Mechanisms and efficacy of heat and cold therapies for musculoskeletal injury

Abstract

Abstract Nonpharmacological treatment strategies for acute musculoskeletal injury revolve around pain reduction and promotion of healing in order to facilitate a return to normal function and activity. Heat and cold therapy modalities are often used to facilitate this outcome despite prevalent confusion about which modality (heat vs cold) to use and when to use it. Most recommendations for the use of heat and cold therapy are based on empirical experience, with limited evidence to support the efficacy of specific modalities. This literature review provides information for practitioners on the use of heat and cold therapies based on the mechanisms of action, physiological effects, and the medical evidence to support their clinical use. The physiological effects of cold therapy include reductions in pain, blood flow, edema, inflammation, muscle spasm, and metabolic demand. There is limited evidence from randomized clinical trials (RCTs) supporting the use of cold therapy following acute musculoskeletal injury and delayed-onset muscle soreness (DOMS). The physiological effects of heat therapy include pain relief and increases in blood flow, metabolism, and elasticity of connective tissues. There is limited overall evidence to support the use of topical heat in general; however, RCTs have shown that heat-wrap therapy provides short-term reductions in pain and disability in patients with acute low back pain and provides significantly greater pain relief of DOMS than does cold therapy. There remains an ongoing need for more sufficiently powered high-quality RCTs on the effects of cold and heat therapy on recovery from acute musculoskeletal injury and DOMS.

Full text

REVIEW ARTICLE
Mechanisms and efficacy of heat and cold therapies for musculoskeletal
injury
Gerard A. Malanga
1,2
, Ning Yan
3
& Jill Stark
4
1
New Jersey Sports Medicine, LLC, Cedar Knolls, NJ,
2
Department of Physical Medicine and Rehabilitation, Rutgers University, New Jersey Medical School,
Newark, NJ, USA,
3
Aleon Pharma International Inc, Parsippany, NJ, USA, and
4
Pain Management, Pfizer Consumer Healthcare, Madison, NJ, USA
Abstract
Nonpharmacological treatment strategies for acute musculoskeletal injury revolve around pain
reduction and promotion of healing in order to facilitate a return to normal function and activity.
Heat and cold therapy modalities are often used to facilitate this outcome despite prevalent con-
fusion about which modality (heat vs cold) to use and when to use it. Most recommendations for
the use of heat and cold therapy are based on empirical experience, with limited evidence to
support the efficacy of specific modalities. This literature review provides information for practi-
tioners on the use of heat and cold therapies based on the mechanisms of action, physiological
effects, and the medical evidence to support their clinical use. The physiological effects of cold
therapy include reductions in pain, blood flow, edema, inflammation, muscle spasm, and meta-
bolic demand. There is limited evidence from randomized clinical trials (RCTs) supporting the use
of cold therapy following acute musculoskeletal injury and delayed-onset muscle soreness
(DOMS). The physiological effects of heat therapy include pain relief and increases in blood flow,
metabolism, and elasticity of connective tissues. There is limited overall evidence to support the
use of topical heat in general; however, RCTs have shown that heat-wrap therapy provides short-
term reductions in pain and disability in patients with acute low back pain and provides signifi-
cantly greater pain relief of DOMS than does cold therapy. There remains an ongoing need for
more sufficiently powered high-quality RCTs on the effects of cold and heat therapy on recovery
from acute musculoskeletal injury and DOMS.
Keywords:
cryotherapy, thermotherapy, sprains and
strains, low back pain, muscle soreness,
acute musculoskeletal injury
History
Received 17 September 2014
Revised 29 October 2014
Accepted 30 October 2014
Published online 15 December 2014
Introduction
Musculoskeletal injury with associated pain is a common
health problem causing extensive disability in industrialized
countries [1,2]. Back pain, including cervical/neck pain and
lumbar/low back pain, is the most common type of muscu-
loskeletal pain experienced [1,2]. The 2012 US National
Health Interview Survey estimated that 27.5% of adults
experienced low back pain and 13.9% experienced neck pain
in the previous 3 months [3]. In Europe, it is estimated that
low back pain affects approximately 12.0% to 39.2% of
adults at any given time and has a lifetime prevalence of
between 60% and 85% [1,4].The Global Burden of Disease
2010 Study quantified the impact of 291 diseases and inju-
ries on health loss and found that low back pain was associ-
ated with the largest number of years lived with disability,
whereas other musculoskeletal disorders and neck pain were
ranked third and fourth in this category, exceeded only by
health loss associated with major depressive disorder [5].
