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The Role of Fiber Types in Muscle Hypertrophy: Implications for Loading Strategies

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Abstract

EMERGING EVIDENCE SUGGESTS THAT TYPE I FIBERS DISPLAY A SUBSTANTIAL PROPENSITY FOR GROWTH IF THEY ARE SELECTIVELY TARGETED VIA LOW-LOAD TRAINING. THE PURPOSE OF THIS ARTICLE WILL BE TO REVIEW THE RESEARCH REGARDING FIBER TYPE-SPECIFIC HYPERTROPHY AND DRAW EVIDENCE-BASED CONCLUSIONS AS TO THEIR IMPLICATIONS FOR PROGRAM DESIGN. Copyright © National Strength and Conditioning Association.
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The Role of Fiber Types in
Muscle Hypertrophy:
Implications for Loading
Strategies
Dan Ogborn, MSc, CSCS and Brad J. Schoenfeld, MSc, CSCS, CSPS
2
AU1
2
Lehman CollegAU2 e, Bronx, New YorAU3 k
ABSTRACT
EMERGING EVIDENCE SUGGESTS
THAT TYPE I FIBERS DISPLAY A
SUBSTANTIAL PROPENSITY FOR
GROWTH IF THEY ARE SELEC-
TIVELY TARGETED VIA LOW-LOAD
TRAINING. THE PURPOSE OF THIS
ARTICLE WILL BE TO REVIEW THE
RESEARCH REGARDING FIBER
TYPE–SPECIFIC HYPERTROPHY
AND DRAW EVIDENCE-BASED
CONCLUSIONS AS TO THEIR
IMPLICATIONS FOR PROGRAM
DESIGN.
INTRODUCTION
Many individuals whAU5 oresistance
traindosowiththeprimary
goal of increasing muscular
size. Current theory suggests that
exercise-induced muscle hypertrophy is
regulated by a phenomenon called me-
chanotransduction, whereby mechanical
forces are converted into chemical signals
that mediate intracellular anabolic and
catabolic pathways, ultimately leading
to a shift in muscle protein balance that
favors synthesis over degradation (42).
The net effect is an accretion of myofi-
brillar contractile proteins that augments
the diameter of individual fibers and
thereby results in an increase in whole-
muscle cross-sectional area (CSA) (28).
Both endurance-oriented type I (slow
twitch) fibers and strength-oriented
type II (fast twitch) fibers have the abil-
ity to hypertrophy. However, research
shows that the growth capacity of fast-
twitch fibers is approximately 50%
greater than that of slow-twitch fibers
(3), although a high degree of interindi-
vidual variability is seen with respect to
the extent of hypertrophic adaptation
(20). Based on this information, it may
be assumed that recruitment of type II
fibers should be the main focus of exer-
cise program design for the accretion of
muscle mass, given the enhanced rate of
hypertrophy in these fibers as compared
with type I fibers.
Despite a logical rationale, emerging
evidence suggests that such an
approach may be simplistic and per-
haps misguided, at least if the goal is
to maximize muscle size. Therefore,
the purpose of this article will be to
review the research regarding fiber
type–specific hypertrophy and draw
evidence-based conclusions as to their
implications for program design.
HYPERTROPHY OF TYPE II FIBERS
WITH HIGH-INTENSITY STRENGTH
TRAINING
Type II muscle fibers have long dis-
played superior growth after high-
intensity strength training
(1,10,11,13,14,20,31,32). These experi-
mental results are often extrapolated to
represent a growth capacity exceeding
that of type I fibers; however, it is
important to note that these findings
are specific to the training intensities
at which the study is performed and
may not apply universally across the
repetition continuum. The superior
capacity for growth of this particular
fiber type may be more a consequence
of the models we study than an intrin-
sic property of the fiber itself. In sup-
port of this hypothesis, bodybuilders
display greater type I fiber hypertrophy
than powerlifters, presumably as a
result of routinely training with higher
repetition ranges (13).
Our previous understanding of the
relationship between training intensity
and the resultant fiber type–specific
hypertrophy is best summarized by
Fry’s (13) comprehensive review of
resistance training program variables.
Using a regression analysis to assess
the intensity-related percent change
in fiber growth across various studies,
it was determined that for the majority
of training intensities above 50% of 1
repetition maximum (1RM), type II
fiber growth exceeded that of the type
I fibers. In addition, the peak growth
rate of type I fibers was lower than for
type II, regardless of training intensity.
This work is limited by the fact that
research to date has been biased
KEY WORDS:
low-intensity exercise; slow-twitch
fibers; low-load training; strength-
endurance continuum
Copyright ÓNational Strength and Conditioning Association Strength and Conditioning Journal | www.nsca-scj.com 1
toward training intensities greater than
60% of 1RM, with a lack of lower-
intensity strength training studies in
the literature (13,38). Thus, the paucity
of low-intensity resistance training
research precludes equal weighting in
analysis, predisposing results toward
higher-intensity training. Furthermore,
regression merely shows the correla-
tion between 2 variables, in this case,
fiber type–specific hypertrophy and
training intensity; it does not imply
causation.
DIRECT COMPARISONS OF
TRAINING INTENSITIES AND FIBER
TYPE–SPECIFIC HYPERTROPHY
Strength training interventions using
intensities above 50% of 1RM abound
(38); however, direct comparisons,
including low-intensity training, that
address fiber type–specific hypertro-
phy are currently lacking, and those
that have been conducted are disparate
and contradictory in their findings.
Campos et al. (10) compared 3 differ-
ent repetition ranges against a seden-
tary control group and found that
groups who performed sets with either
a 3–5 RM or 9–11 RM load to failure
produced significant growth in both
fiber types as compared with training
with 20–28 RM, where the extent of
hypertrophy did not reach statistical
significance. In agreement, Schuenke
et al. (31) found that high-intensity
training (3 36–10 RM; ;80–85% of
1RM) to failure resulted in significant
growth of all fiber types as compared
with a lack of growth after lower-
intensity training (3 320–30 RM;
;40–60% of 1RM). Interestingly, train-
ing with low intensity at a slow speed
(10 seconds concentric and 4 seconds
eccentric) induced a greater hypertro-
phic response compared with training
with a comparable resistance at tradi-
tional speed, but adaptations were less
than that seen with high-intensity
loads.
