See

discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/9023129

Effect of Muscle Oxygenation during

Resistance Exercise on Anabolic Hormone
Response

Article in Medicine & Science in Sports & Exercise November 2003

DOI: 10.1249/01.MSS.0000093613.30362.DF Source: PubMed

CITATIONS READS

40 523

9 authors, including:

Jay R Hoffman Kenneth W Rundell

University of Central Florida Pharmaxis
400 PUBLICATIONS 7,363 CITATIONS 91 PUBLICATIONS 2,224 CITATIONS

SEE PROFILE SEE PROFILE

Jie Kang Shoko Nioka

The College of New Jersey University of Pennsylvania
195 PUBLICATIONS 3,972 CITATIONS 188 PUBLICATIONS 4,527 CITATIONS

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Mitochondria-targeted nutraceuticals in health and disease View project

Monocyte Recruitment following High-Intensity and High-Volume Resistance Exercise View project

All content following this page was uploaded by Jay R Hoffman on 10 August 2015.

The user has requested enhancement of the downloaded file.

Effect of Muscle Oxygenation during
Resistance Exercise on Anabolic
Hormone Response
JAY R. HOFFMAN1, JOOHEE IM2, KENNETH W. RUNDELL3, JIE KANG1, SHOKO NIOKA2,
BARRY A. SPEIRING3, RYOTO KIME2, and BRITTON CHANCE2
1
The College of New Jersey, Ewing, NJ; 2Department of Biochemistry & Biophysics, University of Pennsylvania,
Philadelphia, PA; and 3Marywood University, Scranton, PA

ABSTRACT
HOFFMAN, J. R., J. IM, K. W. RUNDELL, J. KANG, S. NIOKA, B. A. SPEIRING, R. KIME, and B. CHANCE. Effect of Muscle
Oxygenation during Resistance Exercise on Anabolic Hormone Response. Med. Sci. Sports Exerc., Vol. 35, No. 11, pp. 1929 1934,
2003. Purpose: The mechanisms that underlie the affect of acute program variables on muscle growth and strength development for
strength/power athletes have been of great interest. This investigation examined the affects of two different resistance exercise protocols
on muscle oxygenation, and the anabolic hormonal response to such exercise. Methods: Eleven experienced resistance-trained male
athletes performed four sets of the squat exercise using either a low-intensity, high-volume (LI; 15 repetitions at 60% one-repetition
maximum [1-RM]) or high-intensity, low-volume (HI; 4 repetitions at 90% 1-RM) load. Venous blood samples were obtained before
(Pre), immediate (IP), 20- (20P), and 40-min (40P) postexercise. Continuous-wave near-infrared spectroscopy was used to measure
oxygen desaturation during exercise. Results: No differences in muscle deoxygenation were seen between LI and HI. However,
time-dependent postexercise reoxygenation was significantly different between the two exercise sessions (35.3 17.4 s vs 24.5
14.3 s in LI and HI, respectively). Testosterone and growth hormone (GH) concentrations were significantly elevated from Pre at IP,
20P, and 40P in both LI and HI. GH concentrations were higher (P 0.05) for LI than at HI at 20P and 40P. Conclusion: Muscle
oxygen recovery kinetics appeared to be influenced by differences in the intensity and volume of exercise, and delayed reoxygenation
appears to affect the GH response to exercise. Key Words: TESTOSTERONE, GROWTH HORMONE, WEIGHT TRAINING,
NEAR-INFRARED SPECTROSCOPY, MUSCLE ISCHEMIA

