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Journal of Dietary Supplements
ISSN: 1939-0211 (Print) 1939-022X (Online) Journal homepage: https://www.tandfonline.com/loi/ijds20
A Double-Blind, Cross-Over Study to Examine
the Effects of Maritime Pine Extract on Exercise
Performance and Postexercise Inflammation,
Oxidative Stress, Muscle Soreness, and Damage
Randy L. Aldret EdD, ATC, CSCS & David Bellar PhD, FNSCA, CSCSD, RSCCD
To cite this article: Randy L. Aldret EdD, ATC, CSCS & David Bellar PhD, FNSCA, CSCSD,
RSCCD (2019): A Double-Blind, Cross-Over Study to Examine the Effects of Maritime Pine Extract
on Exercise Performance and Postexercise Inflammation, Oxidative Stress, Muscle Soreness, and
Damage, Journal of Dietary Supplements, DOI: 10.1080/19390211.2019.1578847
To link to this article: https://doi.org/10.1080/19390211.2019.1578847
Published online: 19 Mar 2019.
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A Double-Blind, Cross-Over Study to Examine the Effects of
Maritime Pine Extract on Exercise Performance and
Postexercise Inflammation, Oxidative Stress, Muscle
Soreness, and Damage
Randy L. Aldret, EdD, ATC, CSCS and David Bellar, PhD, FNSCA, CSCSD, RSCCD
School of Kinesiology, University of Louisiana at Lafayette, Lafayette, LA, USA
ABSTRACT
The purpose of the present study was to examine whether 14 days
of supplementation with maritime pine extract leading up to and fol-
lowing an exercise test would increase performance and reduce bio-
markers associated with muscle damage, inflammation, and
oxidative stress. The study used a double-blind, placebo-controlled,
cross-over design. Twenty apparently healthy young male partici-
pants ingested either 800 mg pine bark extract or placebo for
14 days prior to the first exercise trial and for 2 days postexercise. On
the exercise day, participants submitted a pre-exercise blood sample
then completed a VO
2
peak test until volitional failure. A postexer-
cise blood sample was collected 1 hour after completion of exercise.
Participants returned at 24 and 48 hours after the exercise testing for
measures of muscle pain in the lower body using an algometer.
Participants then had a 7-day washout period before beginning to
cross over to the alternate treatment. Analysis via ordinal regression
demonstrated a significant difference in oxidative stress in the mari-
time pine extract group compared to placebo (ChiSq ¼2.63;
p¼0.045). Maritime pine extract was effective at affording protection
from oxidative stress postexercise. Further work should be under-
taken to evaluate the findings with other exercise modes or in par-
ticipants with known metabolic syndrome.
KEYWORDS
Maritime pine extract;
muscle damage;
oxidative stress
Introduction
While exercise has multiple known health benefits, there are consequences to prolonged
bouts of exercise. High muscle forces damage the sarcolemma, initiating the release of
cytosolic enzymes and myoglobin, further damaging muscle contractile fibrils and non-
contractile structures. Metabolites such as calcium accumulate to abnormal levels in the
muscle cell to produce more cell damage and reduced force capacity (Chevion 2000;
Lee et al. 2002). At this point, the inflammatory process begins, allowing muscle tissue
to heal and adapt to protect from subsequent exercise.
Exercise produces an imbalance among reactive oxygen species (ROS), free radicals,
and antioxidants (Urso and Clarkson 2003; Pingitore et al. 2015); this phenomenon is
CONTACT Randy L. Aldret raldret@louisiana.edu 225 Cajundome Blvd., Bourgeois Hall 129-B, Lafayette, Louisiana
70506, USA.
Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/ijds.