Employing a quasi within-subject
design, Mitchell et al. (24) compared
training with 3 sets at 80% of 1RM
against one set at 80% of 1RM and
3 sets with 30% of 1RM over 10 weeks,
with all groups taking every set
to concentric failure. Whole-muscle
hypertrophy was equivalent among
all training groups at completion of
the study, and fiber type–specific hyper-
trophy indicated substantial hypertrophy
in all fiber types, with no significant dif-
ferences in fiber type–specific growth
indicated. It should be noted, however,
that the low-intensity condition resulted
in an ;23% increase in type I fiber area
compared with ;16% in the high-
intensity condition. Conversely, high-
intensity training resulted in an ;15%
increase in type II fiber area compared
with ;12% in the low-intensity condi-
tion. The study was likely underpow-
ered to detect significance, suggesting
that an increase type I fiber area sub-
stantially contributed to the hypertro-
phic effects of low-intensity training.
THE INFLUENCE OF TRAINING
INTENSITY ON WHOLE-MUSCLE
HYPERTROPHY
A number of studies have compared
whole-muscle hypertrophy in low-
intensity versus high-intensity training
protocols. Holm et al. (17) employed
a within-subject design, whereby sub-
jects performed 10 sets of unilateral leg
extensions, training one leg at 70% of
1RM and the contralateral leg at 15.5%
of 1RM in a randomized, counterbal-
anced fashion. After 12 weeks, magnetic
resonance imaging (MRI) showed an
approximately 3-fold greater increase
in quadriceps muscle CSA with
higher-intensity exercise compared
with low-intensity exercise. A limitation
of the study was that training at 15.5%
of 1RM was not carried out to concen-
tric muscular failure, which has been
shown to be necessary to maximize
a hypertrophic response in low-
intensity exercise (24).
Leger et al. (23) and Lamon et al. (22)
employed a similar protocol to that of
Campos et al. (10); neither study found
significant differences in muscle CSA
between low-intensity and high-
intensity groups. The discrepancy in
results between studies may be attrib-
utable to the fact that both Leger et al.
(23) and Lamon et al. (22) evaluated
middle-aged males, who conceivably
were detrained relative to the younger
males studied by Campos et al. (10).
Another important difference between
studies was the techniques used to
measure hypertrophy. Campos et al.
(10) employed muscle biopsies, whereas
Leger et al. (23) and Lamon et al. (22)
used computerized tomography (CT).
Because CT does not allow evaluation
of differential effects on fiber typing, it is
not clear whether differences in slow-
twitch versus fast-twitch fibers played
a role in explaining the discrepancies
in these findings. Moreover, noncon-
tractile increases in sarcoplasmic pro-
teins (i.e., mitochondria, fluid, etc.)
may have contributed to the results.
This is an important consideration as
mitochondrial protein synthesis is par-
ticularly sensitive to extended time
under tension (TUT) during strength
training and may increase dispropor-
tionately as TUT and total work are
higher with low-load training (8,9).
As such, it is important to consider
the possibility that even if whole-
muscle hypertrophy is equivalent in
response to various training intensities,
the increase in CSA may be mediated
by differing cellular adaptations (28),
and muscle strength and function
may vary accordingly. This is partially
supported by the observation that
strength is increased to a greater extent
with high-intensity training (10,31),
even when whole-muscle hypertrophy
is comparable (24), although adapta-
tions independent to muscle could also
explain such a response.
Recently, Ogasawara et al. (26) found
similar increases in CSA of the triceps
brachii and pectoralis major as deter-
mined by MRI in subjects performing
training at 75% of 1RM versus 30% of
1RM. The study employed a within-
subject design, whereby participants
performed the higher-intensity exer-
cise for 12 weeks initially and, after
a 12-month washout period of detrain-
ing, performed 12 weeks of the low-
intensity exercise in a nonrandomized
fashion. Although intriguing, these
findings must be viewed with caution
as “muscle memory” via both neural
mechanisms and satellite accretion
may have influenced the results (7,32).
Type I Fiber Hypertrophy
VOLUME 0 | NUMBER 0 | MONTH 2013
2
INTERACTIONS OF LOAD AND
MOTOR UNIT RECRUITMENT
The premise behind high-intensity
training is rooted firmly in Henne-
man’s Size principle that states the
orderly recruitment of motor units dur-
ing a given task (15,16). This principle
dictates that motor units are recruited
based on their size: smaller, low-
threshold slow motor units are recruited
initially, followed by progressively
larger, higher-threshold motor units as
the force demands of the task increases.
Training with heavy loads requires sub-
stantial force production and therefore
calls upon both low- and high-threshold
motor units to maximize force. As
load (training intensity) decreases, the
required force production from the
muscle is reduced, and fewer motor
units are required to complete the lift.
Given that fibers must be recruited in to
respond and adapt to resistance exercise
(21), it seems logical to conclude that
training at very high levels of intensity is
required to maximize recruitment and
therefore muscular development.
However, this argument discounts the
role of fatigue in the stimulation of
hypertrophy and its ability to influence
motor unit recruitment. During low-
load contractions, initial motor unit
recruitment is lower than under high-
load conditions. However, as fatigue
increases, the recruitment threshold
of higher-threshold motor units is pro-
gressively reduced (2). Conceivably,
this results in the gradual recruitment
of higher threshold, presumably fast
motor units as fatigue increases. This
recruitment process provides a mecha-
nism, whereby low-intensity strength
training can activate fast-twitch motor
units and ultimately stimulate the
growth of these fibers.
The exact mechanisms, whereby
fatigue enhances high-threshold motor
unit recruitment, are not well under-
stood. It has been speculated that
results are mediated by metabolic
stress associated with exercise relying
primarily on the fast glycolytic energy
system (29). The accumulation of
hydrogen ions, increased muscle hyp-
oxia, and free radical generation all
have been implicated as playing a role
in the process (29). Regardless of the
mechanism, the fatigue-induced activa-
tion of F AU6
T fibers is believed to be an
attempt to maintain necessary levels of
force generation so that work output is
maintained (2).
Although intuitively it would seem that
a given threshold of intensity is required
to achieve recruitment of the full spec-
trum of fibers, studies to date have
failed to establish a specific percentage
of RM at which this occurs. Surface
electromyography (EMG), which pro-
vides a global measure of motor unit
activity of a given muscle, has been
used to provide an indirect measure of
motor unit recruitment during resis-
tance exercise. Cook et al. (12) recently
demonstrated that EMG amplitude of
the quadriceps femoris during knee
extension exercise to failure was signif-
icantly greater at a high intensity (70%
of 1RM) than at low intensity (20% of
1RM). This suggests that the threshold
for optimal motor unit recruitment
exceeds 20% of 1RM. In contrast,
Wernbom et al. (39) reported that peak
EMG activity was similar among 3 sets
of low-intensity (30% of 1RM) unilateral
knee extensions. In attempting to justify
the discrepancies between the studies of
Cook et al. (12) and Wernbom et al.
