Influence of cold-water immersion on indices of muscle damage following prolonged intermittent shuttle running

Abstract

The aim of this study was to assess the effects of cold-water immersion (cryotherapy) on indices of muscle damage following a bout of prolonged intermittent exercise. Twenty males (mean age 22.3 years, s = 3.3; height 1.80 m, s = 0.05; body mass 83.7 kg, s = 11.9) completed a 90-min intermittent shuttle run previously shown to result in marked muscle damage and soreness. After exercise, participants were randomly assigned to either 10 min cold-water immersion (mean 10 degrees C, s = 0.5) or a non-immersion control group. Ratings of perceived soreness, changes in muscular function and efflux of intracellular proteins were monitored before exercise, during treatment, and at regular intervals up to 7 days post-exercise. Exercise resulted in severe muscle soreness, temporary muscular dysfunction, and elevated serum markers of muscle damage, all peaking within 48 h after exercise. Cryotherapy administered immediately after exercise reduced muscle soreness at 1, 24, and 48 h (P < 0.05). Decrements in isometric maximal voluntary contraction of the knee flexors were reduced after cryotherapy treatment at 24 (mean 12%, s(x) = 4) and 48 h (mean 3%, s(x) = 3) compared with the control group (mean 21%, s(x) = 5 and mean 14%, s(x) = 5 respectively; P < 0.05). Exercise-induced increases in serum myoglobin concentration and creatine kinase activity peaked at 1 and 24 h, respectively (P < 0.05). Cryotherapy had no effect on the creatine kinase response, but reduced myoglobin 1 h after exercise (P < 0.05). The results suggest that cold-water immersion immediately after prolonged intermittent shuttle running reduces some indices of exercise-induced muscle damage.

Full text

Influence of cold-water immersion on indices of muscle damage
following prolonged intermittent shuttle running
D. M. BAILEY
1
, S. J. ERITH
2
, P. J. GRIFFIN
1
, A. DOWSON
1
, D. S. BREWER
1
,
N. GANT
1
, & C. WILLIAMS
1
1
Human Muscle Metabolism Research Group, English Institute of Sport, Loughborough University, Loughborough and
2
Medical and Exercise Science Department, The Football Association, Lilleshall National Sports Centre, Lilleshall, UK
(Accepted 21 August 2006)
Abstract
The aim of this study was to assess the effects of cold-water immersion (cryotherapy) on indices of muscle damage following
a bout of prolonged intermittent exercise. Twenty males (mean age 22.3 years, s ¼ 3.3; height 1.80 m, s ¼ 0.05; body mass
83.7 kg, s ¼ 11.9) completed a 90-min intermittent shuttle run previously shown to result in marked muscle damage and
soreness. After exercise, participants were randomly assigned to either 10 min cold-water immersion (mean 108C, s ¼ 0.5) or
a non-immersion control group. Ratings of perceived soreness, changes in muscular function and efflux of intracellular
proteins were monitored before exercise, during treatment, and at regular intervals up to 7 days post-exercise. Exercise
resulted in severe muscle soreness, temporary muscular dysfunction, and elevated serum markers of muscle damage, all
peaking within 48 h after exercise. Cryotherapy administered immediately after exercise reduced muscle soreness at 1, 24,
and 48 h (P 5 0.05). Decrements in isometric maximal voluntary contraction of the knee flexors were reduced after
cryotherapy treatment at 24 (mean 12%, s
x
¼ 4) and 48 h (mean 3%, s
x
¼ 3) compared with the control group (mean 21%,
s
x
¼ 5 and mean 14%, s
x
¼ 5 respectively; P 5 0.05). Exercise-induced increases in serum myoglobin concentration and
creatine kinase activity peaked at 1 and 24 h, respectively (P 5 0.05). Cryotherapy had no effect on the creatine kinase
response, but reduced myoglobin 1 h after exercise (P 5 0.05). The results suggest that cold-water immersion immediately
after prolonged intermittent shuttle running reduces some indices of exercise-induced muscle damage.
Keywords: Cryotherapy, intermittent exercise, muscle soreness, muscular dysfunction
Introduction
The deleterious effects associated with muscle
damage following a bout of unaccustomed or
eccentric-based exercise are well documented
(Armstrong, 1984; Clarkson & Sayers, 1999; Proske
& Allen, 2005). The time course and severity of
muscle soreness, muscular dysfunction, and appear-
ance of markers of muscle damage in the systemic
circulation can vary considerably depending on the
duration, intensity, and type of exercise performed
(Clarkson, Byrnes, McCormick, Turcotte, & White,
1986; Eston, Critchley, & Baltzopoulos, 1994;
Thompson, Nicholas, & Williams, 1999). These
factors may partially explain why the precise
aetiology of exercise-induced muscle damage re-
mains elusive. Nevertheless, delayed-onset muscle
soreness (DOMS) and associated decrements in
muscular function are one of the most commonly
reported sport-related injuries (Byrne, Twist, &
Eston, 2004).