ß2019 Taylor & Francis Group, LLC
JOURNAL OF DIETARY SUPPLEMENTS
https://doi.org/10.1080/19390211.2019.1578847
referred to as oxidative stress. Both acute aerobic (Davies et al. 1982) and anaerobic
(Bailey et al. 2004) exercise have the potential to increase free radical production. The
contraction of skeletal muscle generates free radicals, resulting in oxidative damage to
the cell (Powers and Jackson 2008). The primary free radical generated in cells is super-
oxide (O
2
-
). Dismutation of superoxide provides a major source of hydrogen peroxide
(H
2
O
2
) in cells. Hydrogen peroxide is cytotoxic and readily generates hydroxyl radicals
in specific circumstances. Hydroxyl radicals damage molecules close to the site of their
generation and are considered the most damaging reactive oxygen species (ROS) present
in biological materials (Powers and Jackson 2008).
Description of French maritime pine bark
Maritime pine extract (Horphag Research USA, Hoboken, New Jersey) has many pur-
ported pharmacological benefits on multiple physiological functions. Most commercial
formulations contain 65%–75% procyanidins, with phenolic acids making up the
remainder (Chen et al. 2009). Procyanidins are biopolymers of catechin and epicatechin
subunits, which are recognized as important constituents in human nutrition. The
phenolic acids are derivatives of benzoic and cinnamic acids, specifically, ferulic acid
and taxifolin (Rohdewald 2002).
Pinus P. potential benefits during exercise
One of the purposes of maritime pine extract supplementation is to increase serum levels
of nitric oxide (NO) by reducing conversion of NO to superoxide and prolonging the
half-life of NO (Carr and Frei 2000) and stimulating inducible nitric oxide synthase
(iNOS or NOS2) (Fitzpatrick et al. 1998). Standard dosing for maritime pine extract is
100–200mg daily, but doses as low as 40–60 mg daily have been shown to be beneficial if
taken over long periods. Nishioka et al (2007)found“180 mg daily for 2 weeks is associ-
ated with an augmentation of an acetylcholine-induced blood vessel relaxation via NO in
vivo”(Nishioka et al. 2007, p. 778). During inflammation, maritime pine extract metabo-
lites inhibit nitrite production with near absolute suppression of NO at 50mcg/mL, which
is a 20-fold increase in potency over hydrocortisone (Uhlenhut and H€
ogger 2012).
Previous studies (Vinciguerra et al. 2006; Vinciguerra et al. 2013) demonstrated that
maritime pine extract reduced training and posttraining muscular pain, reduced cramp-
ing during and after exercise, and had a significant effect on oxidative stress and plasma
free radicals. Vinciguerra et al. (2013) expanded on their earlier findings and theorized
that supplementation with maritime pine extract may make training more effective and
recovery shorter as, typically, a more intense physical activity should produce more oxi-
dative stress (Vinciguerra et al. 2013).
Purpose of the study
The purpose of the study was to determine whether 14 days of supplementation with
maritime pine extract leading up to an exercise test and two days of postexercise
2 R. L. ALDRET AND D. BELLAR
supplementation would increase performance and reduce biomarkers associated with
muscle damage, inflammation, and oxidative stress.
Methods
Participants
For the investigation, 20 apparently healthy college males were recruited out of various
kinesiology classes at a university in the south United States. Participants were
22.7 years (±3.9 yrs.), with body height of 178.1 cm (±7.9cm) and body mass of 82.9 kg
(±13.5 kg). The study group was physically active and engaged in regular exercise
4.3 days/week (±0.8 days/week), had a relative body fat of 16.7% (±7.4%), and had an
average cardiovascular capacity of 30.0 ml/kg/min (±7.0 ml.kg/min).
The participants reported to the Human Performance Lab for an initial visit, at which
time anthropometric measures were collected. All participants gave written informed con-
sent to take part in the study, and the methods were reviewed and approved by the institu-
tional review board at the University of Louisiana at Lafayette (Approval FA15-65 KNES).
