J Appl Physiol 133: 87–103, 2022.

First published May 19, 2022; doi:10.1152/japplphysiol.00114.2022

REVIEW

The influence of longitudinal muscle fascicle growth on mechanical function

Avery Hinks,1 Martino V. Franchi,2 and Geoffrey A. Power1
1
Department of Human Health and Nutritional Sciences, College of Biological Science, University of Guelph, Guelph, Ontario,
Canada and 2Department of Biomedical Sciences, Neuromuscular Physiology Laboratory, University of Padua, Padua, Italy

Abstract
Skeletal muscle has the remarkable ability to remodel and adapt, such as the increase in serial sarcomere number (SSN) or fascicle
length (FL) observed after overstretching a muscle. This type of remodeling is termed longitudinal muscle fascicle growth, and its
impact on biomechanical function has been of interest since the 1960s due to its clinical applications in muscle strain injury, muscle
spasticity, and sarcopenia. Despite simplified hypotheses on how longitudinal muscle fascicle growth might influence mechanical func-
tion, existing literature presents conflicting results partly due to a breadth of methodologies. The purpose of this review is to outline
what is currently known about the influence of longitudinal muscle fascicle growth on mechanical function and suggest future direc-
tions to address current knowledge gaps and methodological limitations. Various interventions indicate longitudinal muscle fascicle
growth can increase the optimal muscle length for active force, but whether the whole force-length relationship widens has been less
investigated. Future research should also explore the ability for longitudinal fascicle growth to broaden the torque-angle relationship’s
plateau region, and the relation to increased force during shortening. Without a concurrent increase in intramuscular collagen, longitu-
dinal muscle fascicle growth also reduces passive tension at long muscle lengths; further research is required to understand whether
this translates to increased joint range of motion. Finally, some evidence suggests longitudinal fascicle growth can increase maximum
shortening velocity and peak isotonic power; however, there has yet to be direct assessment of these measures in a neurologically
intact model of longitudinal muscle fascicle growth.

force-length relationship; force-velocity relationship; passive properties; sarcomerogenesis; serial sarcomere number

INTRODUCTION production for a required task (18–20). Taken together, it is

Skeletal muscle can remodel its architecture in response to
conditions imposed on it. An example of muscle architectural
remodeling that has gained interest in recent years (1–5) is the
longitudinal muscle fascicle growth observed following inter-
ventions such as immobilization in a stretched position (6),
stretching a muscle surgically (7), and eccentric training (8).
In studies on human muscle, longitudinal fascicle growth is
often assumed on a macroscopic scale by an increase in ultra-
sound-measured fascicle length (FL) (9). Increased FL is
believed to reflect increased myofiber lengths, which can ei-
ther run the entire fascicle or present intrafascicular termina-
tions (4, 10). As myofibers, on the smallest scale, comprise
serially aligned sarcomeres, it is believed longitudinal fascicle
growth occurs via an increase in serial sarcomere number
(SSN)—a process termed “sarcomerogenesis” that has been
corroborated by numerous studies on animals (6, 8, 11–15).
The traditional hypothesis for sarcomerogenesis is dictated
by sarcomere force-length properties: active force production
is suboptimal in both overshortened and overstretched posi-
tions due to limited actin-myosin cross-bridge formation (16),
and passive tension increases exponentially with increasing
stretch (17). From a practical point of view, a muscle’s average
sarcomere operating length range is believed to favor force
hypothesized that if a muscle is forced to operate in an
overstretched position, SSN increases to maintain optimal
actin-myosin overlap regions in its new position (21, 22) or
to reduce the passive tension caused by stretch (23) (see
Fig. 1 for a visual representation). This remodeling can
occur in as little as 2 days in animals (6) and appears to relate
to a muscle’s ability to sense a change in tension, then convert
that mechanical signal into biochemical events regulating
protein synthesis (21, 24). Other reviews have discussed poten-
tial mechanisms in detail (2–5, 9, 25–27).
Skeletal muscle attaches to bones via tendons to articulate
the skeletal system, thus a muscle’s architecture governs the
characteristics of its biomechanical function (2, 20, 28). Serial
sarcomere number specifically has been implicated in the shape
of the whole muscle active force-length relationship (12, 29),
maximum shortening velocity (30), mechanical work (31), power
output (32), and passive properties of muscle (33). Longitudinal
fascicle growth has been advocated in clinical settings for ham-
string strain injury prevention in athletes (34, 35), and as ther-
apy for sarcopenia (36), and spastic muscle (5, 37, 38). Therefore,
the functional impact of interventions promoting longitudinal
fascicle growth is of both basic and clinical interest.
Existing literature presents conflicting findings regarding
the influence of longitudinal muscle fascicle growth on

Correspondence: G. A. Power (gapower@uoguelph.ca).

Submitted 23 February 2022 / Revised 20 April 2022 / Accepted 17 May 2022

http://www.jap.org 8750-7587/22 Copyright © 2022 the American Physiological Society. 87

