Is Postexercise Muscle

Soreness a Valid
Indicator of Muscular
D
Adaptations?
o
w
n
Brad J. Schoenfeld, MSc, CSCS, CSPS1 and Bret Contreras, MA, CSCS2
1
l
o
Department of Health Science, Lehman College, Bronx, NY; and 2School of Sport and Recreation,
a
d Auckland University of Technology, Auckland, New Zealand
e
d

f
r
o ABSTRACT not well understood, DOMS nociceptors (6,28).
m

DELAYED ONSET MUSCLE SORE- appears to be a product of

h
t
NESS (DOMS) IS A COMMON SIDE inflammation caused by
t
p
: EFFECT OF PHYSICAL ACTIVITY, microspcopic tears in the connec-
tive tissue elements that sensitize
/
/
j PARTICULARLY OF A VIGOROUS
o
u NATURE. MANY EXERCISERS noci- ceptors and thereby heighten
the sensation of pain (28,42).
r
n
a WHO REGULARLY PERFORM
l
s RESISTANCE TRAINING CONSIDER Histamines, bradykinins,
.
l
w DOMS TO BE ONE OF THE BEST prostaglandins, and other noxious
w
.
INDICATORS OF TRAINING chemicals are believed to mediate
c
o
m EFFECTIVENESS, WITH SOME discomfort by acting on type III and
/
n
RELYING UPON THIS SOURCE AS type IV nerve afferents that
s
c
a A PRIMARY GAUGE. THIS ARTICLE transduce pain signals from muscle to
-
s
DISCUSSES THE RELEVANCE OF the central nervous system (6).
c
j
b USING DOMS TO ASSESS These substances increase vascular
y

WORKOUT QUALITY.
perme- ability and attract
B
neutrophils to the site of insult.
Neutrophils, in turn, gen- erate
h
D
M
f
5 INTRODUCTION reactive oxygen species (ROS),
which can impose further damage
e

