AACN Clinical Issues

Volume 13, Number 2, pp. 237-247

© 2002, AACN

Skeletal Muscle Damage

and Recovery
Christine E. Kasper, PhD, RN, FAAN, FACSM;
Laura A. Talbot, PhD, EdD, RN, CS; Jean M. Gaines, PhD, RN

Muscle disuse atrophy frequently results

from the immobility of an acute hospitaliza-
■ Muscular strength is essential for tion. Mechanical ventilation and hemody-
recovery after an acute illness. Disuse
atrophy of muscle begins within 4 hours namic monitoring along with other therapies
of the start of bed rest resulting in frequently warrant prolonged bed rest. Mo-
decreases in muscle mass, muscle cell bility restrictions for extended periods of
diameter, and the number of muscle time result in disuse atrophy and ultimately
fibers. Strenuous exercise of atrophic cause skeletal muscle damage. To effectively
muscle can lead to muscle damage manage the critically ill patient, the critical
including sarcolemmal disruption, care nurse must focus on the pathology of
distortion of the myofibrils’ contractile skeletal muscle damage, clinical assessment
components, and cytoskeletal damage. of skeletal muscle, and activity management
Assessment of skeletal muscle for disuse (Table 1).
atrophy is done clinically at the bedside
through strength assessment.
Examination of the muscle itself can be
Skeletal Muscle Damage
conducted through the use of nuclear
magnetic resonance imaging, whereas Muscle damage can occur during the pro-
muscle strength can be quantified with a longed immobility of hospitalization and
computerized dynamometer. Biochemical from external sources such as mechanical in-
markers, including creatine kinase and jury (eg, trauma, surgery) or administration
troponin, also are available for the of necrotizing chemicals (eg, anesthesia).
assessment of skeletal muscle damage. Among acute and critically ill adults, the on-
Activity management in the critical care set of skeletal muscle atrophy is rapid and
environment focuses on an individualized
▪▪▪▪▪▪▪▪▪▪
plan, developed in cooperation with the
recovering patient, with the goal of From the School of Nursing, Johns Hopkins Univer-
sity, Baltimore, Md (Dr Kasper, Dr Talbot); and The Er-
preserving and improving atrophic ickson Foundation, Baltimore, Md (Dr Gaines).
skeletal muscle. (KEYWORDS: skeletal
Reprint requests to Christine E. Kasper, PhD, RN,
muscle, damage, atrophy, recovery) FAAN, FACSM, The Johns Hopkins University School
of Nursing, 525 N. Wolfe Street, Baltimore, MD 21205
(e-mail:ckasper@son.jhmi.edu).

237
238  KASPER, TALBOT, AND GAINES AACN Clinical Issues

TABLE 1  Common Musculoskeletal Terminology

Terms Definition

Muscle atrophy A significant decrease in cross-sectional area in skeletal muscle or mass

Cellular muscle damage Rupture of skeletal muscle cells leading to cell death
Muscle injury Rupture or trauma to skeletal muscle with increased serum CK-MB as well
as delayed onset muscle soreness
Hindlimb unloading Method for producing an animal model of “bedrest conditions” with loss of
weight bearing to a rat’s hindlimbs
Eccentric muscle actions Lengthening of the muscle during movement
Concentric muscle actions Shortening of the muscle during movement
Electromechanical dynamometer Measures static and dynamic strength by registering the amount of force
(Kin Com, Cybex) exerted

CK-MB, muscle-specific isoenzyme of creatine kinase.