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 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
Figure 1. Visual representation of the hy-
pothesis behind sarcomerogenesis. A: origi-
nal (nonstretched) fascicle. B: the fascicle is
forced into an overstretched position (i.e.,
with a longer than optimal sarcomere length
and elevated passive tension) via interven-
tion. C: to regain optimal actin-myosin over-
lap and/or alleviate passive tension in the
stretched position, serial sarcomere number
increases in the fascicle.
mechanical function, partly due to a breadth of methodolo-
gies. Depending on the methods employed, important limi-
tations must be considered. Studies on humans (and some
studies on animals) rely on data collected from the level of
the joint rather than a single muscle. Although it can be
argued that joint-level data are representative of the primary
muscle for a joint action (39), muscle length, force, and ve-
locity do not perfectly relate to the corresponding joint
angle, torque, and angular velocity due to muscle synergies
and variation in muscle moment arms depending on joint
angle (40). On top of this, tendons and intramuscular con-
nective tissue can adapt to interventions used to induce
longitudinal fascicle growth (41–43). Stiffer tendons and
connective tissue matrixes alter force transmission
through the muscle-tendon unit, and may therefore pres-
ent disconnects between muscle and joint level data (44–
47). Furthermore, even though strength gains attributed to
neural adaptations occur primarily within the first few
weeks of training, whereas muscle architectural adapta-
tions are thought to contribute more long term (48, 49), the
neural component of mechanical function warrants consider-
ation when interpreting mechanical adaptations obtained
from in vivo voluntary contractions (50). Altogether, there is a
lack of human data where enough confounding variables are
eliminated to make a direct assessment of how muscle archi-
tecture influences mechanical function possible. This review
will employ inclusion criteria in effort to strengthen interpre-
tations of indirect evidence from existing human studies.
The purpose of this review is twofold: 1) outline what is
currently well argued in the literature regarding how longitu-
dinal muscle fascicle growth influences muscle mechanical
function, particularly in interpreting indirect evidence from
studies on humans; and 2) suggest future research directions
to fill current knowledge gaps and improve on methodologi-
cal limitations.
INCLUSION CRITERIA
We conducted an extensive literature search for studies that
observed longitudinal muscle fascicle growth at any structural
scale of skeletal muscle and concomitantly assessed at least
one outcome measure of mechanical function. To narrow the
focus of this review, we have defined longitudinal fascicle
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growth as an increase in SSN. With that said, quantification of
SSN is more common in studies on animals, whereas studies
on humans rely more on ultrasonographic measures of FL.
Only one study on humans has directly quantified SSN adapta-
tions in a longitudinal manner but did not assess mechanical
function (51). Thus, this review will benefit from studies on
humans where an increase in SSN can be indirectly inferred.
Altogether, prominence will be given to studies that observed
longitudinal fascicle growth in one of the following ways: 1)
measured FL and sarcomere length (SL), allowing for mathe-
matical estimation of SSN (SSN = FL/SL) or 2) measured opti-
mal FL, or measured a muscle’s FL at approximately the
optimal joint angle (roughly equating to optimal FL if it is the
primary muscle for that joint action). In option 2, though SSN
would not be known, an increase in SSN can be inferred by an
increase in optimal FL assuming average optimal SL is approxi-
mately constant in skeletal muscle (52–54). To that end, we are
assuming optimal joint angles for human knee extension, knee
flexion, ankle dorsiflexion, and ankle plantar flexion are 60
–
80
(43, 55, 56), 150
–130
(57), 105
–110
(39), and 70
–80
(58),
respectively. In addition, though some studies have assessed
mechanical function alongside maturation-related longitudi-
nal muscle fascicle growth (59–61), we are limiting this review
to studies that induced longitudinal fascicle growth via experi-
mental intervention. In some cases, studies not fitting the
review criteria are still mentioned briefly where they can pro-
vide context. The following outcome measures of mechanical
function were chosen because they were common among mul-
tiple studies and relevant to SSN-related hypotheses: i) the
active force-length relationship, ii) maximum shortening ve-
locity, iii) mechanical work and power output, and iv) the pas-
sive length-tension relationship. Our initial search located 57
articles investigating outcome measures of mechanical func-
tion alongside an observation of longitudinal muscle fascicle
growth, after which our criteria narrowed that down to 23
articles (Table 1). The studies we found investigated i) an exer-
cise training program, ii) static stretch training, iii) denerva-
tion, iv) compensatory overload via synergist ablation, v)
immobilization of a muscle in a stretched position, or vi)
stretching a muscle via surgery. We will distinguish between
different means of inducing longitudinal muscle fascicle
growth where appropriate to elucidate confounding variables
associated with certain interventions.
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
Table 1. Adaptations in mechanical function concurrent to longitudinal muscle fascicle growth
Study Participants Intervention
Tabary et al. (13) Cats 4 wk immobilization in a
stretched position (n = 5)
vs. control (n = 6)
Goldspink et al. Cats 4 wk denervation while im-
(23) mobilized in a stretched
position (n = 12) vs. con-
trol (n = 12)
Kean et al. (62) Cats 28–35 days denervation
(n = 10) vs. contralateral
control
Williams and Mice 2–3 wk immobilization in a
Goldspink (12) stretched position (n = 5)
vs. control (n = 5)
Roy et al. (63) Rats (female) 12–14 wk Compensatory
overload by synergist
ablation (n = 8) vs. con-
trol (n = 8)
Lynn et al. (64) Rats (male) 5 days of decline running
training (n = 8) vs. incline
running training (n = 8)
Williams et al. Rabbits 20% tibial lengthening at a
(65) low (0.8 mm/day), me-
dium (1.6 mm/day), or
high rate (2.7 mm/day;
n = 3 per group)
Cox et al. (32) Rabbits 3 wk incremental surgical
stretch vs. control, then
an additional 3 wk of
maintained stretch
Shrager et al. Rats Lung volume reduction
(66) surgery (n = 11) vs. ster-
notomy (n = 7) 5 mo after
inducing emphysema vs.
control (n = 8)
Butterfield and Rabbits (female) 6 wk entric training with
Herzog (8) stimulation at onset of
stretch to a short muscle
length (SOS; n = 11), stim-
ulation preceding
stretch to a short muscle
length (SPS; n = 7), and
stimulation preceding
stretch to a long muscle
length (SPL; n = 6)
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Animals
Muscles Structural outcomes Functional Outcomes
Soleus 19% :SSN compared No change in joint angle-
with control passive tension curve
compared with control
Soleus 25% :SSN compared No change in joint angle-
with control passive tension curve
compared with control
Flexor digitorum 18% :SSN 13% ;Muscle maximum
longus shortening velocity com-
pared with control
Soleus 16% :SSN compared 5% :LO compared with
with control control.No change in pas-
sive length-tension curve
compared with control.
Plantaris 19% :fiber length/mus- 47% ;Maximum shortening
cle length, trend to- velocity compared with
ward 10% :fiber control
length, no change in
SL compared with
control
Vastus intermedius 9% greater SSN in 25% ;optimal knee angle
decline-trained com- (corresponding to :MTU
pared with incline- length) in decline-trained
trained compared with incline-
trained
Tibialis anterior 19% :SSN at low rate, ;Joint ROM (64% and 89%)
18% :SSN at me- and :passive tension at a
dium rate, 13% :SSN 90
ankle angle (8% and
at high rate com- 7%) with medium and high
pared with control rates compared with
control
Latissimus dorsi Initially 25% :SSN, Initially 40% ;Maximum
then an additional power output compared
5% :SSN with addi- with control, maximum
tional 3 wk stretch power output achieved at
compared with 5–7 Hz in control and 2–3
control Hz in stretched muscle.
Increases back toward
control values with addi-
tional 3 wk stretch.
Initially :hysteresis
(energy) loss during pas-
sive work loops compared
with control. Return to
control values after addi-
tional 3 wk of stretch.
Diaphragm 22% :SSN with lung 10% :LO with lung volume
volume reduction reduction surgery com-
surgery compared pared with sternotomy
with sternotomy
Tibialis anterior 3%–7% :SSN, greatest Rightward shift in torque-
with activation pre- angle relationship by 2.3

ceding stretch and with stimulation at onset
stretching to a long and at short muscle
muscle length length, 7.8
with stimula-
tion preceding stretch
and at short muscle
length, and 9.6
with stim-
ulation preceding stretch
and at long muscle length
Continued
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 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION

Table 1.— Continued

Animals
Study Participants Intervention Muscles Structural outcomes Functional Outcomes
Takahashi et al. Rabbits (male) Stretched tendon transfer Second extensor 20% :SSN 1 wk post- Rightward shifted and nar-
(7) compared with contralat- digitorum surgery, 13% :SSN 4 rower force-length rela-
eral control 1 wk (n = 11) wk postsurgery tionship at 1 and 4 wk
and 4 wk (n = 9) compared with postsurgery
postsurgery controls Passive force-length
curve shifted to left at 1
and 4 wk postsurgery
compared with controls
Larger passive elastic
moduli at 1 and 4 wk in
fiber bundles compared
with controls. In single
fibers, passive elastic
modulus only greater at
1 wk postsurgery.
De Jaeger et al. Rabbits (female) 4 wk static stretch training Soleus 9% :SSN compared 16% ;Peak passive resistive
(67) vs. contralateral control with control torque pre- to post-train-
(n = 7) ing (rightward shift in joint
angle-passive tension
curve)
Salzano et al. Guinea fowl High-acceleration training Iliotibialis lateralis 12%–20% :SSN with 12% :LO, 15% :LO normal-
(68) (n = 15) vs sedentary (n = pars training compared ized to limb length with
15) during growth period postacetabularis with sedentary training compared with
of 4–14 wk sedentary
Chen et al. (69), Rats (males) 4 wk decline running train- Soleus 6% :Soleus SSN in No changes in LO
Noonan et al. ing vs. incline running decline-trained com- No change in work of
(70), and training vs. control (n = pared with incline- shortening of whole sol-
Mashouri et 31 total) trained eus or soleus single fibers
al. (71) Single fiber passive stress
and passive modulus in
decline-trained < control
and incline-trained No
effect on fiber bundles
Humans
Study Participants Intervention Muscles Structural outcomes Functional outcomes
Blazevich et al. Humans (male 4 wk squat lift þ sprint/ Vastus lateralis SJ: 80% :distal FL of VL, No changes in angle of
(72) and female) jump training (SQ; n = 8); and rectus 39% : proximal FL of peak isometric knee
hack squat þ sprint/ femoris RF pre- to post-training extension torque pre- to
jump training (FHS; n = SQ: 22% :distal FL and post-training
7); sprint/jump training 83% :proximal FL of RF 4% ;10-m sprint time with
only (SJ; n = 8) pre- to post-training FHS and SJ