Despite its high prevalence, musculoskeletal pain is
undertreated. A telephone survey of 5803 people with
musculoskeletal pain in 8 European Union countries reported
that approximately 1 in 4 persons with musculoskeletal pain
had not sought medical treatment for it, even though up to
57% of them were in constant pain [6]. Undertreatment of
acute pain can have important long-term consequences
because adequate treatment of acute pain is necessary to
prevent transformation to chronic pain [7]. Severe, persistent
acute pain produces sustained activation of peripheral noci-
ceptors, remodeling of neuronal cytoarchitecture, and the
loss of inhibitory interneurons, all of which then lead to
secondary hyperalgesia and eventually to long-term central
sensitization of second-order spinal neurons [8].
Management of acute musculoskeletal injury includes
both pharmacological and nonpharmacological approaches.
Pharmacological therapies most commonly include nonster-
oidal anti-inflammatory drugs (NSAIDs) or acetaminophen,
but for some types of pain (eg, acute low back pain), skeletal
muscle relaxants/antispasticity drugs, antidepressants, corti-
costeroid injections (for back pain with radiculopathy), and
opioids (for otherwise intractable pain) may be appropriate
[9–11]. Nonpharmacological treatment strategies in acute
musculoskeletal injury should ideally reduce pain and
associated edema, if any, while also promoting muscle heal-
ing in order to facilitate a return to normal function and
activity. Heat or cold therapy modalities are often used in
this context. However, confusion frequently exists about
which modality (heat vs cold) to use, the timing and duration
Correspondence: Gerard A. Malanga, MD, Founder and Partner, New
Jersey Sports Medicine, LLC, 197 Ridgedale Avenue, Suite 210, Cedar
Knolls, NJ 07927, USA. Tel: +1 973 998 8301. Fax: +1 973 998 8302.
E-mail: gmalangamd@hotmail.com
http://informahealthcare.com/pgm
ISSN: 0032-5481 (print), 1941-9260 (electronic)
Postgrad Med, 2015; Early Online: 1–9
2015 Infoma UK, Ltd. DOI: 10.1080/00325481.2015.992719
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of the use, and the mechanism by which each modality
works. Moreover, the optimal medium for a specific modal-
ity (eg, dry heat vs moist heat) may also be in question. This
review provides information for practitioners on nonpharma-
cological treatment approaches, the appropriate use of heat
and cold therapies, and the presumed mechanisms by which
improvement occurs, and presents the available evidence that
supports these approaches.
Methods
Searches of the PubMed electronic database were performed.
Articles relevant to the physiological and clinical effects of
heat and cold therapies on acute musculoskeletal injury and
delayed-onset muscle soreness (DOMS) are summarized in
this interpretive literature review.
Results
Mechanisms of acute musculoskeletal pain
To understand the mechanisms by which cold and heat
reduce acute musculoskeletal pain, it is first necessary to
understand the mechanisms that cause the pain itself. Acute
muscular injuries occur as a consequence of either direct or
indirect trauma (Figure 1) [12]. Injuries related to direct
trauma are generally obvious (eg, falls, sprains, and colli-
sions) and result in contusion at the point of contact. Inflam-
mation resulting from acute injury such as ankle sprain leads
to edema, hyperalgesia, and erythema, which can potentially
increase tissue damage and delay healing [12,13].
Indirect trauma occurs as a result of excessive strain or
force in the muscle without any direct contact, causing a dis-
ruption of myofibers [12,14]. Indirect muscle injuries are
further categorized into passive injuries caused by tensile
overstretch of muscle without contraction or active injuries
caused by eccentric overload of the muscles. Muscle damage
caused by eccentric overload may lead to an acute strain or
DOMS [12], and DOMS may occur with the beginning of a
new exercise program or in athletes following weightlifting
or the performance of other eccentric exercise activities [12].
