (W) 330 (26) 335 (17) 325 (34)
HR max (b/min) 185 (9) 183 (11) 187 (7)
PO (W) @ 2 mmol/L BLa 141 (57) 144 (62) 138 (57)
percent of VO 2max @ 2 mmol/L BLa 50.90 (12.9) 49.08 (14.7) 52.45 (12.0)
PO (W) @ 4 mmol/L BLA 228 (47) 227 (43) 229 (55)
percent of VO 2max @ 4 mmol/L BLa 73.65 (9.7) 71.66 (8.9) 75.63 (10.0)
Data are mean and SD
Table 1 Baseline tness charac-
teristics of study participants.
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
Nutrition
tate measurements we determined the corresponding PO associ-
ated with the accumulation of 2 mmol/L and 4 mmol/L of lactic
acid accumulation by drawing a 3
rd order line of best t through
all data points. For the 2 h ride we asked riders to work at a PO
corresponding to 5 % lower than the PO associated with the accu-
mulation of 4 mmol/L of lactic acid.
Two-hour and 20 km TT performance testing
We have presented a schematic outlining the procedures for the
2 h pre-exhaustion and TT ride performed at baseline and fol-
low-up in
Fig. 2b . For the 2 h pre-exhaustion fasting ride, we
asked participants to report to the Pennington Exercise Testing
Core on the morning of their test where we placed an indwelling
catheter into an antecubital vein 30 min before their ride. We
also determined participant hydration status designated as hav-
ing a urine speci c gravity (USG) less than 1.025. During the TT
we instructed participants to ride the 20 km distance as fast as
possible on his own bicycle. To ensure minimal variability
between tests we asked the participants ride the same bike with
the same con guration for positioning during the rehearsal,
baseline and follow-up testing conditions. Approximately 20 min
after the insertion of the catheter, we collected an initial series
of blood samples to assess resting blood values in order to moni-
tor the pre- and post-treatment safety corresponding to supple-
mentation with AST. These measures included a standard serum
15-panel blood test to measure creatinine, potassium, uric acid,
albumin, calcium, magnesium, creatine phosphokinase (CPK),
alanine aminotransferase (ALT), alkaline phosphatase (ALK),
iron, cholesterol (LDL & HDL), and triglycerides. We also per-
formed a complete blood count (CBC) with di erentials to deter-
mine hemoglobin, hematocrit, mean cell volume, platelet count,
white blood count, granulocytes, neutrophils, eosinophils, and
basophils.
After we collected the rst set of blood samples we asked each
rider to perform a 10 min warm up at a low intensity (50 W)
before initiating the 2 h ride. During the 2 h pre-load ride we col-
lected blood samples every 20 min to determine several indices
indicative of carbohydrate and lipid metabolism including glu-
cose, lactic acid, glycerol, and non-esteri ed fatty acids (NEFA).
At these same time intervals we also measured cardiorespira-
tory parameters (VO
2 and VCO
2 , L/min) to determine the relative
contributions of carbohydrate and fat oxidation during testing
using standard stoichiometric equations [ 6 ] . Riders consumed
250 ml of water every 15 min throughout the test. For the blood
measurements we collected each blood sample during the last
30 s of the 20 min period. For VO
2 and VCO
2 we began data col-
lection 4 min before each 20 min demarcation in order to obtain
steady state values. However, we only used the last minute of
this collection period for our analysis. All blood samples were
spun on a centrifuge and stored at 80 C until we could analyze
them “in batch” (i. e., pre/post test sample together) using a
Beckman Coulter DXC600 (Brea, CA) analyzer.
We analyzed glucose and lactic acid using an oxygen electrode
and enzymatic endpoint method of analysis, respectively. For
glucose, all samples were spun on a centrifuge at 3 500 rpm for
15 min at room temperature. For lactic acid, each sample was
spun at the same speed at 4 °C. For glycerol and NEFA we ana-
lyzed each sample using enzymatic colorimetric detection anal-
ysis, respectively. For glycerol, centrifugation took place at
3 500 rpm for 15 min at room temperature, while for NEFA the
centrifuge speed was 3 000 rpm for 15 min at 4 °C.
Randomization and treatment
After completing the entire baseline testing procedures, we ran-
domized each participant, in a double-blind, placebo controlled,
parallel group designed manner to receive either 4 mg/d of
encapsulated AST or a matched placebo for 4 weeks. We chose
Fig. 2 Overview of study timeline (panel a ) and
testing procedures (panel b ).
a
b
Overview of testing and supplementation timeline.