Many investigations have attempted to alleviate or
prevent exercise-induced muscle damage and its
associated symptoms. Treatment strategies include
stretching, ultrasound, massage, antioxidant supple-
mentation, and administration of non-steroidal anti-
inflammatory drugs (for a review, see Cheung, Hume,
& Maxwell, 2003). More recently, attention has
focused on the effect of cryotherapy in aiding recovery
from muscle-damaging exercise (Eston & Peters,
1999; Howatson and van Someren, 2003; Yanagisawa
et al., 2003a,b). The role of cryotherapy as a treatment
of sport-related injuries is well documented (Bleakley,
McDonough, & MacAuley, 2004), although support
for its specific application to exercise-induced muscle
damage remains predominantly anecdotal.
Cryotherapy is proposed to reduce the inflamma-
tory response to injured tissue as well as decrease
Correspondence: D. M. Bailey, English Institute of Sport, Loughborough University, Loughborough LE11 3TU, UK. E-mail: david.bailey@eis2win.co.uk
Journal of Sports Sciences, September 2007; 25(11): 1163 – 1170
ISSN 0264-0414 print/ISSN 1466-447X online Ó 2007 Taylor & Francis
DOI: 10.1080/02640410600982659

oedema, haematoma formation, and pain (Swenson,
Sward, & Karlsson, 1996). Thus, cryotherapy may
be considered a pertinent treatment modality be-
cause inflammation is integral in the aetiology of
exercise-induced muscle damage (Smith, 1991) and
muscle soreness is the most commonly reported
symptom of this exercise-related injury (Armstrong,
1984). Additionally, inflammation has been shown
to exacerbate existing disruptions to skeletal
muscle tissue, as this immune response is coupled
with secondary damage via transient hypoxia as well
as the non-specific cytotoxic actions of leukocytes
(Lapointe, Frenette, & Cote, 2002; MacIntyre, Reid,
Lyster, Szasz, & McKenzie, 1996; Merrick, Rankin,
Andres, & Hinman, 1999).
Recent research has focused on the role of
cryotherapy on indices of muscle damage following
eccentric exercise of isolated muscle groups. Eston
and Peters (1999) observed that repeated cold-water
immersion (15 min at 158C every 12 h) was effective in
reducing plasma creatine kinase activity and muscle
stiffness, indirectly assessed as relaxed arm angle, in
the days after repeated eccentric elbow flexion. Using
a comparable muscle-damaging exercise protocol,
Yanagisawa and co-workers (2003a,b) also reported
some beneficial effects of cold-water immersion
(15 min at 58C) on exercise-induced muscle oedema
as well as a tendency for reduced muscle soreness and
creatine kinase activity. Conversely, Isabell, Durrant,
Myrer, and Anderson (1992) observed no effect of
cryotherapy (ice-massage) on indices of muscle
damage and suggested repeated cryotherapy may be
contra-indicatory over a prolonged period.
There is limited evidence to support cryotherapy
following more dynamic whole-body exercise, which
may be considered more ecologically valid when
providing recommendations in a sports performance
environment. The aim of this study was to assess
the effects of a single administration of cryotherapy
on the recovery from a bout of strenuous inter-
mittent shuttle-running exerc ise.
Methods
Participants
Twenty healthy men (mean age 22.3 years, s ¼ 3.3;
height 1.80 m, s ¼ 0.05; body mass 83.7 kg, s ¼ 11.9)
volunteered to take part in the study, which had
received approval from the university ethics commit-
tee. Participants completed a mandatory health
questionnaire and provided written informed con-
sent. All participants were habitually active in a
variety of sports, but were unfamiliar with the
exercise to be performed. Participants were required
to abstain from therapeutic treatments including
massage and anti-inflammatory drugs for the dura-
tion of the investigation.
Experimental design
Having refrained from exercise for at least 2 days,
participants arrived at the laboratory in a fasted state
(*10 h). A venous blood sample (*10 ml) was
taken from a vein in the antecubital fossa after
participants had been supine for at least 10 min.
Next, perceived muscle soreness was recorded and
muscular function was assessed using isokinetic
dynamometry and a vertical jump test (described in
detail below). Subsequently, participants completed
the Loughborough Intermittent Shuttle Test (LIST)
as described previously (Thompson et al. , 1999).