D
uring aerobic exercise, blood flow and oxygen de-
livery to working muscle is generally increased to
meet the demands of exercise (23). However, as
exercise intensity increases, intramuscular forces become
elevated, resulting in an attenuation of exercise hyperemia
(4,5,9,24,26). As a consequence, increases in lactic acid and
intramuscular oxygen desaturation are observed. The rela-
tionship between restricted blood flow, lactic acid, and
oxygen desaturation within the exercising muscle has been
demonstrated (9,24). Although it is generally recognized
that exercise resulting in high force production (i.e., resis-
tance exercise) will result in a reduction of blood flow to
exercising muscle (22), studies examining this mode of
exercise are limited. Moreover, most studies investigating
blood flow in the context of resistance exercise have used a
static model (i.e., isometric exercise), despite the fact that a
Address for correspondence: Jay R. Hoffman, Ph.D., FACSM, Department
of Health and Exercise Science, The College of New Jersey, P.O. Box
7718, Ewing, NJ 08628; E-mail: hoffmanj@tcnj.edu.
Submitted for publication February 2003.
Accepted for publication June 2003.
0195-9131/03/3511-1929
MEDICINE & SCIENCE IN SPORTS & EXERCISE
Copyright 2003 by the American College of Sports Medicine
DOI: 10.1249/01.MSS.0000093613.30362.DF
1929
majority of resistance-training programs utilize dynamic
movements with large variations in training intensity and
volume.
The manipulation of these training variables appears to
have important implications on the physiological response
to resistance exercise. Kraemer and colleagues (13,14) have
shown that hormonal responses to acute heavy resistance
exercise are sensitive to changes in these variables (e.g., rest
intervals, exercise intensity, and volume) in both men and
women. Specifically, significantly higher testosterone con-
centrations have been observed when rest periods between
sets are reduced (3 to 1 min), or when the intensity of
exercise is decreased (5 repetition maximum [RM] to 10-
RM) and volume is increased (14). Similarly, circulating
immunoreactive growth hormone concentrations increase in
response to an acute bout of resistance exercise, and appear
to be greatest when training protocols of moderate intensity
(10-RM vs 5-RM) and short rest periods (1 min vs 3 min)
are utilized (13). The elevations in anabolic hormonal re-
sponse to manipulations of the acute program variables may
explain, in part, the variability in muscle hypertrophy observed
with different resistance training programs. For example, body-
builders typically incorporate high-volume, moderate-intensity
training programs with short rest periods.
Recent research has suggested that muscle ischemia
caused by vascular occlusion appears to enhance the hor-
monal response to exercise (30). The extent and duration of
ischemia may ultimately determine the extent of tissue damage
(8) that occurs consequent to a specific stimulus, such as heavy
resistance exercise. In addition, muscle damage that occurs as
a result of heavy resistance exercise is thought to be requisite
for muscle hypertrophy and increases in strength (16). Thus, it
would appear that resistance-training programs designed to
invoke a greater extent and duration of muscle ischemia would
result in increased muscle hypertrophy. Therefore, the purpose
of this study is to compare the effects of a high-intensity,
low-volume with a low-intensity, high-volume exercise para-
digm on muscle oxygenation during resistance exercise. In
addition, the relationship between muscle oxygenation and the
anabolic hormonal response to resistance exercise was exam-
ined. The hypothesis of this study is that exercise programs that
elicit a greater degree of muscle ischemia will result in a greater
anabolic hormonal response to exercise.
METHODS
Subjects. Eleven experienced resistance-trained men
(20.8 1.3 yr; 96.2 14.4 kg, 182.4 7.3 cm) served as (% oxy/deoxy-Hb/Mb) for each exercise period was calcu-
subjects for this investigation. After an explanation of all
procedures, risks, and benefits each subject gave his written
informed consent to participate in this study. The Institu-
tional Review Board of the College approved the research
protocol. Each subject had 6.9 0.8 yr of resistance train-
ing experience (range 6 8 yr), had a 1-RM squat of 184.5
16.5 kg, and was free of any musculoskeletal and endo-
crine disorders. In addition, all subjects reported being free
of anabolic steroid use during the previous year and were
not taking any other ergogenic supplementation during the 6
wk before the study.
Testing procedure. Each subject reported to the Hu-
man Performance Laboratory on three different occasions.
During the initial visit, subjects performed a 1-RM strength
test for the squat exercise. Each subject performed a
warm-up set using a resistance that was approximately 40
60% of his perceived maximum, then performed three to
four subsequent attempts to determine the 1-RM with 35
min of rest between each lift. During the next two sessions,
each subject performed a resistance exercise protocol con-
sisting of five sets of the parallel squat exercise. The first set
was used as a warm-up set. For each testing session both