severe, beginning within 4 hours of hospital- in healthy young adults after sprint running
ization and producing alterations in normal or resistance training. It appears that the act
muscle morphology1 (Figures 1 and 2), such of contracting while the muscle is in a
as decreases in muscle mass,2,3 muscle cell stretched or lengthened position, known as
(fiber) diameter,4 and number of fibers per an eccentric contraction, is responsible for
muscle.5 these injuries.13,15-20
The pathology of skeletal muscle damage
varies depending upon the initiating cause. Skeletal Muscle Damage During Recovery
Numerous studies have examined the patho- From Muscle Atrophy
logical response of skeletal muscle to natu-
rally occurring and experimental injury such The amount of muscle atrophy a patient will
as denervation,6 crushing trauma,6 muscular experience depends on the usage prior to
dystrophies,7,8 intramuscular injection of lo- bed rest and the function of the muscle;
cal anesthetics,9 athletic injuries,10 and is- antigravity muscles (such as the quadriceps)
chemia.9 The muscle damage ranges from a will have greater atrophy than antagonist
relatively minor decrease in contractility to muscles (such as the hamstrings). Research
the increasingly severe neuromuscular has shown that a single bout of exercise pro-
blockade. Atrophy is the result of disuse or tects against muscle damage, with the effects
immobilization. The severity of the atrophy lasting between 6 weeks21,22 and 9 months.23
depends on the severity of the restriction. Muscle resistance to damage may result from
Early signs of skeletal muscle damage are an eccentric exercise-induced morphological
seen on the cellular level and include the change in the number of sarcomeres con-
rupture of the sarcolemmal membrane of nected in series.24 This finding supports initi-
muscle cells, streaming of Z-bands, and torn ating a reconditioning program with gradual
sarcomeres.11-14 Strenuous exercise for the progression from lower intensity activities
patient who has extreme muscle atrophy with minimal eccentric actions to protect
from prolonged bed rest could be in the against muscle damage.25 This model of
form of weight-bearing or ambulation. Stren- gradual reconditioning conflicts with the no-
uous exercise can result in primary or sec- tion of rapid increased activity to produce
ondary sarcolemmal disruption, swelling or better results.26 However, the very exercise
disruption of the sarcotubular system, distor- needed to improve muscular performance
tion of the myofibrils’ contractile compo- may result in further muscle injury. Animal
nents, cytoskeletal damage, and extracellular research studies have examined this possi-
myofiber matrix abnormalities. These frank bility. Changes in muscle morphology, simi-
pathologic changes are similar to those seen lar to what occurs in humans, have been
Vol. 13, No. 2 May 2002 SKELETAL MUSCLE DAMAGE AND RECOVERY  239

Figure 1. Components of skeletal

muscle. Reprinted with permis-
sion from Lieber RL. Skeletal
Muscle Structure and Function:
Implications for Rehabilitation and
Sports Medicine. Baltimore, Md:
Williams & Wilkins; 1992:19.

documented in rat skeletal muscles after dis- covery damaged 20% to 25% of the total
use atrophy produced by hindlimb unload- fibers in the slow twitch soleus muscle after
ing techniques. Hindlimb unloading re- 14 days of exercise. In addition, low-inten-
moves weight-bearing from postural muscles sity run training was found to retard the re-
of the leg, thereby simulating a human bed turn of muscle mass toward control values in
rest condition.27-29 the soleus.2
Animal studies have examined the effects Damage to the soleus and plantaris ap-
of sedentary weight-bearing and run training peared as necrosis, the presence of phagocy-
on atrophic skeletal muscle after long-term tosis and central nuclei, and fiber debris in
hindlimb unloading of 28 days.2,30 Approxi- the intrafascicular and interfibrillar spaces in
mately 7 days of sedentary recovery after postural muscles.11,32 Skeletal muscle dam-
hindlimb unloading is required to return age during remobilization also is seen in the
body weight and muscle weights to control rupture or “wounding” of the sarcolemma,
values. It was demonstrated that sedentary which can be significantly more severe than
weight-bearing and run training immediately the final extent of necrotic cells would im-
after hindlimb unloading produced contrac- ply.11,14 If the sarcolemmal membrane is not
tile forces sufficiently large enough to result further traumatized (ie, no repeated exercise
in transient injury of atrophied muscles.31 during the recovery period) it may reseal it-
Low-intensity treadmill running during re- self and recover from the initial trauma. Ad-
240  KASPER, TALBOT, AND GAINES AACN Clinical Issues

Figure 2. Illustration of the internal structures of a muscle cell. Reprinted with permission from Lieber RL. Skele-
tal Muscle Structure and Function: Implications for Rehabilitation and Sports Medicine. Baltimore, Md: Williams &
Wilkins; 1992:17.

