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Effect of Astaxanthin on Cycling Time Trial Performance


Abstract and Figures

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
Published online:
October 7, 2011
Int J Sports Med 2011; 32:
882–888 © Georg Thieme
Verlag KG Stuttgart · New York
ISSN 0172-4622
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
Key words
ergogenic aid
E ect of Astaxanthin on Cycling Time Trial
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
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-
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
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
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
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
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
Eligible for Baseline
N=53, Failed to meet
inclusion criteria
N=3, Insufficient VO2max
N=2 Failure to complete
2 hr ride
Successfully Completed
Baseline (N=21)
Randomized to
Treatment (N=21)
N=1, Illness
N=1, Computer
N=1, Unable to
Complete Protocol
N=1, Invalid
N=2, Unable to
Complete Protocol
N=1, Invalid
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
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
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 ).
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
Days 6 – 33
Post TestingSupplement (28 d)
Time Trial
(20 km)
Day 3
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
(5 min)
–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)
Lactic acid
Warm up @
100 W
Lactic acid
Lactic acid
NEFA: Non-esterified fatty acid
TT: Time Trial
PO: Power Output in watts
Ave PO
PO ea. 5 km
Time to
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
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
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
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.
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
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).
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
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.
Time (sec)Power Output (W)
20 W
(95% CI, 1.0,
38.1) 1.6 W
(95% CI, –17,
–121 seconds
(95% CI, –185.2,
–19 seconds
(95% CI, –83.5,
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.
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
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
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).
–0.1 Rest Min –10 Min 20 Min 40 Min 60 Min 80 Min 100 Min 120
Rest Min –10 Min 20 Min 40 Min 60 Min 80 Min 100 Min 120
Rest Min –10 Min 20 Min 40 Min 60 Min 80 Min 100 Min 120 Rest Min –10 Min 20 Min 40 Min 60 Min 80 Min 100 Min 120
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Glycerol (mmol/L) Nonesterified facty acids (mmol/L)
Lactic Acid (mmol/L) Glucose (mmol/L)
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Earnest CP et al. Astaxanthin Time Trial Performance … Int J Sports Med 2011; 32: 882–888
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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
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). ...
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. ...
Full-text available
Endurance training (ET) is recommended for the elderly to improve metabolic health and aerobic capacity. However, ET‐induced adaptations may be suboptimal due to oxidative stress and exaggerated inflammatory response to ET. The natural antioxidant and anti‐inflammatory dietary supplement astaxanthin (AX) has been found to increase endurance performance among young athletes, but limited investigations have focused on the elderly. We tested a formulation of AX in combination with ET in healthy older adults (65–82 years) to determine if AX improves metabolic adaptations with ET, and if AX effects are sex‐dependent. Forty‐two subjects were randomized to either placebo (PL) or AX during 3 months of ET. Specific muscle endurance was measured in ankle dorsiflexors. Whole body exercise endurance and fat oxidation (FATox) was assessed with a graded exercise test (GXT) in conjunction with indirect calorimetry. Results: ET led to improved specific muscle endurance only in the AX group (Pre 353 ± 26 vs. Post 472 ± 41 contractions), and submaximal GXT duration improved in both groups (PL 40.8 ± 9.1% and AX 41.1 ± 6.3%). The increase in FATox at lower intensity after ET was greater in AX (PL 0.23 ± 0.15 g vs. AX 0.76 ± 0.18 g) and was associated with reduced carbohydrate oxidation and increased exercise efficiency in males but not in females. Astaxanthin combined with endurance training promoted fat oxidation compared to training alone. Astaxanthin led to carbohydrate sparing and improved exercise efficiency especially in older males.
... With respect to exercise, most research on AX has examined either endurance performance [22,[38][39][40] or changes in markers of substrate oxidation rates [24]. Collectively, AX has been shown to reduce average heart rate at submaximal endurance intensities [39], improve cycling time trial performance [38,40], and in one study, enhance whole body fat oxidation rates [38]. ...