intensity and volume of exercise differed. Subjects exer-
cised using either a light-intensity, high-volume (LI) (15
repetitions with 60% of 1-RM), or high-intensity, low-vol-
ume (HI) (4 repetitions with 90% of 1-RM) exercise proto-
col during each testing session. The exercise protocol was
randomly assigned to prevent an order effect. Rest intervals
between sets were 3 min for both exercise sessions. Each
testing session was separated by at least 72 h and occurred
at the same time of day to account for diurnal variation in
hormonal measurements.
Hemoglobin/myoglobin muscle tissue deoxy-
genation procedure. A 16-channel continuous wave
near infrared spectroscopy (cwNIRS; NIMS, Philadelphia,
PA) was used to measure changes in hemoglobin (Hb)/
myoglobin (Mb) muscle tissue oxygenation/deoxygenation
1930 Official Journal of the American College of Sports Medicine
(oxy/deoxy-Hb/Mb) in the capillary bed of the vastus late-
ralis muscle at rest, during each set, and for 3 min postex-
ercise. After each training session, cuff ischemia (CI) was
performed to obtain maximal oxy/deoxy-Hb/Mb. Linearity
of NIRS technology has been previously validated in other
studies (7,19), and validity for cwNIRS has been recently
established (15). The NIRS unit included a probe consisting
of two LED light sources and eight photodiode detectors.
An 11- 7-cm optical probe with a 3-cm source-to-detector
separation was positioned on the lateral aspect of the right
vastus lateralis at a location equidistant between the greater
trochanter of the femur and the muscles distal connection to
the quadriceps tendon. The location of the probe was re-
corded by noting distances from the anatomical landmarks
to ensure identical probe placement during all trials. Wave-
lengths of 730 and 850 nm were used to monitor relative
change in oxy/deoxy-Hb/Mb. Oxy-Hb/Mb of muscle tissue
was estimated by changes in the difference in signal strength
at those wavelengths. Data acquisition sampling frequency
was set at approximately 2 Hz. Relative oxy/deoxy-Hb/Mb
lated by taking the difference between baseline at rest and
the greatest oxy/deoxy-Hb/Mb that occurred during exer-
cise, and dividing by the maximal oxy/deoxy-Hb/Mb ob-
tained during CI. To obtain CI, a thigh cuff was placed
proximal to the probe and inflated to 260 torr for 8 min or
until a plateau for deoxy-Hb/Mb was reached. CI was ad-
ministered while subjects were seated in a semirecumbent
position with the instrumented leg extended horizontally
and supported. Deoxy-Hb/Mb values from the baseline,
exercise, and CI were obtained by taking 10-s averages.
Recovery kinetics and rates after each exercise session
were also determined using the cwNIRS. Half-time recovery
(T1/2) was ascertained by determining the time necessary to
achieve to 50% of maximal reoxy-Hb/Mb after exercise
cessation (4).
Blood measurements. During each experimental ses-
sion blood samples were obtained preexercise (PRE), im-
mediately postexercise (IP), 20 (20P), and 40 min (40P)
postexercise. All blood samples were obtained using a 20-
gauge Teflon cannula placed in a superficial forearm vein.
The cannula was maintained patent using an isotonic saline
solution placed in a three-way stopcock with a male luer
lock adapter. PRE blood samples were drawn after a 15-min
equilibration period before exercise. IP blood samples were
taken within 30 s of exercise cessation. All blood samples
were drawn with a plastic syringe while the subject was in
a seated position.
After collection, blood was transferred to a Vacutainer
tube containing SST Gel and Clot Activator. The blood
was allowed to clot at room temperature and subsequently
centrifuged at 1500 g for 15 min. The resulting serum was
placed into separate 1.8-mL microcentrifuge tubes and fro-
zen at 80C for later analysis of total testosterone and
22-kDa growth hormone.
Biochemical and hormonal analyses. Serum total
testosterone and 22-kDa growth hormone concentrations were
determined using enzyme immunoassay and enzyme-linked
http://www.acsm-msse.org
immunosorbent assay, respectively (Diagnostic Systems Lab-
oratories, Webster, TX). Determinations of serum immunore-
activity values were made using a SpectraMax340 Spectropho-
tometer (Molecular Devices, Sunnyvale, CA). To eliminate
interassay variance, all samples for a particular assay were
analyzed in the same assay run. All samples were run in
duplicate with a mean intra-assay variance of 10%. The
detection limit of the testosterone and growth hormone assays
were 0.14 nmolL1 and 0.3 gL1, respectively. Lactate
concentrations were determined with an Analox GM7 enzy-
matic metabolite analyzer (Analox Instruments U.S., Lunen-
burg, MA).
Statistical analysis. Data were analyzed using a two-
way ANOVA. In the event of a significant F-ratio, post hoc
comparisons using the Bonferroni method were applied to
determine pairwise differences. In addition, paired Students
t-tests were used to analyze the area under curve (AUC),
which was calculated by using a standard trapezoidal tech-
nique. A criterion alpha level of P 0.05 was used to
determine statistical significance. A sample size of 11 sub-
jects provided 80% statistical power at an level of 0.05
(two-tailed).