Muscle pain associated with DOMS may have a similar
quality and intensity as that found in immediate exercise-
induced muscle soreness, but symptom onset is delayed,
occurring about 24 hours after exercise, peaking within
72 hours, and then slowly resolving over 5 to 7 days [15].
Nonpain symptoms in DOMS may include decreased muscle
motion and decreased force production [12].
Although the underlying mechanism of DOMS remains
uncertain, the physiological events that cause exercise-
induced muscle stress and damage are thought to involve a
combination of metabolic and mechanical factors [16].
Anaerobic metabolism promotes the accumulation of meta-
bolic waste products (eg, inorganic phosphate, lactic acid,
and H
+
), which contributes to muscle fatigue [17,18]. This
accumulation, along with inflammatory mediator release and
increases in cellular osmolality, increases capillary perme-
ability and the potential for edema [19–21]. Edema can
exacerbate mechanical stresses, compressing capillaries and
resulting in impaired oxygen delivery and waste removal
[22]. Reactive oxygen species are generated by high rates of
aerobic energy transformation and heat generation within the
muscle during intense exercise [17,23–25]. They can affect
proteins, nucleic acids, and lipids to destabilize muscle struc-
tures and the excitation-contraction coupling system and
modify Ca
2+
levels [17,26]. Elevated cytosolic Ca
2+
and the
inflammatory response can lead to protease activation and
protein degradation and can potentially impair force-
generating capacity [27]. If inflammation proceeds unabated,
phagocytic activity of neutrophils and macrophages may
cause secondary muscle damage, compounding muscle
soreness and functional impairment [28].
Mechanical stresses during exercise (eg, high intramuscu-
lar pressure and strain from high-force skeletal muscle con-
tractions) can cause direct physical disruption of muscle
structures, including the sarcolemma and connective tissue
[29–31]. Mechanical disruption of the sarcolemma is associ-
ated with swelling [32], whereas sustained Ca
2+
release can
disrupt the excitation-contraction coupling system and
impair force production capability [27,32]. Similar to meta-
bolic stress, dysfunctions in calcium homeostasis can initiate
protease activation and cellular changes and edema, which
along with cytokine-mediated inflammation contribute to
secondary muscle damage [32].
Cold therapy
Cold therapy, also known as cryotherapy, is the application
of any substance or physical medium to the body that
removes heat, decreasing the temperature of the contact area
and adjacent tissues [33]. Cold therapy is used in the man-
agement of acute injury/trauma, chronic pain, muscle spasm,
DOMS, inflammation, and edema [33,34]. Acute ankle
sprains are a prototypic injury for which cold therapy is
used, generally within the context of rest, ice, compression,
and elevation (RICE) therapy [35].
Many devices are available for application of cold therapy,
including bags of crushed ice, commercially available ice and
gel packs, ice massage, cold compression units, and cold whirl-
pool [33,34,36]. The efficacy of each mode of cold therapy for
lowering the temperature within deep and surface tissues may
Acute muscle
injuries
Direct trauma
(contusion) Indirect trauma
Passive injury
(tensile overstretch)
Active injury
(eccentric overload)
Acute strain
Delayed-onset
muscle soreness
(DOMS)
Figure 1. Classification of acute muscular injuries.
Adapted with modification from [12].
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vary [36–39]. For example, wetted ice is more effective than
cubed ice or crushed ice in lowering skin surface temperature
(17.0 C, 14.1 C, 15.0 C, respectively) and intramuscu-
lar temperatures (6.0 C, 4.8 C, 4.3 C, respectively)
over a 20-minute application period [37].
Vapocoolant sprays contain menthol, a counterirritant that
produces the sensation of cooling and analgesia through acti-
vation of transient receptor potential (TRP) ion channels in
cold-sensitive peripheral sensory neurons [40,41] without
actually cooling the skin [41]. Hence, although topical men-
thol may be an effective tool for pain management [42], it is
ineffective for cooling skin and subcutaneous tissue [43,44].