Briefly, the LIST is a field test specifically designed
to replicate the demands associated with intermit-
tent activity such as soccer (Nicholas, Nuttall, &
Williams, 2000). Participants were required to
exercise at varying intensities for 90 min, with
average exercise intensity equal to 75% maximal
oxygen uptake (
_
V O
2max
) determined from a pro-
gressive shuttle-run test (Ramsbottom, Brewer, &
Williams, 1988). Subjective ratings of perceived
exertion were recorded every 15 min during the
LIST (Borg, 1998), heart rate was monitored every
15 s by short-range telemetry (Polar 8810, Vantaa,
Finland), and core body temperature was monitored
at regular intervals using an ingestible thermometer
pill (CorTemp
TM
, HQI, Palmetto, USA). Nude
body mass was determined immediately before and
after exercise. Participants were required to ingest
water in a bolus equal to 5 ml  kg
71
immediately
before exercise and 2 ml  kg
71
every 15 min during
exercise. A venous blood sample was taken immedi-
ately after exercise and additional samples were taken
1, 24, and 48 h after exercise. Participants were
instructed not to resume exercising until the conclu-
sion of testing.
Cryotherapy treatment
Before exercise, participants were matched for
several anthropometric and physiological character-
istics and randomly allocated to either a cryotherapy
or control group (Table I). Immediately after
exercise, the cryotherapy group immersed their lower
limbs (ensuring that the iliac crest was fully
submerged) in a cold-water bath for 10 min. The
water was maintained at a mean temperature of 108 C
(s ¼ 0.5) by the addition of crushed ice and was
repeatedly agitated to avoid the formation of a
warmer boundary layer. This single bout of cryother-
apy was similar to that used in previous investigations
(Yanagisawa et al., 2003a,b) and has been shown to
lower subcutaneous and intramuscular temperature
1164 D. M. Bailey et al.

by 7 – 108C (Meeusen & Lievens, 1986). During this
time, control participants remained at rest in the
same long seated position as the experimental
participants. Heart rate and core body tempera ture
were monitored at regular intervals throughout and
for 15 min following the treatment period. Addi-
tionally, ratings of perceived coldness were assessed
during treatment and recovery using a visual analog
scale that ranged from 1 (‘‘not cold’’) to 10 (‘‘very,
very cold’’).
Assessment of muscle damage
Ratings of perceived soreness were assessed using a
visual analog scale (Thompson et al., 1999) ranging
from 1 (‘‘not sore’’) to 10 (‘‘very, very, sore’’) before,
immediately after (+5 min), and 1, 24, 48, and
168 h after exercise. Participants rated general
whole-body soreness while standing in the relaxed
state and were encouraged to palpate major muscle
groups during assessment.
Maximal voluntary isometric contraction (MVC)
of the knee extensors and flexors was assessed while
seated using an isokinetic dynamometer (Cybex
model 770, LUMEX Inc., Ronkonkoma, USA).
Participants were familiarized with the apparatus and
protocol on at least two occasions before performing
the LIST. Before assessment on the dynamometer,
positional adjustments for knee extension and flexion
were made to ensure movement was restricted to the
saggital plane and that the axis of rotation passed
through the femoral condyles. Following a warm-up
set of five sub-maximal repetitions of knee extension
and flexion (1.05 rad  s
71
), participants completed
two maximal isometric repetitions of the dominant
limb for 5 s for extension at 1.05 rad and flexion at
0.35 rad, where full knee extension was 0 rad. These
angles have previously been identified as optimal
for peak force generation during isometric knee
flexion and extension (Westing & Seger, 1989).
Contractions were separated by 60-s rest periods.
Participants were verbally encouraged and received
visual feedback during each repetition. The greatest
peak torque achieved from both repetitions was
recorded.
Vertical jump height was recorded as pre-
viously described (Byrne & Eston, 2002). Partici-
pants performed the squat jump technique with no
countermovement to minimize the effects of the
stretch – shortening cycle. Participants performed
three consecutive jumps on an electronic timing
mat (Powertimer 1.0 Testing System, Newtest Oy,
Kiviharjuntie, Finland) on each occasion. Jumps were
separated by 60 s rest and the highest jump was
recorded as the peak height.
Sprint performance was assessed during the LIST
and again 48 h after exercise. Sprint times were
measured using two infrared photoelectric cells (RS
Components Ltd., Zurich, Switzerland) interfaced
with a computer. Participants were required to
perform 11615-m maximal sprints during each 15-
min exercise block of the LIST. The values recorded
during the first 15-min block of the LIST were
compared with a subsequent 15-min block per-
formed 48 h after the initial exercise bout.