RESULTS
During LI all subjects completed the 15 required repeti-
tions per set except one subject who completed only 12
repetitions during his last set of exercise. During HI, 9 of the
11 subjects were able to complete the four repetitions re-
quired per set. One subject was only able to complete three
repetitions in his last set, and another subject was only able
to complete 5 of the 16 total repetitions that were required.
The duration of exercise per set was significantly (P 0.05)
greater during LI (41.6 6.6 s) than in HI (21.4 3.6 s).
However, the extent of muscle deoxygenation (expressed as a
percent of maximal desaturation obtained during CI) between
the two exercise sessions was not statistically significant. Dur-
ing LI muscle deoxygenation reached 72.7 18.0%, whereas
HI muscle deoxygenation reached 79.9 13.4%.
After exercise, muscle reoxygenation appeared to be de-
layed during both training sessions. However, the duration
of the delay was significantly (P 0.05) different between
HI and LI (24.5 14.3 s and 35.3 17.4 s, respectively).
Once reoxygenation began the T1/2 recovery was not dif-
ferent between the two training sessions (50.2 15.5 s and
51.7 16.8 s in HI and LI, respectively).
Lactate concentrations at IP were significantly (P 0.05)
elevated above resting levels after both HI and LI testing
conditions. However, lactate concentrations for LI was
significantly (P 0.05) higher at that time point than for
HI (15.3 2.3 mmolL1 and 9.7 3.3 mmolL1, ation. Although both training intensities result in similar
respectively).
The serum testosterone response to the two training ses-
sions is shown in Figure 1. Testosterone concentrations
were significantly (P 0.05) elevated from PRE at IP, 20P,
and 40P in both HI and LI. However, no significant differ-
ences were seen between exercise sessions. AUC analysis
MUSCLE OXYGENATION AND RESISTANCE TRAINING
FIGURE 1A. Comparison of serum testosterone concentrations
(mean SD) for various time points and resistance exercise intensities.
B. Area under the curve (AUC) testosterone responses (mean SD).
* Significantly different from Pre; LI, 60% 1RM; HI, 90% 1RM.
also failed to demonstrate any significant difference be-
tween exercise sessions.
The serum growth hormone response to the two training
sessions is shown in Figure 2. Growth hormone concentra-
tions were significantly (P 0.05) elevated from PRE at IP,
20P, and 40P in both HI and LI. However, growth hormone
concentrations were significantly (P 0.05) higher for LI
than HI at 20P and 40P. In addition, AUC for GH was
significantly (P 0.05) higher during LI than in HI.
DISCUSSION
The purpose of this study was to examine the effect of
training intensity on muscle oxygenation, and to examine
the relationship between muscle deoxygenation and the an-
abolic hormonal response. The results of this study show no
apparent difference between resistance exercise protocols of
low-intensity, high-volume and high-intensity, low-volume
on muscle deoxygenation. However, the duration of exer-
cise appears to have had a greater influence on the deoxy-
genation and the delay in postexercise muscle reoxygen-
deoxygenation values, exercise performed at the lower in-
tensity was performed for a significantly longer duration.
Although previous research has shown that resistance train-
ing will reduce tissue oxygenation within contracting skel-
etal muscle (28), this was the first study to quantify the
extent of muscle deoxygenation during such exercise.
Medicine & Science in Sports & Exercise 1931