ditionally, the histologic observation of frank Kasper et al’s32 research on the effects of
necrosis and cellular infiltration is a late sign hindlimb unloading on rats found that high
of skeletal muscle injury.12,13 levels of exercise during the reloading pe-
The cause of muscle damage during exer- riod resulted in significantly greater muscle
cised recovery from atrophy involves an al- damage than resulted from normal cage-
tered ability of the muscle fibers to bear the bound activity. The work of Pottle et al31 did
mechanical stress of external loads (weight- not support Kasper’s results, instead finding
bearing) and movement associated with ex- no significant difference in muscle force be-
ercise.33 Weight-bearing, such as ambulation, tween rats subjected to normal cage-bound
or loading of the atrophied muscle beyond activity and forced treadmill running. How-
its reduced force-generating capacity may be ever, the two studies differed in length of
responsible for re-use injury. Therefore, time for hindlimb unloading and intensity of
rapid remobilization occurring within 4 to 7 treadmill running, with the Kasper study
days should be viewed with caution, and having a longer length of time and a higher
overloading should be avoided as weight- intensity of running. This raises the possibil-
bearing ambulation for critical care patients ity that a longer period of inactivity coupled
may predispose them to significant tearing with more intense exercise could result in
and rupture of skeletal muscle tissue.32 greater muscle damage.
More recent research examining the ef- Research on a cellular level also has ex-
fects of exercised recovery are mixed. amined the effects of exercised recovery
Vol. 13, No. 2 May 2002 SKELETAL MUSCLE DAMAGE AND RECOVERY  241

with mixed results. After exercised recovery, with the goal of preventing disuse atrophy
animal research has found that there is an in- and reuse injury. Prevention of atrophy im-
crease in muscle fiber regeneration and an proves several patient outcomes including
increase in embryonic myosin in adult recovery time, rehabilitation time, and overall
fibers.34 This argues for muscle healing dur- quality of life. Assessment includes evaluat-
ing exercised recovery. However, the work ing muscle movement, tone, size, and
of Mozkziak et al35,36 found an incomplete strength.44,45
recovery of DNA unit size and myofiber size, To assess muscle movements, passive and
resulting in reduced muscle size after reload- active range of motion for each major joint is
ing. Though recovery of muscle after bed conducted to determine joint range. A go-
rest will occur, it may not be complete and niometer is used to precisely measure and
return the muscle to pre-bed rest conditions. report the joint angle. Limited joint range is a
These issues continue to be explored. sign of muscle contracture caused by muscle
atrophy and shortening of the muscle.
Muscle tone and size are evaluated by
Clinical Findings of Muscle Damage
palpation and measurement.45 Muscle tone
On the clinical level, common signs and refers to the degree of tension displayed by
symptoms associated with recovery from at- resting muscle. The muscle should feel firm
rophy and its associated potential muscle with slight resistance when passively moved.
damage include: muscle soreness, feeling Muscle size should be nearly symmetrical bi-
of weakness upon standing or walking, de- laterally with the dominant side slightly
creased muscle strength, loss of muscle larger. On examination, like muscle groups
mass, and increased fatigability.37-41 Other are contrasted bilaterally. By comparing
symptoms such as delayed onset muscle symmetry of muscle masses, muscle atrophy
soreness present as pain with activity, mus- is determined. Circumference measures of
cle swelling, and tenderness on palpation.42 the extremity are used to quantify differ-
ences. Circumference is a rough estimate of
muscle mass because circumference in-