Reeves et al. Older adult 14 wk conventional resist- Vastus lateralis 8%–10% :Resting FL, 10 Shift in optimal knee
(43) humans (male ance training (n = 9) vs. 10%–18% :FL during extension angle
and female) control (n = 9) maximal contraction,
and 11% :optimal FL
pre- to post-training
Kudo et al. (73) Humans (male 12 wk Eccentric calf raise Medial 9% :FL following only 3% :Dorsiflexion ROM fol-
and female) (n = 11) vs. conventional gastrocnemius eccentric training lowing only eccentric
calf raise training (n = 10) training
Panidi et al. (74) Humans (adoles- 12 wk static stretch training Medial 6%–15% :FL only in Greater :dorsiflexion ROM
cent female) in addition to volleyball gastrocnemius stretch training group with stretch training (22%
training vs. just volleyball vs. 8%), but no change in
training joint angle-passive ten-
sion relationship
Akagi et al. (39), Humans (male 8 wk isometric training at Tibialis anterior 3% :FL following long- Broadening of plateau
Hinks et al. and female) short or long MTU MTU training region of the torque-angle
(75), and lengths (n = 13; nondomi- relationship following
Davidson et nant vs. dominant leg long-MTU training
al. (76) randomized) 11% :Work of shortening,
20% :angular velocity at
10% and 50% MVC loads,
23%–33% :peak isotonic
power following long-
MTU training.
FL, fascicle length; LO, optimal length; MTU, muscle-tendon unit; MVC, maximum voluntary contraction; ROM, range of motion; SL,
sarcomere length; SSN, serial sarcomere number.

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 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
Figure 2. Hypothesis for how longitudinal muscle fascicle growth
increases the optimal muscle length or joint angle for active force or tor-
que production. A hypothetical intervention causes overstretching of sar-
comeres, then sarcomeres are added in series to maintain the optimal
sarcomere length, increasing the range of the active force-length relation-
ship, and shifting the optimal muscle length to the right. Dashed lines
denote the location of optimal muscle length or joint angle. Red repre-
sents the original nonstretched muscle, and green represents the over-
stretched muscle before and after the addition of serial sarcomeres.
INFLUENCE OF LONGITUDINAL MUSCLE
FASCICLE GROWTH ON THE ACTIVE FORCE-
LENGTH RELATIONSHIP
The active force-length relationship includes an ascending
limb (force increases with increasing length), a plateau region
(where length for optimal force production, LO, is located), and
a descending limb (force decreases with increasing length), as
determined by overlap of actin and myosin filaments (16). As
the muscles crossing a joint will lengthen and shorten with
increases and decreases in joint angle, respectively, the force-
length relationship’s shape also applies to assessments of joint
torque and angle (i.e., the torque-angle relationship). As dis-
cussed earlier, maintaining the integrity of this relationship is
often hypothesized to drive longitudinal muscle fascicle
growth: forcing a muscle to act at a longer length will over-
stretch existing sarcomeres, and over time induce an increase
in SSN to maintain optimal actin-myosin overlap at that length
(5, 22). Consequently, a shift in the plateau region to a muscle
length or joint angle previously on the descending limb (i.e., an
increase in LO), and widening of the whole force-length rela-
tionship (i.e., an increase in the range of muscle lengths for
active force production) are expected (Fig. 2).
Immobilization in a Stretched Position and Surgery-
Induced Stretch
Sarcomerogenesis induced via immobilization in a stretched
position or surgery-induced stretch is often be accompanied by
a shift in the active force-length relationship; however, some
studies demonstrating this have limitations worth discussing.
The earliest example came from Williams and Goldspink (12),
who observed a 16% increase in SSN via 2–3 wk of immobi-
lization of the mouse soleus in a stretched position com-
pared with controls, with a concomitant 5% increase in LO.
They did not assess whether there was also widening of
the whole force-length relationship. Despite this being one
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of the most cited examples of a connection between SSN
and whole muscle LO, it is often neglected that they used a
small sample size (n = 5 per group) and did not appear to
run a statistical analysis to compare control and experi-
mental values. Although later studies on immobilization
in stretch improved on these limitations for assessing SSN
(19), they did not also assess the active force-length rela-
tionship. Other later studies instead investigated immobi-
lization in a shortened position and observed a leftward
shift in the active force-length relationship alongside
decreased SSN (77, 78); however, to our knowledge, no
study since Williams and Goldspink (12) has assessed SSN
and the active force-length relationship following immobi-
lization in a stretched position.
Studies investigating surgical stretch-induced sarcomero-
genesis and the force-length relationship also improved on the
above limitations. In the rat diaphragm, Shrager et al. (66)
observed a 22% greater SSN and corresponding 10% longer LO
in rats that received lung volume reduction surgery compared
with sternotomy 5 mo after inducing emphysema. Takahashi
et al. (7) observed 20% and 13% increases in SSN of the rabbit
second extensor digitorum 1 and 4 wk, respectively, following
surgical stretch, alongside a rightward shift in the active force-
length relationship compared with contralateral controls. They
also observed a slight narrowing, rather than the expected wid-
ening of the whole force-length relationship. The authors
speculated that an observed rapid proliferation of the extracel-
lular matrix, which can result in a less organized collagen fibril
network, impaired the muscle’s force transmission ability, thus
narrowing its range for active force production.
It should be noted that it is unclear in Takahashi et al. (7)
how many SL measurements were conducted to determine
average SL. When mathematically estimating SSN, it is im-
portant to both: 1) obtain FL measurements from several
regions of a muscle due to regional variability in FL (8, 79)
and 2) obtain several SL measurements across the length of a
fascicle due to SL nonuniformity (80). For example, the
study by Shrager et al. (66) obtained 10 SL measurements
from 8 fascicles per muscle for strong estimations of SSN.
Exercise Training in Animals
Training emphasizing eccentric contractions is often used
in attempt to induce longitudinal fascicle growth. The gen-
eral consensus for maximizing sarcomerogenesis and force-
length relationship adaptations with eccentric training is
that excursions should be performed at high velocity and
completed through the whole joint range of motion (ROM),
as these factors maximize muscle damage [for a commen-
tary, see Davis et al. (5)].
In animals, there is evidence supporting the above con-
sensus. Butterfield and Herzog (8) employed 6 wk of isoki-
netic eccentric training in the rabbit dorsiflexors, with
comparison of different strain magnitudes and activation
timings used during training. They found that tibialis ante-
rior SSN increased to the greatest extent when muscle activa-
tion preceded stretch rather than occurring at stretch onset,
and that a similar increase in SSN ( þ 7%) occurred whether
the muscle was stretched to a short or long length. The great-
est shift in the torque-angle relationship ( þ 10
); however,
occurred with stretch to a long muscle length. In addition,
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 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
greater torque values observed on the descending limb of
their torque-angle relationships suggest widening of the
whole torque-angle relationship occurred. Through multiple
linear regression, they also added an important finding to
the literature: peak torque achieved during eccentric con-
tractions and fiber strain during relaxation were the greatest
predictors of the % increase in SSN.
Though not eccentric training, results from Salzano et al.
(68) may support the theory that high velocity contractions
induce sarcomerogenesis, observing 12%–20% (in anterior and
posterior regions of the muscle, respectively) increases in SSN
and a 12% increase in LO of the iliotibialis lateralis pars postace-
tabularis in guinea fowl who completed high acceleration
training compared with a sedentary group. With that said, they
only obtained 3 SL measurements per fascicle, which may mis-
represent average SL and subject their SSN calculations to
error. In addition, rather than experimentally determining LO,
LO was estimated via a ratio of a known optimal SL for guinea
fowl to the measured average SL.
In animals, decline running is also often used as a model of
eccentric training. Lynn et al. (64) observed a 9% greater SSN
in the vastus intermedius of rats that completed 5 days of
decline running compared with rats that completed incline
running. Decline-running rats also had a 25% smaller optimal
knee angle (corresponding to a greater knee extensor LO), and
importantly, they observed a significant positive relationship
between SSN and optimal knee angle, supporting the assump-
tion that adaptations in joint-level data, rather than just mus-
cle-level data can be linked to sarcomerogenesis. Though this
study only compared a decline-running group to an incline-
running (i.e., decreased SSN) group rather than controls, and
only measured SL from one point at the center of the fascicle,
similar results were later obtained on the rat vastus interme-
dius with these limitations addressed (15), showing an 8%
greater SSN compared with controls.
Chen et al. (69) later employed 4 wk of decline running in
rats and assessed soleus SSN. They found that soleus SSN
increased to a lesser extent than what was observed in the
vastus intermedius, with only a 6% increase compared with
incline-running rats and no difference compared with con-
trols. There were also no significant differences in LO
between any groups, with only a small ( þ 1.5%) average
difference between decline and incline-trained rats. This
study measured FL using calipers rather than imaging
software (the method used by other studies above) which
can better account for fascicle curvature, so there is a chance
the FL (and thus SSN) measurements were subject to error.
Assuming the FL measurements were accurate, a potential ex-
planation for the difference from Lynn et al. (64)’s results is
rat vastus muscles undergo eccentric excursion of 25% of LO
in locomotion (81), compared with 10% in the soleus (82, 83).
As % increase in SSN may depend on peak force during eccen-
tric contractions (8), there also may not be enough loading
stimulus in bodyweight decline running to induce a large
magnitude of longitudinal fascicle growth and an accompany-
ing shift in LO in the soleus. A recent preprint from our labora-
tory employing 4 wk of weighted-vest decline running
training may support this theory of loading-dependent adap-
tation, showing an 8% greater SSN and on average a 4% longer
soleus LO in trained compared with control rats (preprint
Hinks et al. (84)).
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It should lastly be noted that none of the above studies on
downhill running and sarcomerogenesis investigated whether
there was widening of the whole force-length relationship.
Compared with investigations of a shift in LO, data on whether
sarcomerogenesis widens the force-length relationship is lack-
ing in animal interventions, and the literature would benefit
from more exploration of this adaptation going forward.
Exercise Training in Humans
In humans, there are a number of studies that assessed FL
and the torque-angle relationship following a variety of train-
ing interventions, observing rightward shifts, no shifts, and
leftward shifts in the optimal joint angle alongside apparent
increases in FL (41, 56, 85–90). Many of these studies assessed
the vastus lateralis or biceps femoris but obtained FL meas-
urements at a knee angle of full extension, and therefore do
not fit the inclusion criteria of this review. To reemphasize
the inclusion criteria: FL can vary depending on joint angle,
and measuring from a shortened or stretched position may
underestimate and overestimate, respectively, the magnitude
of longitudinal muscle fascicle growth compared with mea-
surement at optimal joint angle (75). Measurement of optimal
FL or FL around optimal joint angle provides a better case
that sarcomerogenesis occurred (assuming SL is constant)
and allows better interpretation of adaptations in FL in the
context of active force-length relations.
Following 5 wk of three different training programs (squat
lift þ sprint/jump training, hack squat þ sprint/jump train-
ing, and sprint/jump training alone), Blazevich et al. (72)
measured FL at proximal and distal regions of the vastus lat-
eralis and rectus femoris at close to optimal joint angle for
the knee extensors (90
). They observed some instances of
longitudinal fascicle growth, with squat lift þ sprint/jump
training significantly increasing FL in the distal ( þ 22%) and
proximal ( þ 83%) sites of the rectus femoris, and sprint/
jump training alone increasing FL in the distal site of the
vastus lateralis ( þ 80%) and proximal site of the rectus femo-
ris ( þ 39%). FL increases in the hack squat þ sprint/jump
training group did not reach statistical significance. With
data from all groups pooled, there was a near-significant
rightward shift in the knee angle of peak torque. Since there
was variation in FL adaptations among the training groups,
better quantification of torque-angle relationship adapta-
tions may have been possible within each group with a larger
sample size (currently n = 7–8/group).
Reeves et al. (43) provides what should arguably be consid-
ered gold-standard methods for assessment of muscle force-
length relations alongside longitudinal fascicle growth in
humans. Before and after 14 wk of conventional (i.e., concen-
tric þ eccentric) resistance training of the knee extensors in
older adults, they measured vastus lateralis FL at 9 joint angles
across the torque-angle relationship, thus allowing true mea-
surement of optimal FL. Furthermore, they measured FLs both
at rest and during isometric contraction. This approach
addresses another common limitation in studies on both ani-
mals and humans, as at the onset of isometric contraction, sar-
comeres near fiber ends shorten whereas those closer to the
middle lengthen (80), and fascicles as a whole can shorten up
to 35% of their resting length (91–93). Across the knee angles
tested, they found 8%–10% and 10%–18% increases in FL at
rest and during isometric contraction, respectively, with an
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION

11% increase in optimal FL. Correspondingly, there was a 10

shift in the optimal knee extension angle. Because they directly
assessed optimal FL, these results provide, to our knowledge,
the strongest evidence there is of sarcomerogenesis impacting
the torque-angle relationship in human muscle, assuming opti-
mal SL did not change with training.
Rather than a rightward shift in the torque-angle relation-
ship, Akagi et al. (39) showed that longitudinal fascicle growth
in humans can be accompanied by broadening of the torque-
angle relationship’s plateau region. Following 8 wk of isometric
dorsiflexion training at a long muscle-tendon unit length, they
observed a 3% increase in tibialis anterior FL, and concomi-
tantly a widening of the dorsiflexor torque-angle relationship’s
plateau region from a range of 10
–30
of plantar flexion to 5
–
40
of plantar flexion, as characterized by no significant differ-
ences in torque at those angles compared with the optimal
angle. By contrast, they observed a 3% decrease in FL following
training at a short muscle-tendon unit (MTU) length and no
broadening of the plateau region. Results from Kubo et al. (94)
may support these findings (though they did not characterize
muscle architecture and thus do not fit this review’s criteria),
observing increased torque production at angles throughout
the ROM following isometric knee extension training at a long
muscle-tendon unit length, and only close to the training angle
following training at a short muscle-tendon unit length.
Exploring the relationship between FL and peak torque in the
human plantar flexors, a computational model by Drazan et al.
(31) also showed that muscles with longer FLs generate more
joint torque throughout the ROM. A greater SSN may allow
individual sarcomeres, and thus whole fascicles, to be closer to
optimal length across a wider range of joint angles. This adap-
tation may also translate to increased force produced during
active shortening, or in other words greater mechanical work
(see INFLUENCE OF LONGITUDINAL MUSCLE FASCICLE GROWTH ON
MECHANICAL WORK AND PEAK POWER OUTPUT and Fig. 3). Direct
testing of this hypothesis would require in vivo measurement
of both SL and FL across the torque-angle relationship, which
to our knowledge has yet to be done. It is also possible that
broadening of the plateau region is an artifact of widening of
the whole torque-angle relationship, but without assessment of
active torque across the whole ROM, we can only speculate.
Other studies not meeting this review’s inclusion criteria
also observed significant increases in torque at several angles
throughout a joint’s ROM alongside increases in FL, but did
not investigate whether there was broadening of the plateau
region or the whole torque-angle relationship (56, 86, 88). In
addition, some studies have characterized the torque-angle
relationship of the knee extensors at only three angles (41),
or at wide (20
) intervals of angles across the torque-angle
relationship (89), and concluded no rightward shift in the
torque-angle relationship. Results such as these should be
interpreted with caution, as the shape of the knee extensor
torque-angle relationship has been shown to be unpredict-
able in the plateau region (56).
Summary of the Influence of Longitudinal Muscle
Fascicle Growth on the Active Force-Length
Relationship
There is sound evidence for a link between longitudinal
muscle fascicle growth and rightward shifts in the muscle

Figure 3. Visual representation of how sarcomerogenesis may allow for greater force production for the same absolute fascicle excursion. A: original
fascicle (24 mm, 11 sarcomeres). B: original fascicle (33 mm, 15 sarcomeres). Note that the longer fascicle (B) falls on closer to optimal positions for force
production on the sarcomere force-length and force-velocity relationships (sarcomeres are not to scale).