(39), one could infer that 30% of 1RM
represents a lower threshold for type II
recruitment. However, Suga et al. (33)
found that fiber recruitment during
blood flow–restricted training at 30%
of 1RM did not reach levels achieved
with traditional high-intensity resis-
tance exercise, as determined by
inorganic phosphate splitting via
31
P-magnetic resonance spectroscopy.
Only when blood flow–restricted
exercise was carried out at an intensity
of 40% of 1RM did P
i
peaks equate
to those associated with the high-
intensity training. Given the conflict-
ing results, it is difficult to draw any firm
conclusions as to a minimum intensity
threshold for recruiting the full spec-
trum of muscle fibers, although evi-
dence indicates that intensity below
30% of 1RM is suboptimal for inducing
substantial recruitmentofhigh-threshold
motor units.
UNDERSTANDING THE
RELATIONSHIP BETWEEN LOAD
AND TIME UNDER TENSION
The hypothesis that we have underes-
timated both the growth potential of
type I fibers and the ability of low-
intensity training to stimulate hyper-
trophy relies on 2 basic premises: (a)
that hypertrophy requires a minimum
TUT that varies with training intensity
and (b) that this TUT is greater for
type I than type II fibers. To address
this relationship, Burd et al. (9) com-
pared the protein synthetic response
after 4 sets at 3 training intensity con-
ditions: 90% of 1RM lifted to failure,
30% of 1RM to failure, and 30% of
1RM lifted such that the total work
was matched to the 90% of 1RM con-
dition. The protein synthetic response,
although of differing time course, was
similar when either 90% of 1RM or
30% of 1RM was lifted to concentric
failure; however, the low-load work-
matched condition did not stimulate
mixed, myofibrillar, and sarcoplasmic
protein synthesis to a similar extent
as the other conditions. Although the
protein synthetic response to an acute
bout of resistance exercise is not nec-
essarily indicative of long-term hyper-
trophic adaptations (3), there is some
evidence, albeit conflicting, that low-
intensity exercise can produce compa-
rable hypertrophy with higher-intensity
exercise provided sets are taken to fail-
ure (24,26).
Methodology may at least partially
explain the divergent findings regard-
ing the effects of training intensity on
fiber type–specific and whole-muscle
hypertrophy. The studies that do not
equate total intrasession work tend to
show similar growth between high-
and low-intensity exercises (24,26),
with the exception of Schuenke et al.
(31) who displayed greater hypertro-
phy when training at a high intensity.
Conversely, studies that do equate
work show a hypertrophic advantage
for high-intensity exercise (10,17). It is
also important to consider the contri-
bution of muscular failure to these
Strength and Conditioning Journal | www.nsca-scj.com 3
experimental findings. Whereas the
majority of studies identify concentric
failure as the end point for the set
(10,24,31), Holm et al. (17) did not,
and only the low-intensity condition
trained to failure in Ogasawara et al.
(26). Although fatigue may contribute
to the hypertrophic response (29,30), it
is currently unknown how the relation-
ship between training intensity and
hypertrophy compare when exercise
is fatiguing but terminated before the
point of concentric failure.
Nevertheless, given that low-intensity
resistance exercise seems to preferen-
tially increase hypertrophy of type I
fibers (24), it is logical to conclude that
an increased TUT is necessary to fully
stimulate these fibers. This would be
consistent with the endurance-oriented
nature of slow-twitch fibers that renders
them resistant to fatigue.
DO TYPE I FIBERS HAVE A LIMITED
GROWTH CAPACITY?
It remains questionable as to whether
type I fibers have the ultimate hyper-
trophic potential of type II fibers.
There is evidence that they do not.
Studies evaluating the relationship
between CSA and mitochondrial den-
sity suggest that the growth of a given
muscle fiber is achieved at the expense
of its endurance capacity (36). This
implies that the smaller size of highly
oxidative slow-twitch fibers is an evo-
lutionary design constraint, limiting
their inherent ability to hypertrophy
in comparison with fast-twitch fibers
with a low oxidative capacity (36).
One way that type I fiber hypertrophy
may be self-limiting is via competition
between anabolic and catabolic intra-
cellular signaling pathways. Expression
of muscle ring finger and muscle atro-
phy F-box—ubiquitin ligases that mediate
protein degradation—is approximately
2-fold higher in oxidative versus nonox-
idative fibers (36). Moreover, there is evi-
dence that type I fibers have a reduced
ability to increase phosphorylation of
ribosomal protein kinase S6 (p70S6K)
after resistance exercise compared with
type II fibers, which in turn blunts their
protein translational capacity (19).
p70S6K is a downstream effector in
the mTOR pathway, and its activation
via mechanical stimuli has been deemed
critical to the hypertrophic response
(41). These events are consistent with
the “AMPK-PK AU7
B switch” hypothesis,
whereby signaling is switched to either
a catabolic AMPK/PGC-1a–oran
anabolic PKB-TSC2-mTOR–dominated
state depending on whether the imposed
demand is endurance or resistance based
(5). Although signaling interactions are
unquestionably more complex than
asimpleswitchmechanism, especially
given the stimulation of AMPK with tra-
ditional resistance exercise (19), research
does suggest that the endurance-
oriented nature of type I fibers provides
a greater inclination to turnover rates
that favor proteins involved in metabo-
lism (i.e., mitochondrial proteins) over
structural muscle protein (i.e., myofibril-
lar proteins) (36).
Another potential limiting factor in
type I growth is their ability to increase
satellite cell proliferation. Satellite cells
are muscle stem cells that reside
between the basal lamina and the sar-
colemma, which remain dormant in
the resting state. When stimulated by
mechanical stress, however, satellite
cells generate precursor cells (myo-
blasts) that proliferate and ultimately
fuse to existing cells, providing the
necessary agents for remodeling of
muscle tissue (35,40). In addition, sat-
ellite cells are able to donate their
nuclei to the existing muscle fibers,
enhancing their capacity for protein
synthesis (6,25). In young, untrained
subjects, satellite cell number is approx-
imately equal between slow- and fast-
twitch fiber types (18). However, there
is evidence tha AU8
tmixedmodesofexer-
cise training, even of an endurance-
oriented nature, results in a greater
increase of the satellite cell pool in
type II fibers (37), indicating a greater
long-term growth potential for these
fiber types. The heightened exercise-
induced expression of the protein
MyoD in type II fibers (4), which is pre-
dominantly responsible for upregulating
satellite proliferation and thus facilitates
the formation of new myoblasts, could
be a potential mechanism to explain
their enhanced satellite cell response.