Skeletal Muscle Assessment cludes such variables as adipose tissue and
vasculature as well as fat-free lean muscle.
Muscular strength is defined as the maxi- The value of using the circumference as a
mum forces or tension generated by a mus- measure of muscle mass is dependent on the
cle or group of muscles. Human skeletal assumption that both extremities have simi-
muscle is capable of generating 3 to 4 kg of lar amounts of adipose tissue and vascula-
force per cm2 of muscle cross-sectional area, ture. If muscle atrophy is bilateral, prior
irrespective of gender.43 Muscles with the knowledge and experience in muscle assess-
greatest cross-sectional areas exert the great- ment will assist in evaluation of the findings.
est forces. An early sign of skeletal muscle Assessment of muscle strength is simul-
atrophy in a patient is the report of weak- taneously evaluated during joint range of
ness and fatigue, especially in leg muscles. motion.45 The muscle is flexed and the ex-
As these signs may also be attributed to aminer pulls against the tensed muscle.
medication or pathology, it is difficult for the Resistance should be felt. The procedure is
nurse to use patient-reported weakness and then repeated with the corresponding
fatigue in the assessment of strength without muscle group and a comparison of muscle
further data. Clinical, computerized, and bio- strength is made bilaterally. Strength is
chemical methods of strength assessment are graded on a scale of 0 to 5, with 0 represent-
available to assist the nurse in assessing ing no muscle contraction (ie, paralysis) and
skeletal muscle. 5 demonstrating full resistance through a full
range of motion (normal score).
Clinical Assessment
Computerized Assessment
The accurate assessment of muscle function
at the bedside of the critically ill patient is If skeletal muscle damage is found or the
necessary to monitor the status of the muscle area to be assessed is not an extremity, a
242  KASPER, TALBOT, AND GAINES AACN Clinical Issues

more extensive assessment may be needed. muscle injury. Indirect methods include nu-
To quantify current status and progress dur- clear magnetic resonance imaging52-55 or
ing recovery, an assessment of extremity magnetic resonance spectroscopy.56 Mag-
muscle strength can be obtained through the netic resonance imaging can be used to de-
use of computerized dynamometers (Figure termine altered muscle size as well as local-
3). Dynamometers (such as Cybex or Kin- ization and quantification of areas of
Com) provide a rapid method of accurately muscle injury.52-55 Magnetic resonance spec-
quantifying muscular forces (strength) gen- troscopy allows the opportunity to follow
erated during movement.46-49 The objective the subtle changes in skeletal muscle me-
measure of force is obtained by isolating a tabolism that occur in injured and recover-
muscle group, controlling the velocity of ing muscle.56 Both of these techniques
movement, standardizing the technique used could be used to monitor damage or atro-
to assess the force, and limiting extraneous phy in selected critical muscles, such as di-
movements that have the potential to add or aphragm or intercostal muscles during me-
subtract from the developing force.50,51 A dy- chanical ventilation.
namometer provides immediate feedback in
the form of a force curve for isokinetic mea- Biochemical Assessment
sures and a peak torque bar for isometric
readings. Average and peak forces are calcu- Biochemical markers of skeletal muscle
lated by internal software. Physical therapy damage are creatine kinase (CK), aspartate
or departments of rehabilitation commonly aminotransferase, lactate dehydrogenase,
perform these tests. myoglobin, and troponin (Table 2). Creatine
Indirect measures also may be used for kinase is a muscle enzyme in which there is
both extremity and non-extremity skeletal a significant rise in the plasma levels after

Figure 3. KinCom dynamometer for

computerized assessment of skeletal
muscle strength.
Vol. 13, No. 2 May 2002 SKELETAL MUSCLE DAMAGE AND RECOVERY  243

surgical procedures, trauma, myocardial in- duced by multiple parts of the body includ-
farction, and heavy muscular exercise. ing kidneys, red blood cells, brain, stomach,
Though not specific enough to distinguish heart, and skeletal muscle. Any injury in
from skeletal muscle or cardiac injury, two these areas will produce a transient rise in
subunits of CK help in isolating the etiology serum levels. Myoglobin is an oxygen-bind-
of the injury, type M (for muscle) and type B ing protein released after injury to both
(for brain/central nervous system). Serum skeletal and cardiac muscle. Troponin has
levels of CK and CK isoenzyme MB (CK-MB) largely replaced these tests due to the im-
assays are routinely measured when seeking proved specificity in detecting skeletal mus-
evaluation of prolonged angina or chest cle and cardiac damage.
trauma. CK-MB is more specific for cardiac The troponin complex is a regulatory
muscle damage. Yet, serum levels of CK-MB protein found in striated muscle. A contrac-
also will increase with skeletal muscle injury tile protein complex, troponin is located on
or renal failure, even in the absence of my- the thin filament of the contractile apparatus
ocardial injury. A relative index of the ratio that regulates the force and velocity of mus-
of CK-MB to total CK is used to differentiate cle contraction. Troponin is composed of
myocardial injury.57 CK-BB is found predom- three isoforms for both skeletal and cardiac
inantly in the brain and lung with a resultant muscle: tropomyosin-binding subunit (TnT),
rise in serum values after injury to either of calcium-binding subunit (TnC), and acto-
these organs. CK-MM represents the majority myosin-adenosine triphosphate-inhibiting
of the circulatory total CK. A serum increase subunit (TnI).58 Measurement of TnI facili-
in CK-MM is indicative of skeletal muscle in- tates a fast differential diagnosis when com-
jury. A total CK varies according to a per- plex clinical scenarios of skeletal muscle in-
son’s muscle mass, with larger muscular jury with possible cardiac involvement exist.
people having a CK level that will be on the Cardiac troponin I (cTnI) when elevated is
high range of normal. highly specific for myocardial injury, thus
Of the other biochemical markers of distinguishing the etiology of elevations in
skeletal muscle damage, aspartate amino- CK-MB from myocardial or skeletal muscle
transferase (formerly known as serum gluta- injury. Specifically, cTnI can detect cardiac
mate oxaloacetate transaminase or SGOT) injury after trauma, orthopedic injury, or a
and lactate dehydrogenase are enzymes pro- running a marathon.