Procedures
Students were recruited from various kinesiology classes at a university in the south
United States. Once participants agreed to an initial visit appointment, they were
instructed to refrain from NSAIDs and exercise during the 24-hour period immediately
preceding their initial visit. During the initial visit, participants gave written informed
consent after having had the experimental procedures explained to them. Afterward,
they filled out a health questionnaire, the PAR-Qþ, and the Leisure and Physical
Activity Survey (Bellar et al. 2014). Judging from these surveys, the participants were
deemed fit to continue with the experimental procedures. The participants also com-
pleted the Automated Self-Administered 24-hour Recall (ASA 24) and were asked to
maintain a diet consistent with the 24-hour recall. No dietary deficiencies were noted
within the recall data.
Following completion of the questionnaires, each participant’s height and weight was
determined via stadiometer, and body fat percentage was measured using air displace-
ment plethysmography (Bod Pod Gold Standard System, Rome, Italy). Finally, to finish
data collection on the initial visit, the participants underwent a VO
2
peak test on a cycle
ergometer. The test consisted of a 25-watt ramp protocol on a COSMED E100 P
(COSMED; Rome, IT). During this test, expired gases were collected continuously, as
well as heart rate and SpO
2
, using a COSMED QUARK CPET (COSMED; Rome, IT).
Participants continued to exercise until their VO
2
failed to increase by 100 ml/min with
each increase in wattage or volitional failure occurred.
Assignment of order
Participants were randomly assigned to an order of treatment (maritime pine extract
and placebo). The study was conducted in a double-blind fashion, each period lasting
16 days (14 days pre-exercise, 2 days postexercise) with a washout period in between.
JOURNAL OF DIETARY SUPPLEMENTS 3
The maritime pine extract was prepackaged into unique, coded bottles (Horphag
Research USA, Hoboken, New Jersey) and provided to participants. The participants
were asked to take 4 pills per day, in a single dose, during the 14 days leading up to the
exercise trial and the 2 days after. This delivered an 800 mg per day single dose of mari-
time pine extract. Participants received their first doses after initial visit and were
reminded that exercise was restricted 48 hours prior to the exercise trial until the end of
the 48-hour follow up visit. The procedures used in this study are represented visually
in Figure 1.
Pre-exercise trial visit
The participants were asked to report to the Human Performance Lab in the evening
prior to the exercise trials. The participants were fed a standard meal for the evening
(prepackaged to maintain consistency) and sent home with a 240-calorie evening snack
consisting of 10 g of protein, 41 g of carbohydrates, and 4 g of fat. The participants were
provided with an actigraph sleep monitor (Actigraph, Pensacola, FL) to wear and asked
to note the time they went to bed. The data from this monitor were collected the next
morning prior to the start of the exercise trial to confirm time to bed and to ensure suf-
ficient rest prior to exercise. Finally, from this point until the end of the 48-hour
Figure 1. Study flowchart.
4 R. L. ALDRET AND D. BELLAR
follow-up, nonsteroidal anti-inflammatory drugs (NSAIDS) were restricted due to the
measurement of inflammatory markers.
Exercise trials
Participants reported in the morning hours (0600–0800) fasted. They had blood drawn
from the antecubital space (pre-exercise sample) and then repeated the 25-watt ramp
protocol similarly to the VO
2
peak test. During this trial, expired gases were monitored
in a similar fashion, and near-infrared spectroscopy (NIRS) sensors (Moxy Oxygen
Monitor 3, Hutchinson, MN) were secured to the quadriceps muscles, one to the vastus
lateralis and another to the vastus medialis, to monitor muscle oxygenation. Participants
exercised until volitional failure. One hour postexercise, participants again donated a
blood sample from the antecubital space. Participants were given water to drink during
the recovery phase and were reminded to continue to take their assigned doses through
the 24- and 48-hour recovery visits. Participants were also reminded that the restrictions
on NSAIDS and exercise were also active through the conclusion of the 48-hour follow-
up. The participants had a one-week washout period prior to beginning the next supple-
mentation phase with the opposite treatment using identical procedures.
