L'entraînement lourd est plus efficace que le léger

[Nutrimuscle-Conseils]

Changes in muscle size and MHC composition in response to resistance
exercise with heavy and light loading intensity


Muscle mass accretion is accomplished by heavy-load resistance
training. The effect of light-load resistance exercise has been far more
sparsely investigated with regard to potential effect on muscle size
and contractile strength. We applied a resistance exercise protocol in
which the same individual trained one leg at 70% of one-repetition
maximum (1RM) (heavy load, HL) while training the other leg at
15.5% 1RM (light load, LL). Eleven sedentary men (age 25
1 yr)
trained for 12 wk at three times/week. Before and after the intervention
muscle hypertrophy was determined by magnetic resonance
imaging, muscle biopsies were obtained bilaterally from vastus lateralis
for determination of myosin heavy chain (MHC) composition,
and maximal muscle strength was assessed by 1RM testing and in an
isokinetic dynamometer at 60°/s. Quadriceps muscle cross-sectional
area increased (P  0.05) 8
1% and 3
1% in HL and LL legs,
respectively, with a greater gain in HL than LL (P  0.05). Likewise,
1RM strength increased (P  0.001) in both legs (HL: 36
5%, LL:
19
2%), albeit more so with HL (P  0.01). Isokinetic 60°/s muscle
strength improved by 13
5% (P  0.05) in HL but remained
unchanged in LL (4
5%, not significant). Finally, MHC IIX protein
expression was decreased with HL but not LL, despite identical total
workload in HL and LL. Our main finding was that LL resistance training
was sufficient to induce a small but significant muscle hypertrophy in
healthy young men. However, LL resistance training was inferior to HL
training in evoking adaptive changes in muscle size and contractile
strength and was insufficient to induce changes in MHC composition.
unilateral training; resistance training; muscle hypertrophy; muscle
morphology
PRESCRIPTIONS OF HEAVY RESISTANCE training for muscle restoration
purposes have increased over the last decades. Heavy-load
resistance training is undoubtedly the most superior way to train
when muscle mass and strength improvements are aimed for (13,
15, 21, 39). Heavy resistance training potentially evokes altered
muscle architecture [pennation angle (1, 37) and myosin heavy
chain (MHC) transitions (47)], selective type II muscle fiber
hypertrophy (1), and increased efferent neural drive to the muscle
fibers (6), thereby improving muscle quality (i.e., relative change
in muscle mass is less than the concomitant gain in muscle
strength) (1, 33, 35, 72). However, various patient groups, frail
elderly people, and others for whom muscle mass maintenance or
improvement is of crucial importance may not tolerate the optimal
heavy loading training prescriptions. Sparse knowledge, however,
exists on the impact of lighter exercise intensities on muscle mass
and function and is further confused by conflicting and inconclusive
results (16, 20, 34, 57–59, 61). The significant but diminished
effect of medium-load resistance exercise to improve muscle mass
is supported by findings after electrical muscle stimulation (12,
55). However, the reported nonsignificant effect of low-intensity
training may be due to restricted time and insufficient total loading
volume (20, 34, 61), which may possibly also have compromised
the detection of similar adaptations after heavier and more frequent
training interventions (14, 17). Only a very few previous
studies have controlled for differences in total training volume
when comparing the physiological effects of light- and heavy-load
training regimes (5), and to our best knowledge none has done so
when intending to examine the change in muscle mass evoked by
these contrasting training intensities. Hence, currently there is a
lack of reliable and valid knowledge of the impact of muscle
contraction intensity in the lower range of the load continuum on
the hypertrophic response. Acknowledging the superiority of
heavy loading to improve muscle mass and function, we hypothesized
that intense light-load resistance training is sufficient to
accrete skeletal muscle mass and that stronger muscles would
follow because of that (24, 28, 69). To evaluate the relative
potential of the low intensity, a design with the purpose of
comparison with a classic heavy loading protocol was made.
Except for contraction intensity, training volume is of significant
importance when muscle hypertrophy is aimed at (21, 67). Therefore,
we carefully controlled training volume.
The aim of the present study therefore was to compare the
adaptive changes in muscle size, contractile strength, and MHC
composition evoked by resistance training performed at either
low or high contraction intensity while equalized for total
loading volume. Our working hypothesis was that over a
12-wk intervention period, the duration of a general rehabilitation
course, a significant effect on muscle size and function
could be detected in response to an intensive, supervised
training protocol using low external loading.
METHODS
Healthy, young sedentary men were recruited through newspaper
and web advertisements. Twelve men were included in the study after
Address for reprint requests and other correspondence: L. Holm, Inst. of
Sports Medicine, Bispebjerg Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen
NV, Denmark (e-mail: l.holm.isotope@gmail.com).
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
J Appl Physiol 105: 1454–1461, 2008.
First published September 11, 2008; doi:10.1152/japplphysiol.90538.2008.
1454 8750-7587/08 $8.00 Copyright © 2008 the American Physiological Society http://www. jap.org
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examination showed them to be healthy, with no need for daily
medication, and sedentary, defined as no organized participation in
any sports more than once a week. The subjects were informed about
the study protocol, the risks of tests and investigations, and their rights
according to the Declaration of Helsinki II, and the protocol was
approved by the local Ethical Committee of Copenhagen and Frederiksberg
(KF) 01-171/04. One subject was excluded from the study
because of low training compliance (not less than a mean of 2.5
training sessions per week was accepted).
Training protocol. Each subject was included in 36 training sessions
(12 wk with 3 sessions/wk). The exercise protocol consisted of
unilateral resistance training (isolated knee extensions; more details
are given below) as outlined in Fig. 1. Briefly, one leg worked against
a light load [LL: 15.5% of one repetition maximum (1RM)] while
performing 36 repetitions (one repetition every 5th s for 3 min) in
each set. The contralateral leg worked against a heavy load (HL: 70%
of 1RM), performing eight repetitions (25 s) in each set. By
randomization half of the subjects trained their dominant leg with HL
and the contralateral leg with LL, while training was reversed for the
other half of the subjects. The exercise consisted of isolated quadriceps
muscle contractions performed in a commercial knee extension
device (Technogym, Super Executive Line, Gambottola, Italy) with a
range of motion of 100° to 30° (0°  full knee extension). The subject
remained seated in the training device, alternately working each leg by
shifting the predefined loads in the device. A total of 10 sets were
conducted during every training session, lasting 35 min in total (see
Fig. 1). Notably, similar total contraction work (loads lifted 
gravitational internal work) was performed between HL and LL legs
in each training session, by progressively applying extra repetitions to
the LL leg as the HL leg improved strength faster and to a greater
extent than the LL leg. Immediately after each training session
subjects consumed a 100-ml nutrient drink (Komplet Na¨ring, Semper,
Novartis Healthcare, Copenhagen, Denmark) containing 120 kcal, 5 g
protein, 16 g carbohydrate, and 4 g fat plus added minerals and
vitamins. Furthermore, subjects were encouraged to eat a larger meal
as soon as possible.