Blood analysis
Aliquots of blood were used to determine haemo-
globin concentration by the cyanomethaemoglobin
method (Boehringer Mannheim, GmbH Diagnosti-
ca, Mannheim, Germany) and haematocrit by micro-
centrifugation (Hawksley Ltd., Lancing, UK).
Changes in plasma volume were assessed using these
haematrocrit and haemoglobin values (Dill & Costill,
1974). The remaining blood was dispensed into a
tube, left to clot, and then centrifuged (48C) at
4000 rev  min
71
for 10 min to obtain serum.
Serum creatine kinase activity and myoglobin con-
centration were determined at 378C using commer-
cially available techniques (Randox, Crumlin, UK)
designed specifically for use on an automated system
(COBAS Mira Plus, Roche Diagnostics Systems,
Rotkreuz, Switzerland).
Statistical analysis
A two-way analysis of variance (ANOVA) with
repeated measures on time was used to determine
if differences existed between treatment conditions.
When significant F values were observed, the Holm-
Bonferroni step-wise method was used to determine
the location of the differences (Atkinson, 2002).
Values for creatine kinase activity and m yoglobin
were not norm ally distributed and therefore these
values were log transformed before ANOVA. Pearson
product – moment correlations were used to examin e
Table I. Physiological characteristics and physical activity status of
groups (mean + s).
Cryotherapy
(n ¼ 10)
Control
(n ¼ 10) P-value
Age (years) 23.6 + 4.1 21.7 + 2.0 0.123
Height (m) 1.80 + 0.06 1.81 + 0.05 0.665
Body mass (kg) 85.9 + 12.8 81.5 + 11.2 0.517
Body mass index
(kg  m
72
)
26.3 + 2.8 24.9 + 2.7 0.487
Sum of 4 skinfolds (mm)
a
35.3 + 12.8 31.3 + 6.3 0.583
_
V O
2max
(ml  kg
71
 min
71
)
55.2 + 4.8 56.2 + 5.3 0.676
Weekly exercise
sessions (n)
5 + 24+ 1 0.265
a
Sum of four skinfolds (triceps, biceps, suprailiac, subscapular).
Effects of cryotherapy on muscle damage 1165

the relationship between variables. Data analysis was
conducted using SPSS version 12.0 and statistical
significance was set at P 5 0.05. Values are ex-
pressed as means and standard errors of the mean
(s
x
) unless otherwise stated.
Results
Response to intermittent exercise
Mean heart rate during the LIST was
165 beats  min
71
(s
x
¼ 3) for both groups. Mean
rating of perceived exertion increased from 14
(s
x
¼ 1) at 15 min into exercise to 17 (s
x
¼ 1) at the
end of exercise for both groups (P 5 0.05). Core
body temperature during exercise was available for
15 participants (cryotherapy, n ¼ 8; control, n ¼ 7).
Temperature increased from 37.58C(s
x
¼ 0.10) to
38.18C(s
x
¼ 0.13) after exercise (P 5 0.05). During
exercise, participants drank 1.3 litres (s
x
¼ 0.1) of
water and lost 1.2 kg (s
x
¼ 0.3) of body mass. Mean
sprint time during the LIST was 2.70 s (s
x
¼ 0.03).
Estimated changes in plasma volume did not differ
during the testing period for either group.
Response to cryotherapy treatment
Heart rate decreased duri ng the treatment period
from 107 beats  min
71
(s
x
¼ 4) to 94 beats  min
71
(s
x
¼ 3) (P 5 0.05) and continued to decline
(87 beats  min
71
, s
x
¼ 3) 15 min after treatment
(P 5 0.05) in both groups. Cryotherapy had no
effect on heart rate response when compared with
the control group. Core body temperature (n ¼ 15)
decreased from 37.98C(s
x
¼ 0.14) to 37.78C
(s
x
¼ 0.13) during the treatment period and contin-
ued to fall 15 min post-treatment (37.48C, s
x
¼ 0.11)
(P 5 0.05) but was not different between groups.
Perception of coldness was elevated during cryother-
apy (mean 6, s
x
¼ 1) compared with the control
group (mean 1, s
x
¼ 1) and remain ed elevated during
recovery (P 5 0.05).
Indices of muscle damage
Exercise resulted in severe muscle soreness that
peaked immediately after exercise and again 24 h
later (P 5 0.05). Cryotherapy reduced ratings of
perceived soreness at 1, 24, and 48 h post-exercise
(P 5 0.05) (Figure 1).