Baseline Testing
Screening Day 1 Day 2 Day 4 Day 5 Day 32 Day 33 Day 34
2 hr ride
20 km TT
Rest2 hr ride
20 km TT
Rest
VO2max
VO2max
Days 6 – 33
Post TestingSupplement (28 d)
Determine
Eligibility
Ht
Wt
Practice
Time Trial
(20 km)
Day 3
Practice
Time Trial
(20 km)
Sequence of data collection during testing
Pre-Ride procedures 2 hr steady state ride pre-exhaustion ride
Standardized respiratory and blood collections every 20 minutes
Rest
(5 min)
Time
Trial
–30 min –10 – 0 min 16–20 min 36–40 min 56–60 min 76–80 min 96–100 min 116–120 min 120–125 min 125 min+
20 km TT
Respiratory data (4 min of collection)
(VO2 & VCO2)
Measure:
Glucose
Lactic acid
Glycerol
NEFA
Warm up @
100 W
Measure
(–2m):
Glucose
Lactic acid
Glycerol
NEFA
Insert
Catheter
Measure:
Glucose
Lactic acid
Chem-15
CBC
Glycerol
NEFA
Extra
Serum
Plasma
NEFA: Non-esterified fatty acid
TT: Time Trial
PO: Power Output in watts
Ave PO
PO ea. 5 km
Time to
complete
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
Nutrition
4 weeks as studies in mice have shown that AST improves lipid
metabolism and exercise performance within a 4–5 week period
[ 2 , 11 ] . All supplements were provided by Fuji Health Science,
Inc. (Burlington, NJ). Each treatment was delivered in a black soft
gel capsule and each AST soft gel contained 80 mg of 5 % natural
astaxanthin extract from Haematococcus pluvialis algae, yielding
4 mg of active astaxanthin per soft gel, and 120 mg of medium
chain triglyceride as ller. The placebo soft gel was comprised of
200 mg medium chain triglyceride plus a small amount of cara-
mel food coloring to make the capsules identical in appearance
to the active soft gels. We asked all participants to consume their
respective treatments with a meal and provided each person
with enough supplement for 5 extra days in case they required
an extended period to complete the study protocol. This latter
aspect of our study also better enabled us to perform a pill count
at the end of the study to determine the degree of compliance to
the study protocol. Lastly, people independent of the study dis-
persed all treatments using a unique, individualized 4-digit
number sequence. We chose a randomized number sequence in
case we observed any side e ects during the course of the study.
This procedure allows for the breaking of a single treatment
code without sacri cing the integrity of the entire treatment
cohort.
Statistical analysis
Our primary outcome analysis was aimed at determining
whether AST supplementation improved various indices of
cycling performance following a 2 h pre-exhaustion bout of
exercise intended to minimize carbohydrate contribution. The
primary outcomes for our investigation were the rider’s ability
to complete a 20 km TT immediately following a 2 h pre-exhaus-
tion ride. Accordingly, we examined TT performance in terms of
the time it took to complete the 20 TT km ride and the average
PO generated by the rider. As a secondary analysis we examined
several laboratory indices of physical performance such as
VO
2max , maximal PO, and the PO observed at lactate threshold
(2 mmol/L) and onset of blood lactate accumulation (4 mmol/L)
during the VO
2max test. As a tertiary analysis we assessed several
metabolic parameters traditionally used as a means of providing
a mechanism of action should performance changes be observed.
These indices included the analysis of blood variables indicative
of improved carbohydrate and fat usage including: plasma lac-
tate, glucose, non-esteri ed fatty acids, and glycerol. We
approached our analysis of these variables in 2 ways. First, we
analyzed the overall e ectiveness of AST on these variables by
using an integrated area-under-the-curve (AUC) assessment for
all time intervals associated with our data collection beginning
with the resting measurement as “time 0”. Our second strategy
was to examine potential di erences in these variables at each
20 min time point during the 2 h ride. These speci c time points
included resting blood values obtained after a 10 h fast, the end
of warm-up, and every 20 min therein during the 2 h ride. Dur-
ing these same time intervals we also examined the respiratory
derived measurements for the stoichiometric assessment of car-
bohydrate and fat oxidation. For our primary analysis we exam-
ined each variable as change from baseline. Determinations for
within group signi cance were based on the mean change and
accompanying 95 % con dence interval (95 % CI) for each respec-
tive performance parameter. We used a general linear model to
examine between group di erences. E ect sizes were calculated
for time to complete and average power output during the 20 km
TT using Cohen’s d (ES) [ 4 ] . For the AUC analysis we analyzed our
data using a 2 × 2 [treatment (placebo/treatment) × time (pre/
post)] ANOVA. For the time parameter analysis we used a
repeated measures ANOVA. Lastly, we also examined the mean
change in outcomes between the pre-test and post-test condi-
tion using a one-way ANOVA.