Quadriceps muscle cross-sectional area. Magnetic resonance (MR)
imaging scans were conducted on a General Electric (GE) MR
scanner (Sigma Horizon 1.5 T, GE Healthcare) before and after the
training intervention, before any other test measurements were conducted,
and after intervention on the third day after the last training
session to avoid any effect of fluid disturbances directly related to
prior exercise. The protocol was similar to that used previously (29).
Briefly, subjects were left relaxed in the supine position for 20 min
before the scan was conducted with the legs fixed with Velcro straps.
Transaxial images at 10 (distal), 20 (middle), and 30 (proximal) cm
above the lateral tibia plateau were obtained. Scans were conducted by
professional and skilled radiographers, and the circumference of
muscles was manually drawn by skilled personnel blinded in respect
to training intensity, reaching an intraobserver coefficient of variation
(CV) of 0.6% with the MR scanner software (AGFA web1000).
Muscle biopsy. On a separate day after the MRI scan and after the
strength tests were carried out a muscle biopsy was obtained from the
lateral part of the vastus lateralis muscle from each leg with a 4-mm
Bergstro¨m needle (Stille, Stockholm, Sweden) with suction. Briefly,
the skin was shaved and disinfected before the local anesthetization
with lidocaine 1%. An incision hole was made through which the
muscle biopsy was taken. The incision was strapped with SteaStrips
and covered with waterproof plaster. The muscle specimen was
immediately mounted in Tissue-Tek, frozen in precooled isopentane,
and stored at 80°C until further analysis.
Myosin heavy chain analysis. The MHC analysis was performed on
the muscle tissue homogenate with sodium dodecyl sulfate-polyacrylamide
gel electrophoresis (SDS-PAGE) (8). From each biopsy 50–70
cross sections (20 m) were cut in a cryostat and placed in vials, and
100–200 l of lysing buffer pH 6.8 [0.5 M Tris pH 6.8, 10% SDS,
glycerol, mercaptoethanol, distilled H2O, and bromophenol blue (Bio-
Rad no. 161-0404)] was added and heated for 3 min at 90°C (22).
Between 5 and 20 l of the myosin-containing samples were loaded
on 6% polyacrylamide and 30% glycerol SDS-PAGE gels. Gels were
run at 70 V for 42 h at 4°C. Subsequently, the gels were Coomassie
blue stained, and MHC isoform content was determined with a densitometry
system (Cream 1D, KemEnTec Aps, Copenhagen, Denmark).
With SDS-PAGE, three different MHC bands can be separated in
adult human skeletal muscle. These bands correspond to MHC isoforms
I, IIA, and IIX (38).
Before all testing, subjects were familiarized with the strength tests
on a separate day. After a brief warm-up on a Monark cycle ergometer
and at submaximal load in the knee extension equipment, subjects
were fastened to the seat with straps around the hips and thigh. During
1RM they were allowed to grip the seat with their hands. Subjects
were instructed to conduct two unilateral repetitions with the load
applied to the lever arm. When a subject was capable of one but not
two knee extensions the load was noted, given the 1RM strength.
When subjects met for the 10th, 20th, and 30th training sessions they
conducted a 1RM strength test as described above.
Maximal dynamic (concentric and eccentric) quadriceps contraction
strength was measured with an isokinetic dynamometer (model
500-11, Kinetic Communicator, Chattecx, Chattanooga, TN) at a knee
joint angular velocity of 60°/s and range of motion of 90° to 10°
(0°  full knee extension) (5, 29). In addition, maximal isometric
muscle strength was assessed at 70° knee angle (2, 55). On a separate
day before the pretest, the procedures were thoroughly explained and
the subjects were familiarized with the dynamometer and the test
program. After the training period the tests for isolated quadriceps
strength were conducted on the third day after the final training
session, just after completion of the MR scan.
After a brief warm-up, the subject was placed in the KinCom
dynamometer chair with the hips and thigh strapped to the seat (3, 29).
During testing the arms were folded across the chest and strong verbal
and visual encouragement was applied by the researcher. After five
submaximal attempts separated by sufficient rest periods, the maximal
attempts were completed until no increment in peak torque was
observed (maximally 6 attempts). Subsequently, isometric strength
tests were conducted after 3 min of relaxation. Three maximal
attempts were thereafter given by each subject. Online visual feedback
of the knee extensor torque produced was provided to the subjects on
a PC screen during all testing.
Blood samples. Blood samples for different analyses were drawn at
different trials. Therefore, the numbers of subjects enrolled for each
analysis differ. However, the conditions were the same irrespective of
the trial from which the blood for the different parameters were
collected. Subjects arrived at the lab by car in the overnight fasted
state. Three days before that meeting, the subjects were instructed to
refrain from strenuous exercise or physical work. After 4 h of supine
rest, a venous blood sample was collected, after which the exercise
protocol was conducted. At 5, 10, 25, 60, and 120 min after cessation
blood samples were drawn from the antecubital vein with a polyeth-
Fig. 1. Exercise protocol design. HL, heavy
load [70% one repetition maximum (1RM)];
LL, light load (15.5% 1RM).
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ylene catheter. Blood was prepared according to the prescriptions of
the respective analyses. All analyses were done as single determinations,
and the samples for each parameter from each subject were
analyzed in the same analytical sequence.
The following hormone analyses were performed at the Institute of
Sports Medicine, Copenhagen: plasma testosterone (testosterone
ELISA, DRG Instruments) with an intra-assay CV 5.6%, serum
growth hormone (GH) (GH immunoradiometric assay, Biocode-Hycel,
Liege, Belgium) with an intra-assay CV 5%, plasma adrenocorticotropic
hormone [ACTH; radioimmunoassay (RIA), EDTA-plasma,
Nichols Institute Diagnostics, San Clemente, CA] with an intra-assay
CV 10%, plasma glucagons (RIA kit, Linco Research, St. Charles,
MO) with an intra-assay CV 10%, and serum cortisol (Gammacoat
cortisol RIA kit, DiaSorin, Stillwater, MN), intrassay CV 10%.