... With respect to exercise, most research on AX has examined either endurance performance [22,[38][39][40] or changes in markers of substrate oxidation rates [24]. Collectively, AX has been shown to reduce average heart rate at submaximal endurance intensities [39], improve cycling time trial performance [38,40], and in one study, enhance whole body fat oxidation rates [38]. Despite these findings, fewer studies have attempted to assess the role of AX in anaerobic performance. ...
Full-text available
Strenuous exercise involving eccentric muscle actions induces skeletal muscle damage resulting in delayed onset muscle soreness (DOMS). Antioxidant supplementation, such as astaxanthin (AX), may alleviate muscle injury following intense exercise. The purpose of this study was to investigate the effect of a four-week course of AX supplementation at 12 mg/day−1 on subjective markers of DOMS, recovery, and performance after a bout of muscle damaging eccentric exercise. Nineteen resistance-trained men (mean ± SD: age, 22.6 ± 2.2 y) completed a between-group design with a four-week supplementation period of 12 mg/day−1 of either AX or a placebo. Subjects completed four trials, with trials One and Three designed to induce muscle damage, consisting of a one repetition maximum test (1RM) for leg-press, followed by five sets of ten repetitions at 65% of 1RM. Trials Two and Four were performance trials, conducted 48 h later and consisting of repetitions to failure at 65%, 70%, and 75% of 1RM. Subjective markers of DOMS and recovery were collected at multiple timepoints post-trial for trials One and Three. Although performance was not affected (p > 0.05), AX supplementation significantly decreased subjective markers of DOMS (p = 0.01) compared to the placebo. The results demonstrated that AX may enhance recovery by reducing DOMS without detriment to performance in resistance-trained men.
... At the request of the European Commission, the Panel on Nutrition, Novel Food and Food Allergens (NDA) issued statement on the safety of astaxanthin when used as a novel nutrient in food supplements at a maximum concentration of 8 mg/day [46]. In clinical studies of astaxanthin supplementation (4 mg daily) in a group of professional cyclists, an improvement of 5% in the 20 km time trial after 28 days was observed [47]. The effect of astaxanthin on skin condition was assessed in a group of 12 women receiving oral astaxanthin supplementation at a dose of 12 mg/day for 16 weeks; it was found that the treatment significantly improved skin hydration and reduced wrinkle parameters compared to the placebo group. ...
Full-text available
Astaxanthin is gaining recognition as a natural bioactive component. This study aimed to test whether astaxanthin could protect adipose-derived stromal stem cells (ASCs) from apoptosis, mitochondrial dysfunction and oxidative stress. Phaffia rhodozyma was used to extract astaxanthin, whose biocompatibility was tested after 24, 48 and 72 h of incubation with the cells; no harmful impact was found. ASCs were treated with optimal concentrations of astaxanthin. Several parameters were examined: cell viability, apoptosis, reactive oxygen levels, mitochondrial dynamics and metabolism, superoxide dismutase activity, and astaxanthin’s antioxidant capacity. A RT PCR analysis was performed after each test. The astaxanthin treatment significantly reduced apoptosis by modifying the normalized caspase activity of pro-apoptotic pathways (p21, p53, and Bax). Furthermore, by regulating the expression of related master factors SOD1, SOD2, PARKIN, PINK 1, and MFN 1, astaxanthin alleviated the oxidative stress and mitochondrial dynamics failure caused by EMS. Astaxanthin restored mitochondrial oxidative phosphorylation by stimulating markers associated with the OXPHOS machinery: COX4I1, COX4I2, UQCRC2, NDUFA9, and TFAM. Our results suggest that astaxanthin has the potential to open new possibilities for potential bio-drugs to control and suppress oxidative stress, thereby improving the overall metabolic status of equine ASCs suffering from metabolic syndrome.
... 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]. ...
Full-text available
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). ...