Cold therapy mechanisms
Cold therapy has multiple physiological effects on injured tis-
sue (Figure 2) [33]. Decreasing temperatures of skin and
muscle reduces blood flow to the cooled tissues [45–48] by
activating a sympathetic vasoconstrictive reflex [34]. Cold-
induced decreases in blood flow reduce edema and slow the
delivery of inflammatory mediators (eg, leukocytes), reducing
inflammation of the affected area [49,50]. Decreasing tissue
temperature also reduces the metabolic demand of hypoxic
tissues, potentially preventing secondary hypoxic damage in
injured tissue [51,52]. Cold therapy induces a local anesthetic
effect, referred to as cold-induced neurapraxia, by decreasing
the activation threshold of tissue nociceptors and the conduc-
tion velocity of nerve signals conveying pain [33,34,53]. Key
receptors responsive to environmental cold include TRP cat-
ion channel subfamily M, member 8 (TRPM8), and, espe-
cially in the presence of other agonists, TRP cation channel
subfamily A, member 1 (TRPA1), which has a role in cold
hyperalgesia (Figure 3) [54]. Decreasing muscle temperature
also reduces muscle spasm via inhibition of a spinal cord
reflex loop [55]. Sensory neurons express multiple TRP chan-
nels. The TRP cation channel subfamily V, members 1, 3, and
4 all respond to warming temperatures. Activation of any of
these TRP cation channels can trigger action potentials in the
sensory neuron. Some of these channels, such as TRPV1, are
also expressed in the spinal cord, where they seem to have an
important role in the central nervous system as well.
Cold therapy for acute musculoskeletal injury: ankle sprain
Recommendations for the use of cold therapy in the manage-
ment of acute musculoskeletal injury are largely anecdotal
[56]; supporting evidence from quality clinical trials is lack-
ing. One systematic review evaluating cold therapy for the
treatment of acute soft tissue injuries (22 randomized clinical
trials [RCTs] with 1469 participants) found only marginal
evidence supporting the use of ice and exercise after ankle
sprain and postsurgery, but there was little evidence to sug-
gest that the addition of ice to compression significantly
improved swelling and range of motion [57]. Another sys-
tematic review of 4 randomized controlled clinical trials
evaluating the effect of cold therapy on return to participa-
tion after injury concluded that cold therapy positively
affected return to work and sports, with the caveat that the
trials reviewed were of extremely low quality [58]. A more
recent systematic review (11 trials with 868 participants)
analyzed the effectiveness of applying RICE therapy within
the initial 72-hour period after a traumatic ankle sprain and
found that evidence supporting ice in this scenario was
limited. Most trials in the review were conducted prior to
1990 and were of low quality [13].
One RCT compared the efficacy of an intermittent cold
therapy protocol (10 minutes ice, 10 minutes room tempera-
ture, 10 minutes ice, every 2 hours; n =43) with a standard
cold therapy protocol (20 minutes of continuous icing every
2 hours; n =46) over the first 72 hours after acute ankle
sprain [56]. Patients treated with the intermittent icing proto-
col had significantly (P<0.05) less ankle pain on activity
than those treated with the standard 20-minute icing proto-
col. However, there were no significant differences between
icing protocols in terms of ankle function, swelling, or pain
at rest. More recently, the Protection Rest Ice Compression
Elevation (PRICE) RCT compared intermittent cold therapy
and compression alone (n =51) versus intermittent cold
therapy and compression combined with therapeutic exercise
(cryokinetics; n =50) in the management of acute ankle
sprain [59,60]. Patients randomized to the cryokinetic group
experienced significant (P=0.0077) improvements in short-
term ankle function compared with standard intermittent
cold therapy. The implications of these findings on the
efficacy of cold therapy for ankle sprain are limited, as
neither trial included a no-ice control group [13].
