|
Cheng-Chen
Hsu, Graduate Institute of Physical Education, National College
of Physical Education and Sports, Taoyuan County, and School of
Medicine, Taipei Medical University, Taipei, Taiwan, China
Min-Chen Ho, Mei-Chich Hsu, Graduate Institute of Sports
Science, National College of Physical Education and Sports, Taoyuan
County, Taiwan, China
Li-Chin Lin, Taiwan Biotech Co., Ltd, Taiwan, China
Borcherng Su, Department of Anatomic Pathology, E-Da
Hospital, I-Shou University, Kaoshiung County, Taiwan, Republic of
China
Supported by the Taiwan Biotech Co., Taiwan, China
Co-first-authors: Cheng-Chen Hsu and Min-Chen Ho
Co-correspondents: Cheng-Chen Hsu
Correspondence to: Dr. Mei-Chich Hsu, Graduate Institute of
Sports Science, National College of Physical Education and Sports,
Taoyuan County, Taiwan, China.
meichich@mail.ncpes.edu.tw
Telephone: +886-3-3374601
Fax: +886-3-3311843
Received: 2004-12-07
Accepted: 2005-02-18
Abstract
Aim: To
investigate whether American ginseng (AG, Panax quinquefolium)
supplementation was able to improve endurance exercise performance.
Methods:
Thirteen physically active male college students were divided into
two groups (AG or placebo) and received supplementation for 4
wk, before the exhaustive running exercise. Treadmill speed was
increased to a pace equivalent to 80% VO2max
of the subject. A 4-wk washout period followed before the subjects
crossed over and received the alternate supplement for the next 4
wk. They then completed a second exhaustive running exercise. The
physiological variables that were examined included time to
exhaustion and oxygen pulse. Moreover, the plasma creatine kinase
(CK) and lactate were measured prior to the exercise, at 15 and 30
min during exercise, immediately after exercise, and 20, 40, 60, and
120 min after exercise.
Results: The
major finding of this investigation was that the production plasma
CK during the exercise significantly decreased for group AG than for
group P. Secondary physiological finding was that 80% VO2max
running was not improved over a 4-wk AG supplementation regimen.
Conclusion:
Supplementation with AG for 4 wk prior to an exhaustive aerobic
treadmill running reduced the leakage of CK during exercise, but did
not enhance aerobic work capacity. The reduction of plasma CK may be
due to the fact that AG is effective for the decrease of skeletal
muscle cell membrane damage, induced by exercise during the
high-intensity treadmill run.
ã 2005
The WJG Press and Elsevier Inc. All rights reserved.
Key words: Panax quinquefolium; American ginseng;
Creatine kinase; Endurance exercise
Hsu CC, Ho MC, Lin LC, Su B, Hsu MC. American ginseng
supplementation attenuates creatine kinase level induced by
submaximal exercise in human beings. World J Gastroenterol
2005; 11(34): 5327-5331
http://www.wjgnet.com/1007-9327/11/5327.asp
INTRODUCTION
Traditional Chinese medicine plays a key role in the formation of
integrative medicine[1].
Ginseng (Genus Panax) root has been a popular Chinese
medicine with the belief of restoring Qi or life energy. It
is also thought to be a tonic to stimulate appetite, counteract
fatigue, boost the immune system, relieve pain and headaches, and
improve mental function and physical stamina[2].
The mechanism of action of ginseng is not known, but it is thought
to have effects on production of corticotropin and cortisol,
immunomodulation, antioxidants and neuroendocrine activity, modulate
carbo-hydrate and lipid metabolism, and stimulation of nitric
oxidation production in cardiovascular system[3-6].
Adequate dietary supplements or nutritional
ergogenic aids are an important means to optimize exercise
performance and to ward off fatigue. Ergogenic aids are believed to
increase performance by some of the following mechanisms: renewing
or increasing energy stores in the body, facilitating the
biochemical reactions that yield energy, reducing or neutralizing
performance-inhibiting metabolic byproducts, and facilitating
recovery[7,8].
