Sports Med
DOI 10.1007/s40279-013-0112-3
LETTER TO THE EDITOR
Author’s Reply to Steele and Fisher: ‘‘Scientific Rigour: a Heavy
or Light Load to Carry?’’
The Importance of Maintaining Objectivity in Drawing Evidence-Based Conclusions
B. Schoenfeld
Ó Springer International Publishing Switzerland 2013
I appreciate the opportunity to respond to the letter by
Steele and Fisher, ‘‘Scientific rigour; a heavy or light load
to carry?’’ [1] regarding my recent review paper [2]. I
welcome the platform that this letter provides to further
expound on the role of loading in muscular adaptations.
Steele and Fisher [1] begin by questioning my use of the
word ‘‘intensity’’ to describe the relative magnitude of load
lifted. In principle, I agree that this is a valid criticism. The
term ‘‘intensity’’ is rather ambiguous and its employment
should be taken up for scientific discussion to clarify
proper terminology. Although my use of the term followed
commonly accepted jargon, in retrospect I should have
used the phrase ‘‘intensity of load’’ or simply ‘‘load’’ and
will do so in the future.
The remaining content of the letter by Steele and Fisher
[1] attempts to refute my conclusion, namely that evidence
remains equivocal as to whether low-load training is as
effective as high-load training in promoting muscular
adaptations. In trying to make this case, however, the
authors focus their efforts solely on discussing limitations
in studies that showed an advantage to higher load training
and neglect to acknowledge substantial limitations in
studies showing no differences as discussed in detail in my
review. Moreover, they fail to recognize the potential
implications of positive findings in null studies where
results did not rise to a predetermined level of statistical
significance. These omissions ultimately give the impres-
sion of confirmation bias, with the authors endeavoring to
support a pre-conceived hypothesis rather than taking an
B. Schoenfeld (&)
Lehman College, 250 Bedford Park Blvd West, Bronx,
NY 10468, USA
e-mail: brad@workout911.com
objective view of the literature. What follows henceforth is
a point-by-point rebuttal of each of the issues raised.
First, Steele and Fisher [1] question my inclusion of
studies that assessed hypertrophy by muscle biopsy. They
justly state that biopsy is limited by the fact that the sur-
gical extraction of tissue can damage the cells and thus
confound results. However, it should be noted that the
biopsy methods employed in the two studies in question [3,
4] were designed to mitigate confounding issues related to
muscle damage. Specifically, tissue samples were obtained
using the ‘‘double-chop method’’ which allows for
extraction of *1000 fibers per biopsy. This would seem-
ingly provide an ample amount of healthy tissue for ana-
lysis even if some damage was in fact incurred during
surgical incision. Moreover, the authors seem to overlook
the fact that imaging techniques can be confounded by
factors such as the time course of assessment, chemical
shift artefacts, and various errors in obtaining and repeating
site-specific measurements [5–7].
Steele and Fisher [1] then make the statement that ‘‘we
might regard that most persons wishing to increase their
muscularity might be less concerned with in vitro research
and more concerned with change in cross sectional area
(CSA) or thickness of their muscles as a whole.’’ This is a
perplexing claim as biopsy allows for measurement of the
change in individual fiber area. Do the authors really
believe this is of no importance to resistance trained
individuals? A case can be made that biopsy actually
provides the most relevant information about muscle
development as it allows for direct assessment of con-
tractile hypertrophy, which is responsible for producing
muscular force. This is in opposition to imaging tech-
niques, which do not distinguish between intramuscular
tissues and therefore could bias towards increases in non-
contractile elements.

In addition, Steele and Fisher [1] neglect to mention
other shortcomings of various imaging techniques in
assessing muscle hypertrophy. Magnetic resonance imag-
ing, for example, has been shown to correlate poorly with
histologically determined changes in myofiber CSA [8].
This is an important point of fact as mitochondrial protein
synthesis is particularly sensitive to extended time under
tension during resistance training [9], and may increase
disproportionately during low-load training as the time
under tension and total work are higher in comparison to
training with high loads. Moreover, cadaver analyses
indicate that that computerized tomography imaging can
overestimate whole muscle CSA by as much as 20 % [10].
Taking all factors into account, it would be imprudent and
misguided to dismiss muscle biopsy and only look at
imaging techniques when evaluating hypertrophy research
as the authors suggest. Each of these modalities has
inherent strengths and weaknesses as an assessment tool,
and all of them can provide valuable information with
respect to muscular adaptations.
Steele and Fisher [1] then call attention to the fact that
the study by Holm et al. [11] reported differences in CSA
only at the midpoint of the thigh and not proximally or
distally. I am not clear why the authors feel this is a point
of contention? It is well-established that muscles tend to
hypertrophy in a non-uniform fashion [12–15]. It is spec-
ulated that such non-uniform adaptations may be the result
of regional muscle activation or perhaps differences in
muscle oxygenation from a given exercise [12, 16]. The
fact that this study employed the leg extension as the sole
form of resistance training would perhaps explain why site-
specific responses were noted. Regardless, this finding in
no way invalidates the study as the authors seem to suggest.