Serum IGF-I, IGF-binding protein (IGFBP)-1, and IGFBP-3 analyses
were performed at Aarhus University Hospital. Serum IGF-I was
determined by a time-resolved immunofluorometric monoclonal assay
(TR-IFMA, Wallac Oy, Turku, Finland) after acid-ethanol extraction
as previously described (23) with an intraassay CV 5%. Serum
IGFBP-1 was determined by an in-house RIA performed as first
described by Westwood et al. (68) and later modified (42), with an
intra-assay CV 5%. Serum IGFBP-3 was measured by commercially
available immunoradiometric assay (BioSource Europe, Nivelles,
Belgium) with an intra-assay CV 5%.
Other measurements. The weighed food registration was conducted
before the training intervention was initiated. After thorough verbal
instruction, a diary for noting every food item and the amount ingested
was given and an electronic balance was offered for borrowing. On
three consecutive days subjects were instructed to record their daily
intake. Subjects handed in the filled-out diaries, and data were analyzed
with Dankost 3000 software (Dansk Catering Center, Herlev,
Denmark). Finally, before and after the training intervention subjects
were weighed in the morning (wearing only underwear) after an
overnight fast.
Statistical analysis. Absolute quadriceps muscle hypertrophy was
evaluated by a two-way ANOVA with repeated measures, and the
relative changes at each location were compared by paired t-tests.
1RM strength and dynamic and static knee extension strength were
compared by a two-way ANOVA with repeated measures, and the
relative change over the 12-wk period was determined by a paired
t-test. Blood concentrations of hormones were analyzed by a one-way
ANOVA with repeated measures, and the statistical results presented
in Table 3 refer to the outcome of the Holm-Sidak post hoc test
comparing the postexercise concentrations with the preexercise level.
The relative expression of MHC types I, IIA, and IIX in the LL- and
HL-trained legs were compared by a two-way ANOVA with repeated
measures. When significant changes were found by overall testing, a
Holm-Sidak post hoc test was performed to reveal individual differences.
Data are presented as means
SE, and the level of significance
was P  0.05. SigmaStat 3.5 (Systat Software, San Jose, CA) was
used for statistical calculations.
RESULTS
Eleven male (age 24.7
1.1 yr, height 183
2 cm)
weight-stable (pretraining body wt 79.7
4.0 kg, posttraining
body wt 79.7
4.0 kg) subjects completed 12 wk of training
with a mean training frequency of 2.87
0.04 times per week
(no one 2.65 times/wk). They consumed a diet consisting of
18.2
2.5 energy% protein, 55.8
2.4 energy% carbohydrate,
and 26.0
2.1 energy% fat.
Quadriceps cross-sectional area. The cross-sectional areas
(CSAs) of the quadriceps muscle at the three recording locations
(proximal, middle, and distal) are reported in Table 1.
The CSAs at all three locations and their average were similar
at inclusion in the HL- and LL-training legs. Both legs demonstrated
the least hypertrophy at the middle location, with
only HL reaching statistical significance (P  0.001). The
mean CSA of the quadriceps muscle (Fig. 2) improved significantly
in the HL- and LL-trained legs (Fig. 2A), although the
improvement was significantly larger (P  0.05) in the HL
(7.6
1.4%)- compared with the LL (2.6
0.8%)-trained leg
(Fig. 2B).
One repetition maximum strength. 1RM quadriceps strength
before training start and after 10, 20, and 30 exercise sessions
is illustrated in Fig. 3A. At inclusion the LL-trained leg was
slightly stronger than the HL leg. However, after 20 and 30
training sessions the HL-trained leg had improved force production
capacity more and demonstrated larger 1RM strength
than the LL-trained leg (Fig. 3A). However, after both LL and
HL training the strength improved significantly within every
10-session training interval. The overall relative improvement
was higher during the 30-session period for the HL-trained leg
(36
5%) compared with the LL-trained leg (19
2%) (P 
0.05, Fig. 3B).
Isolated dynamic (isokinetic) and isometric muscle strength.
Dynamic quadriceps muscle strength was determined as the
peak torque exerted within the range of motion during maximal
concentric and eccentric muscle contractions, respectively.
Concentric quadriceps contraction strength was equal at inclusion:
HL 218
12 N
m vs. LL 224
17 N
m [not significant
(NS)]. HL improved concentric strength by 13
5% to 244

14 N
m (P  0.05), whereas LL showed no change (postexercise
229
14 N
m; NS). Before training, maximal eccentric
muscle strength was slightly lower in the HL leg (278
15
N
m) than in the LL leg (306
20 N
m) (P  0.1). HL
showed increased (P  0.01) eccentric strength (329
22
N
m), corresponding to an increase of 18
4% (P  0.01). In
contrast, no changes were observed with LL (postexercise
319
21 N
m; NS). Maximal isometric quadriceps strength
was equal at inclusion and increased by 15
4% (P  0.01)
from 253
13 to 290
17 N
m (P  0.01) after HL training,
while remaining unaltered (6
4%) with LL (277
17 vs.
292
18 N
m; NS).
MHC composition. MHC composition in the vastus lateralis
muscle did not differ between HL and LL legs before the start
of the study (see Table 3). After training the proportion of
MHC IIX isoforms decreased from 7
2% to 3
1% (P 
Table 1. Quadriceps cross-sectional area
Heavy Load Light Load
Pre Post Pre Post
Proximal 7,302
371 7,852
371 7,384
379 7,619
354
Middle 7,917
296 8,412
320 8,038
305 8,121
309
Distal 3,957
190 4,355
195 4,045
157 4,203
173
Values (in mm2) are mean
SE of whole quadriceps muscle cross-sectional
area (CSA) at the proximal, middle, and distal locations along the thigh
corresponding to 30, 20, and 10 cm above the lateral tibia condyle. Values are
the mean of 3 individual measurements from a scan before (Pre) and after
(Post) 12 wk of training with either heavy-load 70% 1-repetition maximum
(1RM)
or light-load (15.5% 1RM) resistance exercise. A similar and highly
significant improvement in CSA was found at the distal and proximal locations
after light- and heavy-load resistance training, whereas only in the heavy
load-trained leg was the improvement significant at the middle location.
Furthermore, at the middle section the CSA was significantly (P  0.05) larger
in the heavy load-trained leg than the light load-trained leg after 12 wk of
training. No differences in CSA were apparent at inclusion.
1456 MUSCLE HYPERTROPHY IN RESPONSE TO LIGHT-LOAD TRAINING
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0.05) in the HL leg, whereas no change was observed in the LL
leg (6
1% vs. 6
1%). No changes appeared for either
MHC I or MHC IIA after any of the training intensities.