24- and 48-hour follow-up visits
Participants reported to the lab in the morning hours fasted (0600–0800) and again
donated a blood sample from the antecubital space. Following this, muscle pain was
assessed using an algometer (J Tech, Midvale, UT). This is a device that provides a con-
stant low-force pressure (50N) to a small (1 cm diameter) surface. Once the force was
applied, participants rated their pain according to a pain numeric rating scale, with 0
representing “no pain”and 10 representing “worst possible pain.”The use of these devi-
ces enhances the collection of postexercise muscle soreness and is an improvement over
the traditional method of using visual analog scales alone. Three specific locations were
used, the vastus lateralis 25% and 50% of the distance between the superior border of
the patella and greater trochanter of the femur and the vastus medialis 25% of the dis-
tance between these same landmarks. The exact locations of the tests were marked with
a permanent marker, and the participants were given a marker to maintain the marks
for the remainder of the study.
Blood collection
Blood donated by the participants during the study was collected in 7.5 ml serum separ-
ator tubes. This was allowed to stand at room temperature for 15 minutes then centri-
fuged at 4 C at 3,500 rpm for 10 minutes. Supernatant was removed and stored in
microcentrifuge tubes for later analysis.
Serum was analyzed for oxidative stress levels via the lipid peroxidation of malonalde-
hyde (MDA) with a thiobarbituric acid reactive substances (TBARS) colorimetric assay
(Cayman Chemicals; Ann Arbor, MI). In addition, serum was tested for lactate
dehydrogenase and creatine kinase activity via colorimetric assays to examine muscle
JOURNAL OF DIETARY SUPPLEMENTS 5
damage (Sigma-Aldrich; St. Louis, MO). The absorption endpoints of these assays were
read with a BioTek ELX 808 microplate reader with Gen5 software for data analysis
(BioTek Instruments; Winooski, VT).
Finally, a multiplex chemiluminescent assay (Quansys, Logan, UT) was run to exam-
ine inflammation (interleukin [IL]-1a, IL-1b, IL 2, IL 4, IL 6, IL 8, IL 10, interferon
[INF]-!, tumor necrosis factor [TNF]-a). At the conclusion of the assay procedures, the
plate was imaged with a CCD imager (18 megapixel) and the data analyzed with Qview
Pro Software (Quansys Biosciences; Logan, UT).
Statistical analysis
The principal investigator entered all data into JMP 11.0 pro software at the conclusion
of the study. Data were grouped according to research question and analyzed via
repeated measures analysis of variance (ANOVA) with post hoc analysis where neces-
sary or via nonparametric means provided data deviated from a normal distribution.
Statistical significance was set a priori at alpha <0.05.
Results
Human performance data
Oxygen consumption, muscle oxygenation, and power from exercise trials
ANOVA did not reveal a significant difference between maximum VO
2
achieved during
the 25-watt ramp protocols by treatment type (F ¼0.482, p¼0.49; maritime pine
extract: 25.8 þ/- 4.8 ml O
2
/kgmin; placebo: 27.2 þ/- 6.9 ml O
2
/kgmin). Similarly, stat-
istical analysis of muscle oxygenation data from NIRS sensors (F ¼0.833, p¼0.37) and
total hemoglobin (blood flow) (F ¼0.610, p¼0.44) did not reveal any significant differ-
ence by treatment during the exercise trial. Finally, ANOVA did not reveal a significant
difference between watts (power) achieved during the 25-watt ramp protocols by treat-
ment type (F ¼0.571, p¼0.45; maritime pine extract: 189 þ/- 34.8ml O
2
/kgmin; pla-
cebo: 181.3 þ/- 29.8 ml O
2
/kgmin).
Muscle pain at 24 and 48 hours
Vastus lateralis 25% of the distance between the superior border of the patella and greater
trochanter of the femur on the right leg did not reveal any main effects for treatment
(F ¼0.111, p¼0.74) or interaction effects for treatmenttime (F ¼1.34, p¼0.25). Vastus
lateralis 25% of the distance between the superior border of the patella and greater tro-
chanter of the femur on the left leg did not reveal any main effects for treatment
(F ¼0.756, p¼0.39) or interaction effects for treatmenttime (F ¼0.352, p¼0.56).
