Академический Документы
Профессиональный Документы
Культура Документы
Cryotherapy is an eVective treatment for acute sports injury to soft tissue, although the eV ect of cryotherapy
on exercise-induced muscle damage is unclear. The aim of this study was to assess the eVects of cold water
immersion on the symptoms of exercise-induced muscle damage following strenuous eccentric exercise. After
performing a bout of damage-inducing eccentric exercise (eight sets of Wve maximal reciprocal contractions at
0.58 rad s- 1) of the elbow Xexors on an isokinetic dynamometer, 15 females aged 22.0 2.0 years (mean s)
were allocated to a control group (no treatment, n = 7) or a cryotherapy group (n = 8). Subjects in the cryotherapy group immersed their exercised arm in cold water (15C) for 15 min immediately after eccentric exercise
and then every 12 h for 15 min for a total of seven sessions. Muscle tenderness, plasma creatine kinase activity,
relaxed elbow angle, isometric strength and swelling (upper arm circumference) were measured immediately
before and for 3 days after eccentric exercise. Analysis of variance revealed signiWcant (P < 0.05) main eV ects for
time for all variables, with increases in muscle tenderness, creatine kinase activity and upper arm circumference,
and decreases in isometric strength and relaxed elbow angle. There were signiWcant interactions (P < 0.05) of
group time for relaxed elbow angle and creatine kinase activity. Relaxed elbow angle was greater and creatine
kinase activity lower for the cryotherapy group than the controls on days 2 and 3 following the eccentric exercise.
We conclude that although cold water immersion may reduce muscle stiV ness and the amount of post-exercise
damage after strenuous eccentric activity, there appears to be no eVect on the perception of tenderness and
strength loss, which is characteristic after this form of activity.
Keywords: cold water immersion, cryotherapy, muscle damage.
Introduction
Exercise-induced muscle damage, which commonly
occurs after strenuous eccentric muscle action, consists
of a dull aching pain, stiVness, tenderness and a prolonged loss of muscle strength. The symptoms tend to
develop within the Wrst 24 h post-exercise, peak between
24 and 72 h and then subside after 5 7 days (Ebbeling
and Clarkson, 1989; Armstrong, 1990; Cleak and
Eston, 1992a; Nosaka and Clarkson, 1995). As eccentric muscle actions are usually associated with a higher
force-to-activation ratio, the `loading proWle places a
high stress on the tissues involved and is most likely
a primary factor of muscle damage (Enoka, 1996).
Damage includes disruption of the sarcolemma,
232
Several studies have been undertaken to Wnd ways
to alleviate and treat the symptoms of exercise-induced
muscle damage (see Cleak and Eston, 1992a, for a
review). One such treatment modality, common to the
treatment of acute sports injury, involves cryotherapy
(ice or cold therapy). However, the eVectiveness of
this treatment is unclear due to limited research and
the variations in treatment modality, frequency of
application and duration of treatment.
The response of soft tissue to various forms of
cryotherapy and temperatures of application in both
humans and animals has been reviewed comprehensively by Meeusen and Lievens (1986). A major cause
of inXammation after acute muscle injury is an increase
in capillary permeability, which in conjunction with
an increase in extracellular protein concentration and
vasodilation, results in oedema (Schoberth, 1980).
This response varies directly with tissue temperature
(Janssen and Waaler, 1967). A decrease in tissue temperature results in a reduction in nerve conduction
velocity and activity of the muscle spindle. This
decreases the stretch reXex response and spasticity of
muscle, which reduces the pain spasm cycle and contributes to the relief of pain (Meussen and Lievens,
1986). Thus, when cryotherapy is applied at an appropriate frequency, duration and temperature to injured
muscle, it reduces the inXammatory response and
alleviates spasm and pain after muscle injury (Meeusen
and Lievens, 1986).
In the Wrst published study to investigate the eVects of
heat and cold therapy, in conjunction with stretching
exercise, on the symptoms of exercise-induced muscle
damage, Prentice (1982) observed that a combination
of cold treatment and stretching was most eVective.