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 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
force-length and joint torque-angle relationships in animal
muscle; however, in humans at the joint level, only one study
(43) has shown a direct link between an increase in optimal FL
and a rightward shift in the torque-angle relationship. An
updated study investigating the influence of longitudinal fasci-
cle growth induced via immobilization in a stretched position
on the active force-length relationship is also warranted.
Lastly, further investigation is needed in both animals and
humans on the ability for longitudinal fascicle growth to widen
the force-length relationship, and particularly the plateau
region, which can be assessed by constructing force-length or
torque-angle relationships across a wide range with small inter-
length/interangle intervals.
INFLUENCE OF LONGITUDINAL MUSCLE
FASCICLE GROWTH ON MAXIMUM
SHORTENING VELOCITY
The force-velocity relationship dictates that force decreases
hyperbolically with increasing shortening velocity (95, 96).
With increasing speed of shortening, myofilaments slide past
each other faster, reducing the probability of actin-myosin
binding and the force produced per cross bridge, thereby lim-
iting force production at higher velocities (96, 97). It follows
that when shortening under zero load, a muscle can theoreti-
cally achieve maximum shortening velocity (VO). As it can be
challenging to place a true zero-load on a muscle, a theoretical
VO (Vmax) can also be estimated via extrapolation from the
force-velocity relationship using a Hill equation (87, 90). In
humans, maximum unloaded angular velocity of shortening
can also be used as an estimation of VO in vivo. Studies on
both animals and humans have shown that, assuming a simi-
lar fiber type composition, SSN is directly proportional to
Vmax because a greater SSN can allow individual sarcomeres
to shorten less for a given muscle excursion (2, 30, 97, 98).
Thus, longitudinal muscle fascicle growth may have the
potential to increase a muscle’s Vmax.
Denervation and Compensatory Overload
Some investigations of longitudinal muscle fascicle growth
in animals have demonstrated that changes in factors not
related to muscle architecture can affect Vmax irrespective of
an increase in SSN. In cats, Kean et al. (62) observed an 18%
increase in flexor digitorum longus SSN following denerva-
tion compared with contralateral controls, alongside a 13%
decrease in Vmax. As they also observed decreases in esti-
mated sarcomere shortening velocity and increases in time to
peak twitch tension, they attributed the Vmax decrease to
changes in biochemical factors and contractile proteins, such
as reductions in Ca2 þ -activated ATPase activity and changes
in myosin isoform. Via compensatory overload (i.e., ablation
of synergist muscles) of the rat plantaris, Roy et al. (63)
observed a 10% increase in fiber length and no change in SL
compared with controls, inferring an increase in SSN.
Concomitantly, they observed a 47% decrease in Vmax in units
of mm/s per 1000 sarcomeres (i.e., normalizing for the SSN
increase), attributed to changes in myosin ATPase activity
and a fast-to-slow fiber type shift (63, 99). Altogether, impair-
ment of biochemical factors related to contractile speed can
supersede the ability for longitudinal muscle fascicle growth
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to increase Vmax. To our knowledge, the influence of sarco-
merogenesis on Vmax in a more neurologically intact interven-
tion compared with denervation and compensatory overload
(e.g., eccentric training) has yet to be investigated. Such a
study would especially provide insight if performed on a pre-
dominately type I muscle (e.g., the rat soleus), reducing the
potential for a fiber type shift.
Exercise Training in Humans
To our knowledge, no training study fitting this review’s
inclusion criteria has observed longitudinal muscle fascicle
growth and directly assessed maximum angular velocity of
shortening under no added isotonic load; however, some stud-
ies provide insight. Thom et al. (100) measured FL of the
medial gastrocnemius in young and old men, finding young
men to have a 19% longer FL. Vmax estimated from the torque-
angular velocity relationship via the Hill equation was 38%
lower in old compared with young men. When normalizing
Vmax to FL, the difference in Vmax between young and old men
was reduced by 16%, or in other words, the longer FL (and
assumed greater SSN) of young men accounted for almost half
the difference in Vmax between young and old men. Somewhat
contrary to these findings, Akagi et al. (39) observed no change
in maximum isotonic angular velocity at a low load (10% of
maximum voluntary contraction torque) alongside a 3%
increase in tibialis anterior FL following 8 wk of isometric
training at a long muscle-tendon unit length. As such, cur-
rently there is little direct evidence in humans supporting the
hypothesis that longitudinal fascicle growth can increase Vmax.
Furthermore, neural adaptations and adaptations in tendon
stiffness are common following resistance training, including
isometric training (41, 56, 94), and likely contribute to shorten-
ing velocity at the joint level (49, 50, 101, 102). Techniques such
as correlation coefficients or linear regression (97, 98), or nor-
malizing velocity to FL (63, 100) may help better clarify the
individual contributions from neural, tendon, and FL adapta-
tions to in vivo shortening velocity in humans.
A potential practical application of the influence of longi-
tudinal fascicle growth on Vmax is shown in studies on sprint
performance, as it is generally agreed that sprinting requires
generation of high shortening velocity in locomotor muscles
(103). Strong correlations have been shown between running
sprint time and FL of the vastus lateralis, medial gastrocne-
mius, and lateral gastrocnemius (103–105), and between
front crawl swimming sprint time and FL of the vastus later-
alis and lateral gastrocnemius (106). Blazevich et al. (72) also
observed a 4% decrease in 10-m sprint time concomitant to
increases in FL in the distal site of the vastus lateralis
( þ 80%) and proximal site of the rectus femoris ( þ 39%) fol-
lowing 4 wk of sprint/jump training. Other studies that do
not fit this review’s inclusion criteria have also presented
potential links between training-induced increases in FL and
improved sprint performance (89, 107–109).
Summary of the Influence of Longitudinal Muscle
Fascicle Growth on Maximum Shortening Velocity
Despite reports that FL is directly proportional to a
muscle’s Vmax, little evidence in animals and humans sug-
gests that longitudinal fascicle growth can increase Vmax.
With that said, Vmax has not been assessed within a
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
neurologically intact animal model of sarcomerogenesis,
such as eccentric training, and in humans, confounding fac-
tors such as neural and tendon adaptations have not been
fully teased out. Because there are several cross-sectional
studies on the topic, there should also be further investiga-
tion into the relationship between training-induced longitu-
dinal muscle fascicle growth and Vmax in the context of
sprint performance.
INFLUENCE OF LONGITUDINAL MUSCLE
FASCICLE GROWTH ON MECHANICAL WORK
AND PEAK POWER OUTPUT
Muscle power production is defined as the dot product of
contractile force and velocity. Therefore, per the force-velocity
relationship, peak isotonic power occurs when force and veloc-
ity are both submaximal (100, 110). As SSN is believed to be
proportional to maximum shortening velocity, the hypothesis
can be made that longitudinal fascicle growth can improve
peak power output. Power can also be quantified as the rate of
mechanical work, with work being the product of a contrac-
tion’s linear or angular displacement and the force or torque
produced during displacement (111). These definitions can be
applied to obtain work and power from isokinetic (constant ve-
locity) and isotonic (constant load) shortening contractions (75,
76), sinusoidal contractions (i.e., work loops) that simulate
real-world locomotion in vitro (32, 112), and Wingate or coun-
termovement jump tests in humans (113, 114). As theorized by
Baxter et al. (115) and Drazan et al. (31) based on computational
models, increasing SSN may allow individual sarcomeres to
shorten slower and remain closer to the region of optimal force
production during shortening, increasing mechanical work
(and potentially power) by increasing force during displace-
ment for a given whole muscle excursion and shortening veloc-
ity (see Fig. 3 for a visual representation).
In Animals
Against what is hypothesized, currently it does not appear
that sarcomerogenesis impacts isokinetic work of shortening
in animals. Chen et al. (69) observed a 6% greater soleus SSN
in rats following 4 wk of decline running training compared
with incline running training; however, values for isokinetic
work of shortening were similar between groups. Furthermore,
Mashouri et al. (70) showed the same rats did not have differ-
ences in work of shortening in soleus single fibers, teasing out