TABLE 2  Key Biochemical Markers of Skeletal Muscle Damage

Biochemical Assessment Normal Values

Creatine kinase (CK)54 Measure of muscle damage: Isoenzyme CK-MM Male: 12–70 U/mL
reflects skeletal muscle Female: 10–55 U/mL
Isoenzyme CK-BB reflects brain and lung injury
Isoenzyme CK-MB reflects heart injury
Aspartate aminotransferase54 Measure of muscle damage: especially used 8–20 U/L
with heart and liver assessment but also rises
with injury to pancreas, kidney, and skeletal
muscle
Lactate dehydrogenase54 Measure of muscle damage; especially used 45–90 U/L
with heart and liver assessment but also rises
with injury to pancreas, kidney, and skeletal
muscle
Myoglobin54 Measure of skeletal and heart muscle damage 0–85 ng/mL
Troponin—sTnI44 Measure of muscle damage; sTnI is specific to ⬍ 2.2 ␮g/L
skeletal muscle injury

CK-MM, CK-BB, CK-MB are creatine kinase isoenzymes; type M for muscle and type B for brain/central nervous system.
sTnI, skeletal troponin I.
244  KASPER, TALBOT, AND GAINES AACN Clinical Issues

In the case of skeletal muscle trauma, his- progression of activity is critical to prevent
tological determinants of skeletal muscle muscle damage.
damage are limited to the examination of se- Simple activities such as performing
lected muscle tissues and do not necessarily self-care, eating in a group setting, and
represent the status of all muscle groups. watching television in an activity room en-
Therefore, plasma levels of skeletal troponin courages the patient to move from the
I (sTnI) can be used as a marker of contrac- room and ambulate. Patients should partic-
tion-induced muscle damage.59 After muscle ipate in setting goals for walking the unit
injury, sTnI has been shown to increase and halls or simply increasing the time that
peak in parallel to CK and to stay elevated they are able to bear weight at the bed-
up to 2 days after exercise-induced skeletal side. Maintenance of activity is an effective
muscle injury.60 method of diminishing the effects of dis-
use atrophy even under the extreme con-
ditions of orthopedic traction and