Maximal isometric voluntary contraction for knee
extension was unaffecte d after exercise and treat-
ment. However, MVC for knee flexion was reduced
at 24 and 48 h post-exercise (P 5 0.05) and returned
to pre-exercise values at 168 h post-exercise
(P 5 0.05). Cryotherapy reduced decrements in
MVC at 24 and 48 h comp ared with the control
group (P 5 0.05) (Figure 2).
Peak vertical jump height was reduced from pre-
exercise values (0.36 m, s
x
¼ 0.01) at 24 (0.35 m,
s
x
¼ 0.01) and 48 h (0.34 m, s
x
¼ 0.01) for both
groups (P 5 0.05). Vertical jump height was un-
affected by cryotherapy. Mean sprint time during the
first 15-min block of the LIST (2.67 s, s
x
¼ 0.03) was
unaffected 48 h (2.70 s, s
x
¼ 0.04) after exercise and
treatment.
Creatine kinase activity was elevated immediately
after exercise (P 5 0.05), peaking 24 h later but
this response was not influenced by cryotherapy
(Figure 3). Myoglobin concentration increased
Figure 1. Perceived muscle soreness following exercise for cryotherapy (solid bars) and control (open bars) groups. Values are mean and
standard errors. *Different from pre-exercise for both groups (P 5 0.05); {Different between groups (P 5 0.05).
1166 D. M. Bailey et al.

immediately after exercise in both groups (P 5 0.05).
Concentrations peaked 1 h after exercise in the
control group but were reduced at this time in the
cryotherapy group (P 5 0.05) (Figure 3).
Discussion
The main findings of this study were that individuals
who received cryotherapy treatment after exercise
reported a dimi nished perception of muscle soreness
up to 48 h later, a lower decrement in MVC at both
24 h and 48 h post-exercise, and a reduced serum
myoglobin response 1 h after exercise. These find-
ings are consistent with those of similar investiga-
tions using cryotherapy as a modality to treat
exercise-induced muscle damage (Eston & Peters,
1999; Howatson & van Someren, 2003; Yanagisawa
et al., 2003b).
The intermittent shuttle-running protocol used to
elicit muscle damage resulted in severe muscle
soreness and an associated period of muscular
dysfunction comparable to that previously documen-
ted (Bailey et al., 2002; Bailey, Williams, Hurst, &
Powell, 2003; Thompson et al., 1999). Additionally,
the increase in intracellular proteins was similar
and over the same time course as observed in pre-
vious investi gations using both this exercise protocol
(Bailey et al., 2002; Thompson et al., 1999) and other
analogous eccentric-based exercise models (Byrnes
et al., 1985; Thompson et al., 2004). The greatest
soreness was generally reported in the weight-bearing
musculature of the lower limbs, specifically the
hamstrings (Bailey et al., 2003; Thompson et al.,
1999), conceivably related to the eccentric actions of
this muscle group during intermittent running. The
moderate relationship (r ¼ 70.58; P 5 0.05) be-
tween decrements in MVC of the knee flexors and
muscle soreness at 48 h post-exercise provides some
support for the proposed association between muscle
injury, dysfunction, and soreness that is not well
Figure 2. Isometric maximal voluntary contraction of the knee flexors (A) and extensors (B) following exercise for cryotherapy (solid line)
and control (broken line) groups. Values are mean and standard errors. *Different from pre-exercise for both groups (P 5 0.05); {Different
between groups (P 5 0.05).
Effects of cryotherapy on muscle damage 1167

documented (Nosaka, Newton, & Sacco, 2002;
Warren, Lowe, & Armstrong, 1999).
The acute onset of muscle soreness observed
immediately after exercise is related to the accumu-
lation of by-products that are either metabolic or
contraction induced (Miles & Clarkson, 1994) rather
than DOMS, which is more commonly associated
with muscle damage (Cheung et al., 2003). This
could account for the biphasic increase in muscle
soreness observed following exercise and support the
proposal that cryotherapy was effective in reducing
muscle injury rather than facilitating removal of
exercise-induced accumulation of by-products. The
observed reductions in DOMS at 24 and 48 h post-
exercise with cryotherapy is consistent with similar
previous investigations (Denegar & Perrin, 1992;
Prentice, 1982; Yanagisawa et al., 2003b). Some
authors attribute this reduced pain perception to the
analgesic effects of cooling rather than inhibition of
muscle damage (Denegar & Perrin, 1992; Gulick,
Kimura, Sitler, Paolone, & Kelly, 1996; Meeusen &
Lievens, 1986). The application of cold, sufficient to
lower muscle tissue to temperatures around 10 –
158C, reduces nerve conduction velocity, muscle
spindle activity, the stretch-reflex response, and
spasticity, thus inhibiting the pain – spasm cycle
(Meeusen & Lievens, 1986). However, the duration
of this analgesia is limited to 1 – 3 h (Meeusen &
Lievens, 1986), so this mechanism might only
account for the initial reductions in muscle soreness
observed 1 h after exercise. Denegar and Perrin
(1992) observed similar beneficial effects of cryother-
apy (ice packs) on DOMS. These authors docu-
mented a further reduction in perceived soreness
when the treatment was supplemented with a period
of stretching. They proposed that stretching results
in stimulation of the Golgi tendon organ, motor
inhibition, and reduced muscul ar tension resulting in
Figure 3. Serum creatine kinase activity (A) and myoglobin concentration (B) following exercise for cryotherapy (solid line) and control
(broken line) groups. Values are mean and standard errors. *Different from pre-exercise for both groups (P 5 0.05); {Different between
groups (P 5 0.05).