Blood concentrations. Circulating concentrations of testosterone,
GH, IGF-I, IGFBP-1, IGFBP-3, ACTH, glucagon, and
cortisol are presented in Table 2. No significant changes in
concentration in the early minutes (5–120 min) after a single
exercise session compared with preexercise concentration were
observed for testosterone, GH, ACTH, glucagon, cortisol, and
IGFBP-1 (Table 2). Only IGF-I and IGFBP-3 were elevated at
5 min (10% for each), and IGFBP-3 was elevated at 120 min
(7%) as well (Table 2).
DISCUSSION
To our best knowledge the present data are the first to
evaluate the adaptive change in muscle size, contractile
strength, and MHC isoform expression evoked by resistance
training using either low or high contraction intensity, matched
for total training volume. The main findings were that in
sufficiently nourished, healthy young men training for 12 wk at
a nonexhaustive light load intensity (15.5% of 1RM) was
sufficient to induce gains in muscle size and 1RM strength. It
should be noted, however, that these changes were significantly
smaller than those observed after heavy-load (70% of 1RM)
resistance training of similar duration and volume. Nevertheless,
the results suggest that in situations where heavy-load
resistance training is not applicable (e.g., in very early postoperative
rehabilitation or in severely ill patients), light-load
resistance training may be tolerable and will improve muscle
mass and result in concomitant functional benefits.
Training-induced changes in muscle size. Despite major
diversities in exercise type and training volume, it can be
concluded that when resistance training is conducted at a
training intensity heavier than 60% of 1RM muscular hypertrophy
is induced along with substantial gains in maximal
muscle contraction strength (1, 4, 21, 25, 39, 44, 49, 51, 52, 63,
67, 71). Gains in anatomic muscle CSA of 10–15% have been
reported with 10–14 wk of dynamic heavy-resistance training
(29, 43, 49). However, some diversity has been shown in the
relative improvements along the length of the muscle bulk
(45). In the present study we demonstrated a significant mean
increase in quadriceps muscle size of 2.6
0.8% (see Fig. 2)
after 12 wk of LL resistance training (15.5% 1RM). In comparison,
an almost threefold greater gain was observed with HL
training (7.6
1.4%, Fig. 2).
The hypertrophic response seen in the HL leg was slightly
lower than expected, despite the fact that both total volume and
loading intensity (% 1RM) were comparable to previously
reported heavy-load training protocols (e.g., Refs. 1, 29). We
suggest two possible explanations for this diminished increase.
First, a single exercise session did not induce marked changes
in the circulating levels of the major anabolic hormones (Table
2). Data support the concept that training involving only a
minor fraction of the total muscle mass, as in our protocol,
results in a very limited anabolic hormone response (26).
Similar hormonal responses are seen after light resistance (48)
or endurance (41) exercise. In direct contrast is the response
produced when a larger muscle mass is exercised and/or
Fig. 2. Quadriceps muscle cross-sectional area (Q-CSA). A: absolute Q-CSA
as a mean of proximal, middle, and distal measurements (depicted individually
in Table 1) before (Pre, open bars) and after (Post, checked bars) 12 wk of
training at either light (15.5% 1RM, white bars) or heavy (70% 1RM, gray
bars) contraction intensity. No difference was apparent between Q-CSA at
inclusion. #P  0.05 compared with corresponding Pre value. B: relative
change in mean Q-CSA after 12 wk of training at either light (15.5% 1RM) or
heavy (70% 1RM) contraction intensity. #P  0.05 difference between the
relative changes at the 2 contraction intensities. Data are means
SE.
Fig. 3. 1RM quadriceps muscle strength determined in the knee-extensor
device. A: absolute strength before training start (pretraining) and after 10, 20,
and 30 sessions of exercise training. Light, leg trained at 15.5% 1RM; heavy,
leg trained at 70% 1RM. #P  0.05 compared with the strength of the Pre
value. B: relative change in 1RM over the course of 12 wk of resistance
training with either light or heavy loads. #P  0.05 difference comparing the
relative change following light and heavy load training. Data are means
SE.
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more complex training exercises are employed (40). These
training modalities would produce a larger relative muscle
hypertrophy. Second, the local hypertrophic response in the
HL-trained leg was presumably attenuated by the combination
of a high training volume (80 repetitions at 70% 1RM)
in an unvaried monotonous protocol. Studies using lower
volume and different types of exercise (i.e., leg press, knee
extension, hack squat) have reported more substantial gains
in muscle size (1, 29).
Given that we did not observe any marked systemic endocrine
response, the hypertrophy of 2.5% observed after 12
wk of LL resistance training seems a reliable and valid estimate
of the magnitude of muscle size gain that can be expected to
occur in response to low-intensity resistance training (21, 34,
57). Furthermore, this finding is important because it demonstrates
that a marked and intensity-dependent muscle hypertrophy
can be obtained without any systemic anabolic endocrine
response. The observed 10% increase in circulating IGF-I
and IGFBP-3 presumably originated from a release from the
active myocytes, because they are known to increase expression
and production of the IGF-axis proteins acutely
after exercise (7, 46).
The present data are the first to demonstrate that LL (20%
1RM) resistance exercise training has the capability to induce
muscle hypertrophy (21). These findings are supported by
recent data from Drummond et al. (18), who reported that
low-intensity exercise induced a myogenic response similar to
blood flow-restricted light-load exercise, known to induce
muscle hypertrophy. We are aware of only one comparable
training study published by Takarada et al. (61), who, however,
found no hypertrophy in their control group completing knee
extension exercises for 8 wk with light-load intensity (10–20%
1RM) without vascular occlusion. However, their lack of
hypertrophy probably was due to markedly reduced training
volume and frequency (5 sets of 18 repetitions twice a week for
8 wk) compared with those of the present study (10 sets of 36
reps three times a week for 12 wk). In relation to the recent
focus on the effect of vascular occlusion during exercise on the
hypertrophy response to even light-load training (60–62), it
should be stated that our design allowed the muscle to relax
and be oxygenated between contractions.
However, recapping the present data, it turns out that
exercise volume seems inversely proportional to exercise
intensity when aiming for exercise-induced muscle mass
gains. Therefore, several studies have failed to show a
muscle-gaining effect of endurance training on skeletal
muscle size (16, 30, 56).