Full-text available
A healthy lifestyle is essential for maintaining physical and mental health. Health promotion, with a particular emphasis on regular exercise and a healthy diet, is one of the emerging trends in healthcare. However, the way in which exercise training and nutrients from dietary intake interact with each other to promote additive, synergistic, or antagonistic effects on physiological functions leading to health promotion, and the possible underlying biomolecular mechanisms of such interactions, remain poorly understood. A healthy diet is characterized by a high intake of various bioactive compounds usually found in natural, organic, and fresh foodstuffs. Among these bioactive compounds, astaxanthin (ASX), a red carotenoid pigment especially found in seafood, has been recognized in the scientific literature as a potential nutraceutical due to its antioxidant, anti-inflammatory, and neurotrophic properties. Therefore, scientists are currently exploring whether this promising nutrient can increase the well-known benefits of exercise on health and disease prevention. Hence, the present review aimed to compile and summarize the current scientific evidence for ASX supplementation in association with exercise regimes, and evaluate the additive or synergistic effects on physiological functions and health when both interventions are combined. The new insights into the combination paradigm of exercise and nutritional supplementation raise awareness of the importance of integrative studies, particularly for future research directions in the field of health and sports nutrition science.
Astaxanthin (AX) is an antioxidant which may spare endogenous carbohydrates and improve fat oxidation rates, thus improving metabolic flexibility. To date, no studies have attempted to examine the impact of AX in an overweight cohort, whom often suffer from metabolic inflexibility. Nineteen subjects (mean ± SD: age: 27.5 ± 6.3 years; height: 169.7 ± 9.0 cm; body mass: 96.4 ± 17.9 kg; BF%: 37.9 ± 7.0%; BMI: 33.4 ± 5.6 kg/m2; VO2peak: 25.9 ± 6.7 ml·kg-1·min-1) were recruited and supplemented with either 12 mg of AX or placebo (PLA) for 4 weeks. Subjects completed a graded exercise test on a cycling ergometer to examine changes in substrate oxidation rates. A total of 5 stages, each lasting 5 min and resistance increased 15 W each stage, were completed to examine changes in levels of glucose and lactate, fat and carbohydrate (CHO) oxidation rates, heart rate, and rating of perceived exertion (RPE). Although there were no changes found in rates of fat oxidation, blood lactate or glucose, or RPE (all p > 0.05), a significant decrease was observed in CHO oxidation from pre to post supplementation in the AX group only. Further, the AX group demonstrated a 7% decrease in heart rate across the graded exercise test. These findings suggest that 4 weeks of AX supplementation may offer some cardiometabolic benefits to overweight individuals, and be a favorable supplement for these individuals beginning an exercise program.
Waldman, HS, Bryant, AR, Parten, AL, Grozier, CD, and McAllister, MJ. Astaxanthin supplementation does not affect markers of muscle damage or inflammation after an exercise-induced muscle damage protocol in resistance-trained males. J Strength Cond Res XX(X): 000-000, 2022-It is well documented that exercise-induced muscle damage (EIMD) decreases exercise performance by elevated inflammation and subjective discomfort. Due to its potent antioxidative properties, astaxanthin (AX) may serve as a potential dietary supplement strategy for mitigating delayed-onset muscle soreness (DOMS) and enhancing recovery and performance. This study aimed to investigate the effects of AX on markers of muscle damage, inflammation, DOMS, and anaerobic performance and substrate metabolism. Thirteen resistance-trained men (mean ± SD, age, 23.4 ± 2.1 years) completed a double-blind, counterbalanced, and crossover design with a 1-week washout period between 2, 4-week supplementation periods at 12 mg·d-1 of AX or placebo. After each supplementation period, subjects completed 2 trials, with trial 1 including a graded exercise test (GXT) and a 30-second Wingate and trial 2 including an EIMD protocol followed by the collection of fasting blood samples (pre-post) to measure creatine kinase, advanced oxidative protein products, C-reactive protein, interleukin-6, insulin, and cortisol. Astaxanthin supplementation had no statistical effects on markers of substrate metabolism during the GXT, Wingate variables, or markers of muscle damage, inflammation, or DOMS when compared with placebo (all p > 0.05). However, 4 weeks of AX supplementation did significantly lower oxygen consumption during the final stage of the GXT (12%, p = 0.02), as well as lowered systolic blood pressure (∼7%, p = 0.04), and significantly lowered baseline insulin values (∼24%, p = 0.05) when compared with placebo. Collectively, these data suggest that 4 weeks of AX supplementation at 12 mg·d-1 did not affect markers of muscle damage, inflammation, or DOMS after an EIMD protocol in a resistance-trained male cohort.