Vastus lateralis 50% of the distance between the superior border of the patella and
greater trochanter of the femur on the right leg did not reveal any main effects for
treatment (F ¼0.237, p¼0.63) or interaction effects for treatmenttime (F ¼0.002,
p¼0.96). Vastus lateralis 50% of the distance between the superior border of the patella
and greater trochanter of the femur on the left leg did not reveal any main effects for
6 R. L. ALDRET AND D. BELLAR
treatment (F ¼0.125, p¼0.72) or interaction effects for treatmenttime
(F ¼0.593, p¼0.45).
Vastus medialis 25% of the distance between the superior border of the patella and
greater trochanter of the femur on the right leg did not reveal any main effects for treat-
ment (F ¼0.052, p¼0.82) or interaction effects for treatmenttime (F ¼0.640, p¼0.43).
Vastus medialis 25% of the distance between the superior border of the patella and
greater trochanter of the femur on the left leg did not reveal any main effects for treat-
ment (F ¼0.002, p¼0.962) or interaction effects for treatmenttime (F ¼0.001, p¼0.97).
A table of results for muscle pain at 24 and 48 hours is provided in Table 1.
Biomarkers of muscle damage
Multiplex inflammatory panel creatine kinase (CK) and lactate dehydrogenase
Analysis of IL-1a, IL-1b, IL-2,4,6,8,10, INFg, and TNFa data from collected serum did not
reveal a main effect for treatment (F <1.0, p>0.4) or an interaction effect for treatmenttime
(F <1.2, p>0.30). A table of results for the inflammatory multiplex panel is provided in
Table 2.
Creatine kinase (CK) and lactate dehydrogenase
Analysis of creatine kinase data from collected serum did not reveal a main effect for
treatment (F ¼0.172, p¼0.68) or an interaction effect for treatmenttime (F ¼0.223,
p¼0.88). Analysis of lactate dehydrogenase data from collected serum did not reveal a
main effect for treatment (F ¼0.114, p¼0.74) or an interaction effect for treat-
menttime (F ¼1.57, p¼0.21).
Oxidative stress results
Analysis of MDA via TBARS assay utilizing repeated measures ANOVA was under-
taken; however, the assumption of ANOVA that residuals will be normally distributed
Table 1. Muscle pain at 25% and 50% of the vastus lateralis and 25% of vastus medialis at 24 hours
and 48 hours.
Location Time (hours) Left leg Right leg
Treatment group
Vastus lateralis 25% 24 1.43 ± 1.63 1.52 ± 1.41
48 0.93 ± 1.02 1.17 ± 1.14
Vastus lateralis 50% 24 0.97 ± 1.08 0.97 ± 0.96
48 0.8 ± 0.96 0.9 ± 1.15
Vastus medialis 25% 24 1.5 ± 2.04 1.3 ± 1.5
48 1.38 ± 1.72 1.28 ± 1.84
Placebo group
Vastus lateralis 25% 24 1.72 ± 1.97 1.43 ± 1.51
48 1.45 ± 1.56 1.53 ± 1.78
Vastus lateralis 50% 24 0.97 ± 0.91 1.15 ± 1.52
48 1.02 ± 1.68 1.1 ± 1.67
Vastus medialis 25% 24 1.47 ± 1.37 1.35 ± 1.85
48 1.37 ± 1.68 1.02 ± 1.19
Measured on a pain numeric rating scale where 0 is “no pain”and 10 is “worst possible pain.”
JOURNAL OF DIETARY SUPPLEMENTS 7
Table 2. Inflammatory multiplex panel.