Training-induced changes in maximal muscle strength, effects
of cross-learning. The primary research question in the
present study was to address the importance of exercise muscle
contraction intensity for inducing changes in muscle size over
time. To reduce the biological variability the within-subject
experimental design was chosen. However, we are fully aware
of the disadvantages this protocol design creates with regard to
the strength measurements (i.e., cross-training). Even though
some controversy exists in the findings and interventions leading
to cross-training (19), we acknowledge that maximal and
submaximal heavy-load unilateral training induces neural adaptations,
which involve contralateral cross-training effects
(36, 66, 70).
Training strength (1RM) is presumably the strength parameter
most influenced by cross-training and neural effects in
general, which is shown by the paramount increases already
after 10 training sessions. The later improvements, however,
were smaller but remained significant after both training intensities.
We believe that the continuous 1RM strength improvements
caused not only a steady neural adaptation but, specifically
for the light-trained leg, a cross-training effect. Part of
the improvements we do ascribe to accretion of the contractile
apparatus, i.e., muscle size.
Unlike 1RM testing, the slow muscle strength performances
conducted in the isokinetic dynamometer tests are assumed not
to be affected by cross-learning (50) and hence represent a
more reliable estimate of the true training-induced change in
maximal contractile capacity. We found that the isometric and
slow-speed concentric strength improved as expected with
regard to the observed hypertrophy for the HL- as well as
Table 2. Circulating concentrations
Preexercise
Minutes After Exercise
5 10 25 60 120
Testosterone, g/l 4.4
0.4 4.9
1.0 4.8
1.0 4.4
0.9 4.4
0.7 4.5
0.2
GH, mIU/l 2.2
1.4 12.1
5.3 15.3
6.6 21.1
7.9 20.2
12.6 8.4
5.6
IGF-I, g/l 140
10 154
15* 144
13 144
13 137
13 140
13
IGFBP-1, g/l 37.0
3.9 33.8
2.9 31.6
3.0 32.2
2.9 30.0
2.4 36.4
3.3
IGFBP-3, g/l 3,220
80 3,520
90* 3,410
130 3,430
130 3,420
100 3,410
90*
ACTH, ng/l 22.0
2.6 22.6
2.3 21.2
1.6 20.2
2.4 17.6
2.6 23.4
3.3
Glucagon, ng/l 73.2
2.5 70.2
1.8 70.6
5.9 66.5
3.9 63.8
4.3
Cortisol, g/dl 10.3
1.7 9.9
1.6 9.5
2.3 9.0
1.1 9.0
1.3 9.0
0.7
Values are mean
SE of circulating levels of testosterone, growth hormone (GH), adrenocorticotropic hormone (ACTH), glucagon, and cortisol (n  6) and
of insulin-like growth factor (IGF)-I, IGF-binding protein (IGFBP)-1, and IGFBP-3 (n  12). *Significantly (P  0.05) different from the preexercise
concentration revealed by the Holm-Sidak post hoc test. No data exist on glucagon at 60 min after exercise for technical reasons.
Table 3. Myosin heavy chain isoform distribution
Heavy Load Light Load
Pre Post Pre Post
Type I 63
4 65
4 64
4 60
4
Type IIA 30
3 32
3 31
3 33
3
Type IIX 7
2 3
1* 6
1 6
1
Values are mean
SE of myosin heavy chain isoform distributions in
heavy-load trained (70% 1RM) and light-load trained (15.5% 1RM) vastus
lateralis before (Pre) and after (Post) the 12-wk training intervention. *P 
0.05 vs. Pre value.
1458 MUSCLE HYPERTROPHY IN RESPONSE TO LIGHT-LOAD TRAINING
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LL-trained legs. However, for the LL-trained leg, the day-today
variation and the dependence on noncontrollable confounders
for muscle strength measurements with the isokinetic
dynamometer assessment method (31, 32) may simply have
been larger than the actual strength improvement that would be
related to the lean hypertrophy. Therefore, the significant LL
training-induced muscle hypertrophy leading to a small increase
in functional strength (1RM) was too small to be
detected in the dynamometer tests.
Changes in maximal eccentric muscle strength with training
interventions have previously been demonstrated to rely
strongly on adaptation of neural mechanisms (3, 10). We
observed an increased eccentric strength only in the HL-trained
leg (see RESULTS), which therefore suggests that HL resistance
training affected the neuromuscular function leading to improved
strength, whereas LL exercise training did not. Furthermore,
no cross-learning effect whatsoever was seen for this
adaptive parameter. Also, we did not detect any increase in rate
of force development (data not shown), implying that the
neural adaptations revealed by any of the training modalities
were very limited.
Training-induced changes in MHC protein expression.
Heavy resistance training is known to induce a decrease in
MHC IIX protein expression (9, 11, 41, 54), which we verified
(Table 3) even when applying a protocol using a small muscle
group insufficient to exert a systemic endocrine response
(Table 2). Furthermore, endurance training is also potent to
downregulate MHC IIX protein expression (53) and fiber type
IIX presence (41). However, data suggest that the potential of
endurance training to decrease MHC IIX protein expression
and IIX fiber phenotype is lower compared with heavy resistance
training (11, 41, 47). We did not observe any changes in
MHC protein expression in the LL-trained leg (Table 3).
Because the total performed work was equal between the light
and heavy contraction intensities, our data directly demonstrate
that contraction intensity rather than performed work is a
significant determinant for decreasing MHC IIX protein expression.
The uneven ability of muscle contraction intensities to induce
changes in MHC IIX protein expression may potentially
have an implication for muscle contractility (11). It has been
hypothesized that high abundance of fiber type IIX improves
acute and short-lasting muscle contractility (8, 11). However,
other adaptations to heavy-load training, where fiber type IIX
seems to disappear, favor that regime for the most musclestrengthening
purposes, and the priority of enhancing fiber type
IIX may be advisable only after long-term adaptation to heavy
resistance training. Thus it is not recommended to refrain from
heavy resistance training if the purpose is more powerful and
stronger muscles. Therefore, we do not ascribe the differences
in MHC protein expression after the two contraction intensities
in the present study to exert any functional effect on muscle
contractility or to be a motive for choosing any intensity in
preference to another.
Conclusions. The within-subject design of the present study,
in which unilateral training was performed involving either
light-load or heavy-load exercise at equalized total work,
insufficient to exert a systemic endocrine response, provides
new direct knowledge on the lean effect of contraction intensity
on the long-term anabolic response in skeletal muscle.