However, more recent research has observed that
cryotherapy has a negligible eVect. Yackzan et al. (1984)
applied ice therapy in three separate groups (immediate,
after 24 h or after 48 h) after strenuous eccentric
exercise of the elbow Xexors. They reported no differences in the joint range of motion and concluded
that cryotherapy was not eVective for reducing the
symptoms of exercise-induced muscle damage. However, it is possible that the single cold application treatment was insuYcient to inXuence the mechanisms
responsible for reducing the joint angle in their study. In
a similar study, Isabell et al. (1992) assessed the eVects
of ice-massage alone, ice-massage with exercise and
exercise alone on range of motion of the elbow Xexors
after damaging exercise in three separate groups. No
diVerences in range of motion were observed between
the three groups. Braun and Clarkson (1989) also
observed that cold treatment applied before and during
damaging exercise of the elbow Xexors did not aVect
the relaxed arm angle. It is possible that the lack of
agreement between studies may be attributable to the
Methods
Fifteen female student volunteers (mean age 22.0
2.0 years) at the University of Wales, Bangor, provided
informed consent to participate in the study. After
a bout of eccentric exercise on the elbow Xexors of
the dominant arm, the participants were allocated at
random to either a cryotherapy treatment group or a
control group. The symptoms of exercise-induced
muscle damage were then compared to baseline values
over a period of 3 days.
The bout of damage-inducing exercise
The bout of eccentric exercise consisted of eight sets
of Wve maximal contractions (eccentric and concentric)
at 0.58 rad s- 1 with 60 s rest between each set on
an isokinetic dynamometer (KincomTM, Chattanooga,
Bicester, UK). This was similar to other muscle
damage-inducing protocols (Nosaka and Clarkson,
1995; Gulick et al., 1996).
Cryotherapy
The cryotherapy group submerged their exercised arm
(ensuring that the origins and insertions of the biceps
were fully submerged) into a plastic tub of water for
15 min (Meeusen and Lievens, 1986). The water
was maintained at the recommended temperature of
15 1C (by adding ice cubes, cold or hot water,
previously practised in a pilot study) to elicit a drop in
intramuscular temperature of about 7 10C (Meeusen
and Lievens, 1986). This treatment was applied
immediately post-exercise and every 12 h thereafter for
a duration of 3 days in accordance with the suggested
clinical applications of cryotherapy (Kellet, 1986).
Measurements of exercise-induced muscle damage
The criterion measures were plasma creatine kinase
activity, isometric strength of the elbow Xexors, relaxed
arm angle, local muscle tenderness and upper arm
233
Results
The results for both the treatment group and the control
group are shown in Table 1.
Relaxed arm angle
The control group had a signiWcantly lower relaxed
arm angle than the cryotherapy group (mean s:
2.56 0.21 vs 2.78 0.08 rad; F1,14 = 5.99, P < 0.05).
There was also a main eVect for time (F3,39 = 12.98,
P < 0.001). The relaxed arm angle decreased from
2.82 0.09 rad at baseline to 2.67 0.16, 2.63 0.14
and 2.60 0.15 rad on days 1, 2 and 3, respectively.
There was also a group time interaction (F3,39 = 4.46,
P < 0.01) (Fig. 1). There was a larger decrease in
relaxed arm angle for the control group, which was
still 13% lower than baseline and 14% lower than the
cryotherapy group on day 3.
234
Variable
Baseline
24 h
48 h
4.57 0.53
4.65 0.34
4.97 0.65
4.78 0.43
4.81 0.61
5.50 1.36
4.72 0.55
5.99 1.69
Isometric strength
Cryotherapy
101.6 34.2
Control
100.4 32.8
78.3 21.4
73.0 29.0
92.5 31.2
81.3 42.1
112.3 27.2
86.4 45.3
2.75 0.08
2.59 0.25
2.74 0.05
2.49 0.25
2.78 0.06
2.40 0.27
27.3 2.2
30.2 2.4
27.3 2.1
30.4 2.4
27.1 2.2
30.4 2.7
Tenderness (N)
Cryotherapy
Control
22.6 7.3
26.9 3.9
24.9 6.4
26.7 5.6
22.1 5.4
21.9 6.9
Ln CK (IU l2 1)
Cryotherapy
Control
15.1 9.4
15.7 6.1
72 h
Figure 1 Relaxed arm angle of the cryotherapy group (s ) and the control group (h ) immediately before and 3 days after
strenuous eccentric exercise of the elbow Xexors (mean sx). The values for the control group were 13% lower than baseline
values and 14% lower than for the cryotherapy group by day 3 (P < 0.05).
235
Figure 2 Natural log values for plasma creatine kinase activity of the cryotherapy group (s ) and the control group
(h ) immediately before and 3 days after strenuous eccentric exercise of the elbow Xexors (mean sx). The values for the control
group were higher than baseline values and the values for the cryotherapy group by day 3 (P < 0.05).
Strength
The isometric strength values for the subjects in
this study are similar to those of a previous study
that used similar subjects and methods (Nosaka and
Clarkson, 1997). There was a signiWcant main eVect
for time on strength (F3,39 = 2.87, P < 0.05). Strength
was lower than the baseline value at day 1 (76.1 29.6
vs 101 32.2 N), returning to baseline values by
days 2 and 3. There was no signiWcant group time
interaction.