We examined blood chemistry values (i. e., Chem-15/CBC) and
food frequency evaluations using the same statistical techniques
as described for the primary outcome data. The reason for the
blood chemistry analysis was to determine whether AST sup-
plementation might adversely a ect hepatorenal function, in
order to ensure that supplementation with AST was safe. Lastly,
we examined by pill count the number of assigned treatment
capsules vs. the number of supplement days during the study
period. We excluded any outliers in the studies who fell outside
3 SD for time changes from pre to post treatment. All individual
time point data in our paper are presented as mean ± SD. Statisti-
cal signi cance was set at P 0.05.
Results
We randomized 21 participants into our study (AST = 11,
PLA = 10). However, only 7 participants from each treatment
group completed the entire testing protocol. The reasons for this
completion rate are presented in
Fig. 1 , but generally fall
under the categories of illness, equipment failure or inability to
complete the 2 h pre-exhaustion ride or the subsequent TT. We
did however remove 2 outlier performances from our analysis.
In one instance, we removed a rider from the AST group for
demonstrating a 7 min time improvement from the pre to post
test condition. In the other instance we removed one rider from
the PLA group for an abnormal performance loss of 5 min.
Though we could have kept these 2 riders in our analysis, their
relative changes in performance given their respective treat-
ment groups, only served to separate our hypothesis further
from the null. In essence, leaving these 2 riders in the analysis
increased the treatment e ect for the AST group, while simulta-
neously making the PLA group appear slower.
For those who completed the study, we observed no statistical
di erence at baseline between treatment groups for any of our
measurements associated with the study including age (28 ± 6
years), body mass (74.6 ± 8.8 kg), and height (175.6 ± 8.5 cm). For
our post-test analysis, we observed a signi cant within group
improvement for the time it took to complete the 20 km TT for
the A ST supplemented riders (2 387 ± 206 s vs. 2 266 ± 190 s;
range, 02, 251 s) and the average power output measured
during the TT ride (162 ± 37 W vs. 186 ± 34 W; range, 05–40 W,
P < 0.05). For our analysis of time to complete the 20 km TT, we
observed that the AST group’s time improvement was signi -
cantly di erent from the PLA group (P < 0.02). Though some
improvement in time was observed for the PLA group, neither
TT time (2251 ± 260 s vs. 2 233 ± 283 s; range, 101, 62) or PO
(186 ± 57 W vs. 187 ± 75 W) was statistically signi cant following
the 28 d supplementation period. The ES for the di erence
between treatment groups in their time to complete the time
trial was 1.25, whilst the ES for the between group di erence in
PO was 0.95. According to Cohen, these ES would be considered
large [ 4 ] .We have presented the mean and 95 % CI change for
time and PO along with accompanying individual responses for
each treatment group in
Fig. 3 .
For our analysis of fuel utilization we were unable to detect a
signi cant treatment di erence for any blood marker indicative
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
Nutrition
of enhanced carbohydrate or fat oxidation (
Fig. 4 a, b ), neither
were we able to detect a change in any blood parameter sugges-
tive of a shift in fuel metabolism (
Fig. 5 a–d ) for any given
20 min time interval. While we did observe a signi cant increase
in plasma concentrations of NEFA with increasing exercise time,
these increases were similar within each group but not di erent
between groups or the pre/post treatment condition. When we
further analyzed our blood work data as an AUC for the entire 2 h
pre-exhaustion ride we were also unable to detect a signi cant
di erence for treatment group. Lastly, we did not observe any
di erences in either the blood chemistries suggesting the treat-
ment group signi cantly altered hepatorenal function during
the treatment period (data not shown).