This suggests that over time, fast-
twitch fibers may have a favorable pre-
disposition to growth because of an
enhanced capacity to synthesize new
contractile proteins.
Considering the aforementioned fac-
tors, evidence suggests that although
type I fibers possess significant growth
potential, they may have a lower ceil-
ing for hypertrophy in comparison
with type II fibers. Unfortunately, no
study to date has directly examined
this hypothesis. Furthermore, as the
study documenting enhanced phos-
phorylation of p70S6K only relied on
higher training intensities, it remains to
be determined whether low-intensity
strength training can augment protein
synthetic signaling pathways (24) in
type I fibers specifically to a greater
extent than high-intensity training in
type II fibers (19). This topic should
be explored in future research.
PRACTICAL APPLICATIONS
Based on the current body of research,
there is emerging evidence indicating
that type I fibers can substantially
contribute to overall muscle CSA.
Research also suggests that low-load
resistance exercise may help to maxi-
mize type I fiber hypertrophy, pro-
vided that training is carried out to
concentric muscular failure (24). From
a practical perspective, the following
recommendations can be made.
If one’s goal is simply to maximize
overall muscle mass, exercise prescrip-
tions should include training across
a wide spectrum of repetition ranges.
Higher-intensity exercise seems neces-
sary to fully stimulate fast-twitch fiber
growth (13), whereas lower-intensity
exercise preferentially enhances hyper-
trophy in slow-twitch fibers (24). A
periodized approach combining high-
and low-intensity training may help
ensure an optimal hypertrophic response
in the full continuum of fiber types. Both
linear and nonlinear models are viable
approaches here, as neither has been
showntobesuperiortotheotherinthis
regard. Thus, intensities can be varied
Type I Fiber Hypertrophy
VOLUME 0 | NUMBER 0 | MONTH 2013
4
within and/or across multiple training
sessions or by alternating target repeti-
tion zones every few microcycles. Train-
ing loads can easily be manipulated
based on the characteristics of the exer-
cises within a training session, favoring
high-load training on multi-joint exer-
cises like the squat and deadlift, saving
higher repetition ranges for single-joint,
isolation type exercises that may be bet-
ter suited to lighter training loads.
Although training percentages or
repetition ranges can be varied in
a periodized manner, advanced train-
ing techniques may provide additional
hypertrophic benefit. Drop sets, where
training load is progressively decreased
on subsequent sets with little to no rest
once the point of fatigue or technical
failure is achieved at each training
load, may provide the best of both
worlds (27). Training load can be max-
imized initially to capitalize on type II
fiber activation; however, as fatigue sets
in, training loads can be progressively
decreased to increase the TUT to max-
imally stimulate the type I fibers. In
addition, rest-pause training, where a
set with a given training load is extended
beyond the point of fatigue by taking
small rests within the set, may provide
a similar benefit by increasing the dura-
tion of loading. Care must be taken
when using these techniques to balance
the need for increased muscle recruit-
ment and TUT to promote optimal
hypertrophy against the potential for ele-
vated levels of fatigue and overuse (27).
On the other hand, if hypertrophy
is a means to maximize strength,
then higher-intensity loads should be
favored over lighter loads, as gains in
strength are greater with high-load
training as compared with low-load
training (10) even when a comparable
hypertrophic response occurs (24). If
strength is to be maximized in specific
exercises, as in sports such as power-
lifting, higher-intensity training is
essential because of the specificity of
strength (13) and the fact that exercise
technique can differ across the training
intensity continuum (34). Fiber-type
specificity plays a role in this process.
Fast-twitch fibers are innervated by
larger motor neurons compared with
their slow-twitch counterparts, allowing
for enhanced high force production.
Because of the smaller size of the neu-
rons associated with type I fibers, they
simply cannot cycle fast enough to carry
out tasks involving high levels of force.
Hence, the major focus here should be
on high-load training (greater than
;75% of 1RM).
Conflicts of Interest and Source of Funding:
The authors report no conflicts of interest
and no source of fundin AU4g.
Dan Ogborn is
currently com-
pleting a postdoc-
toral fellowship
and physiother-
apy degree at
McMaster
University.
Brad
Schoenfeld is
a lecturer in exer-
cise science at
CUNY AU9Lehman
College and is
director of their
human perfor-
mance laborator AU10y.
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Type I Fiber Hypertrophy
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... Furthermore, UBPT-induced adaptations may lead to improved kinetic characteristics during throwing such as increased force, power, and rate of force development [88]. In addition, the increase in maximal strength (Fig. 2) and MBT performance (Fig. 3) discussed in previous sections may also contribute to sport-specific throwing performance [138]. For instance, a significant association between upper-body maximal strength and ball throwing velocity (r = 0.64-0.69) ...
... The physiological basis of such an increment of muscle volume may be attributed to specific muscle fibre recruitment during the plyometric exercises [144]. UBPT is characterized by short duration high-velocity movement that activates the motor units associated with fast-twitch muscle fibres [144] which are suggested to have greater potential for hypertrophy [138,145]. However, such speculations about hypertrophy response being specific to muscle fibre type have been suggested to be controversial in the literature [138,146]. ...
... UBPT is characterized by short duration high-velocity movement that activates the motor units associated with fast-twitch muscle fibres [144] which are suggested to have greater potential for hypertrophy [138,145]. However, such speculations about hypertrophy response being specific to muscle fibre type have been suggested to be controversial in the literature [138,146]. Another mechanism that may be responsible for the increase in muscle volume is the increase in the rate of protein synthesis [147], which has the potential to increase the muscle volume. This is noteworthy because body composition can influence physical performance such as speed, change of direction, and upper limb explosive strength [148]. ...