1168 D. M. Bailey et al.

a concurrent reduction in the pain – spasm cycle
(Denegar & Perrin, 1992). Although cooling, either
alone or accompanied by passive stretching, has
inhibitory influences on pain perception, some
researchers reporting benefic ial effects of cryotherapy
on exercise-induced muscle damage have not ob-
served a concomitant effect on muscle soreness
(Eston & Peters, 1999; Howatson & van Someren,
2003).
Cryotherapy improved recovery of MVC of the
knee flexors 24 – 48 h after exercise. Exercise re-
sulted in a reduction of knee flexion peak torque at
24 (12%, s
x
¼ 4) and 48 h (3%, s
x
¼ 3) in the
cryotherapy group, which was markedly less than
that experienced by the control group at 24 (21%,
s
x
¼ 5) and 48 h (14%, s
x
¼ 5). Values had returned
to pre-exercise values 7 days after exercise in both
groups. This patt ern of strength loss and recovery is
similar to that previously reported following this
exercise protocol (Bailey et al., 2002; Thompson
et al., 1999), although decrements were lower
compared with previous studies (Bailey et al., 2002;
Thompson et al., 2003). Additionally, these findings
provide further support for the use of muscle
function as an applicable and reliable measurement
tool for quantifying exercise-induced muscle dam age
(Warren et al., 1999). However, Warren and co-
workers’ (1999) endorsement of specificity when
measuring muscle function was not supported, as
assessment of isometric maximal voluntary contrac-
tion was more sensitive to decrements in muscular
function than sprint and vertical jump assessments.
The effects of cryotherapy on the appearance of
intracellular proteins are similar to those reported
previously (Eston & Peters, 1999; Howatson &
van Someren, 2003). It is still uncle ar what
mechanism is responsible for the difference in
myoglobin concentration following cryotherapy
treatment. Others have postulated that cryotherapy
might reduce post-exercise muscle damage via a
decreased permeability of blood and lymph vessels
due to an attenuated inflamma tory response. These
investigations employed creatine kinase activity as
the sole marker for intracellular protein release
(Eston & Peters, 1999; Howatson & van Someren,
2003). This particular marker is subject to large
variability between individuals and caution is advised
when interpreting the response of this intracellular
protein (Clarkson & Ebbeling, 1988; Warren et al.,
1999). This explanation could, in part, account for
the lack of a treatment effect observed with creatine
kinase activity. Also, as secondary damage to skeletal
muscle resulting from inflammation may be more
pronounced in the hours rather than days after
exercise (Lapointe et al., 2002; Merrick et al., 1999),
it is possible that myoglobin is a more accurat e
indicator of subsequent injury. Although cryotherapy
treatment had no effect on core body temperature
compared with the control group, as cooling rates
were 0.038C  min
71
(s
x
¼ 0.01) for both groups,
previous investigations have reported reductions in
subcutaneous and intramuscular temperatures dur-
ing similar cryotherapy treatments (for a review, see
Meeusen & Lievens, 1986). Therefore, it is reason-
able to assume that cold-water immersi on was
effective in lowering intramuscular temperature.
With this in mind, it is possible that cryo therapy
mediated a reduced inflamma tory response and
subsequent secondary muscle damage attenuating
the efflux of myoglobin. However, it is also con-
ceivable that cold-water immersion elicited profound
haemodynamic changes (Stocks, Taylor, Tipton, &
Greenleaf, 2004) that could provide an alternative
explanation for the differing appearance in this
systemic marker of muscle damage.
The results of this study suggest that cryotherapy
applied as a single bout of cold-water immersion
immediately after exercise is effective in reducing
some of the deleterious symptoms associated with
exercise-induced muscle damage. The precise me-
chanisms responsible for this benefit requires further
clarification but findings highlight the multitude of
factors involved in the aetiology of exercise-induced
muscle damage.