D
P
H
elayed onset muscle soreness
K
a
(DOMS) is a common occur- to the sarcolemma (8). Biochemical
v
1 rence in response to changes resultant to a structural
z
E
o
unfamiliar disrup- tion of the extracellular
u
m or vigorous physical activity. It has matrix (ECM) also have been
1
t been noted observationally that many implicated to play a causative role
Q
f
N
individuals who regularly perform (53). It has been pro- posed that
resistance training consider DOMS
damage to myofibers facil- itates the
to be one of the best indicators of
training effectiveness, with some escape and entrance of intracellular
relying upon this source as a and extracellular proteins, whereas
primary gauge (37). In fact, there is disturbance of the ECM pro- motes
a long-held belief that DOMS is a the inflammatory response (53). In
necessary precursor to muscle combination, these factors are
remodeling (13). thought to magnify the extent of
Current theory suggests that DOMS is sore- ness. In addition, DOMS can
related to muscle damage from be exac- erbated by edema, whereby
unfa- miliar or unaccustomed swelling exerts increased osmotic
exercise (48). Although the exact pressure within muscle fibers that
mechanisms are serve to fur- ther sensitize
DOMS is most pronounced exercise bout and port sex-related differences in the
when exercise training peaks at approximately expression of DOMS (11,45).
provides a novel stim- ulus to 48 hours postexercise
the musculoskeletal system (42). However, the THEORETICAL BASIS FOR USING
(4). Although both precise time course and DOMS AS A GAUGE FOR
concentric and eccen- tric extent of DOMS is MUSCULAR ADAPTATIONS
training can induce DOMS, highly variable and can The first step in determining
studies show that last for many days whether DOMS provides a valid
lengthening actions have the depending on factors, gauge of mus- cle development is to
most profound effect on its such as exercise establish whether the theory has
mani- festation (7). As a intensity, training biological plausibility. Plausibility
general rule, soreness status, and genetics. can possibly be inferred from the
becomes evident about 6–8 The pre- vailing body of correlation between DOMS and
hours after an intense literature does not sup- exercise-induced muscle damage
(EIMD). It has been
KE Y W OR DS :
DOMS; delayed onset muscle sore- ness;
16 VOLUME 35 | NUMBER 5 | OCTOBER 2013 Copyright © National Strength
workout and Conditioning
quality; AssociationEIMD
muscle damage;
posited that structural changes associ- suggested that they induce similar hypertrophic effects on skeletal
ated with EIMD influence gene muscle (56).
expression, resulting in a
strengthening of the tissue that helps Muscle damage also may mediate
protect the muscle against further hypertrophy by facilitating activation of
injury (1,44). When considering the satellite cells (i.e., muscle stem cells). When
mechanisms of muscle hypertrophy, stimulated by mechanical stress, satellite cells
there is a sound theoretical basis generate precursor cells (myoblasts) that
suggesting that such damage is in proliferate and ulti- mately fuse to existing
fact associated with the accretion of cells, providing the necessary agents for
contractile proteins (48). What remodeling of muscle tissue (63,67). In
follows is an overview of the evi- addition, under certain conditions, satellite
dence supporting a hypertrophic cells are able to donate their nuclei to the
role for EIMD. An in-depth existing muscle fibers, enhancing their capacity
discussion of the topic is beyond the for protein synthesis (2,34). Evidence
scope of this article, and interested substantiates that satellite cell activity is
readers are referred to the recent upregulated in response to EIMD (12,46,49).
review by Schoenfeld (48). This is consistent with the survival
mechanisms of the muscle cell where damaged
It is hypothesized that the acute fibers must quickly obtain additional
inflam- matory response to damage is myonuclei to facilitate tissue repair.
a primary mediator of hypertrophic Activation of satellite cells provides these
adaptations. Macrophages, in needed myonuclei and co-expressing various
particular, are believed to promote myogenic regulatory factors, such as Myf5,
remodeling pursuant to damaging MyoD, myogenin, and MRF4, which are
exercise (60), and some re- searchers involved in muscle repara- tion and growth
have hypothesized that these (10). To this end, stud- ies indicate that a
phagocytic cells are required for person’s ability to expand the satellite cell
muscle growth (23). Current theory pool is a critical factor in maximizing muscle
suggests that macrophages mediate growth (41). It should be noted, however,
hypertrophy through the secretion of that satellite cells are responsive to both
cytokines syn- thesized within muscle damaging and nondamaging ex- ercises
skeletal muscle (also known as (40), and it is not clear whether their activity
myokines). Myokines have been is enhanced by EIMD in a manner that
shown to possess anabolic proper- promotes meaningful dif- ferences in muscle
ties, exerting their effects in an auto- hypertrophy.
crine/paracrine fashion to bring about
Cell swelling is another potential mech- anism
unique effects on skeletal muscle
by which muscle damage may promote
adap- tation (36,43,51). It should be
hypertrophic adaptations. EIMD is
noted that some research has shown
accompanied by an accumula- tion of fluid and
that myokine production may be
plasma proteins within the fiber, often to an
largely independent of damage to
extent whereby this buildup exceeds the
muscle tissue (62). This may be a
capacity of lym- phatic drainage (16,31,42).
function of the specific myo- kine
This results in tissue edema, with significant
response because numerous myo-
swelling persisting in trained subjects for at
kines have been identified with
least 48 hours after an exercise bout (19). Cel-
each displaying unique responses to
lular swelling is theorized to regulate cell
exercise training (40). Neutrophils,
function (17), stimulating anabolism via
another phagocytic leukocyte, also
increasing protein synthesis and decreas- ing
may play a role in inflammatory-
protein breakdown (15,33,54). Although the
mediated post- exercise hypertrophy,
exact mechanisms remain poorly understood, it
conceivably by signaling other
appears that
inflammatory cells nec- essary for
muscle regeneration. One such
possibility is ROS (65), which can
function as key cellular signaling
molecules in exercise-induced
adaptive gene expression (14,20,21,59).
Studies show that ROS promote
growth in both smooth muscle and
cardiac muscle (55), and it has been
membrane-bound, integrin-associated from damaging exer- cise it may interfere with the recu-
volume sensors are involved in the would be additive rather perative process (24,38). Studies
pro- cess (27). These osmosensors than con- stitutive. indi- cate that regeneration of muscle
activate intracellular protein kinase Furthermore, it is important tissue in those with severe EIMD
transduction pathways, possibly to note that excessive can exceed 3 weeks, with full
mediated by auto- crine effects of damage has a decidedly recovery taking up to 47 days when
growth factors (5). The effects of cell negative effect on exercise force production deficits reach 70
swelling subsequent to EIMD have performance and recovery. (47). In extreme cases, EIMD can
not as yet been directly investigated, By defini- tion, severe result in rhabdomyolysis (40), a
however, and it therefore remains EIMD decreases force- potentially serious condition that
unclear whether the associated edema producing capacity by 50 may lead to acute renal failure (61).
promotes similar anabolic and anti- or more (40). Such When taking all factors into
catabolic effects to those reported in functional decrements will account, it can be postulated that
the literature. necessarily impair an EIMD may enhance hypertrophic
Despite the sound theoretical ratio- individual’s abil- ity to train adaptations, although this theory is
nale, direct research showing a at a high level, which in far from con- clusive. The hormesis
cause- effect relationship between turn would be detrimental theory states that biological systems’
EIMD and hypertrophy is currently to muscle growth. response to stressors follows an
lacking. It has been shown that Moreover, although training inverted U-shaped curve (44). This is
muscle damage is not obligatory for in the early recovery phase consistent with Selye’s (50) concept
hypertrophic adapta- tions (3,13,25). of EIMD does not seem to of the general adaptation
Thus, any anabolic effects resulting exacerbate muscle damage, syndrome and would