Full-text available
Astaxanthin is a member of the carotenoid family that is found abundantly in marine organisms, and has been gaining attention in recent years due to its varied biological/physiological activities. It has been reported that astaxanthin functions both as a pigment, and as an antioxidant with superior free radical quenching capacity. We recently reported that astaxanthin modulated mitochondrial functions by a novel mechanism independent of its antioxidant function. In this paper, we review astaxanthin’s well-known antioxidant activity, and expand on astaxanthin’s lesser-known molecular targets, and its role in mitochondrial energy metabolism.
Astaxanthin is a carotenoid widely found in marine organisms and microorganisms. With extensive use in nutraceuticals, cosmetics, and animal feed, astaxanthin will have the largest share in the global market for carotenoids in the near future. Owing to its unique molecular features, astaxanthin has excellent antioxidant activity and holds promise for use in biochemical studies. This review focuses on the observed health benefits of dietary astaxanthin, as well as its underlying bioactivity mechanisms. Recent studies have increased our understanding of the role of isomerization and esterification in the structure–function relationship of dietary astaxanthin. Gut microbiota may involve the fate of astaxanthin during digestion and absorption; thus, further knowledge is needed to establish accurate recommendations for dietary intake of both healthy and special populations. Associated with the regulation of redox balance and multiple biological mechanisms, astaxanthin is proposed to affect oxidative stress, inflammation, cell death, and lipid metabolism in humans, thus exerting benefits for skin condition, eye health, cardiovascular system, neurological function, exercise performance, and immune response. Additionally, preclinical trials predict its potential effects such as intestinal flora regulation and anti-diabetic activity. Therefore, astaxanthin is worthy of further investigation for boosting human health, and wide applications in the food industry.
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One possible reason for the continued neglect of statistical power analysis in research in the behavioral sciences is the inaccessibility of or difficulty with the standard material. A convenient, although not comprehensive, presentation of required sample sizes is provided. Effect-size indexes and conventional values for these are given for operationally defined small, medium, and large effects. The sample sizes necessary for .80 power to detect effects at these levels are tabled for 8 standard statistical tests: (1) the difference between independent means, (2) the significance of a product-moment correlation, (3) the difference between independent rs, (4) the sign test, (5) the difference between independent proportions, (6) chi-square tests for goodness of fit and contingency tables, (7) 1-way analysis of variance (ANOVA), and (8) the significance of a multiple or multiple partial correlation.
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It is accepted that oxidative stress and inflammation play an integral role in the pathophysiology of many chronic diseases including atherosclerotic cardiovascular disease. The xanthophyll carotenoid dietary supplement astaxanthin has demonstrated potential as an antioxidant and anti-inflammatory therapeutic agent in models of cardiovascular disease. There have been at least eight clinical studies conducted in over 180 humans using astaxanthin to assess its safety, bioavailability and clinical aspects relevant to oxidative stress, inflammation or the cardiovascular system. There have been no adverse outcomes reported. Studies have demonstrated reduced markers of oxidative stress and inflammation and improved blood rheology. A larger number of experimental studies have been performed using astaxanthin. In particular, studies in a variety of animals using a model of myocardial ischemia and reperfusion have demonstrated protective effects from prior administration of astaxanthin both intravenously and orally. Future clinical studies and trials will help determine the efficacy of antioxidants such as astaxanthin on vascular structure, function, oxidative stress and inflammation in a variety of patients at risk of, or with, established cardiovascular disease. These may lead to large intervention trials assessing cardiovascular morbidity and mortality.