Article
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Background Upper-body plyometric training (UBPT) is a commonly used training method, yet its effects on physical fitness are inconsistent and there is a lack of comprehensive reviews on the topic. Objective To examine the effects of UBPT on physical fitness in healthy youth and young adult participants compared to active, specific-active, and passive controls. Methods This systematic review followed PRISMA 2020 guidelines and utilized the PICOS framework. PubMed, WOS, and SCOPUS were searched. Studies were assessed for eligibility using the PICOS framework. The effects of UBPT on upper-body physical fitness were assessed, including maximal strength, medicine ball throw performance, sport-specific throwing performance, and upper limb muscle volume. The risk of bias was evaluated using the PEDro scale. Means and standard deviations were used to calculate effect sizes, and the I ² statistic was used to assess heterogeneity. Publication bias was assessed using the extended Egger's test. Certainty of evidence was rated using the GRADE scale. Additional analyses included sensitivity analyses and adverse effects. Results Thirty-five studies were included in the systematic review and 30 studies in meta-analyses, involving 1412 male and female participants from various sport-fitness backgrounds. Training duration ranged from 4 to 16 weeks. Compared to controls, UBPT improved maximal strength (small ES = 0.39 95% CI = 0.15–0.63, p = 0.002, I ² = 29.7%), medicine ball throw performance (moderate ES = 0.64, 95% CI = 0.43–0.85, p < 0.001, I ² = 46.3%), sport-specific throwing performance (small ES = 0.55, 95% CI = 0.25–0.86, p < 0.001, I ² = 36.8%), and upper limbs muscle volume (moderate ES = 0.64, 95% CI = 0.20–1.08, p = 0.005, I ² = 0.0%). The GRADE analyses provided low or very low certainty for the recommendation of UBPT for improving physical fitness in healthy participants. One study reported one participant with an injury due to UBPT. The other 34 included studies provided no report measure for adverse effects linked to UBPT. Conclusions UBPT interventions may enhance physical fitness in healthy youth and young adult individuals compared to control conditions. However, the certainty of evidence for these recommendations is low or very low. Further research is needed to establish the optimal dose of UBPT and to determine its effect on female participants and its transfer to other upper-body dominated sports.
... However, it remains unknown whether manipulating resistance training (RT) variables can lead to positive adaptations in CT. Lower intensity resistance training (LIRT), characterized by intensities below 50% of 1RM and higher repetitions, performed until or near volitional fatigue, stimulates hypertrophy in type I (oxidative) muscle fibers [15][16][17], promotes muscle mitochondrial adaptations [18,19] and capillarization [20], and increases muscular endurance capacity [21]. Notably, a strong relationship has been demonstrated between skeletal muscle capillarity, type I muscle fibers (proportion and cross-sectional area), and CT [22,23]. ...
... Interventions that improve physiological processes supporting oxidative metabolism, such as endurance training, have been shown to increase CT in young adults [1]. LIRT performed with sets close to volitional fatigue has been demonstrated to stimulate hypertrophy of type I muscle fibers [15][16][17], induce muscle mitochondrial adaptations [18,19], and promote capillarization [20], and increase endurance capacity [21]. The effect of LIRT on type I muscle fibers, when performed with maximal repetitions until or close to voluntary concentric failure, is believed to be related to greater oxidative and metabolic stresses [18,[35][36][37]. ...
... HIRT, being of higher intensity, stimulates greater activation of fast-fatigable fibers (type IIX fibers), resulting in a lower number of repetitions per set and potentially lesser metabolic stress on type I muscle fibers. In contrast, LIRT performed at lower intensity preferentially stimulates type I muscle fibers [15][16][17][18][19]. Type I muscle fibers have a higher oxidative capacity and fatigue threshold, allowing for a higher number of repetitions per set in LIRT and potentially greater metabolic stress on type I muscle fibers. ...
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Purpose The torque–duration relationship in muscle group exercise is characterized by two parameters, the critical torque (CT) and the W prime (Wʹ), which define the limit of tolerance. These parameters have significant utility in assessing health and disease. However, there is a lack of information regarding the optimization of CT and/or Wʹ gains through manipulation of resistance training (RT) variables, especially in older adults. Therefore, this study aimed to investigate the impact of different intensities of RT, specifically higher intensity RT (HIRT) versus lower intensity RT (LIRT), on CT and Wʹ in postmenopausal women. Methods The study spanned 12 weeks of RT. Postmenopausal women were randomized into three groups: control group (CG, n = 14), LIRT (loads necessary to perform 27–31 repetitions, n = 17), and HIRT (loads necessary to perform 8–12 repetitions, n = 14). Results Compared to the CG group, the LIRT group exhibited a significant increase in CT (15%, P < 0.05), while the HIRT group showed a significant increase in Wʹ (36%, P < 0.05). Conclusions Different intensities of RT result in distinct adaptations of torque–duration relationship parameters (Wʹ and CT) in postmenopausal women.
... The higher T-test values in the two-muscle group reflect greater consistency among participants, suggesting that while the overall hypertrophic response was lower, the two-muscle training protocol is a reliable method for promoting balanced muscle growth. This finding is supported by research showing that moderate training volumes can still induce significant hypertrophy when combined with progressive overload, even if the volume per muscle is reduced (Ogborn & Schoenfeld, 2014). ...
Article
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This study investigates the effects of different bodybuilding training methodologies—single muscle versus multiple muscle training—on upper body muscle growth. Despite the established benefits of resistance training for muscle hypertrophy, the optimal structuring of workouts remains debated. An experimental design was utilized, dividing 44 participants from the Iraqi Federation for Bodybuilding and Fitness into two groups, with one focusing on training a single muscle per session and the other on training two muscles per session over 12 weeks. Pre- and post-test measurements were taken to assess changes in chest, upper arm, and forearm circumferences, alongside strength gains. Statistical analysis using SPSS revealed significant increases in muscle size for both training approaches, with the single muscle group demonstrating superior hypertrophic outcomes. These findings suggest that training one muscle group per session may provide a more effective stimulus for muscle growth compared to training multiple groups simultaneously. The results contribute valuable insights into bodybuilding training practices, indicating that specific training strategies can optimize hypertrophy and enhance strength in bodybuilders.
... In the present study, we observed greater increases in type II fCSA compared with type I fCSA (Fig. 1). Higher-intensity resistance exercise requires greater motor unit recruitment, ultimately engaging more type II fibers and leading to greater type II fiber growth at intensities >50% one-repetition maximum (1RM) (34)(35)(36)(37). With MIS, we observed increases of 36% and 48% in type I and II fCSA, respectively, and with COL, we observed increases of 21% and 32% in type I and II fCSA, respectively. ...