Discussion
The primary aim of our study was to examine the e ect of AST
supplementation on 20 km TT performance following a 2 h pre-
exhaustion ride undertaken after a 10 h fast. The goal in using
this type of protocol was to minimize the contributions of carbo-
hydrate for energy provision; hence, creating an increased reli-
ance on fat oxidation. This decision was based on observations
from animal studies showing an increased reliance on fat utiliza-
tion while simultaneously increasing time to exhaustion during
exercise [ 1 , 2 , 11 , 12 ] . We observed an approximate 2 min mean
improvement (5 %) in the time necessary to complete the 20 km
TT that was accompanied by a 20 W increase (15 %) in the aver-
age power output generated by riders during the TT condition.
Changes in time and power output for the PLA group were 0.8 %
and 0.5 %, respectively. An examination of
Fig. 3 also shows
that each of the riders in the AST group improved 20 km per-
formance time and power output, while the PLA group showed
minimal improvements and were fairly evenly split between
faster and slower performances. Despite these improvements in
cycling performance the mechanism of action to explain our
ndings remain enigmatic.
Most of the research conducted on AST to date has used murine
models to examine exercise performance and energy distribu-
tion patterns. For example, Aoi et al. [ 2 ] examined mice divided
into 4 groups of mice that were either (a) sedentary, (b) seden-
tary, yet, treated with AST, or assigned to run on treadmill (c)
without or (d) with AST supplementation [ 2 ] . In their study, the
authors reported that each exercise group was able to run longer
on the treadmill before exhaustion; however, those mice treated
with AST also increased fat utilization during exercise compared
to mice on a normal diet. At a cellular level these ndings were
supported by the observation that AST fed mice increased the
localization of fatty acid translocase (FAT/CD36) and carnitine
palmitoyltransferase I (CPT I) in skeletal muscle. In essence, AST
improved various mechanisms associated with transporting
long chain fatty acids into the mitochondria. In our current
study, however, we see no evidence for the preferential use of
fat.
A question that may be raised pertains to dosing equivalents
between murine and human studies. In one such study, Ikeuchi
Fig. 3 Data represent the mean and 95% CI within group changes in
time performance (panel a ) and power output (panel b ) for cyclists receiv-
ing 28 d of AST (left side) or PLA (right side) supplementation. *P<0.05
for between group di erences.
300
a
b
–300
250
–250
200
–200
100
–100
50
–50
0
150
–150
60
–60
50
–50
40
–40
20
–20
10
–10
0
30
–30
Time (sec)Power Output (W)
20 W
(95% CI, 1.0,
38.1) 1.6 W
(95% CI, –17,
20.3)
–121 seconds
(95% CI, –185.2,
–56.5)
–19 seconds
(95% CI, –83.5,
45.2)
Astaxanthin Placebo
Astaxanthin Placebo
Fig. 4 Data represent mean and standard deviations for carbohydrate
(panel a ) and fat oxidation (panel b ) observed during the 2 h pre-exhaus-
tion ride.
4.00
a
b
3.00
1.00
3.50
2.50
0.50
0.00
2.00
1.50
0.80
0.60
0.20
0.70
0.50
0.10
0.00
0.40
0.30
Min 20 Min 40 Min 60 Min 80 Min 100 Min 120
Min 20 Min 40 Min 60 Min 80 Min 100 Min 120
Astaxanthin Pre
Astaxanthin Post
Placebo Pre
Placebo Post
Carbo hydrate Oxidation (g/min)Fat Oxidation (g/min)
Astaxanthin Pre
Astaxanthin Post
Placebo Pre
Placebo Post
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
Nutrition
et al. [ 11 ] examined the e ects of AST supplementation on exer-
cise-induced fatigue in mice by administering AST (1.2, 6, or
30 mg/kg body weight) for 5 weeks via stomach intubation. Post-
test analysis showed an overall dose dependent increase in exer-
cise time to exhaustion in mice receiving 6 and 30 mg/kg of AST
vs. control. This would equate to approximately 420 mg and 2.1 g
of AST in humans, respectively, assuming the AST was given to a
70 kg “reference male”. Thus, the dosage given to the mice was
signi cantly higher than what we administered in our study. The
authors of this study also observed a signi cant reduction in lac-
tic acid and higher concentration of non-esteri ed fatty acids
and plasma glucose concentrations throughout exercise in the
AST treated groups [ 11 ] . Though this larger dosage pattern may
ultimately a ect energy substrate utilization, it does not recon-
cile the improvements in performance that we observed in our
trial.