Strength and Conditioning Journal | www.nsca-scj.com 17

Muscle Soreness as an Indicator of Workout Quality

suggest that if EIMD does indeed reason for caution when use DOMS as a gauge of muscular adaptations
pro- mote muscle development, attempting to given the theorized role of the acute
optimum benefits would be realized inflammatory response in tissue remodeling
from mild to moderate damage. subsequent to EIMD. It also deserves mention
However, an optimal degree of that noneccentric aerobic endurance exer- cise
damage for maximiz- ing muscle can cause extensive muscle sore- ness. Studies
growth, assuming one does in fact show the presence of DOMS after marathon
exist, remains to be determined. running and long-duration cycling (57). These
types of exercise are not generally associated with
IS THERE A CAUSAL LINK significant hypertrophic adapta- tions, indicating
BETWEEN DOMS AND MUSCLE
HYPERTROPHY? that soreness alone is not necessarily suggestive
of growth.
Given that DOMS is related to
EIMD and assuming EIMD is Moreover, DOMS displays a great deal of
indeed a medi- ator of hypertrophy, interindividual variability (58). This variability
the question then becomes whether persists even in highly experienced lifters, with
these events can be linked to some consis- tently reporting perceived soreness after
conclude that DOMS is a valid a workout, whereas others experiencing little, if
indicator of growth. Although it is any, postexercise muscular ten- derness.
tempting to draw such a relation- Anecdotally, many bodybuild- ers claim that certain
ship, evidence suggests reason for muscles are more prone to soreness than others.
skepticism. First, it remains debatable They report that some muscles almost never
as to whether DOMS is an accurate experience DOMS, whereas other muscles almost
gauge of muscle damage. There is always experience DOMS after training. Recent
little doubt that DOMS is a by- research supports these assertions (52). Because the
product of EIMD (6,40). However, bodybuilders possess marked hyper- trophy of the
studies show that soreness, as muscles that are and are not prone to DOMS, it
reported on a visual analog scale, is casts doubt on the supposition that soreness is
poorly correlated with both the time manda- tory for muscle development. More-
course and the magni- tude of over, genetic differences in central and peripheral
accepted markers of EIMD, adjustments and variations in receptor types and in
including maximal isometric strength, the ability to mod- ulate pain at multiple levels in
range of motion, upper arm the ner- vous system have been proposed to
circumfer- ence, and plasma creatine explain these discrepant responses (35). Yet, there
kinase levels (39). Magnetic is no evidence that mus- cle development is
resonance imaging changes
attenuated in those who fail to get sore
consistent with edema also do not
postexercise.
correlate well with the time course
of DOMS, with soreness peak- ing Resistance exercises and activities that place peak
long before swelling manifests (6). So tension at longer muscle lengths have been shown
although DOMS may provide a to produce more soreness than exercises that place
general indication that some degree peak tension at shorter muscle lengths (22).
of damage to muscle tissue has Whether these alterations affect the magnitude of
occurred, it cannot be used as a hypertrophic adaptations has yet to be studied, but
defini- tive measure of the it has been postulated that torque-angle curves in
phenomenon. resistance training might augment hypertrophy
through varying mecha- nisms (9). It is therefore
What is more, humans can experience
DOMS without presenting local signs conceivable that
of inflammation (40). In a study of
sub- jects who performed different
forms of unaccustomed eccentric
exercise (including downhill
treadmill running, eccentric cycling,
downstairs running), Yu et al. (66)
found no significant evi- dence of
inflammatory markers postex- ercise
despite the presence of severe
DOMS. Other studies have reported
similar findings after the performance
of submaximal, eccentrically based
exercise (29,30). These results provide
exercises that stress a muscle results. A number of hypertrophic gains. Pain associated
maximally at a short muscle explanations have been with DOMS has been shown to
length can promote provided to explain the impair movement patterns, albeit in
hypertrophic gains without repeated bout effect, individuals with high pain- related
inducing much, if any, including a fear (64). Altered exercise
soreness. strengthening of con- kinematics arising from DOMS-
Training status has an effect nective tissue, increased related discomfort can reduce
on the extent of DOMS. efficiency in the activa- tion of the target
Soreness tends to dis- sipate recruitment of motor musculature and potentially lead to
when a muscle group is units, greater motor injury. Moreover, some researchers
subjected to subsequent bouts unit synchronization, a have speculated that DOMS could
of the same exer- cise more even distribution reduce the motivation levels
stimulus. This is consistent of the workload among involved in subsequent training,
with the "repeated bout fibers, and/or a greater reducing exercise adherence (18).
effect," where regi- mented contri- bution of Therefore, excessive DOMS should
exercise training attenuates the synergistic muscles not be actively pursued because it
extent of muscle damage (3,57). ulti- mately interferes with progress.
(32). Even lighter loads In addition to reducing
protect muscles from expe- joint torque and muscle PRACTICAL APPLICATIONS
riencing DOMS during force, DOMS may In conclusion, there are several
subsequent bouts of exercise nega- tively affect takeaway points for the strength coach
(26). Therefore, train- ing a subsequent workouts or personal trainer as to the validity
muscle group on a frequent in other ways and of using DOMS as a measure of
basis would reduce soreness, therefore impede workout quality. Because muscle
yet could still deliver strength and damage is theorized to mediate
impressive hypertrophic hypertrophic adaptations (48), there is

18 VOLUME 35 | NUMBER 5 | OCTOBER 2013

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the desired goal. Given that DOMS is suing his PhD in activation and replenishment. Trends
a gross indicator of EIMD, soreness Sports Science at Cell Biol 15: 666–673, 2005.
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