IL-1aIL-1bIL 2 IL 4 IL 6 IL 8 IL 10 INF- !TNF- a
Treatment group
Pre-exercise 2.02 ± 0.76 2.6 ± 1.09 2.03 ± 1.02 2.35 ± 1.36 2.91 ± 1.07 2.33 ± 1.09 2.41 ± 1.02 2.64 ± 1.19 2.88 ± 1.0
24 h 2.24 ± 0.96 2.63 ± 1.14 2.08 ± 0.8 2.66 ± 1.33 3.09 ± 0.91 2.4 ± 1.09 2.4 ± 1.15 2.52 ± 0.99 2.91 ± 0.96
48 h 1.95 ± 0.78 2.49 ± 1.12 1.97 ± 1.05 2.21 ± 1.29 2.88 ± 1.16 2.34 ± 1.02 2.39 ± 0.92 2.42 ± 0.87 2.6 ± 1.07
Placebo group
Pre-exercise 2.11 ± 0.86 2.54 ± 1.08 2.04 ± 1.02 2.29 ± 1.2 2.53 ± 1.06 2.44 ± 1.08 2.34 ± 0.92 2.68 ± 1.05 2.67 ± 1.11
24 h 1.98 ± 0.87 2.51 ± 1.08 1.61 ± 0.25 2.46 ± 1.41 2.77 ± 1.09 2.32 ± 1.02 2.43 ± 0.88 2.44 ± 0.9 2.64 ± 1.11
48 h 1.88 ± 0.81 2.43 ± 1.07 1.54 ± 0.12 1.98 ± 1.12 2.55 ± 1.0 2.2 ± 1.1 2.41 ± 0.9 2.46 ± 1.19 2.66 ± 1.04
Measures in pg/mL. IL ¼interleukin; INF ¼interferon; TNF ¼tumor necrosis factor.
8 R. L. ALDRET AND D. BELLAR
was violated. Therefore, analysis was undertaken with nonparametric means. Chi-square
analysis did not reveal a difference at 24 hours for oxidative stress (ChiSq ¼0.90,
p¼0.34); however, at the 48-hour timepoint there was a significant reduction with
maritime pine extract as compared to placebo (ChiSq ¼2.63, p¼0.045). At 24 hours,
the mean for the placebo group was x¼0.95nmol/ml, SD ¼0.42, and the mean for
the maritime pine extract group was x¼0.83nmol/ml, SD ¼0.43. At 48 hours, the
mean for the placebo group was x¼0.99nmol/ml, SD ¼0.44, and the mean for the
maritime pine extract group was x¼0.76nmol/ml, SD ¼0.38. In addition, the placebo
group demonstrated a significant increase in oxidative stress from pre-exercise to
48 hours postexercise (p¼0.01) and a trend toward increase at 24 hours postexercise
(p¼0.08); There were no significant changes between pre-exercise and 24 or 48 hours
post-exercise. A table of results for creatine kinase, lactate dehydrogenase, and oxidative
stress is provided in Table 3.
Discussion
During low-intensity and duration protocols, antioxidant defenses appear sufficient, but
as intensity and duration increase, as in the present study, this is no longer the case
(Noda 1997). It appears that antioxidant capacity may be temporarily reduced during
and immediately following exercise (Packer et al. 1999), after which time, levels typically
increase above basal conditions during the recovery period (Iravani and Zolfaghari
2011). In the present study, this response took 24 to 48 hours, as with other studies of
post-sprint-type exercises (Sivonov
a et al. 2004); it happens immediately in postendur-
ance marathon runners (Sivonov
a et al. 2004). A few studies have missed these changes
by taking only one sample immediately postexercise (Voss et al. 2006) or 20 minutes
postexercise (Enseleit et al. 2012). In addition, elevated oxidative stress during high-
intensity exercise may suppress the respiratory chain, thereby reducing the efficiency of
energy (ATP) production (Knez et al. 2007).
Maritime pine extract’s uses during exercise and postexercise conditions such as
cramping can be traced to its antiedema and anti-inflammatory actions (Steinburg et al.
2006). Alterations in muscular metabolism associated with muscular pain from repeated
stressing exercise are unclear (Nikolaidis et al. 2007), which may explain why the pain
measurement data were not significantly different between groups. The positive oxida-
tive-resistant effects of maritime pine extract during and after stressing exercise events
Table 3. Creatine kinase, lactate dehydrogenase, and oxidative stress (MDA).