Cold therapy for DOMS
A number of reviews or meta-analyses evaluating cold
therapy in the prevention or treatment of DOMS have been
recently published [61–63]; as expected based on the timing
of publication, there is a considerable overlap of trials
reported in each review. The largest was a Cochrane Database
review of 17 trials (n =366) comparing the effects of cold-
water immersion in the prevention or management of muscle
soreness after exercise [61]. Comparisons of cold-water
immersion versus passive intervention (ie, rest or no interven-
tion) found no difference in pain measures at immediate
follow-up (standardized mean difference [SMD], 0.07; 95%
CI, 0.43 to 0.28; 7 trials), but found significantly lower
levels of pain with cold-water immersion at 24 hours (SMD,
0.55; 95% CI, 0.84 to 0.27; 10 trials), 48 hours
(SMD, 0.66; 95% CI, 0.97 to 0.35; 8 trials), 72 hours
(SMD, 0.93; 95% CI, 1.36 to 0.51; 4 trials), and
Cold therapy Heat therapy
↑ Temperature of
skin and muscle
↓ Temperature of
skin and muscle
↓ Blood flow ↓ Metabolism ↑ Blood flow ↑ Metabolism
↓ Pain
↑ Healing
↑ Elasticity
↓ Inflammation
↓ Edema
↓ Pain
↓ Muscle spasm
↓ Elasticity
Figure 2. Physiological effects of heat and cold therapies [33].
DOI: 10.1080/00325481.2015.992719 Mechanisms and efficacy of heat and cold therapies for musculoskeletal injury 3
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96 hours (SMD, 0.58; 95% CI, 1.00 to 0.16; 5 trials)
after cold therapy. In addition, immediate ratings of recovery
after cycling under hot and humid conditions (mean differ-
ence, 0.97 units; 95% CI, 0.10 to 2.05) and improvement of
fatigue (MD, 1.70 units; 95% CI, 2.49 to 0.90) were
also significant in favor of cold-water immersion [61].
Results from more recent trials of cold therapy efficacy
for exercise-induced muscle soreness are conflicting. One
RCT (n =20) reported that 20 minutes of cold therapy (5 C
ice bath) was ineffective in attenuating decreased muscle
strength and soreness seen after muscle-damaging exercise
(40-minute downhill run) [64]. A second RCT (n =24) of
localized air-pulsed cold therapy (3 applications of 30 C
air, 4 minutes each) found no significant differences between
the cold therapy group and controls in muscle soreness or
function following strenuous exercise (eccentric elbow flexor
muscle contractions) [65]. In contrast, Oakley et al. [66]
reported that daily multiple applications of ice (20 minutes,
3 times/day for 72 hours; n =21) were significantly
(P=0.009) superior to no-treatment control (n =10) for
reducing perceived muscle soreness 48 hours after exercise
that consisted of eccentric hamstring contractions. Although
not statistically significant, there was also a trend for a
greater range of motion and lower creatinine kinase and
aspartate aminotransferase levels at 72 hours in the cold ther-
apy group versus control.
Complications of cold therapy
Cold therapy, if used inappropriately, can put patients at risk
for local cold-induced injuries, such as frostbite [67,68].
Commonly reported complications of cold therapy include
allergic reactions, burns, and intolerance/pain [69]. Cases of
neuropathy of superficial nerves have been reported follow-
ing ice application for muscle soreness [70] and acute injury
[71]. This cryotherapy-related nerve palsy is temporary in
almost all cases, but can last for hours, days, or months
[70,71]. Cold therapy should be used with caution in patients
with hypertension, mental impairment, or decreased sensa-
tion. Cold therapy should not be used in patients with cold
hypersensitivity, cold intolerance, or Raynaud’s disease, or
over areas of vascular compromise [34]. Cold therapy has
also been associated with short-term adverse changes to joint
position sense [72], muscle strength [73], and neuromuscular
performance [74,75], which may adversely affect perform-
ance of athletes immediately postcooling [73].
Heat
TRPV2?
TRPV3
TRPV4
TRPV1
TRPA1
TRPV1
TRPA1
TRPM8
TRPV1 (acid)
TRPA1
(acid/base)
pH
Reactive
chemicals
Environmental
cold
Cold
hyperalgesia
Spinal
cord
Withdrawal
in response
to insult
Action
potential
Pain avoidance
emotional
reaction
DRG TRPV1 on
nerve terminals
Other TRP channels
in spinal cord?
Figure 3. TRP channels as nociceptors.