FIGURE 2A. Comparison of serum growth hormone concentrations
(mean SD) for various time points and resistance exercise intensities.
B. Area under the curve (AUC) growth hormone responses (mean
SD). * Significantly different from Pre; # Significantly different be-
tween LI and HI. LI, 60% 1RM; HI, 90% 1RM.
Interestingly, the extent of muscle deoxygenation during
resistance exercise appears similar to values previously re-
ported in speed skaters skating in a low position (5), alpine
skiers during a simulated giant slalom event (26), and sprint-
ers performing the Wingate anaerobic power test (21). De-
oxygenation of skeletal tissue during exercise is a function
of a change in blood flow and intramuscular pressure (25).
Intramuscular pressure is known to increase linearly with
increases in the force of muscle contraction, which occur as
a result of increased tension in activated muscle fibers
(2,11). As intramuscular pressure increases, blood perfusion
to the activated skeletal muscle is reduced. This appears to
begin when muscle contraction exceeds 3550% of its max-
imal force capability (10). In this study, resistance exercise
was performed at 60% and 90% of the subjects 1-RM and
would be expected to cause elevated intramuscular pres-
sures. Thus, the extent of muscle deoxygenation observed
during each testing session was not surprising. Even though
there appeared to be a tendency for greater tissue deoxy-
genation after HI than LI, this 7% difference in muscle
deoxygenation was not statistically different.
Previous research has reported a moderate correlation (r
0.70, P 0.05) between lactic acid concentrations and
the rate of muscle deoxygenation during submaximal aero-
bic exercise (18). However, despite a higher lactate concen-
tration seen after LI (P 0.05), there was no significant
difference between the two exercise intensities in muscle
deoxygenation. In addition, no correlations (r 0.10) were
observed in this study between muscle deoxygenation and
1932 Official Journal of the American College of Sports Medicine
lactate acid concentrations in both LI and HI. Apparently the
high intramuscular pressures, as well as the relatively short
duration of exercise resulting from heavy resistance exer-
cise, has a much greater impact on muscle deoxygenation
than lactate concentrations. It is possible that the higher
lactate concentrations seen during LI had a greater impact
on muscle reoxygenation postexercise.
A unique aspect to this study was the difference seen in
reoxygenation between LI and HI. Despite similar deoxy-
genation levels during each training session, there was a
44.1% longer delay in the start of reoxygenation after LI
compared with HI. The phenomenon of delayed reoxygen-
ation, as a function of intensity and volume during resis-
tance exercise, has not been previously seen. It is likely that
the higher lactate accumulation seen during LI facilitated a
greater O2Hb dissociation (Bohr effect). In addition, previ-
ous research has also demonstrated that O2Mb dissociation
will follow a similar pattern of O2Hb dissociation when
exercise intensity is maximal (4,19). Considering that sub-
jects were exercising at intensities that approximated their
RM for each exercise intensity, it appears that the duration
of exercise performed at a maximal effort may be more
important than the relative intensity of exercise in affecting
muscle oxygen recovery kinetics. In addition, the greater
metabolic acidosis seen during LI may have resulted in a
2-adrenoreceptor-mediated constriction of arteriole mi-
crovessels. McGillivray-Anderson and Faber (20) have
demonstrated that 2-adrenoreceptors on terminal arterioles