Performance in aerobic-type events depends on the ability to
maintain a high output per unit of time. There is a growing
inclination among athletes to use herbs to improve endurance
performance or increase recovery after exercise.
The most studied herb for human aerobic physical
performance is ginseng. Although the mechanism underlying the
alleged ergogenicity of ginseng on physical performance has not been
defined, theories include stimulation of the
hypothalamic-pituitary-adrenal cortex axis and increased resistance
to the stress of exercise, enhanced myocardial metabolism, increased
hemoglobin levels, vasodilatation, increased oxygen extraction by
muscles, and improved mito-chondrial metabolism in the muscle, all
of which theoretically could enhance aerobic exercise performance[9-13].
In the review studies of Bahrke and Morgan,
administration of ginseng or its components enhanced exercise
endurance by altering fuel homeostasis during exercise, increased
free fatty acid utilization in preference over glucose for cellular
energy demands in rats and mice[14,15].
However, the evidence for ginseng as an endurance aerobic exercise
ergogenic supplementation in men is variable. As ginseng is touted
as a dietary ergogenic aid, incomplete study on performance has
yielded little proof to reinforce performance affirmations.
A number of chemically similar steroid glycosides
or saponin chemicals, known as ginsenosides, have been identified as
active ingredients in ginseng. The original medicinal species of
ginseng is Chinese or Korean ginseng (Panax ginseng C.A. Meyer).
American ginseng (Panax quinquefolius) contains many of the
same compounds, although in slightly different proportions. It is
the North American variety of ginseng, which grows in eastern and
central USA and Canada.
There is relatively little research that shows a
performance benefit of American ginseng (AG) in human beings. The
purpose of the present study was to determine, whether 4 wk of oral
supplementation with AG had any benefit on endurance
exercise and/or recovery after exercise.
MATERIALS AND METHODS
Subjects and anthropometric measurements
Thirteen male volunteers completed this randomized, double blind,
crossover experimental research study with a washout period of 4 wk.
Both body height and body weight were measured by an auto-anthropometer,
Nakamura KN-3000 (Nakamura, Tokyo, Japan). Body weight was measured
to the nearest 0.1 kg with subjects not wearing shoes or outerwear.
Body weight was recorded to the nearest 0.1 cm. Age, weight, and
heights (mean±SD) were 23.0±1.6 years, 70.2±6.3 kg, and 172.5±5.2 cm, respectively. A medical examination was performed on
each subject before entering the study. Written voluntary consent to
participate was obtained from all subjects after informing them of
the purpose of the experiment, the procedure, and the possible
risks. This investigation received the approval of the National
College of Physical Education and Sports (Taoyuan, Taiwan). All
subjects were healthy, physically active, college students with
normal dietary habits.
American ginseng supplementation
Each subject was instructed to ingest either 4 AG capsules (400 mg
AG per capsule) daily or a hydroxymethylcellulose placebo in the
same capsule form (both provided by Taiwan Biotech Co., Taiwan), and
received his allotment of CS or placebo in 4 weekly portions.
The Panax-bearing ginsenosides content was
determined from its degree of concentration in a hot water extract.
The compositions of the AG that we used were, ginsenosides Rb1
(8.67%, w/w), Rc (0.99%, w/w), Rd (1.05%, w/w), and Re (5.08%, w/w).
At an initial meeting, 4 wk prior to commencing any supplementation,
subjects were asked to cease taking any dietary supplementations
that contained ginsenosides and were instructed to maintain a
consistent diet before and during the experimental period.
Procedures
VO2max
was determined in the pre-experimental period. Each subject came to
the laboratory 7 d before the start of the actual study, and
performed an incremental running test on a motor-driven treadmill
(Quinton Instruments, Model 1 860, Washington, USA) according to the
Bruce protocol until exhaustion. In order to determine the baseline
endurance performance time, maximum oxygen consumption (VO2max)
was determined by the automated system (Model 29C, SensorMedics,
Yorba Linda, CA,USA). The VO2max
was defined as the attainment of at least two of the three following
criteria: (1) an increase of ≤140
mL VO2max
with an increasing workload; (2) heart
rate within 10 beats of age-predicted maximum; and (3) rating of
perceived exertion (RPE) greater than 17 using the Borg scale. Heart
rate (HR) measured
by the Sport Tester (PE 3 000, Polar Electro, Kempele,
Finland) were monitored during the
treadmill exercise. The RPE was recorded by using the modified Borg
scale[16].