Reprinted by permission from MacMillan Publishers Ltd: Nat Neurosci [54] 2002.
DRG = Dorsal root ganglion; TRP = Transient receptor potential; TRPA = TRP cation channel subfamily A; TRPV = TRP vanilloid.
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Heat therapy
Heat therapy is the application of heat to the body resulting
in increased tissue temperature [33]. Superficial modes of
heat therapy include hot water bottles, heat pads, electric
heat pads, heat wraps, heated stones, soft heated packs filled
with grain, poultices, hot towels, hot baths, sauna, paraffin,
steam, and infrared heat lamps [33,76]. An alternative mode
of heat therapy is deep-heat therapy, which involves conver-
sion of another form of energy to heat (eg, shortwave
diathermy, microwave diathermy, ultrasound) [33].
Heat therapy mechanisms
Physiological effects of heat therapy include pain relief,
increases in blood flow and metabolism, and increased elastic-
ity of connective tissue (Figure 2) [33]. Neural transduction of
heat is mediated by TRP vanilloid 1 (TRPV1) receptors,
which are ion channels activated by noxious heat (Figure 3)
[54,77]. The TRPV1 receptors are present in primary afferent
neurons, the spinal cord, and throughout the brain. Activation
of TRPV1 receptors within the brain may modulate antinoci-
ceptive descending pathways [78]. Increasing tissue tempera-
ture stimulates vasodilation and increases tissue blood flow
[79,80], which is thought to promote healing by increasing the
supply of nutrients and oxygen to the site of injury [33,81,82].
The rate of local tissue metabolism is also increased by warm-
ing, which may further promote healing [33]. Heat-induced
changes in the viscoelastic properties of collagenous tissues
may underlie the demonstrated efficacy of heat therapy for
improving range of movement [83,84].
Heat therapy for acute musculoskeletal injury: low back
pain
The therapeutic benefit of heat therapy for the management
of acute and subacute low back pain was evaluated in a
2006 Cochrane Database review [76]. This review of 9 trials
(n =1117), based, in part, on 3 prospective RCTs detailed
below [85–87], examined the efficacy of superficial heat and
cold therapies for low back pain and found that heat-wrap
therapy provides small but significant short-term reductions
in pain and disability for patients with low back pain [76].
In the first trial (n =219), heat-wrap therapy versus oral
placebo was applied for approximately 8 hours daily for
3 consecutive days [87]. Active heat therapy provided signif-
icantly greater pain relief (day 1: P<0.001), less
muscle stiffness (day 1: P=0.008), and increased flexibility
(P<0.01 at all time points) compared with oral placebo. In
addition, mean disability scores, measured by the Roland-
Morris Disability Questionnaire, were significantly reduced
compared with placebo on the third day of treatment (active
heat therapy, mean, 5.3 vs placebo, mean, 7.4; P<0.0002).
The second trial evaluated the application of low-level heat
therapy or oral placebo overnight (~8 hours) for 3 nights [86].
In comparison to placebo, overnight heat therapy provided
significantly better daytime pain relief (P<0.05) on each suc-
cessive day as well as during the 2-day follow-up period
where no treatment was administered (P=0.0001). Improve-
ments in morning muscle stiffness (P£0.02 for all time
points), lateral trunk flexibility (day 4: P<0.002), and low
back disability (day 4: P<0.005) were also significantly supe-
rior following overnight heat therapy compared with placebo.
In the third trial, Mayer et al. [85] evaluated continuous
low-level heat-wrap therapy combined with directional
preference-based exercise. Heat therapy (8 hours/day for
5 days) plus exercise therapy significantly improved meas-
ures of spinal function and disability 2 days after the last
treatment versus either intervention alone or no-treatment
(educational booklet) control (P<0.05 for all). Pain relief
was also significantly greater with heat plus exercise com-
pared with exercise alone and booklet control 2 days after
the last treatment.