References
Armstrong, R. B. (1984). Mechanisms of exercise-induced
delayed onset muscular soreness: A brief review. Medicine and
Science in Sports and Exercise, 16, 529 – 538.
Atkinson, G. (2002). Analysis of repeated measurements in
physical therapy research: Multiple comparisons amongst level
means and multi-factorial designs. Physical Therapy in Sport, 3,
191 – 203.
Bailey, D. M., Williams, C., Hurst, T. L., & Powell, J. R. (2003).
Effect of antioxidant supplementation on indices of muscle
damage following prolonged intermittent shuttle running.
Medicine and Science in Sports and Exercise, 35, S197.
Bailey, D. M., Williams, C., Markovitch, D., Dean, A., Webb, J.
M. M., & Powell, J. R. (2002). Recovery from prolonged
intermittent shuttle running following 9 days of ascorbic acid
supplementation. Journal of Physiology, 539P, S145.
Bleakley, C., McDonough, S., & MacAuley, D. (2004). The use of
ice in the treatment of acute soft-tissue injury: A systematic
review of randomized controlled trials. American Journal of
Sports Medicine, 32, 251 – 261.
Borg, G. A. (1998). Borg’s perceived exertion and pain scales.
Champaign, IL: Human Kinetics.
Byrne, C., & Eston, R. (2002). The effect of exercise-induced
muscle damage on isometric and dymanic knee extensor
strength and vertical jump performance. Journal of Sports
Sciences, 20, 417 – 425.
Byrne, C., Twist, C., & Eston, R. (2004). Neuromuscular
function after exercise-induced muscle damage: Theoretical
and applied implications. Sports Medicine, 34, 49 – 69.
Byrnes, W. C., Clarkson, P. M., White, J. S., Hsieh, S. S.,
Frykman, P. N., & Maughan, R. J. (1985). Delayed onset
muscle soreness following repeated bouts of downhill running.
Journal of Applied Physiology, 59, 710 – 715.
Effects of cryotherapy on muscle damage 1169

Cheung, K., Hume, P., & Maxwell, L. (2003). Delayed onset
muscle soreness: Treatment strategies and performance factors.
Sports Medicine, 33, 145 – 164.
Clarkson, P. M., Byrnes, W. C., McCormick, K. M., Turcotte,
L. P., & White, J. S. (1986). Muscle soreness and serum
creatine kinase activity following isometric, eccentric, and
concentric exercise. International Journal of Sport Nutrition and
Exercise Metabolism, 7, 152 – 155.
Clarkson, P. M., & Ebbeling, C. (1988). Investigation of serum
creatine kinase variability after muscle-damaging exercise.
Clinical Science, 75, 257 – 261.
Clarkson, P. M., & Sayers, S. P. (1999). Etiology of exercise-
induced muscle damage. Canadian Journal of Applied Physiology,
24, 234 – 248.
Denegar, C. R., & Perrin, D. H. (1992). Effect of transcutaneous
electrical nerve stimulation, cold, and a combination treatment
on pain, decreased range of motion, and strength loss
associated with delayed onset muscle soreness. Journal of
Athletic Training, 27, 200, 202, 204 – 206.
Dill, D. B., & Costill, D. L. (1974). Calculation of percentage
changes in volumes of blood, plasma, and red cells in
dehydration. Journal of Applied Physiology, 37, 247 – 248.
Eston, R., & Peters, D. (1999). Effects of cold water immersion on
the symptoms of exercise-induced muscle damage. Journal of
Sports Sciences, 17, 231 – 238.
Eston, R. G., Critchley, N., & Baltzopoulos, V. (1994). Delayed-
onset muscle soreness, strength loss characteristics and creatine
kinase activity following uphill and downhill running. Journal of
Sports Sciences, 12, 135.
Gulick, D. T., Kimura, I. F., Sitler, M., Paolone, A., & Kelly,
J. D. (1996). Various treatment techniques on signs and
symptoms of delayed onset muscle soreness. Journal of Athletic
Training, 31, 145 – 152.
Howatson, G., & van Someren, K. A. (2003). Ice massage: Effects
on exercise-induced muscle damage. Journal of Sports Medicine
and Physical Fitness, 43, 500 – 505.
Isabell, W. K., Durrant, E., Myrer, W., & Anderson, S. (1992).
The effects of ice massage, ice massage with exercise, and
exercise on the prevention and treatment of delayed onset
muscle soreness. Journal of Athletic Training, 27, 208 – 217.