are highly sensitive to tissue acidosis.
The athletic background of these subjects may have also
contributed to the postexercise delay in muscle reoxygen-
ation. All of the subjects in this study were anaerobic ath-
letes. Though speculative, it is likely that the fiber compo-
sition of these athletes was primarily of the Type II variety.
Previous research has shown that such fibers do not dem-
onstrate the level of postexercise hyperemia seen in slow-
oxidative and fast-oxidative fibers common in more aerobic
athletes (17). Therefore, it is possible that the delay in
reoxygenation after high-intensity resistance exercise may
also be a function of fiber type composition and associated
vasculature density.
Another purpose of this study was to investigate whether
differences in muscle oxygenation as a result of exercise
intensity will influence the hormonal response to such ex-
ercise. Previous studies have indicated that under ischemic
conditions the hormonal response to exercise may be en-
hanced (27,30). However, in these studies the ischemic
conditions were examined via vascular occlusion. This is the
first study known that has examined the affect of muscle
deoxygenation occurring as a natural response to the exer-
cise stress on the hormonal response to resistance exercise.
The results attained in this study confirm previous investi-
gations that have demonstrated that growth hormone
(27,30), but not testosterone (30), concentrations are influ-
enced by tissue ischemia in actively contracting muscle.
The prolonged ischemic response seen after LI, reflected
by the greater delay in muscle reoxygenation, resulted in a
greater growth hormone response than that seen after HI. In
http://www.acsm-msse.org
addition, lactate concentrations were 58% higher after LI
than after HI, presumably a result of the local tissue hypoxia
caused by elevated intramuscular pressure. Growth hormone
secretion patterns have been shown to be quite responsive to
changes in the acid-base balance of muscle (6). Increases in
intramuscular acidity can stimulate sympathetic nerve ac-
tivity through a chemoreceptive reflex that is mediated by
intramuscular metaboreceptors (29). Thus, it appears that
the duration of acute hypoxia and the accumulation of
metabolites during resistance training are important stimuli
for the growth hormone response.
The importance of acute program variables such as training
intensity and volume on the hormonal response to exercise has
been demonstrated (13,14). Although the response of growth
hormone in this study supports these previous investigations,
the response of testosterone to differences in these training
variables did not. Similar to growth hormone, testosterone is
responsive to changes in acute program variables (13,14).
Generally, resistance exercise of moderate intensity (i.e., 10-
RM) appears to induce a significantly greater testosterone
response than exercise of higher intensity (i.e., 5-RM) (13,14).
However, when the hormonal response was examined using
AUC analysis, no significant differences were seen (14). Our
results confirm these findings.
Another factor that may have contributed to the similar
response of testosterone in this study was the effect of the
subjects training and athletic experience. Previous studies
that have examined the effect of acute program variables on
the hormonal response to resistance exercise have primarily
used recreationally trained subjects (13,14). The subjects of
this study were all competitive intercollegiate athletes par-
ticipating in a strength/power sport. Training experience has
previously been shown to result in an attenuated hormonal