Endurance performance time was also recorded at the end of the test
for each subject. On the day of the experiment, subjects reported to
the laboratory at 7-9 a.m. following a 10-12 h overnight fast, and
abstained from rigorous exercise for 48 h prior to the test. An
antecubital vein connected to a three-way stopcock with a 10-cm
extension tube for blood sampling was inserted in the subjects. The
cannula was kept patent by periodic flushing with a sodium chloride
solution (9 g/L) and remained in place throughout the experimental
period. No heparin was used in the catheter.
Protocol
Baseline physiological data was collected, while subjects stood
quietly on the treadmill (Quinton Instruments, Model 1 860,
Washington, USA) for 3 min prior to commencing the running test.
Subjects then commenced a 5 min warm-up at a running speed
equivalent to 60% VO2max,
the treadmill speed was increased to a pace equivalent to 80% VO2max
of the subjects. The subjects ran until volitional fatigue.
Volitional fatigue was defined as the point at which subjects could
no longer maintain the required running speed. VO2max
and HR were monitored throughout the
exercise and were recorded, and oxygen pulse was calculated from
oxygen consumption and heart rate. In addition, oxygen pulse (mLO2/beat)
was calculated by dividing oxygen consumption (mLO2/min)
by heart rate (beat/min).
Blood sampling and analysis
Blood samples were taken prior to the exercise, at 15 and 30 min
during exercise, immediately after exercise, and 20, 40, 60, and 120
min after exercise. At each sampling time, about 5 mL of venous
blood was taken. Whole blood for determination of hematocrit and
hemoglobin was collected in EDTA tubes cooled at -4 ℃
and examined within 4 h after venepuncture to correct relative
changes in plasma volume by using hematocrit and hemoglobin values
from each test, according to the methods described by Dill and
Costill[17].
The other venous blood was to obtain EDTA-plasma and stored at -20 ℃
for later analysis. The plasma creatine kinase (CK) and plasma
lactate were measured by a spectrophotometer technique (Johnson
& Johnson DT-60II, Orthoclinical Diagnostics, Rochester, NY,USA)
by means of ultraviolet test kits (Orthoclinical Diagnostics,
Rochester, NY,USA).
Statistical analyses
SPSS 11.0 for Windows statistical program was used to perform all
analyses. The independent variables between the two supplements (AG vs
placebo), including an endurance run time to exhaustion and VO2max
after supplements were compared using Student's
t-test for paired data. Differences in
oxygen pulse and plasma CK, and plasma lactate values between the
two treatment levels were analyzed by factorial (two-way, time×treatment) ANOVA with repeated
measures. A Tukey's
post hoc test
was used to locate any significant difference. Significance was
accepted at the P<0.05 level. All data are presented as
mean±SD.
RESULTS
Basic physical characteristics
There was no difference between groups in VO2max
and the run time to exhaustion (Table 1).
Table 1 Maximal oxygen consumption and run time to exhaustion1,2
| Group |
VO2max
(mL/min/kg) |
Time
to exhaustion (s) |
| AG |
44.6±3.1 |
2
279.5±252.7 |
| P |
45.1±5.0 |
2
218.3±345.9 |
1AG:
American ginseng supplement; P: placebo supplement. 2Values
are expressed as mean±SD
(n = 13).
Oxygen pulse
Data of oxygen consumption were collected in the time period of 0-1,
14-15, and 29-30 min. The oxygen pulse had no significant difference
between groups during these periods (Figure 1).
Figure 1 (PDF)
Oxygen pulse during exercise phase
in group AG (-■-) and group P (-●-). Each point represents the mean±SD
(n = 13).