Article
Introduction Skeletal muscle satellite cells (SC) contribute to the adaptive process of resistance exercise training (RET) and may be influenced by nutritional supplementation. However, little research exists on the impact of multi-ingredient supplementation on the SC response to RET. Purpose We tested the effect of a multi-ingredient supplement (MIS) including whey protein, creatine, leucine, calcium citrate, and vitamin D on SC content and activity as well as myonuclear accretion, SC and myonuclear domain compared with a collagen control (COL) throughout a 10-wk RET program. Methods Twenty-six participants underwent a 10-wk linear RET program while consuming either the MIS or COL supplement twice daily. Muscle biopsies were taken from the vastus lateralis at baseline and 48 h after a bout of damaging exercise, before and after RET. Muscle tissue was analyzed for SC and myonuclear content, domain, acute SC activation, and fiber cross-sectional area (fCSA). Results MIS resulted in a greater increase in type II fCSA following 10 wk of RET (effect size (ES) = 0.89) but not myonuclear accretion or SC content. Change in myonuclei per fiber was positively correlated with type I and II and total fiber hypertrophy in the COL group only, indicating a robust independent effect of MIS on fCSA. Myonuclear domain increased similarly in both groups, whereas SC domain remained unchanged following RET. SC activation was similar between groups for all fiber types in the untrained state but showed a trend toward greater increases with MIS after RET (ES = 0.70). Conclusions SC responses to acute damaging exercise and long-term RET are predominantly similar in MIS and COL groups. However, MIS can induce greater increases in type II fCSA with RET and potentially SC activation following damage in the trained state.
... 2 According to Henneman's size principle on the characteristics of motor neurons and their muscle fibre size, low to moderate intensity activities recruit mainly type I fibres, whereas type IIa and IIb fibres are progressively recruited as intensity increases. 11 The neural recruitment pattern among the different diaphragmatic fibres follows this key order to generate different motor behaviours ranging from normal ventilation up to intense efforts. 1,2 However, it is worth noting that in the diaphragm, maximum diaphragm fibre recruitment, and therefore activation of all motor fibres, occurs sporadically during forced expiratory manoeuvres, which play a minimal role compared to normal diaphragmatic function. ...
... In addition, X:0:X:0 is used as a movement tempo variable in explosive strength training at the maximum possible speed with the load worked at the time of exercise. Some sources have suggested the use of 3-digit numbers for the repetition rate variable, which represents the sum of concentric, eccentric and isometric components of a repetition (Ogborn and Schoenfeld, 2014). Westcott et al. (2001) recommended 2:1:4 as the best standard for tempo in resistance exercise repetitions. ...
Article
Full-text available
Although many studies have demonstrated whether movement tempo, a training variable during resistance exercise, has an effect on muscle performance, there are still gray areas related to muscle hypertrophy and muscular fitness in different populations. The aim of this narrative systematic review was to investigate the effect of movement tempo on muscular performance such as maximal strength, skeletal muscle hypertrophy, muscle power and muscular endurance in resistance training performed at specific frequencies. Three electronic databases were searched using terms related to movement tempo and resistance training. The included studies were those published in English using randomized and non-randomized comparative dynamic resistance exercise interventions in healthy adults. The results suggest that changing the tempo of movement during resistance training may have an effect on muscle hypertrophy, but the results are not conclusive. There are conflicting research results, although faster tempos seem to be advantageous in terms of power outcomes at different movement tempos. More studies are needed to evaluate muscular endurance performance in terms of movement tempo. Differences in the size of the muscles studied, the structure of the training programs, and the standardization of the experimental approach and data collection tools used may partially explain the inconsistency in the results between tempos in different contraction phases or in the same contraction phases.
... In addition, X:0:X:0 is used as a movement tempo variable in explosive strength training at the maximum possible speed with the load worked at the time of exercise. Some sources have suggested the use of 3-digit numbers for the repetition rate variable, which represents the sum of concentric, eccentric and isometric components of a repetition (Ogborn and Schoenfeld, 2014). Westcott et al. (2001) recommended 2:1:4 as the best standard for tempo in resistance exercise repetitions. ...
Article
Full-text available
Although many studies have shown whether movement speed manipulation has an effect on muscular performance during resistance exercise, its effects are not entirely clear. The aim of this systematic review is to investigate the effect of movement speed on muscular performance such as maximal strength, hypertrophy and muscular endurance in resistance training performed at certain frequencies. Seven electronic databases were searched using terms related to movement speed and resistance training. The studies included in the review were studies published in English using randomized and non-randomized comparative dynamic resistance exercise interventions in healthy adults. Hypertrophy of the quadriceps was examined in five studies and of the biceps brachii in two studies. Three studies found significantly greater increases in hypertrophy of the quadriceps for moderate-slow compared to fast training. For the remaining studies examining the quadriceps, significant within-group increase in hypertrophy was found for only moderate-slow training in one study and for only fast training in the other study. The two studies that examined hypertrophy of the biceps brachii found greater increases for fast compared to moderate-slow training. This article provides an overview of the available scientific data describing the impact of movement tempo on hypertrophy and strength development with a thorough analysis of changes in duration of particular phases of movement. Additionally, the review provides movement tempo-specific recommendations as well real training solutions for strength and conditioning coaches and athletes, depending on their goals.
Article
High-load resistance exercise (>60% of 1-repetition maximum) is a well-known stimulus to enhance skeletal muscle hypertrophy with chronic training. However, studies have intriguingly shown that low-load resistance exercise training (RET) (≤60% of 1-repetition maximum) can lead to similar increases in skeletal muscle hypertrophy as compared to high-load RET. This has raised questions about the underlying mechanisms for eliciting the hypertrophic response with low-load RET. A key characteristic of low-load RET is performing resistance exercise to, or close to, task failure, thereby inducing muscle fatigue. The primary aim of this evidence-based narrative review is to explore whether muscle fatigue may act as an indirect or direct mechanism contributing to skeletal muscle hypertrophy during low-load RET. It has been proposed that muscle fatigue could indirectly stimulate muscle hypertrophy through increased muscle fibre recruitment, mechanical tension, ultrastructural muscle damage, the secretion of anabolic hormones, and/or alterations in the expression of specific proteins involved in muscle mass regulation (e.g., myostatin). Alternatively, it has been proposed that fatigue could directly stimulate muscle hypertrophy through the accumulation of metabolic by-products (e.g., lactate), and/or inflammation and oxidative stress. This review summarizes the existing literature eluding to the role of muscle fatigue as a stimulus for low-load RET-induced muscle hypertrophy and provides suggested avenues for future research to elucidate how muscle fatigue could mediate skeletal muscle hypertrophy.