Even in normally functioning, sedentary young men, the quadriceps
muscle that is loaded every day adapts to light-load
training when targeted directly. These data oppose the common
notion that light-load training only leads to adaptation in
muscles that are infrequently used and spared for load-bearing
functions (65). Therefore, the significance of the present findings
is that even very low contraction intensity (15% 1RM),
performed even as isolated resistance training, is sufficient to
induce muscle mass accretion in human skeletal muscle. The
responses, however, appear to be greatly attenuated relative to
those achieved by use of heavy-load (70% 1RM) resistance
exercise regimes. Regardless, the present data demonstrate that
low-intensity resistance exercise in the present settings provides
a consistent stimulus for muscle hypertrophy, which
suggests that this training modality and volume are fundamentally
different from other low-intensity types of training, i.e.,
high-volume endurance training that conversely may induce
muscle atrophy (27, 64).
ACKNOWLEDGMENTS
All the volunteer subjects are sincerely thanked. Without their great enthusiasm
and eagerness to participate and complete the training as prescribed,
these data would never have been generated. We express our gratitude to Joan
Hansen, Merete Møller, Kirsten Nyborg, Ann-Christina Ronnie´ Henriksen, and
Ann-Marie Sedstrøm, who helped us in collecting and analyzing data.
REFERENCES
1. Aagaard P, Andersen JL, Dyhre-Poulsen P, Leffers AM, Wagner A,
Magnusson SP, Halkjaer-Kristensen J, Simonsen EB. A mechanism for
increased contractile strength of human pennate muscle in response to
strength training: changes in muscle architecture. J Physiol 534: 613–623,
2001.
2. Aagaard P, Simonsen EB, Andersen JL, Magnusson P, Dyhre-Poulsen
P. Increased rate of force development and neural drive of human skeletal
muscle following resistance training. J Appl Physiol 93: 1318–1326, 2002.
3. Aagaard P, Simonsen EB, Andersen JL, Magnusson SP, Halkjaer-
Kristensen J, Dyhre-Poulsen P. Neural inhibition during maximal eccentric
and concentric quadriceps contraction: effects of resistance training.
J Appl Physiol 89: 2249–2257, 2000.
4. Aagaard P, Simonsen EB, Trolle M, Bangsbo J, Klausen K. Effects of
different strength training regimes on moment and power generation
during dynamic knee extensions. Eur J Appl Physiol Occup Physiol 69:
382–386, 1994.
5. Aagaard P, Simonsen EB, Trolle M, Bangsbo J, Klausen K. Specificity
of training velocity and training load on gains in isokinetic knee joint
strength. Acta Physiol Scand 156: 123–129, 1996.
6. Aagaard P, Thorstensson A. Neuromuscular aspects of exercise—adaptive
responses evoked by strength training. In: Textbook of Sports Medicine.
Basic Science and Clinical Aspects of Sports Injury and Physical
Activity, edited by Kjaer M, Krogsgaard M, Magnusson P, Engebretsen L,
Roos H, Takala T, Woo SL. Oxford, UK: Blackwell Science, 2003,
p. 70–106.
7. Adams GR, Haddad F. The relationships among IGF-1, DNA content,
and protein accumulation during skeletal muscle hypertrophy. J Appl
Physiol 81: 2509–2516, 1996.
8. Andersen JL, Aagaard P. Myosin heavy chain IIX overshoot in human
skeletal muscle. Muscle Nerve 23: 1095–1104, 2000.
9. Andersen JL, Klitgaard H, Saltin B. Myosin heavy chain isoforms in
single fibres from m. vastus lateralis of sprinters: influence of training.
Acta Physiol Scand 151: 135–142, 1994.
10. Andersen LL, Andersen JL, Magnusson SP, Aagaard P. Neuromuscular
adaptations to detraining following resistance training in previously
untrained subjects. Eur J Appl Physiol 93: 511–518, 2005.
11. Andersen LL, Andersen JL, Magnusson SP, Suetta C, Madsen JL,
Christensen LR, Aagaard P. Changes in the human muscle forcevelocity
relationship in response to resistance training and subsequent
detraining. J Appl Physiol 99: 87–94, 2005.
12. Arvidsson I, Arvidsson H, Eriksson E, Jansson E. Prevention of
quadriceps wasting after immobilization: an evaluation of the effect of
electrical stimulation. Orthopedics 9: 1519–1528, 1986.
MUSCLE HYPERTROPHY IN RESPONSE TO LIGHT-LOAD TRAINING 1459
J Appl Physiol • VOL 105 • NOVEMBER 2008 • www.jap.org
Downloaded from jap.physiology.org on December 19, 2008
13. Bird SP, Tarpenning KM, Marino FE. Designing resistance training
programmes to enhance muscular fitness: a review of the acute programme
variables. Sports Med 35: 841–851, 2005.
14. Brandenburg JP, Docherty D. The effects of accentuated eccentric
loading on strength, muscle hypertrophy, and neural adaptations in trained
individuals. J Strength Cond Res 16: 25–32, 2002.
15. Campos GE, Luecke TJ, Wendeln HK, Toma K, Hagerman FC,
Murray TF, Ragg KE, Ratamess NA, Kraemer WJ, Staron RS.
Muscular adaptations in response to three different resistance-training
regimens: specificity of repetition maximum training zones. Eur J Appl
Physiol 88: 50–60, 2002.
16. Carter SL, Rennie CD, Hamilton SJ, Tarnopolsky. Changes in skeletal
muscle in males and females following endurance training. Can J Physiol
Pharmacol 79: 386–392, 2001.
17. Cote C, Simoneau JA, Lagasse P, Boulay M, Thibault MC, Marcotte
M, Bouchard C. Isokinetic strength training protocols: do they induce
skeletal muscle fiber hypertrophy? Arch Phys Med Rehabil 69: 281–285,
1988.
18. Drummond MJ, Fujita S, Takashi A, Dreyer HC, Volpi E, Rasmussen
BB. Human muscle gene expression following resistance exercise and
blood flow restriction. Med Sci Sports Exerc 40: 691–698, 2008.
19. Enoka RM. Neural adaptations with chronic physical activity. J Biomech
30: 447–455, 1997.
20. Friedmann B, Kinscherf R, Borisch S, Richter G, Bartsch P, Billeter
R. Effects of low-resistance/high-repetition strength training in hypoxia on
muscle structure and gene expression. Pflu¨gers Arch 446: 742–751, 2003.
21. Fry AC. The role of resistance exercise intensity on muscle fibre adaptations.
Sports Med 34: 663–679, 2004.
22. Fry AC, Allemeier CA, Staron RS. Correlation between percentage fiber
type area and myosin heavy chain content in human skeletal muscle. Eur
J Appl Physiol Occup Physiol 68: 246–251, 1994.
