Page 1 of 5
Hypothesis
Licensee OA Publishing London 2013. Creative Commons Attribution License (CC-BY)
For citation purposes: Martins WR, Carvalho MM, Mota MR, Cipriano GFB, Mendes FAS, Diniz LR, et al. Diacutaneous
fibrolysis versus passive stretching after articular immobilisation: muscle recovery and extracellular matrix
remodelling. OA Medical Hypothesis 2013 Dec 21;1(2):17.
Competing interests: none declared. Conflict of interests: none declared.
All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
All authors abide by the Association for Medical Ethics (AME) ethical rules of disclosure.
Biomedical Sciences
Diacutaneous fibrolysis versus passive stretching
after articular immobilisation: muscle recovery and
extracellular matrix remodelling
WR Martins1*, MM Carvalho1, Mota MR2, GFB Cipriano1, FAS Mendes1, LR Diniz1,
GC Junior1, RL Carregaro1, JLQ Durigan1
Abstract
Introduction
Atrophy and muscle shortening
due to articular immobilisation are
common problems in musculoskel-
etal rehabilitation. Muscle stretching
mechanical stimuli might be consid-
ered as the golden standard proce-
dure to improve muscle flexibility
in rehabilitation. Muscle stretching
generates mechanotransduction, po-
tentiating specific gene expression
and promotes sarcomerogenesis and
extracellular matrix remodelling on
shortened and atrophied muscles.
Hypothesis
Diacutaneous fibrolysis, like stretch-
ing, uses an external force to stress
connective and muscle tissues me-
chanically to treat muscle short-
ening; thus, it is widely used in
clinical practice even if there is no
evidence to support it. Consider-
ing this subject, we have hypoth-
esised that diacutaneous fibrolysis
can generate mechanotransduction,
affecting muscle hypertrophy and
extracellular matrix remodelling after
immobilisation.
Evaluation of hypothesis
We have designed a laboratory ex-
perimental study with a sample of
50 rats. The sample was randomly di-
vided into five groups: Control group
(n = 10) with non–immobilised rats;
3–week immobilisation group (n =
10); 3–week immobilisation/3–week
non–immobilisation group (n = 10);
3–week immobilisation/3–week
stretching group (n = 10); and 3–
week immobilisation/3–week dia-
cutaneous fibrolysis group (n = 10).
All rats had their left tibiotarsal joint
immobilised in maximum plantar
flexion with the orthotics for 3 con-
secutive weeks. After the immobilisa-
tion period, the intervention groups
received their respective interven-
tion on their left triceps suralis for
3 weeks. Dependent variables of the
study were sarcomere analysis, poly-
merase chain reaction, connective
tissue density, collagen birefringence
and matrix metalloproteinases. Sta-
tistical analysis was performed using
analysis of variance and Duncan post
hoc test was applied for differences
between groups. For all calculations,
a 5% (p < 0.05) significance level was
established.
Conclusion
If the hypothesis is confirmed, the
present study might provide evidence
to support the use of this physical
therapy resource widely used to treat
muscle dysfunctions.
Introduction
Muscle plasticity is a remarkable me-
chanical property; it is the ability of
muscle cells to alter their structure
and function in accordance to differ-
ent stimuli. Articular immobilisation
leads to muscle atrophy and rigidity,
characterised by decrease in muscle
fibre protein content and size1 and
increase in their connective tissue2.
Data show that during the first 6
hours of articular immobilisation,
the synthesis of muscle protein is re-
duced, and within 72 hours, it might
reduce the muscle mass up to 30% of
its original size3,4. Seven days of im-
mobilisation results in loss of muscle
fibres, reduces the number of serial
and parallel sarcomeres and leads
to muscle atrophy and shortening5,6.
Evidence shows that the increase in
connective tissue diminishes blood
flow, water and proteoglycans into
muscle fibres; binding of abnormal
collagen fibres occurs, which induces
rigidity and loss of flexibility of the
connective tissue7,8.
Passive muscle stretching is con-
sidered as an effective resource and
is often used to increase muscle and
joint flexibility. Previous studies have
showed that muscle stretching pro-
motes sarcomerogenesis (contractile
protein synthesis triggered by spe-
cific muscle gene potentiation)9–12 by
mechanotransduction (mechanical
stimulus conversion into chemical
activity)13–15. During muscle stretch-
ing, mechanical stimuli are first
transmitted to the extracellular ma-
trix (ECM), and the integrins on their
membrane detect those stimuli and
transmit them to the cell interior, ac-
tivating a series of nuclear proteins
responsible for modifying the specif-
ic gene transcription that regulates
sarcomerogenesis16.
Stretching–induced mechanotrans-
duction affects connective tissue
remodelling through matrix metal-
loproteinases (MMPs) because they
degrade ECM components. MMPs
play a role in both tissue function and
development, which include patho-
logical processes. Coutinho et al.2.
* Corresponding author
Email: wrmartins@me.com
1
Division of Physical Therapy, University of
Brasilia, Brasilia, Distrito Federal, Brazil
2
College of Health Sciences, University Center
of Brasília, Brasília, Brazil