potential confounding factors at the whole muscle level (e.g.,
intramuscular connective tissue).
In addition to isokinetic and isotonic contractions,
work and power can be assessed in cyclic contractions via
the work loop technique [for a review, see Ahn (112)]. Cox
et al. (32) measured maximum work loop power output
[(work of shortening – work of lengthening)  cycle fre-
quency] across a range of cycle frequencies (i.e., speeds of
sinusoidal active shortening followed by passive length-
ening) after 3 wk of incrementally surgically stretching
the rabbit latissimus dorsi. They observed a 25% increase
in SSN, but concomitantly maximum power output
decreased 40%. The cycle frequency with optimal power
output also shifted to 2–3 Hz compared with 5–7 Hz in
controls, indicating preference for slower velocities in the
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stretched muscle. They concluded these detriments to
work loop performance were caused by an increase in
force during the passive stretch phase of the work loops
(i.e., increased negative power, and loss of net power out-
put) due to an increase in collagen content, which con-
tributes to muscle passive stiffness (see INFLUENCE OF
LONGITUDINAL MUSCLE FASCICLE GROWTH ON THE PASSIVE
LENGTH-TENSION RELATIONSHIP). This conclusion was sup-
ported by a shift back toward control values for maximum
power output with an additional 3 wk of maintained (i.e.,
not further increased) stretch, as SSN increased another
5% and collagen content decreased back to control val-
ues. Further research is required to understand the influ-
ence of sarcomerogenesis on maximum power output
with other, less detrimental experimental interventions
(e.g., eccentric training). A recent preprint from our labo-
ratory provides insight, as rats who completed 4 wk of
weighted decline running training had an 8% greater SSN
than controls, alongside increased net work output in
some work loops (84). Furthermore, adaptations in intra-
muscular connective tissue likely did not interfere, as
there were no differences in collagen content or % cross-
linked collagen between trained and control rats.
To elucidate whether the observed longitudinal fascicle
growth contributed to the improved work loop perform-
ance, we estimated mathematically what the SL operating
ranges and sarcomere shortening velocities would have
been based on the FL, SSN, cycle frequency, and length
change values [described in preprint Hinks et al. (84)].
Briefly, by estimating FL at the end-ranges of a certain
length change, the SL range can then be estimated by
dividing FL by the known SSN. As seen in the preprint’s
Table 1, the sarcomeres of trained rats were estimated to
shorten/lengthen relatively less from optimal SL and oper-
ate at relatively slower shortening velocities than controls.
Therefore, it is possible that in the cycle frequency/length
change combinations investigated, the increased SSN
placed sarcomeres at more advantageous positions on the
force-length and force-velocity relationships, increasing
force production throughout the ROM and contributing to
a greater net work output.
In Humans
There is inconclusive evidence implicating longitudinal
muscle fascicle growth in increased mechanical work of
shortening and peak isotonic power in humans. First,
though they do not meet this review’s inclusion criteria, it
is worth noting the large quantity of studies that have
observed increases in peak concentric torque or 1-repeti-
tion maximum strength (which may imply increased work
of shortening) concurrent to apparent increases in FL (85,
107, 116–122). Following 8 wk of isometric training at a long
muscle-tendon unit length, our laboratory observed an
11% increase in isokinetic work of shortening in the dorsi-
flexors alongside a 3% increase in tibialis anterior FL,
although we observed a similar increase in work of short-
ening following training at a short MTU length alongside a
3% decrease in FL (75). In the same training study, how-
ever, training at a long muscle-tendon unit length led to
greater increases in isotonic power at loads of 10% and
50% of maximum torque (76). It should be noted that those
95
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
measures cannot deduce the true peak isotonic power, as
that would require assessment across a range of isotonic
loads due to the force-velocity relationship (110). In addi-
tion, it is crucial to consider the confounding factor of ten-
don adaptations in joint-level data. For more compliant
tendons, the joint level excursion may be primarily taken
up by the tendon rather than muscle fascicles, whereas
stiffer tendons present a more proportional relationship
between fascicle shortening and joint angular rotation.
Using ultrasound to track actual fascicle excursions (rather
than just joint excursions) during isokinetic contractions
is becoming more common (123) and may help address
this confounding factor going forward. This technique
may also help address more complex questions such as:
does longitudinal fascicle growth impact mechanical work
during a slow contraction to the same extent as during a
fast contraction? Altogether, though studies linking
increased isokinetic mechanical work of shortening and
peak isotonic power to longitudinal fascicle growth in
humans are currently lacking, they provide grounds for
further exploration.
There has also been some investigation into the role of FL
in practical measures of peak power. Wingate peak power out-
put has been shown to be related to quadriceps and gastrocne-
mii anatomical cross-sectional (ACSA) and vastus lateralis
and medial gastrocnemius pennation angle (PA), but not FL
in sprint cyclists (124, 125). These relationships are somewhat
understandable, as ASCA and PA are associated with maxi-
mum force or torque production (2, 126), which plays a role in
power generation as well. Instead, vastus lateralis and medial
gastrocnemius FL had negative relationships with time to
peak power output in sprint cyclists (124), suggesting longitu-
dinal fascicle growth may shorten the time to develop maxi-
mal power. Conversely, vastus lateralis FL was found to
explain Wingate peak power output together with the percent-
age of type II fibers in road cyclists (113), and partly explain
Wingate peak power output in male rowers (127). Correlations
have also been drawn between vastus lateralis FL and coun-
termovement jump power (114), and some studies not fitting
this review’s inclusion criteria have observed increased coun-
termovement jump power concomitant to apparent increases
in vastus lateralis FL (107, 122). More longitudinal training
studies on humans with assessment of optimal FL are needed
to determine if longitudinal fascicle growth influences these
practical assessments of peak power output.
Summary of the Influence of Longitudinal Muscle
Fascicle Growth on Mechanical Work and Peak Power
Output
Longitudinal muscle fascicle growth does not appear to
affect mechanical work of isokinetic shortening, however, may
increase net work output in sinusoidal contractions. To our
knowledge, no study on animals has assessed peak isotonic
power alongside an observation of longitudinal fascicle growth.
Some evidence in humans implicates longitudinal fascicle
growth in improved peak isotonic power; however, further
investigation is needed obtaining true peak power (i.e., across a
range of isotonic loads). There are also many cross-sectional
studies suggesting longitudinal fascicle growth can improve
practical measures of peak power output, and more longitudi-
nal studies are needed to corroborate those findings.
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INFLUENCE OF LONGITUDINAL MUSCLE
FASCICLE GROWTH ON THE PASSIVE
LENGTH-TENSION RELATIONSHIP
Noncontractile elements such as the elastic protein titin,
the intramuscular collagen matrix, tendons, and aponeuro-
ses contribute to a muscle’s passive tension development
when stretched (17, 128, 129). It follows that passive tension
increases exponentially with muscle length, forming the ba-
sis for the passive length-tension relationship (20). Since
titin spans the half-sarcomere, a greater SSN may allow indi-
vidual sarcomeres to stretch less during joint or muscle dis-
placement, reducing passive tension especially at longer
muscle lengths. Hence a rightward shifted, less steep passive
length-tension relationship is expected with longitudinal
fascicle growth. With lower passive tension at longer muscle
lengths, longitudinal fascicle growth may also be expected to
increase joint ROM.
Old Compared with Young Muscle
Though not an intervention, comparison between old
and young muscle provides insight in this area. When com-
paring the medial gastrocnemius of old and young rats,
Power et al. (130) found that young rats had a 10% higher
SSN. Correspondingly, the older muscles (with fewer serial
sarcomeres) had greater passive forces at longer lengths (130).
With that said, the age-related decreases in SSN could not
entirely explain the elevated passive tension, and age-related
increases in passive tension are also associated with stiffening
of the intramuscular collagen matrix (131), which may have