Muscle tenderness
There was a signiWcant main eVect for time on muscle
tenderness (F3,39 = 16.55, P < 0.001). Tenderness values
were signiWcantly higher than baseline values on day
1 (24.3 5.7 vs 15.4 7.8 N) and remained above
baseline values on day 2 (25.4 6.0 N) and day 3
(22.0 6.1 N). There was no signiWcant interaction of
group time on tenderness.
Discussion
The results of this study are in line with those of previous studies that examined the temporal characteristics
of exercise-induced muscle damage on the upper arm
musculature (Newham et al., 1983; Yackzan et al.,
1984; Newham and Jones, 1985; Friden et al., 1988;
Nosaka et al., 1991; Cleak and Eston, 1992b; Howell
et al., 1993; Nosaka and Clarkson, 1997). However, the
most interesting Wndings are revealed by the group
time interactions on two of the dependent variables
namely, relaxed arm angle and creatine kinase activity.
The overall decrease in relaxed arm angle in the control group by day 3 (0.35 rad) was very similar (0.38
rad) to that observed by Cleak and Eston (1992b), but
greater than (0.21 rad) that observed by Nosaka and
Clarkson (1997), who used a faster eccentric speed to
induce muscle damage (1.05 vs 0.58 rad s- 1). Several
investigators have speculated that the cause of muscle
shortening may be an abnormal increase of calcium ions
in the muscle cell (Armstrong, 1984; Newham et al.,
1985; Clarkson and Tremblay, 1988; Ebbeling and
Clarkson, 1989; Nosaka et al., 1991), which has been
attributed to a defect in the sarcoplasmic reticulum
after damaging exercise. Increased intracellular levels of
calcium have been observed in the muscles of horses
subjected to high-intensity exercise (Byrd, 1992).
The results provide support that cryotherapy may
reduce the extent to which the muscle and connective
tissue unit becomes shortened after strenuous eccentric
exercise. This is indicated by the signiWcant group
236
time interaction for the relaxed arm angle measurement.
It can be seen from Fig. 1 that the cryotherapy group
experienced less of a decrease in relaxed arm angle
(increased range of motion) than the control group.
Studies on humans and animals have shown that
local cooling aV ects the motor neuron pool, the muscle
spindle and its aVerents, the skin aVerents, the myoneural junction and the extrafusal Wbres of the muscle
(see Meeusen and Lievens, 1986, for a review). The
progressive fall in conduction velocity of the motor and
sensory nerves exposed to cold application is in proportion to the temperature of the tissues, and continues
until the nervous tissue temperature decreases to 10 15C (Fox, 1961). The rate of Wring from muscle spindle aVerents decreases when the whole muscle is cooled.
This eVect is immediate and results in a reduction in
spasticity.
Our results lend some support to a previous study
(Prentice, 1982), which examined the use of heat and
cold therapy in conjunction with stretching to determine what combination would elicit the greatest
amounts of relaxation within muscles that were in a
state of exercise-induced damage. Electromyographic
activity indicated that the application of cold followed
by stretching was the most successful combination.
It was proposed that cold application reduced the level
of electrical activity of the muscle spindle by increasing
the threshold stimulus for Wring and decreasing the
aVerent Wring rate. However, the results are not in
line with those of previous studies (Yackzan et al.,
1984; Braun and Clarkson, 1989; Isabell et al., 1992)
that examined the eVects of cold therapy on muscle
spasticity following exercise-induced muscle damage.
This may be a result of the variation in timing and
nature of cold applications.
These factors may also explain why our results diVer
from those of Isabell et al. (1992), who observed that
cryotherapy, applied after damaging eccentric exercise,
had no eVect on plasma creatine kinase activity.
Although the overall mean values (the main eVect for
group) indicated that creatine kinase activity increased
above baseline values on days 2 and 3, this eVect appears
to be a phenomenon of the group time interaction.
It can be seen from Fig. 2 that creatine kinase activity
continued to increase in the control group, whereas
in the cryotherapy group there was no increase above
baseline values.
It is unclear what mechanism can account for the
diVerence in creatine kinase activity between the two
groups after the bout of damaging exercise. Several lines
of explanation might be proposed: there was a reduced
eZux of creatine kinase from the muscle into the
lymphatic system, a reduction in the amount of postexercise damage as a result of cold application in
the treatment group, or an increase in creatine kinase
237
Acknowledgements
We thank Ron Maughan, Priscilla Clarkson, Mike Gleeson
and the anonymous referees for their helpful comments. We
also thank Declan Connolly for his advice in the early stages of
the project.