REFERENCES
1. ANAKWE, O. O., and W. H. MAGER. Beta-2-adrenergic stimulation
of androgen production by cultured mouse testicular interstitial
cells. Life Sci. 35:20412049, 1984.
2. BALLARD, R. E., D. E. WATENPAUGH, G. A. BRETT, G. MURTHY, D. C.
HOLLEY, and A. R. HARGENS. Leg intramuscular pressures during
locomotion in humans. J. Appl. Physiol. 84:1976 1981, 1998.
3. CADOUX-HUDSON, T. A., J. D. FEW, and F. J. IMMS. The effect of
exercise on the production and clearance of testosterone in well-
trained young men. Eur. J. Appl. Physiol. 54:321325, 1985.
4. CHANCE, B., M. T. DAIT, C. ZHANG, T. HAMAOKA, and F. HAGER-
MAN. Recovery from exercise-induced desaturation in the quadri-
ceps muscle of elite competitive rowers. Am. J. Physiol. 262:
C766 C775, 1992.
5. FOSTER, C., K. W. RUNDELL, A. C. SNYDER, et al. Evidence of
restricted blood flow during speed skating. Med. Sci. Sports.
Exerc. 31:14331440, 1999.
6. GORDON, S. E., W. J. KRAEMER, N. H. VOS, J. M. LYNCH, and H. G.
KNUTTGEN. Effect of acid-base balance on the growth hormone
response to acute high-intensity cycle exercise. J. Appl. Physiol.
76:821 829, 1994.
7. HAMAOKA, T., C. ALBANI, B. CHANCE, and H. IWANE. A new method
for evaluation of muscle aerobic capacity in relation to physical
activity measured by near-infrared spectroscopy. Int. Med. Sport
Sci. 39:421 429, 1992.
8. HARRIS, A. G., R. LEIDERER, F. PEER, and K. MESSMER. Skeletal
muscle microvascular and tissue injury after varying durations of
ischemia. Am. J. Physiol. 271:H2388 H2398, 1996.
MUSCLE OXYGENATION AND RESISTANCE TRAINING
response to an acute bout of heavy resistance exercise (12).
Although this doesnt explain the similar response of tes-
tosterone to the two exercise protocols, it does suggest that
the testosterone response to acute resistance exercise is
attenuated in highly trained men.
Testosterone concentrations after both LI and HI were
significantly elevated from PRE. Nevertheless, it did not
appear that the mechanisms responsible for elevated testos-
terone levels were related to muscle deoxygenation. These
results support recent research by Viru and colleagues (30),
who also reported that changes in testosterone concentra-
tions were not influenced by muscle ischemia. Though
previous studies have suggested that exercise-induced in-
creases in testosterone concentrations are related to direct
Leydig cell stimulation by elevated catecholamine concen-
trations (1) and/or through changes in hormonal clearance
rate (3), it appears that the mechanisms responsible for such
changes are still not clear.
In summary, although heavy resistance exercise results in
significant muscle deoxygenation, training intensity and
volume does not seem to impact the extent of deoxygen-
ation. The results of this study do suggest that oxygen
recovery kinetics within skeletal muscle are influenced by
these training variables. Furthermore, stimulation of growth
hormone release during resistance training does appear to be
affected by the duration of muscle ischemia and accumula-
tion of metabolites. These same stimuli do not appear to
influence changes in testosterone concentrations during
such exercise.
We would like to thank a dedicated group of subjects.
This study was supported by National Institute of Health Grant
HL-44125-12.
9. IM, J., S. NIOKA B. CHANCE, and K. W. RUNDELL. Muscle oxygen
desaturation is related to whole body VO2 during cross-country ski
skating. Int. J. Sports Med. 22:356 360, 2001.
10. KARLSSON, J., A. ERIKSSON, A. FORSBERGH, L. KALLBERGH, and P. A.
TESCH. The Physiology of Alpine Skiing. Park City, UT: U. S. Ski
Coaches Association Press, 1978, pp. 18 30.