Lapointe, B. M., Frenette, J., & Cote, C. H. (2002). Lengthening
contraction-induced inflammation is linked to secondary
damage but devoid of neutrophil invasion. Journal of Applied
Physiology, 92, 1995 – 2004.
MacIntyre, D. L., Reid, W. D., Lyster, D. M., Szasz, I. J., &
McKenzie, D. C. (1996). Presence of WBC, decreased strength
and delayed soreness in muscle after eccentric exercise. Journal
of Applied Physiology, 80, 1006 – 1013.
Meeusen, R., & Lievens, P. (1986). The use of cryotherapy in
sports injuries. Sports Medicine, 3, 398 – 414.
Merrick, M. A., Rankin, J. M., Andres, F. A., & Hinman, C. L.
(1999). A preliminary examination of cryotherapy and second-
ary injury in skeletal muscle. Medicine and Science in Sports and
Exercise,
31, 1516 – 1521.
Miles, M. P., & Clarkson, P. M. (1994). Exercise-induced muscle
pain, soreness, and cramps. Journal of Sports Medicine and
Physical Fitness, 34, 203 – 216.
Nicholas, C. W., Nuttall, F. E., & Williams, C. (2000). The
Loughborough Intermittent Shuttle Test: A field test that
simulates the activity pattern of soccer. Journal of Sports Sciences,
18, 97 – 104.
Nosaka, K., Newton, M., & Sacco, P. (2002). Delayed-onset
muscle soreness does not reflect the magnitude of eccentric
exercise-induced muscle damage. Scandinavian Journal of
Medicine and Science in Sports, 12, 337 – 346.
Prentice, W. E. (1982). Electromyographic analysis of the
effectiveness of heat or cold and stretching for inducing
relaxation in injured muscle. Journal of Orthopaedic and Sports
Physical Therapy, 3, 133 – 140.
Proske, U., & Allen, T. J. (2005). Damage to skeletal muscle from
eccentric exercise. Exercise and Sports Science Reviews, 33,98–
104.
Ramsbottom, R., Brewer, J., & Williams, C. (1988). A progressive
shuttle run test to estimate maximal oxygen uptake. British
Journal of Sports Medicine, 22 , 141 – 144.
Smith, L. L. (1991). Acute inflammation: The underlying
mechanism in delayed onset muscle soreness? Medicine and
Science in Sports and Exercise, 23, 542 – 551.
Stocks, J. M., Taylor, N. A., Tipton, M. J., & Greenleaf, J. E.
(2004). Human physiological responses to cold exposure.
Aviation, Space and Environmental Medicine, 75, 444 – 457.
Swenson, C., Sward, L., & Karlsson, J. (1996). Cryotherapy in
sports medicine. Scandinavian Journal of Medicine and Science in
Sports, 6, 193 – 200.
Thompson, D., Bailey, D. M., Hill, J., Hurst, T. L., Powell, J. R.,
& Williams, C. (2004). Prolonged vitamin C supplementation
and recovery from eccentric exercise. European Journal of
Applied Physiology, 92, 133 – 138.
Thompson, D., Nicholas, C. W., & Williams, C. (1999).
Muscular soreness following prolonged intermittent high-
intensity shuttle running. Journal of Sports Sciences, 17, 387 –
395.
Thompson, D., Williams, C., Garcia-Roves, P., McGregor, S. J.,
McArdle, F., & Jackson, M. J. (2003). Post-exercise vitamin C
supplementation and recovery from demanding exercise.
European Journal of Applied Physiology, 89, 393 – 400.
Warren, G. L., Lowe, D. A., & Armstrong, R. B. (1999).
Measurement tools used in the study of eccentric contraction-
induced injury. Sports Medicine, 27, 43 – 59.
Westing, S. H., & Seger, J. Y. (1989). Eccentric and concentric
torque – velocity characteristics, torque output comparisons,
and gravity effect torque corrections for the quadriceps and
hamstring muscles in females. International Journal of Sports
Medicine, 10
, 175 – 180.
Yanagisawa, O., Niitsu, M., Takahashi, H., Goto, K., & Itai, Y.
(2003a). Evaluations of cooling exercised muscle with MR
imaging and 31P MR spectroscopy. Medicine and Science in
Sports and Exercise, 35, 1517 – 1523.
Yanagisawa, O., Niitsu, M., Yoshioka, H., Goto, K., Kudo, H., &
Itai, Y. (2003b). The use of magnetic resonance imaging to
evaluate the effects of cooling on skeletal muscle after strenuous
exercise. European Journal of Applied Physiology, 89, 53 – 62.
1170 D. M. Bailey et al.