Activity Management in the non–weight-bearing.60 Additionally, im-
Critical Care Environment proved muscle strength through continu-
ing performance of activities of daily living
The primary clinical goal of activity man- supports the cardiovascular system’s abil-
agement in the critical care environment is ity to defend against orthostatic hypoten-
to encourage as much physical activity as sion after inactivity.60
is reasonable for the individual patient. In the forefront of muscle therapy is the
Passive range of motion is routinely used use of neuromuscular electrical stimula-
to prevent pressure ulcers and contrac- tion. This has been used as a therapeutic
tures, and to stimulate circulation. How- method to increase skeletal muscle size
ever, passive range of motion cannot pre- and strength in a variety of situations: to
vent atrophy of the affected muscles. improve fitness62; to increase muscle
Initially, exercises that can be done strength in athletes63; to help in rehabilita-
while the patient is supine are imple- tion after spinal cord injury64; and to aid in
mented to help prevent muscle decondi- recovery from surgical procedures (eg, an-
tioning. Parsons et al61 demonstrated that terior cruciate ligament repair).65-68 Neuro-
non–weight-bearing isotonic exercise in- muscular electrical stimulation involves the
creased lean body mass during bed rest. use of high frequency electrical neuromus-
Exercise can take the form of simply push- cular stimulation to induce muscle contrac-
ing against an immovable object such as a tions. A large variety of stimulating proto-
footboard or the nurse’s hands (isometric cols have been studied with the majority of
exercise) or performing a bicycle move- work using short-term therapy (3 to 6
ment while supine (isotonic exercise). Al- weeks) with higher frequency stimulation
ternately, the patient can exercise by push- that cause about 20 individual maximal
ing against the nurse’s hands while the contractions over a period of 10 or more
nurse is performing range of motion (iso- minutes. Strength increases of up to 50% to
kinetic exercise). When possible, the nurse 60% have been observed in healthy subjects
positions the patient in a sitting position using this type of protocol.69 While the use
while still in bed, preferably with legs of neuromuscular electrical stimulation as a
down. Sitting upright allows the upper critical care therapy is limited, theoretically it
body muscles to support the body against has the potential to maintain and improve
gravity while allowing gravitational force skeletal muscle status in the bed-ridden pa-
to act upon the lower extremities. tient in which ambulation is contraindicated.
As soon as physiologically possible, the
nurse gets the patient out of bed to per-
form low-level activity such as sitting in a
Summary
chair two to three times a day. Frequent
assessment of patient condition (heart rate, Providing competent nursing care for pa-
blood pressure, and patient report of fa- tients with multiple injuries and organ fail-
tigue) during these low-level activities and ures is complex, and the prevention of
Vol. 13, No. 2 May 2002 SKELETAL MUSCLE DAMAGE AND RECOVERY  245

skeletal muscle atrophy and injury has a 7. Edström L, Thornell LE, Albo J, Landin S,
lower priority than maintaining vital systems. Samuelsson M. Myopathy with respiratory
However, muscular strength is essential for failure and typical myofibrillar lesions. J Neu-
recovery from an acute illness. Accurate rol Sci. 1990;96:211-228.
8. Komiyama A, Nonaka I, Hirayama K. Muscle
evaluation of the patient is possible through
pathology in marinesco-sjogren syndrome. J
the use of clinical assessment of muscle Neurol Sci. 1989;89:103-113.
strength. Detailed evaluation is available 9. Carlson BM, Faulkner JA. The regeneration of
through the use of computerized muscle as- skeletal muscle fibers following injury: a re-
sessment (magnetic resonance imaging or view. Med Sci Sports Exerc. 1983;15(3):187-198.
spectroscopy) with strength measurement 10. Fisher BD, Baracos VE, Shnitka TK, Mendryk
through the use of a dynamometer. Bio- SW, Reid DC. Ultrastructural events following
chemical markers of skeletal muscle injury acute muscle trauma. Med Sci Sports Exerc.
such as troponin can also be used in evalua- 1990;22(2):185-193.
tion of musculoskeletal status. An individual- 11. Kasper, CE. Sarcolemmal disruption in re-
loaded atrophic skeletal muscle. J Appl Phys-
ized plan of progressive exercise initiated as
iol. 1995;79(2):607-14.
soon as possible in the recovery process is 12. McNeil PL. Cell wounding and healing. Amer
the best way to ensure the total recovery of Sci. 1991;79:222-235.
the patient in the least amount of time and 13. McNeil PL, Khakee R. Disruptions of muscle
with the fewest complications. fiber plasma membranes: Role in exercise-in-
duced damage. Am J Pathol. 1992;140(5):
1097-1109.
Acknowledgment 14. Kalpana V, Thompson JL, Riley DA. Sarcom-
ere lesion damage occurs mainly in slow
Dr Talbot was supported by the Fund for
fibers of reloaded rat adductor longus mus-
Geriatric Medicine and Nursing, Johns Hop- cles. J Appl Physiol. 1998;85(3):1017-1023.
kins University. 15. Fridén J, Lieber RL, Thornell, LE. Subtle indi-
cations of muscle damage following eccen-
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