Blood chemistry
In both placebo and AG groups, plasma CK and plasma lactate were
significantly increased with the duration of exercise and reached a
peak at exhaustive time (Figures 2 and 3). Blood lactate
concentration at 15, 30 min of exercise, and 120 min after exercise
in AG group (9.3±2.1, 11.4±2.7, and 2.2±0.4 mmol/L)
were significantly lower than in the placebo group (10.6±2.4, 13.3±2.7, and 2.6±0.4 mmol/L),
respectively (Figure 3). Moreover, plasma CK activity at 30 min of
exercise, immediately, 20, 60, and 120 min after exercise in the AG
group (181.2±78.0, 217.5±64.0, 167.5±56.2, 155.3±57.8, and
167.7±61.5 U/L)
were significantly lower than in the placebo group (254.3±81.6, 280.2±90.0, 246.5±66.3, 227.8±58.4, and
231.9±67.8 U/L),
respectively (Figure 2).
Figure 2
(PDF) Plasma
CK levels observed during exercise and recovery phases in group AG (-■-) and group P (-●-). Each point represents the mean±SD
(n = 13). aP<0.05
vs P groups; cP<0.05
vs before exercise.
Figure
3
(PDF) Plasma lactate levels observed during exercise and
recovery phases in group AG (-■-) and group P (-●-). Each point represents the mean±SD
(n = 13). aP<0.05
vs P groups; cP<0.05
vs before exercise.
DISCUSSION
The research was designed to determine whether or not
supplementation with AG for 4 wk prior to 80% VO2max
run would increase the time to exhaustion and/or have any ergogenic
benefit in healthy male college students. The variables that were
examined included time to exhaustion, oxygen pulse, plasma CK, and
plasma lactate. To our knowledge, this is the first study of AG in
human clinical trials to determine endurance aerobic physical
performance.
The major finding of this investigation was that
the production of plasma CK during exercise significantly decreased
for group AG over group P (P<0.05). Secondary
physiological findings suggested that 80% VO2max
running was not improved over a 4-wk AG supplementation regimen.
The CK marker is used to determine muscle damage.
The amount of plasma CK of healthy adults at rest is approximately
40-200 U/L for men[18].
In this study, the plasma CK conce-ntrations before exercise are
within the normal range in both groups and have no significant
difference between groups (AG group, 108.1±62.4; P
group, 138.6±94.6,
respectively).
Although most studies indicate that muscle injury
is assessed through prolonged endurance exercise, it is obvious that
it can be caused during high intensity short-term exercise as well[19,20].
During running exercise, the extensor muscles of the lower limb
performed eccentric actions as the foot touches the ground and the
dorsiflexors of the ankle contract eccentrically. In eccentric
exercise, the contracting muscle is forcibly lengthened as it
develops tension, potentially causing damage. Therefore,
endurance exercise, such as an exhaustive running exercise can
induce damage and pathological alteration in skeletal muscle.
With high-intensity exercise, the high-force
contractions cause muscle cell injury early in the exercise period[20].
Mechanical rupture of muscle fiber is one of the major mechanisms to
explain how the muscle injury was induced by exercise. This stress
on the cross bridges of the myofiber causes disruption of the muscle
fibrils leading to Z-line in disintegration or Z-line streaming[21].
Moreover, strenuous exercise can also disrupt the sarcolemma and
sarcoplasmic reticulum[22].
Mair et al., demonstrated a transient rise in the serum
concentrations of muscle proteins such as CK, an indicator of muscle
damage due to sarcolemma disruption, which cause a leakage of CK
into the blood[23].
In this study, the total CK activity
significantly increased in both groups during exhaustive running
exercise. We assign this to plasma CK increasing in both groups of
the subjects due to exercise-induced skeletal muscle damage. The
increases in plasma CK in this study indicate that muscle damage had
occurred during the exhaustive running in both groups.
Intense exercise may increase the production of
free radicals or reactive oxygen species. A free radical
prefers to steal electrons from the lipid membrane of a cell,
initiating a free radical attack on the cell known as lipid
peroxidation. Kanter et al., have demonstrated that
post-exercise plasma CK elevations may be related to an
exercise-induced lipid peroxidation[24].