contributed to these results as well. As made apparent in the
sections below, there is a clear trade-off between SSN adapta-
tions and adaptations in intramuscular collagen for influenc-
ing a muscle’s passive length-tension relationship.
Immobilization in a Stretched Position
Tabary et al. (13) immobilized the cat soleus in a stretched
position for 4 wk and observed a 19% increase in SSN com-
pared with controls. Against what is hypothesized, the joint
angle-passive tension curves were identical between the immo-
bilized and contralateral control muscles. Similar results were
observed by Goldspink et al. (23) with a larger sample size (n =
12/group instead of n = 5–6/group) and an even greater increase
in SSN ( þ 25%) when denervating the soleus while immobi-
lized in a stretched position. A limitation of these studies is
they did not specify how many fascicles they performed SSN
estimations on, thus the magnitudes of SSN increase they
reported may be subject to error. With that said, the results
of Williams and Goldspink (12), who estimated SSN from 5
fascicles per muscle, are consistent with the above find-
ings. Following immobilization in a stretched position, they
observed a 16% increase in mouse soleus SSN compared with
controls, and no differences in the whole muscle passive
length-tension relationship. Although the same laboratory
showed that 7 days of immobilization in a stretched position
did not alter intramuscular connective tissue content observed
via Picro-sirius red staining in the rabbit soleus (42), a closer
look at time-course changes by Ahtikoski et al. (132) found
hydroxyproline concentration (the primary protein constituent
in collagen) began to significantly increase in the rat soleus
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
starting at 7 days of immobilization in a stretched position.
Therefore, since the above studies immobilized the muscle for
4 wk, it is possible they did not observe changes to the passive
length-tension relationship due an interplay between increased
collagen content and increased SSN. As we are only speculating,
further investigation is needed on the influence of intramuscu-
lar collagen adaptations on the passive force-length relationship
following immobilization in a stretched position.
Surgery-Induced Stretch
More profound incidences of intramuscular collagen coun-
teracting the influence of sarcomerogenesis on the passive
length-tension relationship are seen in studies on surgery-
induced stretch. After surgically stretching the rabbit second
extensor digitorum, Takahashi et al. (7) observed 20% and 13%
increases in SSN 1 and 4 wk postsurgery, respectively, com-
pared with controls. Despite the increase in SSN, the stretched
muscles produced greater passive tension at longer muscle
lengths than controls. A follow-up analysis comparing the
muscle’s single fibers and fiber bundles found the same effect
to occur in fiber bundles but not in single fibers. Since fiber
bundles contain intramuscular collagen whereas single fibers
do not, they concluded the passive length-tension curve’s left-
ward shift was due to collagen proliferation following the sur-
gery. In rabbits, Williams et al. (65) observed a 64%–89% loss
in ankle joint ROM and a leftward shift in the whole muscle
passive length-tension relationship concomitant to an 13%
increase in tibialis anterior SSN induced via tibial lengthening
compared with controls. They attributed the increased passive
tension to collagen accumulation seen by Picrosirius red stain-
ing. Lastly, as mentioned in In Animals, Cox et al. (32) observed
decreased net work output due to increased work of lengthen-
ing in passive work loops as a result of collagen accumulation,
despite a 25% increase in SSN following 3 wk of incremental
surgical stretch of the rabbit latissimus dorsi.
Static Stretch Training
Unlike the studies on surgical stretch, De Jaegar et al. (67)
observed no changes in collagen content and a 9% increase
in rabbit soleus SSN following 4 wk of static stretch training
compared with contralateral controls. Aligning with what is
hypothesized for sarcomerogenesis, they observed a right-
ward shift in the joint angle-passive tension relationship (a
16% decrease in peak passive torque).
Results from studies on humans disagree with the above
observations in animals. Panidi et al. (74) employed 12 wk of
static stretch training of the plantar flexors in young female
volleyball players. Performing ultrasound measurements at
approximately the optimal plantar flexion angle, they observed
a 6% increase in FL at the middle region of the medial gastro-
cnemius, and a concomitant 22% increase in maximum dorsi-
flexion ROM. However, the joint angle-passive tension
relationship did not change following training, and ROM
increased to the same extent in the contralateral (i.e., not
exposed to stretching) plantar flexors, suggesting a cross-edu-
cation effect of training on ROM. Increases in ROM of the
trained and untrained limb also occur following static stretch
training in the absence of FL adaptations (133–135). These
observations have led authors to conclude that increased ROM
following static stretch training in humans is due to neural
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adaptations (e.g., increased stretch tolerance) rather than mor-
phological adaptations. Furthermore, correlations between FL
and ROM have only been reported when adjusting for muscle
slack angle (136). Panidi et al. (74) also pointed out that
increased FL following static stretch training in humans tends
to only occur with training interventions longer than 6 wk and
with long stretching durations to maximize mechanical ten-
sion (137, 138). Altogether, the hypothesis that longitudinal fas-
cicle growth induced by static stretch training can increase
joint ROM and shift the passive length-tension relationship is
only supported by studies on animals. Although some human
studies have reported increases in FL following intense static
stretch training, none have directly assessed whether a shift in
optimal FL occurred [Reeves et al. (43)], and doing so in future
research may help refine current interpretations.
Eccentric Training
In animals, there is evidence linking eccentric training-
induced longitudinal muscle fascicle growth to a shift in the
passive length-tension relationship. Chen et al. (69) observed
a 6% greater soleus SSN in rats following decline running
training compared with incline running training. In those
same rats, Noonan et al. (71) observed lower passive stress
and an 50% lower passive elastic modulus in single fibers
of decline-trained rats than incline-trained rats, thus the
greater SSN may have allowed for less passive tension devel-
opment during stretch of single fibers. There were no differ-
ences in passive stress or modulus in fiber bundles, however,
suggesting a potential interference of intramuscular collagen
such that there may not be similar adaptations in passive
properties at the whole muscle level. A recent preprint from
our laboratory addresses this question. Following 4 wk of
weighted decline running training in rats, we observed an
8% increase in soleus SSN compared with controls [preprint
Hinks et al. (84)]. Concomitantly, the soleus of trained rats
had a rightward shifted passive length-tension relationship
compared with controls, with 45–62% lower passive forces
produced across the muscle lengths tested. We also observed
no differences in collagen content or % cross-linked collagen
between groups, bolstering the interpretation that the pas-
sive length-tension relationship shifted due to the observed
longitudinal fascicle growth.
The influence of eccentric training-induced longitudinal
fascicle growth on the passive length-tension relationship in
humans is less clear. Kudo et al. (73) assessed medial gastro-
cnemius FL at approximately the optimal plantar flexion
angle following 12 wk of eccentric compared with conven-
tional calf-raise training. They observed an increase ( þ 9%) in
FL and a concomitant increase ( þ 3%) in dorsiflexion ROM in
only the eccentric training group. An association between
these two measures should be made with caution, however,
since they did not assess whether there were statistically sig-
nificant relationships between FL and ROM. As well, due to
potential cross-education effects of training on ROM as
reported in the static stretch training studies above, assessing
ROM in a contralateral control limb would have provided
insight. Assessment of passive resistive torque throughout the
ROM could have also elucidated whether the increased ROM
was associated with morphological adaptations. Although a
study employing a similar training program on the plantar
97
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
flexors did observe a rightward shift in the joint angle-passive
tension curve (23% decrease in passive resistive torque),
they did not measure FLs (139), so we can only speculate.
Summary of the Influence of Longitudinal Muscle
Fascicle Growth on the Passive Length-Tension
Relationship
Studies on animals provide strong evidence that longi-
tudinal muscle fascicle growth can reduce passive tension