Only two studies have examined the e cacy of AST for
improving exercise performance in humans, while only one of
those studies examined some type of endurance perform-
ance. In 2 002, Keisuke et al. examined the e ectiveness of
AST on the build up of lactic acid following 1 200 m of running
before and after 4 weeks of supplementation and found that
the 2 min post-running lactic acid concentration was signi -
cantly lower in the AST supplemented runners vs. control
[ 14 ] . In a second study, Bloomer et al. supplemented resis-
tance trained men with AST (4 mg/d) for 3 weeks and found no
supplementation related e ects on plasma levels of creatine
kinase, lactate dehydrogenase, delayed onset muscle soreness
or exercise performance [ 3 ] .
Strengths and Limitations
A strength of our current investigation is that we examined the
e ectiveness of AST supplementation under conditions aimed at
decreasing the reliance on carbohydrate metabolism by use of
an overnight fast without the presence of CHO ingestion during
the 2 h pre-exhaustion ride. Though we were successful in dem-
onstrating that AST appears to have an ergogenic e ect, we
acknowledge that the true e ectiveness of AST supplementation
relative to competitive exercise performance is not yet known
given that our feeding schema does not adequately represent
dietary practices associated with competition. Therefore, to test
the true ergogenic e ect of a supplement would necessitate
doing so under conditions that best approximate those condi-
tions involved in competition. We further acknowledge that our
results are currently predicated on a relatively small sample size.
One of the strengths of our ndings is the observation that all of
the participants in the AST group improved their time in com-
pleting the 20 km TT via an improvement in power output.
Though an examination of the range of improvement varies
from 2 to 251 s, the 95 % con dence intervals suggest that the
likely range for the true value of the AST treatment is 56–185 s.
Our calculation of e ect sizes for both performance indices
Fig. 5 Data represent mean and standard deviations for plasma glucose (panel a ), lactic acid (panel b ), non-esteri ed fatty acid (panel c ) and glycerol
concentrations observed during the 2 h pre-exhaustion ride. *P < 0.05 for within group time point di erences from rest through 40 min (all groups).
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Glycerol (mmol/L) Nonesterified facty acids (mmol/L)
Lactic Acid (mmol/L) Glucose (mmol/L)
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Nutrition
References
1 Aoi W , Naito Y , Sakuma K , Kuchide M , To kuda H , Maoka T , Toyokuni S ,
Oka S , Yasuhara M , Yoshikawa T . Astaxanthin limits exercise-induced
skeletal and cardiac muscle damage in mice . Antioxid Redox Signal
2003 ; 5 : 139 – 144
2 Aoi W , Naito Y , Takanami Y , Ishii T , Kawai Y , Akagiri S , Kato Y , Osawa
T , Yoshikawa T . Astaxanthin improves muscle lipid metabolism in
exercise via inhibitory e ect of oxidative CPT I modi cation . Biochem
Biophys Res Commun 2008 ; 366 : 892 – 897
3 Bloomer RJ , Fry A , Schilling B , Chiu L , Hori N , Weiss L . Astaxanthin sup-
plementation does not attenuate muscle injury following eccentric
exercise in resistance-trained men . Int J Sport Nutr Exerc Metab 2005 ;
15 : 401 – 412
4 Cohen J . A power primer . Psychological Bulletin 1992 ; 112 : 155 – 159
5 Fassett RG , Coombes JS . Astaxanthin, oxidative stress, in ammation
and cardiovascular disease . Future Cardiol 2009 ; 5 : 333 – 342
6 Frayn KN . Calculation of substrate oxidation rates in vivo from gaseous
exchange . J Appl Physiol 1983 ; 55 : 628 – 634
7 Guerin M , Huntley ME , Olaizola M . Haematococcus astaxanthin: appli-
cations for human health and nutrition . Trends Biotechnol 2003 ; 21 :
210 – 216
8 Harriss DJ , Atkinson G . Update – Ethical Standards in Sport and Exer-
cise Science Research . Int J Sports Med 2011 ; 32 : 819 – 821
9 Higuera-Ciapara I , Felix-Valenzuela L , Goycoolea FM . Astaxanthin: a
review of its chemistry and applications . Crit Rev Food Sci Nutr 2006 ;
46 : 185 – 196
10 Hussein G , Sankawa U , Goto H , Matsumoto K , Watanabe H . Astaxanthin,
a carotenoid with potential in human health and nutrition . J Nat Prod
2006 ; 69 : 443 – 449
11 Ikeuchi M , Koyama T , Takahashi J , Ya zawa K . E ects of astaxanthin