The American ginseng Panax quinquefolium exhibits effective
antioxidant, free radical scavenging activity, and inhibiting lipid
peroxidation[25-29].
Lactate is an important indicator of muscle
performance under stress. Lactate levels rise as intensity increases
during exercise. The lower blood lactate concentration during
running exercise presumably reflects a lower intramuscular lactate
concentration and an increased relative contribution of anaerobic
metabolism to ATP production. In this study, the AG group exhibited
lower plasma levels of lactate at 15, 30 min of exercise than that
in the placebo group. It seems unlikely to be due to amelioration of
oxygen extraction from the blood by the working muscles as a
consequence of AG supplementation, since VO2max
and oxygen pulse was unaffected by prior supplementation. Decreased
blood lactate accumulation is not necessarily a result of muscle
tissue anti-hypoxia. Factors other than an increased cellular PO2,
a decrease in intracellular calcium
concentration, decreased activation of glycogen phosphorylase, or
decreased intrac-ellular pH can also cause a decrease in
intramuscular lactate production[30].
Otherwise, the rate of efflux of lactate from the contractile muscle
could be decreased due to the decreased muscle cell membrane
permeability after exercise-induced damage[31].
In conclusion, a 4-wk AG supplementation reduced
the leakage of CK from skeletal sarcoplasm into blood streaming
during an exhaustive treadmill run, but did not enhance aerobic work
capacity. The reduction of plasma CK level may be due to AG that is
effective for the decrease of skeletal muscle cell membrane damage
induced by exercise during the high intensity treadmill run. In the
future, we will investigate if the reduction in CK efflux is simply
an indication of increased sarcolemma stability or whether the
muscles are in fact receiving less damage.
ACKNOWLEDGMENTS
We wish to extend our deep appreciation to all participating
subjects for their dedication to this study.
REFERENCES
1
Lu AP, Jia HW, Xiao C, Lu QP. Theory of traditional
Chinese medicine and therapeutic method of diseases.
World J Gastroenterol 2004; 10:
1854-1856
2
Coleman CI, Hebert JH, Reddy P. The effects of Panax
ginseng on quality of life. J Clin Pharm Ther 2003; 28:
5-15
3
Tode T, Kikuchi Y, Hirata J, Kita T, Nakata H, Nagata
I. Effect of Korean red ginseng on psychological functions
in patients with severe
climacteric syndromes. Int J Gynaecol Obstet 1999; 67:
169-174
4
Yuan CS, Attele AS, Wu JA, Lowell TK, Gu Z, Lin Y.
Panax quinquefolium L. inhibits thrombin-induced endothelin
release in vitro. Am
J Chin Med 1999; 27: 331-338
5
Ji LL, Peterson DM. Aging, exercise, and
phytochemicals: promises and pitfalls. Ann N Y Acad Sci 2004;
1019: 453-461
6
Tan BK, Vanitha J. Immunomodulatory and antimicrobial
effects of some traditional chinese medicinal herbs: a
review. Curr Med Chem 2004;
11: 1423-1430
7
Lawrence ME, Kirby DF. Nutrition and sports
supplements: fact or fiction. J Clin Gastroenterol 2002; 35:
299-306
8
Maughan RJ, King DS, Lea T. Dietary supplements. J
Sports Sci 2004; 22: 95-113
9
Kim DH, Moon YS, Jung JS, Min SK, Son BK, Suh HW, Song
DK. Effects of ginseng saponin administered
intraperitoneally on the
hypothalamo-pituitary-adrenal axis in mice. Neurosci Lett
2003; 343: 62-66
10
Zhang HG, Li XH, Yang ZC. Effects of Panax notoginseng
saponins on myocardial Gsalpha mRNA expression and
ATPase activity after
severe scald in rats. Burns 2003; 29: 541-546
11
Bae JW, Lee MH. Effect and putative mechanism of
action of ginseng on the formation of glycated hemoglobin in
vitro.