at long lengths at levels of the single fiber, whole muscle,
and joint, unless there is concurrently considerable prolif-
eration of the intramuscular collagen matrix. Further
investigation is needed to clarify whether such prolifera-
tion of the intramuscular collagen matrix occurs later (i.e.,
beyond 7 days) when immobilizing a muscle in a stretched
position, and how that impacts passive tension. More
research also is needed with assessment of optimal FL and
contralateral controls to elucidate whether longitudinal
fascicle growth induced via static stretch training and
eccentric training impacts the passive-length tension rela-
tionship and joint ROM in humans.
FUTURE DIRECTIONS
Due to longitudinal muscle fascicle growth’s potential to
increase the range for active force production, increase optimal
muscle length, and reduce passive tension at longer muscle
lengths, interventions promoting longitudinal fascicle growth
may be beneficial in certain clinical settings (e.g., muscle strain
injury prevention, sarcopenia, muscle spasticity) (5, 34, 36).
Figure 4. What is currently known about how longitudinal muscle fascicle growth influences mechanical function. Red X’s indicate a particular modality
did not show the indicated functional adaptation. Question marks indicate inconclusive findings in current literature.
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Our review highlights additional benefits such as increases in
shortening velocity, force production throughout the ROM,
and power production are also hypothetically possible with
longitudinal fascicle growth. However, many of the beneficial
mechanical adaptations associated with longitudinal fascicle
growth are supported more by whole muscle data from ani-
mals rather than more clinically applicable joint level data
from humans. This gap raises the question: in understanding
how longitudinal fascicle growth can influence mechanical
function, is joint level data more important than data from iso-
lated muscle? In everyday life, neural inputs and all the
muscles and tendons surrounding a joint are involved, rather
than one muscle alone.
The confounding factors of in vivo joint-level data (i.e.,
neural adaptations, tendon adaptations, muscle synergy)
have yet to be teased out from most of the interpretations
in existing literature. As outlined throughout this review,
there are cases in studies on humans both where the
hypotheses for how longitudinal fascicle growth influences
mechanical function are proven correct, and incorrect. It is
possible that in some of these studies on humans, con-
founding factors are interfering with the hypothesis, like
what has been observed with intramuscular collagen adap-
tations and the passive length-tension relationship in stud-
ies on animals (described in INFLUENCE OF LONGITUDINAL
MUSCLE FASCICLE GROWTH ON THE PASSIVE LENGTH-TENSION
RELATIONSHIP). Although it is arguably impossible to fully
isolate adaptations from an intervention to increases in FL,
several methodologies exist to better understand how longi-
tudinal fascicle growth influences in vivo mechanical func-
tion in humans.
 INFLUENCE OF LONGITUDINAL FASCICLE GROWTH ON MECHANICAL FUNCTION
As discussed, an approach such as Reeves et al. (43) (i.e.,
construction of a torque-angle relationship, with measurement
of FL via ultrasound at all joint angles) should be employed
when determining optimal FL in vivo. Alongside this, microen-
doscopy provides a noninvasive way to measure SL in vivo (51,
140, 141), and can thereby allow measurement of in vivo opti-
mal SL and estimation of SSN. Furthermore, tracking fascicle
excursion during shortening contractions would elucidate any
uncertainty related to tendon compliance (123).
Unfortunately, microendoscopy systems currently have
limited availability. Other methods exist, however, to pro-
vide better precision in interpreting data from humans in
the context of longitudinal fascicle growth. The average
human SL (2.64 μm) determined by Walker and Schrodt (53)
from cadaver inspection is sometimes used to estimate SSN
from ultrasound-measured FL (75). For better precision, one
could also take biopsies from a muscle after determining in
vivo optimal FL via ultrasound and construction of the tor-
que-angle relationship, then test single fibers obtained from
the biopsies to determine an average optimal SL for that
same muscle. Those FL and SL measurements can then be
used to estimate SSN. Once SSN has been determined, it can
also be used alongside FL measurements (SL = SSN/FL) to
estimate SLs throughout the ROM, as described in a recent
commentary (27). Like the microendoscopy method described
above, this may provide insight into adaptations such as
broadening of the plateau region and increased work of
shortening.
On top of the methods described above, linear regression
or correlation coefficients can be employed to elucidate the
influence of FL, compared with other variables (e.g., tendon
stiffness, CSA, pennation angle, fiber type), on measures of
mechanical function. These types of analysis are currently
common in cross-sectional studies investigating FL and me-
chanical function (103–106, 114, 124, 125, 127), but less so in
intervention studies (8, 64).
Finally, FL, SL, and SSN, and how they adapt to interven-
tions, are subject to regional variability (8, 51, 72, 79). Future
studies should consider interpreting how longitudinal fascicle
growth influences mechanical function in the context of how
different regions of muscle adapt: it seems sarcomeres are
added distally on a fascicle (51), but do distal, mid-belly, or
proximal FL adaptations influence mechanical function to dif-
ferent extents? This limitation applies to studies on animals as
well: most take an average across several FL and SL measure-
ments to estimate SSN, inherently ignoring assessment of re-
gional variability in SSN adaptations. Furthermore, at least 6
FL measurements and 6 SL measurements per fascicle appear
to be the current consensus for estimating SSN (69, 142); how-
ever, to our knowledge, no study has verified the validity of
this quantity of measurements against other quantities.
CONCLUSIONS
An often-investigated example of skeletal muscle remodel-
ing is longitudinal muscle fascicle growth, in which SSN
increases in response to a change in mechanical tension pre-
sented by overstretching. Longitudinal fascicle growth has
been hypothesized to influence aspects of mechanical function
including the active and passive force-length relationships,
shortening velocity, and mechanical work and power output.
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These outcome measures have been assessed concomitant to
longitudinal fascicle growth across a wide range of interven-
tions including immobilization in a stretched position, surgical
stretch, denervation, compensatory overload, various exercise
training programs, and static stretch training (summarized in
Fig. 4). This review aimed to outline gaps and limitations in
the literature on how longitudinal fascicle growth influences
mechanical function to guide future research.
There is currently strong evidence across various types of
interventions that longitudinal fascicle growth can induce a
rightward shift in the muscle force-length and joint torque-
angle relationship in animals; however, in humans, existing
evidence is less concrete due to methodological limitations.
More investigation is also needed on the ability for longitudinal
fascicle growth to widen the whole force-length relationship,
and particularly the plateau region. There is currently little evi-
dence in animals or humans supporting that longitudinal fasci-
cle growth can increase Vmax; however, this question has yet to
be investigated in a neurologically intact model of longitudinal
fascicle growth such as eccentric training. There has also been
almost no investigation of the influence of longitudinal fascicle
growth on peak isotonic power across a range of loads in ani-
mals or humans. Longitudinal fascicle growth may also reduce
passive tension at long muscle lengths unless there is consider-
able proliferation of the intramuscular collagen matrix. In ani-
mals, it appears that increased SSN in the absence of collagen
accumulation can also increase joint ROM. In humans, how-
ever, it is unclear whether increased joint ROM is associated
with longitudinal muscle fascicle growth, or solely neural
adaptations. To fill current knowledge gaps and improve real-
world applicability, future research can assess optimal FL and
estimate SSN in vivo, track fascicle excursions in dynamic con-
tractions, account for regional variability in muscle architec-
ture, and employ statistical models to assess the relationships
between different variables.
GRANTS
This review received funding from the National Sciences and
Engineering Research Council of Canada (NSERC) (to G. A. Power).
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by
the authors.
AUTHOR CONTRIBUTIONS
A.H. prepared figures; A.H. and G.A.P. drafted manuscript; A.H.,
M.V.F., and G.A.P. edited and revised manuscript; A.H., M.V.F.,
and G.A.P. approved final version of manuscript.
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