CK (nmol/mL) LDH (nmol/mL) MDA
Treatment group
Pre-exercise 200.89 ± 93.52 0.96 ± 0.57 0.82 ± 0.38
24 h 203.6 ± 85.32 1.0 ± 0.49 0.83 ± 0.43
48 h 191.14 ± 81.15 1.09 ± 0.54 0.76 ± 0.38
Placebo
Pre-exercise 203.01 ± 127.58 1.01 ± 0.67 0.77 ± 0.3
24 h 223.68 ± 133.28 1.04 ± 0.44 0.95 ± 0.42
48 h 213.04 ± 113.12 0.91 ± 0.51 0.99 ± 0.44
CK ¼creatine kinase; LDH ¼lactate dehydrogenase; MDA ¼malonaldehyde.
Significant difference treatment versus placebo (p¼0.045).
Significant increase from pre-exercise versus 48 h within placebo group (p¼0.01).
JOURNAL OF DIETARY SUPPLEMENTS 9
can be attributed to its ability to inhibit macrophage oxidative burst, lipoprotein oxida-
tion, and hydroxyl-radical-induced DNA damage (Marzatico et al. 1997).
Antithrombotic and antioxidant action of maritime pine extract may be particularly
effective in situations of dehydration following prolonged maximal exercise (Alessio
et al. 1997), though this would still need to be experimentally evaluated. This combin-
ation of action may explain why the 24-hour oxidative stress data were not significant,
but the 48-hour data demonstrated a difference between groups.
Prolonged physical activity also produces an excess amount of reactive oxidative species
(Waring et al. 2003), beyond the ability of the body’s ability to cope under normal
physiological circumstances (Mach et al. 2010). Additional oral antioxidant supplementa-
tion, especially vitamins C and E, may be a suitable, noninvasive means of reducing oxi-
dative stress, but excess exogenous antioxidants may have detrimental effects on health
and performance (Pingitore et al. 2015). The lowering of oxidative stress biomarkers does
not demonstrate any detrimental effects to the body, particularly in an exposure this
short, as there is limited opportunity for adaptations to the supplementation that would
be detrimental. Alternatives to supplementation include whole foods that contain antioxi-
dants in natural ratios and proportions (Pingitore et al. 2015). An adequate intake of vita-
mins and minerals through a varied diet remains an optimal approach (Pingitore et al.
2015). However, food availability, intolerance to certain types of foods, and extreme train-
ing regimens where athletes are exposed to high oxidative stress make exogenous supple-
mentation with maritime pine extract and other antioxidants necessary.
Conclusions
The primary finding of the present investigation was that maritime pine extract as com-
pared to placebo was effective at affording protection from oxidative stress postexercise.
It is suggested that further work be undertaken to evaluate these findings with other
exercise modes known to greatly increase lipid peroxidation (marathon, triathlon, road
races >10k); it could also be suggested that clinical evidence be garnered from a study
of individuals with metabolic syndrome, as that is known to greatly enhance oxida-
tive stress.
Declaration of interest
The authors declare no conflict of interest. The authors alone are responsible for the content and
writing of the article.
Funding
This research was funded by Horphag research grant number R4498.
About the authors
Randy L. Aldret, EdD, ATC, CSCS, Assistant Professor, School of Kinesiology, University of
Louisiana at Lafayette, Lafayette, LA, USA. Research interests: athletic performance, concussion
diagnosis, diabetes management in athletics.
10 R. L. ALDRET AND D. BELLAR
David Bellar, PhD, FNSCA, CSCSD, RSCCD, Professor and Director, School of Kinesiology,
University of Louisiana at Lafayette, Lafayette, LA, USA. Research interests: nutrition and human
performance, nutrition and antioxidant status, athlete monitoring.
ORCID
Randy L. Aldret http://orcid.org/0000-0002-6454-7449
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12 R. L. ALDRET AND D. BELLAR