23. Frystyk J, Dinesen B, Orskov H. Non-competitive time-resolved immunofluorometric
assays for determination of human insulin-like growth
factor I and II. Growth Regul 5: 169–176, 1995.
24. Fukunaga T, Miyatani M, Tachi M, Kouzaki M, Kawakami Y,
Kanehisa H. Muscle volume is a major determinant of joint torque in
humans. Acta Physiol Scand 172: 249–255, 2001.
25. Hakkinen K, Alen M, Komi PV. Changes in isometric force- and
relaxation-time, electromyographic and muscle fibre characteristics of
human skeletal muscle during strength training and detraining. Acta
Physiol Scand 125: 573–585, 1985.
26. Hakkinen K, Pakarinen A, Newton RU, Kraemer WJ. Acute hormone
responses to heavy resistance lower and upper extremity exercise in young
versus old men. Eur J Appl Physiol Occup Physiol 77: 312–319, 1998.
27. Harber MP, Gallagher PM, Creer AR, Minchev KM, Trappe SW.
Single muscle fiber contractile properties during a competitive season in
male runners. Am J Physiol Regul Integr Comp Physiol 287: R1124–
R1131, 2004.
28. Harridge SD, Bottinelli R, Canepari M, Pellegrino MA, Reggiani C,
Esbjornsson M, Saltin B. Whole-muscle and single-fibre contractile
properties and myosin heavy chain isoforms in humans. Pflu¨gers Arch
432: 913–920, 1996.
29. Holm L, Esmarck B, Mizuno M, Hansen H, Suetta C, Holmich P,
Krogsgaard M, Kjaer M. The effect of protein and carbohydrate supplementation
on strength training outcome of rehabilitation in ACL patients.
J Orthop Res 24: 2114–2123, 2006.
30. Hoppeler H, Howald H, Conley K, Lindstedt SL, Claassen H, Vock P,
Weibel ER. Endurance training in humans: aerobic capacity and structure
of skeletal muscle. J Appl Physiol 59: 320–327, 1985.
31. Housh DJ, Housh TJ, Johnson GO, Chu WK. Hypertrophic response to
unilateral concentric isokinetic resistance training. J Appl Physiol 73:
65–70, 1992.
32. Housh TJ, Housh DJ, Weir JP, Weir LL. Effects of unilateral concentric-
only dynamic constant external resistance training. Int J Sports Med
17: 338–343, 1996.
33. Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB, Hoffman
EP, Angelopoulos TJ, Gordon PM, Moyna Nutrimuscle, Pescatello LS, Visich
PS, Zoeller RF, Seip RL, Clarkson PM. Variability in muscle size and
strength gain after unilateral resistance training. Med Sci Sports Exerc 37:
964–972, 2005.
34. Jackson CG, Dickinson AL, Ringel SP. Skeletal muscle fiber area
alterations in two opposing modes of resistance-exercise training in the
same individual. Eur J Appl Physiol Occup Physiol 61: 37–41, 1990.
35. Jones DA, Rutherford OM. Human muscle strength training: the effects
of three different regimens and the nature of the resultant changes.
J Physiol 391: 1–11, 1987.
36. Kannus P, Alosa D, Cook L, Johnson RJ, Renstrom P, Pope M,
Beynnon B, Yasuda K, Nichols C, Kaplan M. Effect of one-legged
exercise on the strength, power and endurance of the contralateral leg. A
randomized, controlled study using isometric and concentric isokinetic
training. Eur J Appl Physiol Occup Physiol 64: 117–126, 1992.
37. Kawakami Y, Abe T, Kuno SY, Fukunaga T. Training-induced changes
in muscle architecture and specific tension. Eur J Appl Physiol 72: 37–43,
1995.
38. Klitgaard H, Bergman O, Betto R, Salviati G, Schiaffino S, Clausen T,
Saltin B. Co-existence of myosin heavy chain I and IIa isoforms in human
skeletal muscle fibres with endurance training. Pflu¨gers Arch 416: 470–
472, 1990.
39. Kraemer WJ, Adams K, Cafarelli E, Dudley GA, Dooly C, Feigenbaum
MS, Fleck SJ, Franklin B, Fry AC, Hoffman JR, Newton RU,
Potteiger J, Stone MH, Ratamess NA, Triplett-McBride T. American
College of Sports Medicine position stand. Progression models in resistance
training for healthy adults. Med Sci Sports Exerc 34: 364–380, 2002.
40. Kraemer WJ, Hakkinen K, Newton RU, Nindl BC, Volek JS,
McCormick M, Gotshalk LA, Gordon SE, Fleck SJ, Campbell
WW, Putukian M, Evans WJ. Effects of heavy-resistance training on
hormonal response patterns in younger vs. older men. J Appl Physiol
87: 982–992, 1999.
41. Kraemer WJ, Patton JF, Gordon SE, Harman EA, Deschenes MR,
Reynolds K, Newton RU, Triplett NT, Dziados JE. Compatibility of
high-intensity strength and endurance training on hormonal and skeletal
muscle adaptations. J Appl Physiol 78: 976–989, 1995.
42. Krassas GE, Pontikides N, Kaltsas T, Dumas A, Frystyk J, Chen JW,
Flyvbjerg A. Free and total insulin-like growth factor (IGF)-I, -II, and
IGF binding protein-1, -2, and -3 serum levels in patients with active
thyroid eye disease. J Clin Endocrinol Metab 88: 132–135, 2003.
43. McCall GE, Byrnes WC, Dickinson A, Pattany PM, Fleck SJ. Muscle
fiber hypertrophy, hyperplasia, and capillary density in college men after
resistance training. J Appl Physiol 81: 2004–2012, 1996.
44. McDonagh MJ, Davies CT. Adaptive response of mammalian skeletal
muscle to exercise with high loads. Eur J Appl Physiol Occup Physiol 52:
139–155, 1984.
45. Narici MV, Hoppeler H, Kayser B, Landoni L, Claassen H, Gavardi
C, Conti M, Cerretelli P. Human quadriceps cross-sectional area, torque
and neural activation during 6 months strength training. Acta Physiol
Scand 157: 175–186, 1996.
46. Psilander N, Damsgaard R, Pilegaard H. Resistance exercise alters
MRF and IGF-I mRNA content in human skeletal muscle. J Appl Physiol
95: 1038–1044, 2003.
47. Putman CT, Xu X, Gillies E, MacLean IM, Bell GJ. Effects of strength,
endurance and combined training on myosin heavy chain content and
fibre-type distribution in humans. Eur J Appl Physiol 92: 376–384, 2004.