References
Ackerman, N.B. (1975). The inXuences of changes in temperature on intestinal lymph Xow and relationship to
operations for carcinoma of the intestine. Surgery,
Gynecology and Obstetrics, 140, 885 888.
Armstrong, R.B. (1984). Mechanisms of exercise-induced
delayed onset muscle soreness: A brief review. Medicine and
Science in Sports and Exercise, 16, 529 538.
Armstrong, R.B. (1990). Initial events in exercise induced
muscular injury. Medicine and Science in Sports and Exercise,
22, 429 435.
Baker, S.B., Kelly, N. and Eston, R.G. (1997). Pressure pain
tolerance at diVerent sites on the quadriceps femoris
muscle prior to and following eccentric exercise. European
Journal of Pain, 1, 229 233.
Barcroft, H. and Edholm, K. (1943). The eVects of temperature on blood Xow and deep temperature on the human
forearm. Journal of Physiology, 102, 5 20.
Braun, B. and Clarkson, P.M. (1989). EVect of cold treatment
during eccentric exercise. Medicine and Science in Sports and
Exercise, 21 (suppl.), S32.
238
Byrd, S.K. (1992). Alterations in the sarcoplasmic reticulum:
A possible link to exercise-induced muscle damage.
Medicine and Science in Sports and Exercise, 24, 531 536.
Byrne, R.M. and Levy, M.N. (1993). Physiology. St. Louis,
MO: Mosby Year Book.
Clarkson, P.M. and Newham, D.J. (1994). Associations
between muscle soreness, damage and fatigue. In Fatigue:
Neural and Muscular Mechanisms (edited by S.C. Gandevia,
R.M. Enoka, A.J. McComas, D.G. Stuart and C.K.
Thomas), pp. 457 469. New York: Plenum Press.
Clarkson, P.M. and Tremblay, I. (1988). Exercise induced
muscle damage, repair and adaptation in humans. Journal
of Applied Physiology, 65, 1 6.
Cleak, M.J. and Eston, R.G. (1992a). Delayed onset muscle
soreness: Mechanisms and management. Journal of Sports
Sciences, 10, 325 341.
Cleak, M.J. and Eston, R.G. (1992b). Muscle soreness,
swelling, stiV ness and strength loss after intense eccentric
exercise. British Journal of Sports Medicine, 26, 267 272.
Ebbeling, C.B. and Clarkson, P.M. (1989). Exercise induced
muscle damage and adaptation. Sports Medicine, 7, 207 234.
Edwards, T., Baker, S. and Eston, R.G. (1996). A method of
detecting the muscle pain threshold using an objective
software-mediated technique. Perceptual and Motor Skills,
82, 955 960.
Enoka, R.M. (1996). Eccentric contractions require unique
activation strategies by the nervous system. Journal of
Applied Physiology, 81, 2339 2346.
Eston, R.G., Critchley, N. and 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.
Eston, R.G., Finney, S., Baker, S. and Baltzopoulos, V. (1996).
Muscle tenderness and peak torque changes after downhill running following a prior bout of isokinetic eccentric
exercise. Journal of Sports Sciences, 14, 291 299.
Fox, R.H. (1961). Local cooling in man. B ritish Medical
Bulletin, 17, 14 18.
Friden, J. and Leiber, R.L. (1992). Structural and mechanical
basis of exercise-induced muscle injury. Medicine and
Science in Sports and Exercise, 24, 521 530.
Friden, J., Seger, J. and Ekblom, B. (1988). Sublethal muscle
Wbre injuries after high tension anaerobic exercise.
European Jour nal of Applied Physiology, 57, 360 368.
Fu, F.H., Cen, H.W. and Eston, R.G. (1997). The eVects
of cryotherapy on muscle damage in rats subjected to
endurance training. Scandinavian Journal of Medicine and
Science in Sports, 7, 358 362.
Gulick, D.T., Kimura, I.F., Sitler, M., Paolone, A. and Kelly,
J.D. (1996). Various treatment techniques on signs and
symptoms of muscle soreness. Journal of Athletic Training,
31, 145 152.
Hill, D.W. and Richardson, J.D. (1989). EVectiveness of 10%
trolamine salicylate cream on muscular soreness induced
by a reproducible program of weight training. Journal of
Orthopaedic and Sports Physical Therapy, 11, 19 23.
Howell, J.N., Chlebourn, G. and Conatser, R. (1993). Muscle
stiV ness, strength loss, swelling and soreness following