Another way of improving time trial performance is by reducing the power demand of riding at a certain velocity. Riding with hands on the brake hoods would improve aerodynamics and increase performance time by ≈5 to 7 minutes and riding with hands on the handlebar drops would increase performance time by 2 to 3 minutes compared with a baseline position (elbows on time trail handle bars). Conversely, riding with a carefully optimised position could decrease performance time by 2 to 2.5 minutes. An aerodynamic frame saved the modelled riders 1:17 to 1:44 min:sec. Furthermore, compared with a conventional wheel set, an aerodynamic wheel set may improve time trial performance time by 60 to 82 seconds. From the analysis in this article it becomes clear that novice cyclists can benefit more from the suggested alterations in position, equipment, nutrition and training compared with elite cyclists. Training seems to be the most important factor, but sometimes large improvements can be made by relatively small changes in body position. More expensive options of performance improvement include altitude training and modifications of equipment (light and aerodynamic bicycle and wheels). Depending on the availability of time and financial resources cyclists have to make decisions about how to achieve their performance improvements. The data presented here may provide a guideline to help make such decisions.
Endurance performance and fuel selection while ingesting glucose (15, 30, and 60 g/h) was studied in 12 cyclists during a 2-h constant-load ride [approximately 77% peak O2 uptake] followed by a 20-km time trial. Total fat and carbohydrate (CHO) oxidation and oxidation of exogenous glucose, plasma glucose, glucose released from the liver, and muscle glycogen were computed using indirect respiratory calorimetry and tracer techniques. Relative to placebo (210+/-36 W), glucose ingestion increased the time trial mean power output (%improvement, 90% confidence limits: 7.4, 1.4 to 13.4 for 15 g/h; 8.3, 1.4 to 15.2 for 30 g/h; and 10.7, 1.8 to 19.6 for 60 g/h glucose ingested; effect size=0.46). With 60 g/h glucose, mean power was 2.3, 0.4 to 4.2% higher, and 3.1, 0.5 to 5.7% higher than with 30 and 15 g/h, respectively, suggesting a relationship between the dose of glucose ingested and improvements in endurance performance. Exogenous glucose oxidation increased with ingestion rate (0.17+/-0.04, 0.33+/-0.04, and 0.52+/-0.09 g/min for 15, 30, and 60 g/h glucose), but endogenous CHO oxidation was reduced only with 30 and 60 g/h due to the progressive inhibition of glucose released from the liver (probably related to higher plasma insulin concentration) with increasing ingestion rate without evidence for muscle glycogen sparing. Thus ingestion of glucose at low rates improved cycling time trial performance in a dose-dependent manner. This was associated with a small increase in CHO oxidation without any reduction in muscle glycogen utilization.
This paper reviews the assumptions involved in calculating rates of carbohydrate and fat oxidation from measurements of O2 consumption, CO2 production, and urinary nitrogen excretion. It is shown that erroneous results are obtained in the presence of metabolic processes such as lipogenesis and gluconeogenesis. The apparent rates calculated under these conditions can, however, be interpreted as net rates of "utilization." Thus the apparent rate of carbohydrate oxidation is the sum of the rates of utilization for oxidation and for lipogenesis minus the rate at which carbohydrate is formed from amino acids. The apparent rate of fat oxidation is the difference between the rates of oxidation and synthesis from carbohydrate, so that the apparently negative rates encountered in patients infused with glucose do quantitatively represent net rates of synthesis. Other processes such as synthesis of ketone bodies or lactate at rates greater than their utilization can also disturb the calculations, but the magnitude of the effect can be estimated from appropriate measurements. Methods of correcting the observed gaseous exchange in these circumstances are given.
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.
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.