48. Reeves GV, Kraemer RR, Hollander DB, Clavier J, Thomas C,
Francois M, Castracane VD. Comparison of hormone responses following
light resistance exercise with partial vascular occlusion and moderately
difficult resistance exercise without occlusion. J Appl Physiol 101: 1616–
1622, 2006.
49. Ronnestad BR, Egeland W, Kvamme NH, Refsnes PE, Kadi F, Raastad
T. Dissimilar effects of one- and three-set strength training on strength and
muscle mass gains in upper and lower body in untrained subjects. J Strength
Cond Res 21: 157–163, 2007.
50. Rutherford OM, Jones DA. The role of learning and coordination in
strength training. Eur J Appl Physiol Occup Physiol 55: 100–105, 1986.
51. Seynnes OR, de Boer M, Narici MV. Early skeletal muscle hypertrophy
and architectural changes in response to high-intensity resistance training.
J Appl Physiol 102: 368–373, 2007.
52. Shepstone TN, Tang JE, Dallaire S, Schuenke MD, Staron RS, Phillips
SM. Short-term high- vs. low-velocity isokinetic lengthening training
results in greater hypertrophy of the elbow flexors in young men. J Appl
Physiol 98: 1768–1776, 2005.
53. Short KR, Vittone JL, Bigelow ML, Proctor DN, Coenen-Schimke
JM, Rys P, Nair KS. Changes in myosin heavy chain mRNA and protein
expression in human skeletal muscle with age and endurance exercise
training. J Appl Physiol 99: 95–102, 2005.
54. Staron RS, Karapondo DL, Kraemer WJ, Fry AC, Gordon SE, Falkel
JE, Hagerman FC, Hikida RS. Skeletal muscle adaptations during early
1460 MUSCLE HYPERTROPHY IN RESPONSE TO LIGHT-LOAD TRAINING
J Appl Physiol • VOL 105 • NOVEMBER 2008 • www.jap.org
Downloaded from jap.physiology.org on December 19, 2008
phase of heavy-resistance training in men and women. J Appl Physiol 76:
1247–1255, 1994.
55. Suetta C, Magnusson SP, Rosted A, Aagaard P, Jakobsen AK, Larsen
LH, Duus B, Kjaer M. Resistance training in the early postoperative
phase reduces hospitalization and leads to muscle hypertrophy in elderly
hip surgery patients—a controlled, randomized study. J Am Geriatr Soc
52: 2016–2022, 2004.
56. Suter E, Hoppeler H, Claassen H, Billeter R, Aebi U, Horber F, Jaeger
P, Marti B. Ultrastructural modification of human skeletal muscle tissue
with 6-month moderate-intensity exercise training. Int J Sports Med 16:
160–166, 1995.
57. Taaffe DR, Pruitt L, Pyka G, Guido D, Marcus R. Comparative effects of
high- and low-intensity resistance training on thigh muscle strength, fiber area,
and tissue composition in elderly women. Clin Physiol 16: 381–392, 1996.
58. Takarada Y, Ishii N. Effects of low-intensity resistance exercise with
short interset rest period on muscular function in middle-aged women. J
Strength Cond Res 16: 123–128, 2002.
59. Takarada Y, Sato Y, Ishii N. Effects of resistance exercise combined
with vascular occlusion on muscle function in athletes. Eur J Appl Physiol
86: 308–314, 2002.
60. Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N.
Effects of resistance exercise combined with moderate vascular occlusion
on muscular function in humans. J Appl Physiol 88: 2097–2106, 2000.
61. Takarada Y, Tsuruta T, Ishii N. Cooperative effects of exercise and
occlusive stimuli on muscular function in low-intensity resistance exercise
with moderate vascular occlusion. Jpn J Physiol 54: 585–592, 2004.
62. Tanimoto M, Ishii N. Effects of low-intensity resistance exercise with
slow movement and tonic force generation on muscular function in young
men. J Appl Physiol 100: 1150–1157, 2006.
63. Tesch PA, Ekberg A, Lindquist DM, Trieschmann JT. Muscle hypertrophy
following 5-week resistance training using a non-gravity-dependent
exercise system. Acta Physiol Scand 180: 89–98, 2004.
64. Trappe S, Harber M, Creer A, Gallagher P, Slivka D, Minchev K,
Whitsett D. Single muscle fiber adaptations with marathon training.
J Appl Physiol 101: 721–727, 2006.
65. Turner DL, Hoppeler H, Claassen H, Vock P, Kayser B, Schena F,
Ferretti G. Effects of endurance training on oxidative capacity and
structural composition of human arm and leg muscles. Acta Physiol Scand
161: 459–464, 1997.
66. Weir JP, Housh TJ, Weir LL, Johnson GO. Effects of unilateral
isometric strength training on joint angle specificity and cross-training.
Eur J Appl Physiol Occup Physiol 70: 337–343, 1995.
67. Wernbom M, Augustsson J, Thomee R. The influence of frequency,
intensity, volume and mode of strength training on whole muscle crosssectional
area in humans. Sports Med 37: 225–264, 2007.
68. Westwood M, Gibson JM, Davies AJ, Young RJ, White A.
The phosphorylation pattern of insulin-like growth factor-binding protein-
1 in normal plasma is different from that in amniotic fluid and
changes during pregnancy. J Clin Endocrinol Metab 79: 1735–1741,
1994.
69. Widrick JJ, Stelzer JE, Shoepe TC, Garner DP. Functional properties
of human muscle fibers after short-term resistance exercise training. Am J
Physiol Regul Integr Comp Physiol 283: R408–R416, 2002.
70. Wilkinson SB, Tarnopolsky MA, Grant EJ, Correia CE, Phillips SM.
Hypertrophy with unilateral resistance exercise occurs without increases in
endogenous anabolic hormone concentration. Eur J Appl Physiol 98:
546–555, 2006.
71. Willardson JM. The application of training to failure in periodized
multiple-set resistance exercise programs. J Strength Cond Res 21: 628–
631, 2007.
72. Young A, Stokes M, Round JM, Edwards RH. The effect of highresistance
training on the strength and cross-sectional area of the human
quadriceps. Eur J Clin Invest 13: 411–417, 1983.
MUSCLE HYPERTROPHY IN RESPONSE TO LIGHT-LOAD TRAINING 1461
J Appl Physiol • VOL 105 • NOVEMBER 2008 • www.jap.org
Downloaded from jap.physiology.org on December 19, 2008