Next, Steele and Fisher [1] contend that the study by
Lamon et al. [17] used the same data from previous work
by Leger et al. [18] and thus should not have been included
in the review. If this is indeed the case, then I accept
responsibility for the oversight. However, I take umbrage
with the assertion that, ‘‘Though a relatively simple mis-
take to make, it seems that someone reading an article with
the expected intricacy to discuss it in review might have
noticed this.’’ Note that nowhere in the study by Lamon
et al. [17] was it mentioned that pre-existing data was used
for analysis, which is customary in such instances. Con-
sidering that the study was published three years after the
fact with a different lead author, it is unreasonable to
expect this would be readily apparent when reviewing
hundreds of studies over many months as I did for this
review.
The authors then extol the virtues of the Leger et al. [18]
study because it ‘‘controlled for volume between high- and
low-load groups, had participants train to MMF and again
report no difference between high- and low-load groups.’’ I
B. Schoenfeld
concur with these sentiments. However, it is important to
duly note that this study used the exact same protocol as
Campos et al. [4], who found significantly greater hyper-
trophic increases in high- compared to low-load groups.
This only serves to further highlight contradictory findings
between studies on the topic.
Finally, Steele and Fisher [1] questioned why I did not
include three additional studies as part of my review. The
first study by Hisaeda et al. [19] employed a protocol where
the low-load group trained in a range of 15–20 repetitions,
which correlates to an intensity of approximately 60–65 %
1RM. This is at or above the threshold commonly cited as
necessary for hypertrophy, and thus it did not meet the
\50 % 1RM intensity level required for inclusion. The
second study mentioned was by Kraemer et al. [20]. I am
miffed as to why Steele and Fisher [1] feel this study is
relevant to the topic at hand? The protocol involved a
repetition range of 3–12 reps, which in no way provides
insight into the hypertrophic effects of low-load training.
The final study by Popov et al. [21], although applicable to
the topic, was listed as being published in Russian. Since
the search criteria for my review focused only on English-
language publications, this study was not considered for
inclusion. Thus, the claim by Steele and Fisher [1] that
these studies were ‘‘inexplicably’’ omitted from the review
is patently unfounded.
With respect to the study by Popov et al. [21], I have
managed to obtain an English-language version of the
paper and it makes for intriguing discussion. Briefly, the
researchers evaluated two groups: a high-load group that
trained at 80 % 1RM, and a low-load group that performed
sets at 50 % 1RM without relaxation during performance.
Although no significant differences were found between
groups, the absolute differences in hypertrophy were quite
striking. Quadriceps volume was 150 % greater in the
higher-load group compared to low-load (15 % vs. 6 %,
respectively), and volume of the gluteus maximus was
38 % greater in those who trained at a higher versus lower
percentage of 1RM (18 % vs. 13 %, respectively). Given
the small sample size, it is certainly possible if not likely
that null findings may be attributed to a type II error.
Without question, a strong case can be made that these
differences would be practically meaningful for anyone
seeking to maximize muscle hypertrophy.
When examining the body of literature as a whole, here
is a summary of what we can ascertain: three studies show
a significant advantage for high-load training [3, 4, 11] and
six studies (including the study by Popov et al. [21]) show
no significant differences between using low- versus high-
loads [18, 21–25]. The important caveat here is that two of
the six studies that failed to show significant differences
demonstrated clear absolute hypertrophic advantages for
higher load training, with CSA increases of the magnitude
Author’s Reply to Steele and Fisher
of 34 to 150 % [21, 22]. The small sample sizes of these
studies suggest that null findings quite possibly were the
result of a type II error. Thus, it would be fair to say that
five studies showed positive findings for the higher load
training and four showed no appreciable differences.
Given the conflicting findings and methodological lim-
itations in the current literature, I firmly stand by my initial
conclusions: There is compelling evidence that low-load
training can promote substantial hypertrophy in untrained
subjects but the jury is still out as to whether it is as
effective as higher-load training in maximizing muscular
adaptations. If one remains unbiased, I do not see how it is
possible to come to any other conclusion. Furthermore, I
want to stress that I endeavored to take an impartial
approach when conducting the review and did not allow
individual opinion to sway my objectivity in any way. This
is the essence of a scientific approach, and it is what we
should strive for both in carrying out our research efforts as
well as when critically scrutinizing published papers. In
closing, I believe that my review does proper justice to this
important topic and hope it spurs additional research that
helps to fill in the existing gaps in the literature.
Acknowledgements The author has no conflicts of interest that are
directly relevant to the content of this letter.
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