supplementation on exercise-induced fatigue in mice . Biol Pharm Bull
2006 ; 29 : 2106 – 2110
12 Ikeuchi M , Koyama T , Takahashi J , Yaza wa K . E ects of astaxanthin in
obese mice fed a high-fat diet . Biosci Biotechnol Biochem 2007 ; 71 :
893 – 899
13 Jeukendrup AE , Martin J . Improving cycling performance: how should
we spend our time and money . Sports Med 2001 ; 31 : 559 – 569
14 Keisuke S , Hiroshi Y , Kazuhiro A , Natsue K , Akito A , Kesato ki K , Masahiro
Y . Sports Performance Bene ts from Taking Natural Astaxanthin Char-
acterized by Visual Acuity and Muscle Fatigue Improvement in
Humans . J Clin Therap Med 2002 ; 18 : 1085 – 1100
15 Mortensen A , Skibsted LH , Truscott TG . The interaction of dietary caro-
tenoids with radical species . Arch Biochem Biophys 2001 ; 385 : 13 – 19
16 Pashkow FJ , Watumull DG , Campbell CL . Astaxanthin: a novel potential
treatment for oxidative stress and in ammation in cardiovascular
disease . Am J Cardiol 2008 ; 101 : 58D – 68D
17 Smith JW , Zachwieja JJ , Peronnet F , Passe DH , Massicotte D , Lavoie C ,
Pascoe DD . Fuel selection and cycling endurance performance with
ingestion of [13C]glucose: evidence for a carbohydrate dose response .
J Appl Physiol 2010 ; 108 : 1520 – 1529
18 Tarnopolsky MA , Atkinson SA , Phillips SM , MacDougall JD . Carbohydrate
loading and metabolism during exercise in men and women . J Appl
Physiol 1995 ; 78 : 1360 – 1368
would be characterized as large by Cohen [ 4 ] . It should also be
noted that our trial using AST accompanied by fasting and with-
out carbohydrate ingestion during the cyclists ride produced
similar results to those of Smith et al., who recently reported
similar ndings to ours using carbohydrate supplementation
during a 20 km TT under a similar feeding schema [ 17 ] .
These ndings are particularly intriguing as Jeukendrup and
Martin [ 13 ] estimate that carbohydrate and ca eine will pro-
duce similar performance bene ts in 40 km TT [ 13 ] . For exam-
ple, they project that carbohydrates will improve 40 km TT
performance by 00:42 s, 0:36 s, and 0:32 s for novice, well-
trained, and elite cyclists, respectively. In their model, it has also
been suggested that ca eine improves 40 km TT performance by
1:24 (min:s), 1:03 (min:s), and 0:55 s, respectively. Thus, if one
is to place value on the e ectiveness of an ergogenic aid during
cycling performance, the results of our study suggest that sup-
plementation with AST may promote similar time gains as to
those noted above using other nutritionally based ergogenic
aids. However, a greater body of conformational research nd-
ings needs to be accumulated before making such a conclusion.
Despite our inability to identify a mechanism of action for the
observed changes in exercise performance our study does sug-
gest that AST supplementation may be an e ective supplement
for improving exercise performance. If fat metabolism is of
future research interest, those investigators undertaking that
task may wish to consider a lower intensity exercise regime
more closely identi ed with the purported range of maximal fat
oxidation. If performance is an area of interest, we suggest that
these issues be examined under conditions more closely related
to feeding strategies of those athletes engaged in the sport of
interest.
Acknowledgements
Funding for this study was obtained from the Gatorade Sports
Science Institute. Astaxanthin and placebo supplements were
donated by Fuji Health Science, Inc.
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... However, these findings are not consistently documented in humans. For example, two studies noted ergogenic effects in trained and/or recreationally trained cyclists supplementing with ASTA (Brown et al., 2021;Earnest et al., 2011). Findings from Earnest et al. (2011) suggested an ergogenic effect in trained cyclists without a significant effect on substrate utilization during exercise. ...
... For example, two studies noted ergogenic effects in trained and/or recreationally trained cyclists supplementing with ASTA (Brown et al., 2021;Earnest et al., 2011). Findings from Earnest et al. (2011) suggested an ergogenic effect in trained cyclists without a significant effect on substrate utilization during exercise. In addition, findings from Res et al. (2013) failed to suggest an ergogenic effect or any significant effect on fat oxidation during exercise. ...