Kettenmann et al. [88] compared low-level heat-wrap ther-
apy (40 C, ‡4 hours/day for 4 days + NSAID rescue) with a
no-heat control condition (NSAID rescue only) in a random-
ized trial in 38 patients with acute low back pain. Subjects in
the heat-wrap group experienced significant (P<0.05) reduc-
tions in perceived pain and stress, improvements in sleep at
night, and a reduced need for daytime naps compared with
controls. Electroencephalogram recordings also showed
significant (P<0.05) decreases in Beta 1 and Beta 2 fre-
quency bands in the heat-wrap group versus the control
group, indicating reduced arousal and increased relaxation
with heat therapy.
Heat therapy for DOMS
Mayer et al. [89] evaluated continuous low-level heat-
wrap therapy for the prevention and early-phase treatment
(ie, 18–48 hours postexercise) of low back DOMS. Healthy
asymptomatic subjects were randomized to prevention
(n =35) or treatment (n =38) substudies and asked to per-
form vigorous eccentric exercise to experimentally induce
low back DOMS. In the prevention substudy, heat therapy
initiated 4 hours before the eccentric exercise (8 hours total)
significantly (P<0.05) reduced pain intensity, disability, and
subject-reported deficits in physical function 24 hours post-
exercise compared with a stretching control treatment. In the
treatment substudy, heat-wrap therapy applied 18 and
32 hours postexercise (8 hours each) provided significantly
greater pain relief (hour 24: P=0.026) than did cold pack
application (15–20 minutes every 4 hours from 18–42 hours
postexercise). There were no significant between-group dif-
ferences in self-reported physical function and disability.
Petrofsky et al. [90] compared the efficacy of 3 heating
modalities (air-activated heat wrap, hydrocollator heat wrap,
and chemical moist heat wrap) for alleviating DOMS. The
trial enrolled 3 cohorts of subjects: younger subjects (aged
20–45 years; n =40), older subjects (aged 45–70 years;
n=40), and subjects with diabetes mellitus (aged
45–70 years; n =40). Patients with diabetes had significantly
higher average soreness after the exercise compared with the
older and younger groups (P<0.01). Moist heat reduced
soreness to the greatest extent both immediately and up to
2 days after exercise compared with the other modalities.
The greatest reductions in pain with moist heat were in the
older subjects (52.3% reduction) compared with those who
were younger (33.3%) and those who had diabetes (30.5%).
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Complications of heat therapy
As reported in the 2006 Cochrane Database review, adverse
events reported in trials of superficial heat for low back pain
were minor and mainly consisted of “skin pinkness [76]”.
Precautions should be taken during the use of heat therapy
in patients with multiple sclerosis [33,91], poor circulation,
spinal cord injuries, diabetes mellitus [33], and rheumatoid
arthritis [33,92], where heat may cause disease progression,
burns, skin ulceration, and increased inflammation
[33,91,92]. Skin should be protected when using heat ther-
apy in heat-sensitive or high-risk patients, especially over
regions with decreased sensory function [33].
Cold therapy versus heat therapy
A handful of trials have directly compared the effects of
cold therapy versus heat therapy. In the abovementioned trial
by Mayer et al. [89], heat wrap was compared with cold
pack for treatment of low back DOMS. The pain relief score
was 138% greater with the heat wrap versus the cold pack at
hour 24 postexercise, but, as stated previously, no differences
in physical function or disability between the treatment
groups were reported. Another RCT compared the analgesic
efficacy of 30 minutes of heat or cold therapy in 60 patients
presenting to an emergency department for acute back and
neck strains [93]. No significant differences in pain scores
were observed between the heat and cold groups after a sin-
gle 30-minute treatment; neither modality was associated
with predefined clinically significant reductions in pain. The
low analgesic effect of heat and cold therapy observed in
this trial is difficult to interpret given the trial’s lack of a
control group.
Hassan et al. [94] compared immersion in warm water
(38 C, 30 minutes) versus cold water (20 C, 30 minutes)
versus a no-treatment control group beginning 15 minutes
after eccentric hamstring exercises in 60 young athletic
males. Warm water significantly decreased markers of
muscle stress reaction, including skeletal troponin I, creatine
kinase, and myoglobin levels, compared with cold water or
control (P<0.05). In contrast, cold-water immersion ele-
vated levels of muscle stress reaction markers.