11. KoRNER, L., P. PARKER, C. ALSTROM, et al. Relation of intramus-
cular pressure to the force output and myoelectrical signal of
skeletal muscle. J. Orthop. Res. 2:289 296, 1984.
12. KRAEMER, W. J., A. C. FRY, B. J. WARREN, et al. Acute hormonal
responses in elite junior weightlifters. Int. J. Sports Med. 13:103
109, 1992.
13. KRAEMER, W. J., S. E. GORDON, S. J. FLECK, et al. Endogenous
anabolic hormonal and growth factor responses to heavy resis-
tance exercise in male and females. Int. J. Sports Med. 12:228 35,
1991.
14. KRAEMER, W. J., L. MARCHITELLI, S. GORDON, et al. Hormonal and
growth factor responses to heavy resistance exercise protocols.
J. Appl. Physiol. 69:144250, 1990.
15. LIN, Y., G. LECH, S. NIOKA, X. INTES, and B. CHANCE. Noninvasive,
low noise, fast imaging of blood volume and deoxygenation
changes in muscles using light-emitting diode continuous wave
image. Rev. Sci. Inst. 73:30653074, 2002.
16. MACDOUGALL, J. D. Morphological changes in skeletal muscle
following strength training and immobilization. In: Human Muscle
Power, N. L. Jones, N. McCartney, and A. J. McComas (Eds.).
Champaign, IL: Human Kinetics, 1986, pp. 269 284.
Medicine & Science in Sports & Exercise 1933
17. MACKIE, B. G., and R. L. TERJUNG. Blood flow to different skeletal
muscle fiber types during contraction. Am. J. Physiol. 245:H265
H275, 1983.
18. MAEHARA, K., M. RILEY, P. GALASSETTI, T. J. BARSTOW, and K.
WASSERMAN. Effect of hypoxia and carbon monoxide on muscle
oxygenation during exercise. Am. J. Respir. Crit. Care Med.
155:229 235, 1997.
19. MANCINI, D. M., L. BOLINGER, H. LI, K. KENDRICK, B. CHANCE, and
J. R. WILSON. Validation of near infrared spectroscopy in humans.
J. Appl. Physiol. 77:2740 2747, 1994.
20. MCGILLIVRAY-ANDERSON, K. M., and J. E. FABER. Effect of acidosis
on contraction of microvascular smooth muscle by alpha 1- and
alpha 2-adrenoceptors: implications for neural and metabolic reg-
ulation. Circ. Res. 66:16431657, 1990.
21. NIOKA, S., D. MOSER, G. LECH, et al. Muscle deoxygenation in
aerobic and anaerobic exercise. In: Oxygen Transport to Tissue,
Vol. XX, A. G. Hudetz and D. F. Bruley (Eds.). New York:
Plenum Press, 1998, pp. 6370.
22. PEREZ-GONZALEZ, J. F. Factors determining the blood pressure
responses to isometric exercise. Circ. Res. 48(Suppl. I):I87I92,
1981.
23. ROWELL, L. B. Circulation. Med. Sci Sports 1:1522, 1969.
1934 Official Journal of the American College of Sports Medicine
View publication stats
24. RUNDELL, K. W., S. NIOKA, and B. CHANCE. Hemoglobin/myoglo-
bin desaturation during speed skating. Med. Sci. Sports Exerc.
29:248 258, 1997.
25. SALTIN, B., G. RADEGRAN, M. D. KOSKOLOU, and R. C. ROACH.
Skeletal muscle blood flow in humans and its regulation during
exercise. Acta Physiol. Scand. 162:421 436, 1998.
26. SZMEDRA, L., J. IM, S. NIOKA, B. CHANCE, and K. W. RUNDELL.
Hemoglobin/myoglobin oxygen desaturation during alpine skiing.
Med. Sci. Sports Exerc. 33:232236, 2001.
27. TAKARADA, Y., Y. NAKAMURA, S. ARUGA, T. ONDA, S. MIYAZAKI,
and N. ISHII. Rapid increase in plasma growth hormone after
low-intensity resistance exercise with vascular occlusion. J. Appl.
Physiol. 88:61 65, 2000.
28. TAMAKI, T., S. UCHIYAMA, T. TAMURA, and S. NAKANO. Changes in
muscle oxygenation during weight-lifting exercise. Eur. J. Appl.
Physiol. 68:465 469, 1994.
29. VICTOR, R. G., and D. R. SEALS. Reflex stimulation of sympathetic
outflow during rhythmic exercise in humans. Am. J. Physiol.
257:H2017H2024, 1989.
30. VIRU, M., E. JANSSON, A. VIRU, and C. J. SUNDBERG. Effect of
restricted blood flow on exercise-induced hormone changes in
men. Eur. J. Appl. Physiol. 77:517522, 1998.
http://www.acsm-msse.org