... In addition, findings from Res et al. (2013) failed to suggest an ergogenic effect or any significant effect on fat oxidation during exercise. However, both of these studies utilized a betweensubjects, parallel design, which may explain the lack of significant treatment effects due to between-group differences at baseline (Earnest et al., 2011;Res et al., 2013). It is also worth noting that these studies involved supplementation with 4 and 20 mg/day for 4 weeks (Earnest et al., 2011;Res et al., 2013). ...
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This study investigated the effects of 6 mg/day of astaxanthin supplementation on markers of oxidative stress and substrate metabolism during a graded exercise test in active young men. A double-blind, randomized, counterbalanced, cross-over design was used. Fourteen men (age = 23 ± 2 years) supplemented with 6 mg/day of astaxanthin and a placebo for 4 weeks, with a 1 week washout period between treatments. Following each supplementation period, a fasting blood sample was obtained to measure markers of oxidative stress: glutathione, hydrogen peroxide, advanced oxidation protein products, and malondialdehyde. Participants also completed a graded exercise test after each treatment to determine substrate utilization during exercise at increasing levels of intensity. Glutathione was ∼7% higher following astaxanthin compared with placebo (1,233 ± 133 vs. 1,156 ± 185 μM, respectively; p = .02, d = 0.48). Plasma hydrogen peroxide and malondialdehyde were not different between treatments ( p > .05). Although not statistically significant ( p = .45), advanced oxidation protein products were reduced by ∼28%. During the graded exercise test, mean fat oxidation rates were not different between treatments ( p > .05); however, fat oxidation decreased from 50 to 120 W ( p < .001) and from 85 to 120 W ( p = .004) in both conditions. Astaxanthin supplementation of 6 mg/day for 4 weeks increased whole blood levels of the antioxidant glutathione in active young men but did not affect oxidative stress markers or substrate utilization during exercise. Astaxanthin appears to be an effective agent to increase endogenous antioxidant status.
... The effect of AX on muscle metabolism and performance is less clear in humans, with some showing a reduction in injury markers (Djordjevic et al., 2012) but not others (Bloomer et al., 2005), or benefits in strength (Malmsten & Lignell, 2008) in healthy male athletes. Earnest et al. in 2011 reported improved 20 km time trial performance with no difference in fat or carbohydrate oxidation during sub-max cycling in endurance trained male cyclists (Earnest et al., 2011). Res et al. observed no effect on either time trial or fat oxidization in endurance trained male athletes (Res et al., 2013). ...
... The effect of AX on muscle metabolism and performance is less clear in humans, with some showing a reduction in injury markers (Djordjevic et al., 2012) but not others (Bloomer et al., 2005), or benefits in strength (Malmsten & Lignell, 2008) in healthy male athletes. Earnest et al. in 2011 reported improved 20 km time trial performance with no difference in fat or carbohydrate oxidation during sub-max cycling in endurance trained male cyclists (Earnest et al., 2011). Res et al. observed no effect on either time trial or fat oxidization in endurance trained male athletes (Res et al., 2013). ...
... We recognize this limitation and analyzed both sexes separately. To account for the likelihood that substrate utilization changes did not reach a steady-state at each step in exercise intensity, especially in male participants where the steps were only 1 minute each, we used the sum of the substrate oxidation for all the stages in the exercise period rather than rely on the rate of substrate utilization for a given stage (Brown et al., 2020;Earnest et al., 2011;Res et al., 2013). In addition, comparing the difference within subjects also minimized the influence of non-steady state conditions on the comparison. ...
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... Astaxanthin has thirteen conjugated double bonds and because of their arrangement, astaxanthin has strong antioxidant properties [54]. The astaxanthin dose that 2.5 g of krill oil provides is around 1.7 mg, which is below the recommended dose of 4 mg for athletes that is linked to improved muscle damage, time trial performance and power output [55][56][57]. Nevertheless, it has been suggested that the phospholipids of krill oil may increase intestinal absorption of astaxanthin [40], thereby optimizing its availability to the body for integration into cell membranes and fight against excessive free radical production in athletes [53]. ...