J Ethnopharmacol 2004; 91:
137-140
12
Li Z, Chen X, Niwa Y, Sakamoto S, Nakaya Y.
Involvement of Ca2+ -activated K+ channels in ginsenosides-induced
aortic relaxation in
rats. J Cardiovasc Pharmacol 2001; 37: 41-47
13
Wang BX, Zhou QL, Yang M, Wang Y, Cui ZY, Liu YQ,
Ikejima T. Hypoglycemic mechanism of ginseng glycopeptide.
Acta Pharmacol Sin 2003; 24:
61-66
14
Bahrke MS, Morgan WP. Evaluation of the ergogenic
properties of ginseng. Sports Med 1994; 18: 229-248
15
Bahrke MS, Morgan WR. Evaluation of the ergogenic
properties of ginseng: an update. Sports Med 2000; 29:
113-133
16
Borg GA, Perceived exertion: a note on "history"
and methods. Med Sci Sports Exerc 1973; 5: 90-93
17
Dill DB, Costill DL. Calculation of percentage changes
in volumes of blood, plasma, and red cells in dehydration. J
Appl Physiol 1974; 17:
247-248
18 Tietz
NW. Clinical guide to laboratory tests. 3rd
ed. Philadelphia: Saunders 1995: 180
19
Byrd SK. Alterations in the sarcoplasmic reticulum: a
possible link to exercise-induced muscle damage. Med Sci
Sports Exerc 1992; 24:
531-536
20
Friden J, Lieber RL. Structural and mechanical basis
of exercise-induced muscle injury. Med Sci Sports Exerc
1992;
24: 521-530
21
MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle
soreness. The inflammatory response to muscle injury and
its clinical
implications. Sports Med 1995; 20: 24-40
22
Clarkson PM, Hubal MJ. Exercise-induced muscle damage
in humans. Am J Phys Med Rehabil 2002;
81(11 Pt 1):
S52-S69
23
Mair J, Mayr M, Muller E, Koller A, Haid C,
Artner-Dworzak E, Calzolari C, Larue C, Puschendorf B. Rapid
adaptation
to eccentric
exercise-induced muscle damage. Int J Sports Med 1995; 16:
352-356
24
Kanter MM, Lesmes GR, Kaminsky LA, La Ham-Saeger J,
Nequin ND. Serum creatine kinase and lactate
dehydrogenase changes
following an eighty kilometer race. Relationship to lipid
peroxidation. Eur J Appl Physiol
Occup Physiol 1988; 57:
60-63
25
Li J, Huang M, Teoh H, Man RY. Panax quinquefolium
saponins protects low density lipoproteins from oxidation. Life
Sci 1999; 64: 53-62
26
Li JP, Huang M, Teoh H, Man RY. Interactions between
Panax quinquefolium saponins and vitamin C are observed
in vitro. Mol Cell
Biochem 2000; 204: 77-82
27
Kitts DD, Wijewickreme AN, Hu C. Antioxidant
properties of a North American ginseng extract. Mol Cell Biochem
2000; 203: 1-10
28
Fu Y, Ji LL. Chronic ginseng consumption attenuates
age-associated oxidative stress in rats. J Nutr 2003;
133:
3603-3609
29
Ng TB, Liu F, Wang HX. The antioxidant effects of
aqueous and organic extracts of Panax quinquefolium,
Panax notoginseng,
Codonopsis pilosula, Pseudostellaria heterophylla and Glehnia
littoralis. J Ethnopharmacol 2004;
93: 285-288
30
Connett RJ, Honig CR, Gayeski TE, Brooks GA. Defining
hypoxia: a systems view of VO2,
glycolysis, energetics,
and
intracellular PO2.
J Appl Physiol 1990; 68: 833-842
31
Newham DJ, Jones DA, Edwards RH. Large delayed plasma
creatine kinase changes after stepping exercise.
Muscle Nerve 1983; 6:
380-385
Science
Editor Guo SY Language
Editor Elsevier HK
| |
PubMed