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Book (colored) on weight training exercises (legs, abs, lower back, neck, respiratory muscles). It includes anatomical illustrations and photos.
Article
This study aims to explore the role of FoxO1 and its acetylation in the alleviation of hypoxia‐induced muscle atrophy by resistance training. Forty male Sprague–Dawley rats were randomly divided into four groups: normoxic control group (C), normoxic resistance training group (R), hypoxic control group (H) and hypoxic resistance training group (HR). Rats in R and HR groups were trained on an incremental weight‐bearing ladder every other day, while those in H and HR groups were kept in an environment containing 12.4% O 2 . After 4 weeks, muscles were collected for analysis. Differentiated L6 myoblasts were analysed in vitro after hypoxia exposure and plasmids transfection (alteration in FoxO1 acetylation). The lean body mass loss, wet weight and fibre cross‐sectional area of extensor digitorum longus of rats were decreased after 4 weeks hypoxia, and the adverse reactions above was reversed by resistance training. At the same time, the increase in hypoxia‐induced autophagy was suppressed, which was accompanied by a decrease in the expression of nuclear FoxO1 and cytoplasmic Ac‐FoxO1 by resistance training. The L6 myotube diameter increased and the expression of autophagic proteins were inhibited under hypoxia via intervening by FoxO1 deacetylation. Overall, resistance training alleviates hypoxia‐induced muscle atrophy by inhibiting nuclear FoxO1 and cytoplasmic Ac‐FoxO1‐mediated autophagy.
Article
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The purpose of this study was to determine whether the training responses observed with low-load resistance exercise to volitional fatigue translates into significant muscle hypertrophy, and compare that response to high-load resistance training. Nine previously untrained men (aged 25 [SD 3] years at the beginning of the study, standing height 1.73 [SD 0.07] m, body mass 68.9 [SD 8.1] kg) completed 6-week of high load-resistance training (HL-RT) (75% of one repetition maximal [1RM], 3-sets, 3x/wk) followed by 12 months of detraining. Following this, subjects completed 6 weeks of low load-resistance training (LL-RT) to volitional fatigue (30% 1 RM, 4 sets, 3x/wk). Increases (p < 0.05) in magnetic resonance imaging-measured triceps brachii and pectorals major muscle cross-sectional areas were similar for both HL-RT (11.9% and 17.6%, respectively) and LL-RT (9.8% and 21.1%, respectively). In addition, both groups increased (p < 0.05) 1RM and maximal elbow extension strength following training; however, the percent increases in 1RM (8.6% vs. 21.0%) and elbow extension strength (6.5% vs. 13.9%) were significantly (p < 0.05) lower with LL-RT. Both protocols elicited similar increases in muscle cross-sectional area, however differences were observed in strength. An explanation of the smaller relative increases in strength may be due to the fact that detraining after HL-RT did not cause strength values to return to baseline levels thereby producing smaller changes in strength. In addition, the results may also suggest that the consistent practice of lifting a heavy load is necessary to maximize gains in muscular strength of the trained movement. These results demonstrate that significant muscle hypertrophy can occur without high-load resistance training and suggests that the focus on percentage of external load as the important deciding factor on muscle hypertrophy is too simplistic and inappropriate.
Article
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It is well established that regimented resistance training can promote increases in muscle hypertrophy. The prevailing body of research indicates that mechanical stress is the primary impetus for this adaptive response and studies show that mechanical stress alone can initiate anabolic signalling. Given the dominant role of mechanical stress in muscle growth, the question arises as to whether other factors may enhance the post-exercise hypertrophic response. Several researchers have proposed that exercise-induced metabolic stress may in fact confer such an anabolic effect and some have even suggested that metabolite accumulation may be more important than high force development in optimizing muscle growth. Metabolic stress pursuant to traditional resistance training manifests as a result of exercise that relies on anaerobic glycolysis for adenosine triphosphate production. This, in turn, causes the subsequent accumulation of metabolites, particularly lactate and H(+). Acute muscle hypoxia associated with such training methods may further heighten metabolic buildup. Therefore, the purpose of this paper will be to review the emerging body of research suggesting a role for exercise-induced metabolic stress in maximizing muscle development and present insights as to the potential mechanisms by which these hypertrophic adaptations may occur. These mechanisms include increased fibre recruitment, elevated systemic hormonal production, alterations in local myokines, heightened production of reactive oxygen species and cell swelling. Recommendations are provided for potential areas of future research on the subject.
Article
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The purpose of this study was to test the hypothesis that skeletal muscle adaptations induced by long-term resistance training (RT) are associated with increased myogenic regulatory factors (MRF) and insulin-like growth factor-I (IGF-I) mRNA expression in rats skeletal muscle. Male Wistar rats were divided into 4 groups: 8-week control (C8), 8-week trained (T8), 12-week control (C12) and 12-week trained (T12). Trained rats were submitted to a progressive RT program (4 sets of 10-12 repetitions at 65-75% of the 1RM, 3 day/week), using a squat-training apparatus with electric stimulation. Muscle hypertrophy was determined by measurement of muscle fiber cross-sectional area (CSA) of the muscle fibers, and myogenin, MyoD and IGF-I mRNA expression were measured by RT-qPCR. A hypertrophic stabilization occurred between 8 and 12 weeks of RT (control-relative % area increase, T8: 29% vs. T12: 35%; p>0.05) and was accompanied by the stabilization of myogenin (control-relative % increase, T8: 44.8% vs. T12: 37.7%, p>0.05) and MyoD (control-relative % increase, T8: 22.9% vs. T12: 22.3%, p>0.05) mRNA expression and the return of IGF-I mRNA levels to the baseline (control-relative % increase, T8: 30.1% vs. T12: 1.5%, p<0.05). Moreover, there were significant positive correlations between the muscle fiber CSA and mRNA expression for MyoD (r=0.85, p=0.0001), myogenin (r=0.87, p=0.0001), and IGF-I (r=0.88, p=0.0001). The significant (p<0.05) increase in myogenin, MyoD and IGF-I mRNA expression after 8 weeks was not associated with changes in the fiber-type frequency. In addition, there was a type IIX/D-to-IIA fiber conversion at 12 weeks, even with the stabilization of MyoD and myogenin expression and the return of IGF-I levels to baseline. These results indicate a possible interaction between MRFs and IGF-I in the control of muscle hypertrophy during long-term RT and suggest that these factors are involved more in the regulation of muscle mass than in fiber-type conversion.