Discussion
Heat and cold therapy are considered part of the standard of
care for acute musculoskeletal pain [7]. However, most
recommendations for use of heat and cold therapy in acute
musculoskeletal injury are based on empirical experience or
unconfirmed information because the evidence base support-
ing the efficacy of these modalities is quite limited [76]. For
example, the RICE and PRICE protocols are commonly
used to manage acute injury but have not been validated in
adequately designed randomized controlled trials.
The available studies are few in number, and they have
numerous methodological limitations. For example, although
1 systematic review of cold therapy for acute soft tissue inju-
ries identified 22 RCTs for inclusion, mean study quality on
the Physiotherapy Evidence Database (PEDro) Scoring Scale
was a 3.4 out of 10 (range, 1–5) [57]. The most recent
Cochrane review of superficial heat or cold for low back
pain was published in 2006, and of the 9 trials it included,
most were small and 4 were considered “low”quality [76].
Available studies have used varying forms of cold and heat
that may or may not be comparable in terms of their physio-
logical effects. Another challenge is that it is difficult to
maintain blinding in studies of cold and heat. Many of the
studies reviewed here were not blinded and therefore were
subject to bias and potential overestimation of treatment
effects, particularly given the subjective nature of pain
[57,76,95].
Even when evidence is available, it has not always been
consistent. Recent studies regarding the effects of cold ther-
apy in DOMS have had conflicting results, the reasons for
which are unknown. The various small studies differed with
regard to study design, including the forms of cold therapy
used, the manner in which exercise-induced muscle damage
was provoked, and the manner in which muscle soreness
was evaluated. It should also be noted that results from
crossover trials have been more favorable for cold therapy
versus results from parallel trials.
Given the limitations of the available data, it is difficult
to make evidence-based recommendations regarding the use
of cold and heat therapy. Cold therapy is generally recom-
mended for ankle and other joint sprains, despite a lack of
strong supporting evidence [10,35]. Heat therapy is recom-
mended for reducing pain and increasing function in
patients with acute low back pain and in patients with
DOMS [11,96]. Guidelines of the American College of
Rheumatology recommend use of thermal agents for relief
of pain and stiffness associated with osteoarthritis of the
hand and thermal agents in combination with physical
therapist-supervised exercise for treatment of osteoarthritis
of the hip and knee [97]. Based on currently available evi-
dence and our clinical experience, we recommend cold
therapy in the setting of acute injury with inflammation
and heat for muscular pain and soreness as well as for joint
pain and stiffness. Either cold or heat may be helpful for
acute low back pain and muscle soreness, but heat appears
to be better validated.
Conclusion
Although there is some clinical evidence that cold therapy is
effective for pain following acute musculoskeletal injuries,
there is a need for additional sufficiently powered, high-qual-
ity, and appropriately reported RCTs of effects of cold ther-
apy. Heat therapy has demonstrated therapeutic benefit for
both analgesia and promoting healing in certain injuries.
Thermotherapy can be used as monotherapy or in combina-
tion with oral analgesics to relieve acute low back pain and
muscle soreness. As with cold therapy, more RCTs of heat
therapy would enhance the body of literature. Patients can
be counseled to apply ice during the initial 48 to 72 hours
after an acute injury of the musculoskeletal system
(eg, sprains, strains), whereas after the first 72 hours there is
little evidence for continued benefit. Heat is the modality of
choice for acute low back pain and muscle soreness. Better
education of health care providers and consumers could help
6G. A. Malanga et al. Postgrad Med, 2015; Early Online: 1–9
Postgraduate Medicine Downloaded from informahealthcare.com by Stuart Dickinson on 12/16/14
For personal use only.

reduce confusion and optimize the use of these accessible
and low-cost therapies in the treatment of musculoskeletal
injuries.
Acknowledgments
Editorial/medical writing support was provided by John H.
Simmons, MD, of Peloton Advantage, LLC, and was funded
by Pfizer.
Declaration of interest:Gerard A. Malanga, MD, has
received consulting fees from Pfizer Consumer Healthcare.
Ning Yan, PhD, was formerly affiliated with Pfizer Con-
sumer Healthcare. Jill Stark, DPM, is an employee of Pfizer
Consumer Healthcare.
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