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There is evidence that both omega-3 polyunsaturated fatty acids (n-3 PUFAs) and choline can influence sports performance, but information establishing their combined effects when given in the form of krill oil during power training protocols is missing. The purpose of this study was therefore to characterize n-3 PUFA and choline profiles after a one-hour period of high-intensity physical workout after 12 weeks of supplementation. Thirty-five healthy power training athletes received either 2.5 g/day of Neptune krill oilTM (550 mg EPA/DHA and 150 mg choline) or olive oil (placebo) in a randomized double-blind design. After 12 weeks, only the krill oil group showed a significant HS-Omega-3 Index increase from 4.82 to 6.77% and a reduction in the ARA/EPA ratio (from 50.72 to 13.61%) (p < 0.001). The krill oil group showed significantly higher recovery of choline concentrations relative to the placebo group from the end of the first to the beginning of the second exercise test (p = 0.04) and an 8% decrease in total antioxidant capacity post-exercise versus 21% in the placebo group (p = 0.35). In conclusion, krill oil can be used as a nutritional strategy for increasing the HS-Omega-3 Index, recover choline concentrations and address oxidative stress after intense power trainings.
... Among the human studies examined for the present review, there are only six studies about ASX supplementation and exercise ( Table 2), all of which tested its ergogenic effects in non-sedentary individuals. Three revealed no performance improvement with ASX [59][60][61], two did reveal performance improvement (cycling time-trial test) [62,63], and the final one revealed only an antioxidant effect [64]. Interestingly, a low dosage (4-12 mg/day) appears to be more promising than a higher dosage (20 mg/day). ...
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... The group treated with astaxanthin was able to perform significantly more knee bends (squats) compared to the placebo group ( Fig. 23.6) when carrying a barbell weighing 42.5 kg. In another randomized, single-blind, placebo-controlled study, 14 competitive amateur cyclists performed a 20 km maximal biking test after a 2 h constant intensity preexhaustion ride followed by a 10-h fast (Earnest et al. 2011). The group treated with astaxanthin bicycled significantly faster (121 s faster) compared to the placebo group (19 s faster). ...
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During endurance exercise at approximately 65% maximal O2 consumption, women oxidize more lipids, and therefore decrease carbohydrate and protein oxidation, compared with men (L.J. Tarnopolsky, M.A. Tarnopolsky, S.A. Atkinson, and J.D. MacDougall. J. Appl. Physiol. 68: 302-308, 1990; S.M. Phillips, S.A. Atkinson, M.A. Tarnopolsky, and J.D. MacDougall. J. Appl. Physiol. 75: 2134-2141, 1993). The main purpose of this study was to examine the ability of similarly trained male (n = 7) and female (n = 8) endurance athletes to increase muscle glycogen concentrations in response to an increase in dietary carbohydrate from 55-60 to 75% of energy intake for a period of 4 days (carbohydrate loading). In addition, we sought to examine whether gender differences existed in metabolism during submaximal endurance cycling at 75% peak O2 consumption (VO2 peak) for 60 min. The men increased muscle glycogen concentration by 41% in response to the dietary manipulation and had a corresponding increase in performance time during an 85% VO2 peak trial (45%), whereas the women did not increase glycogen concentration (0%) or performance time (5%). The women oxidized significantly more lipid and less carbohydrate and protein compared with the men during exercise at 75% VO2-peak. We conclude that women did not increase muscle glycogen in response to the 4-day regimen of carbohydrate loading described. In addition, these data support previous observations of greater lipid and lower carbohydrate and protein oxidation by women vs. men during submaximal endurance exercise.
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Dietary carotenoids react with a wide range of radicals such as CCl3O2*, RSO2*, NO2*, and various arylperoxyl radicals via electron transfer producing the radical cation of the carotenoid. Less strongly oxidizing radicals, such as alkylperoxyl radicals, can lead to hydrogen atom transfer generating the neutral carotene radical. Other processes can also arise such as adduct formation with sulphur-centered radicals. The oxidation potentials have been established, showing that, in Triton X-100 micelles, lycopene is the easiest carotenoid to oxidize to its radical cation and astaxanthin is the most difficult. The interaction of carotenoids and carotenoid radicals with other antioxidants is of importance with respect to anti- and possibly pro-oxidative reactions of carotenoids. In polar environments the vitamin E (alpha-tocopherol) radical cation is deprotonated (TOH*+ --> TO* + H+) and TO* does not react with carotenoids, whereas in nonpolar environments such as hexane, TOH*+ is converted to TOH by hydrocarbon carotenoids. However, the nature of the reaction between the tocopherol and various carotenoids shows a marked variation depending on the specific tocopherol homologue. The radical cations of the carotenoids all react with vitamin C so as to "repair" the carotenoid.