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To distinguish the respective potential of endurance and resistance training to increase the satellite cell pool, we investigated the effects of 14 weeks of concurrent lower body endurance and upper body resistance training (3 sessions/week) on vastus lateralis (VLat) and deltoid (Del) muscles of 10 active elderly men. NCAM+ satellite cells and myonuclear number were assessed in VLat and Del. After 14 weeks of training the NCAM+ satellite cell pool increased similarly (+38%) in both muscles, mainly in type II muscle fibers (P < 0.05). There was no significant change in myonuclear number or myonuclear domain in either muscle. Combining resistance training in the upper limbs with endurance training in the lower limbs is an efficient strategy to enhance the satellite cell pool in upper and lower body muscles in elderly subjects. Our results provide a practical reference for the determination of optimal exercise protocols to improve muscle function and regeneration in the elderly. Muscle Nerve, 2008
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We conducted a 12-wk resistance training program in elderly women [mean age 69 +/- 1.0 (SE) yr] to determine whether increases in muscle strength are associated with changes in cross-sectional fiber area of the vastus lateralis muscle. Twenty-seven healthy women were randomly assigned to either a control or exercise group. The program was satisfactorily completed and adequate biopsy material obtained from 6 controls and 13 exercisers. After initial testing of baseline maximal strength, exercisers began a training regimen consisting of seven exercises that stressed primary muscle groups of the lower extremities. No active intervention was prescribed for the controls. Increases in muscle strength of the exercising subjects were significant compared with baseline values (28-115%) in all muscle groups. No significant strength changes were observed in the controls. Cross-sectional area of type II muscle fibers significantly increased in the exercisers (20.1 +/- 6.8%, P = 0.02) compared with baseline. In contrast, no significant change in type II fiber area was observed in the controls. No significant changes in type I fiber area were found in either group. We conclude that a program of resistance exercise can be safely carried out by elderly women, such a program significantly increases muscle strength, and such gains are due, at least in part, to muscle hypertrophy.
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In mammalian systems, skeletal muscle exists in a dynamic state that monitors and regulates the physiological investment in muscle size to meet the current level of functional demand. This review attempts to consolidate current knowledge concerning development of the compensatory hypertrophy that occurs in response to a sustained increase in the mechanical loading of skeletal muscle. Topics covered include: defining and measuring compensatory hypertrophy, experimental models, loading stimulus parameters, acute responses to increased loading, hyperplasia, myofiber-type adaptations, the involvement of satellite cells, mRNA translational control, mechanotransduction, and endocrinology. The authors conclude with their impressions of current knowledge gaps in the field that are ripe for future study. © 2012 American Physiological Society. Compr Physiol 2:2829-2870, 2012.
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A VARIETY OF SPECIALIZED TRAINING TECHNIQUES HAVE BEEN ADVOCATED AS A MEANS TO HEIGHTEN MUSCLE GROWTH. FORCED REPETITIONS/DROP SETS, SUPERSETS, AND HEAVY NEGATIVES, IN PARTICULAR, HAVE BEEN PURPORTED TO ENHANCE THE HYPERTROPHIC RESPONSE TO RESISTANCE EXERCISE. THIS ARTICLE WILL EXPLORE THE POTENTIAL ROLE OF THESE TECHNIQUES IN PROMOTING MUSCLE HYPERTROPHY AND PROVIDE AN INSIGHT INTO POSSIBLE APPLICATIONS TO RESISTANCE TRAINING PROGRAMS.
Article
Purpose: This study compared endurance and neuromuscular function after bouts of low-load (LL), high-load (HL), and LL blood flow-restricted (LL(BFR)) resistance exercise. Methods: Eight recreationally active male subjects completed three sets of dynamic knee extensions to volitional failure under three conditions: HL (70% peak torque), LL (20% peak torque), and LL(BFR) (20% peak torque with an occlusive cuff inflated to 180 mm Hg wrapped around the thigh). Before and immediately after exercise, isometric torque, central activation, electrically evoked torque, and muscle activation via surface EMG were measured. Results: Isometric torque and evoked torque decreased an average of 37% and 40%, respectively (P < 0.01) in all conditions after exercise. There were no differences in the toque decrements between the conditions (P > 0.05). Percent central activation did not change after any condition (P = 0.09). Rate of torque development declined an average of 26% after all three conditions (P = 0.003), and rate of half-relaxation time was depressed by 48% after the HL condition (P = 0.004) only. EMG amplitude was greater in the HL condition at the beginning and end of exercise compared with the LL and LL(BFR) conditions (P = 0.001). At the end of exercise, EMG amplitude rose 19% (P = 0.02) and was not different among conditions (P > 0.05). Subjects performed more repetitions during the LL and LL(BFR) conditions (P < 0.05). Conclusion: Although LL and LL(BFR) resistance exercise to volitional failure exhibit lower levels of muscle activation than HL exercise, similar torque decrements occur after all bouts of resistance exercise, and the muscle fatigue can be attributed to peripheral factors.
Article
We have reported that the acute postexercise increases in muscle protein synthesis rates, with differing nutritional support, are predictive of longer-term training-induced muscle hypertrophy. Here, we aimed to test whether the same was true with acute exercise-mediated changes in muscle protein synthesis. Eighteen men (21 ± 1 yr, 22.6 ± 2.1 kg/m(2); means ± SE) had their legs randomly assigned to two of three training conditions that differed in contraction intensity [% of maximal strength (1 repetition maximum)] or contraction volume (1 or 3 sets of repetitions): 30%-3, 80%-1, and 80%-3. Subjects trained each leg with their assigned regime for a period of 10 wk, 3 times/wk. We made pre- and posttraining measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and posttraining biopsies of the vastus lateralis, and a single postexercise (1 h) biopsy following the first bout of exercise, to measure signaling proteins. Training-induced increases in MR-measured muscle volume were significant (P < 0.01), with no difference between groups: 30%-3 = 6.8 ± 1.8%, 80%-1 = 3.2 ± 0.8%, and 80%-3= 7.2 ± 1.9%, P = 0.18. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30%-3 (P = 0.04), whereas training-induced isometric strength gains were significant but not different between conditions (P = 0.92). Biopsies taken 1 h following the initial resistance exercise bout showed increased phosphorylation (P < 0.05) of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signaling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure.