Alternating hot and cold water immersion for athlete recovery: A review

Abstract

Objectives. The aim of this review was to investigate whether alternating hot – cold water treatment is a legitimate training tool for enhancing athlete recovery. A number of mechanisms are discussed to justify its merits and future research directions are reported. Alternating hot– cold water treatment has been used in the clinical setting to assist in acute sporting injuries and rehabilitation purposes. However, there is overwhelming anecdotal evidence for it's inclusion as a method for post exercise recovery. Many coaches, athletes and trainers are using alternating hot – cold water treatment as a means for post exercise recovery. Design. A literature search was performed using SportDiscus, Medline and Web of Science using the key words recovery, muscle fatigue, cryotherapy, thermotherapy, hydrotherapy, contrast water immersion and training. Results. The physiologic effects of hot – cold water contrast baths for injury treatment have been well documented, but its physiological rationale for enhancing recovery is less known. Most experimental evidence suggests that hot– cold water immersion helps to reduce injury in the acute stages of injury, through vasodilation and vasoconstriction thereby stimulating blood flow thus reducing swelling. This shunting action of the blood caused by vasodilation and vasoconstriction may be one of the mechanisms to removing metabolites, repairing the exercised muscle and slowing the metabolic process down. Conclusion. To date there are very few studies that have focussed on the effectiveness of hot– cold water immersion for post exercise treatment. More research is needed before conclusions can be drawn on whether alternating hot– cold water immersion improves recuperation and influences the physiological changes that characterises post exercise recovery.

Full text

Literary review
Alternating hot and cold water immersion
for athlete recovery: a review
Darryl J. Cochrane*
Department of Management, Sport Management and Coaching, Massey University, Private Bag 11 222, Palmerston North, New Zealand
Abstract
Objectives. The aim of this review was to investigate whether alternating hot–cold water treatment is a legitimate training tool for
enhancing athlete recovery. A number of mechanisms are discussed to justify its merits and future research directions are reported.
Alternating hot–cold water treatment has been used in the clinical setting to assist in acute sporting injuries and rehabilitation purposes.
However, there is overwhelming anecdotal evidence for it’s inclusion as a method for post exercise recovery. Many coaches, athletes and
trainers are using alternating hot–cold water treatment as a means for post exercise recovery.
Design. A literature search was performed using SportDiscus, Medline and Web of Science using the key words recovery, muscle fatigue,
cryotherapy, thermotherapy, hydrotherapy, contrast water immersion and training.
Results. The physiologic effects of hot– cold water contrast baths for injury treatment have been well documented, but its physiological
rationale for enhancing recovery is less known. Most experimental evidence suggests that hot–cold water immersion helps to reduce injury
in the acute stages of injury, through vasodilation and vasoconstriction thereby stimulating blood flow thus reducing swelling. This shunting
action of the blood caused by vasodilation and vasoconstriction may be one of the mechanisms to removing metabolites, repairing the
exercised muscle and slowing the metabolic process down.
Conclusion. To date there are very few studies that have focussed on the effectiveness of hot – cold water immersion for post exercise
treatment. More research is needed before conclusions can be drawn on whether alternating hot–cold water immersion improves
recuperation and influences the physiological changes that characterises post exercise recovery.
q2003 Published by Elsevier Ltd. All rights reserved.
Keywords: Recovery; Training; Post exercise; Hydrotherapy; Regeneration; Immersion
1. Introduction
Recovery is an important aspect of any physical
conditioning programme however, many athletes train
extremely hard without giving their body time to recover
which can lead to over reaching, burnout or poor
performances (Mackinnon and Hooper, 1991). Without the
necessary recovery interventions it is very difficult for an
athlete to maintain a high level of performance on a daily or
weekly basis. As athletes look for the leading edge, rest is
frequently overlooked for increases in overload, intensity
and volume.
Recently a lot of emphasis has been placed on speeding
up the recovery process so athletes can proceed to do
successive bouts of training or competition without the
associated fatigue or burn out effects. Numerous physical,
psychological and nutritional methods have been used to
accelerate the recovery process (Calder, 1996). There has
been an increase in the use of modalities such as massage,
floatation, hyperbaric oxygenation therapy and acupuncture
with little scientific evaluation of its use and effectiveness
for exercise recovery. Alternating hot – cold water immer-
sion is one technique that is very popular and is practised
with increased frequency in aiding recovery after physical
training and competition (Calder, 2001a). Anecdotal reports
from coaches, medical personnel and athletes suggest that
this method of water immersion has positive effects on
subsequent performance.
The aim of this review was to source the literature and
provide the scientific rationale and mechanisms of using
alternating hot–cold water immersion for post exercise
recovery.
2. Therapeutic modalities
Ice packs, whirlpools, baths, heat packs, infra-red lamps,
paraffin wax and ice massage are various techniques of
Physical Therapy in Sport 5 (2004) 26–32
www.elsevier.com/locate/yptsp
1466-853X/$ - see front matter
doi:10.1016/j.ptsp.2003.10.002
*Tel.: þ64-6-350-5799; fax: þ64-6-350-5661.
E-mail address: d.cochrane@massey.ac.nz (D.J. Cochrane).

cryotherapy and thermotherapy that have been used in the
sports medicine and rehabilitation fields for the treatment of
acute injuries (Prentice, 1999). Additionally, contrast baths,
warm and cold packs have also played a major role in injury
management but increasingly these modalities are now used
for post exercise recovery. Warm spas with cold plunge
pools or contrast hot–cold baths and showers are common
practises used by athletes after training or exercise.
According to Calder (1996) the contrast hot – cold water
technique is thought to speed recovery by increasing the
peripheral circulation by removing metabolic wastes and
stimulating the central nervous system. Calder (2001b)
further claims that contrast hot – cold increases lactate
clearance, reduces post exercise oedema and enhances
blood flow to the fatigued muscle. Additionally, it is thought
to slow down the metabolic rate and revitalise and energise
the psychological state.
3. Physiology of cooling and heating
There is a general consensus that the application of cold
ice or water immersion decreases skin, subcutaneous and
muscle temperature (Enwemeka et al., 2002; Myrer et al.,
1997; Hartvickson, 1962; Johnson et al., 1979; Lowden and
Moore, 1975). The decrease in tissue temperature is thought
to stimulate the cutaneous receptors causing the sympathetic
fibres to vasoconstrict which decreases the swelling and
inflammation by slowing the metabolism and production of
metabolites thereby limiting the degree of the injury
(Enwemeka et al., 2002).
Superficial tissues can remain cool up to four hours from
ice packs or cold water immersion (Beltisky et al., 1987;
Hocutt et al., 1982; McMaster et al., 1979). The mechanism
of this process still remains unclear. Enwemeka et al. (2002)
found that cold pack treatment up to 20 min significantly
decreased superficial tissue temperature by dulling and
reducing the sensation of pain. They concluded that cold
pack treatment limits the amount of swelling in acute
injuries by slowing the metabolic rate by shunting less blood
to the cold superficial area. Earlier research has shown that
metabolites are cleared by the blood exchange from
superficial to deep tissue. Incoming warm blood is diverted
to the deeper tissues thereby slowing down the cooling
effect of the deep tissues (Pugh et al., 1960). A cooling
effect also decreases nerve conduction velocity in super-
ficial tissues by slowing the rate of firing of muscle spindle
afferents and reflex responses thus decreasing muscle spasm
and pain (Prentice, 1999; de Jesus et al., 1973).
Thermotherapy has shown to increase tissue temperature,
increase local blood flow, increase muscle elasticity, cause
local vasodilation, increase metabolite production and
reduce muscle spasm (Prentice, 1999; Brukner and Khan,
2001; Zuluaga et al., 1995). Additionally, superficial
heating decreases sympathetic nerve drive which causes
vasodilation of local blood vessels and increases circulation.
The increased blood flow allows an increased supply of
oxygen, antibodies and the ability to clear metabolites
(Zuluaga et al., 1995).
Myrer et al. (1994) proposed that if contrast therapy is
reported to produce physiologic effects (vasodilation and
constriction of local blood vessels, changes in blood flow,
reduction in swelling, inflammation and muscle spasm)
significant fluctuations of muscle temperature must be
produced by the alternating hot – cold contrast treatments.
Participants immersed their right leg into a hot (40.6 8C)
whirlpool for 4 min followed by a cold (15.6 8C) whirlpool
for 1 min, and this was repeated four times (Myrer et al.,
1994). This protocol did not produce any significant
differences in intramuscular temperature 1 cm below the
skin in the gastrocnemius muscle. In a subsequent study,
Myrer et al. (1997) changed the modality of the contrast
therapy to cold and hot packs. The exposure duration was
extended to 5 min for both the hot–cold treatment. The
rationale for using the packs was to give deeper penetration,
greater heat transfer and elicit superior temperature
fluctuations. The results verified their previous study that
hot–cold contrast treatment does not produce the required
physiologic effects required to induce intramuscular tem-
perature changes. Wertz (1998) and Higgins and Kaminski
(1998) have also reported similar results. Lehmann et al.
(1974) suggested that for the physiologic effects to take
place the muscle temperature must reach at least 40 8C,
however, the above studies reported muscle temperatures
below 40 8C. More research is required to investigate the
required physiologic effects associated with using deep heat
treatments in hot–cold contrast therapy.
4. Recovery
Recovery is defined as ‘the return of the muscle to its pre
exercise state following exercise’ (Tomlin and Wenger,
2001). Aerobic metabolism remains elevated in the recovery
phase after exercise. Known as excess post-exercise oxygen
consumption (EPOC) it assists in replenishing the body
stores (Bahr and Maehlum, 1986). EPOC consists of a fast
and slow component (Gaesser and Brooks, 1984). The fast
component restores 70% of ATP and PCr energy stores
within 30 s (Hultman et al., 1967) and reloads plasma
haemoglobin and muscle myoglobin (Bahr, 1992). The slow
component is observed after strenuous exercise and has
been associated with increased cardiac and respiratory
functions, elevated core temperature and removal of
metabolic waste products (Gaesser and Brooks, 1984;
Sahlin, 1992). Dependent on the exercise intensity it may
take up to 24 h for the slow component to return to its
resting levels (Gaesser and Brooks, 1984). Phosphagen
stores take 3– 5 min to fully recover (Hultman et al., 1967)
compared to an hour or more for the resting return of lactate
and pH. The rise in lactate production and H
þ
accumulation
can disrupt the muscle contractile processes and the existing
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–32 27

transport and metabolic pathways can become less efficient
(Tomlin and Wenger, 2001).The use of passive (no exercise,
massage, contrast hydrotherapy) or active recovery (light
exercise) for replenishing fuel stores and removal of
metabolic wastes has implications for accelerating post
exercise recovery rates.
4.1. Metabolic removal in active and passive recovery
Lactate production is evident when training or compet-
ing, however, the amount produced is dependent on the
duration and intensity of the exercise and the length of the
recovery interval. The ability to clear lactate in the recovery
phase relies on the working muscle to quickly remove,
tolerate and/or buffer H
þ
(Sahlin and Henriksson, 1984).
hot–cold immersion may have some merit in aiding
recovery if waste products are cleared faster. However,
the mechanism by which active recovery promotes lactate
removal is not clearly understood. This process is complex
as it depends on a range of factors for example, local blood
flow, chemical buffering, movement of lactate from muscle
to blood, lactate conversion to pyruvate in liver, muscle and
heart (McArdle et al., 2001).
Research has shown that lactate removal is increased
when active recovery periods are implemented compared to
passive rest for continuous or repeated bouts of exercise
(Hermansen and Stensvold, 1972; Weltman et al., 1979;
Cortes et al., 1989). Dodd et al. (1984) found that a recovery
period of moderate continuous intensity facilitated lactate
removal faster than passive recovery. Additionally, a
combination of high intensity (65% VO
2
max) and low
intensity (35% VO
2
max) was no more beneficial than a
recovery of low intensity (35% VO
2
max) for 40 min.
There is conflicting evidence on the effect that active and
passive recovery has on muscle glycogen synthesis. Choi
et al. (1994) have shown active recovery delays glucose
synthesis after high intensity (130% VO
2
max) intermittent
cycling in untrained males. However, Futre et al. (1987)
found no statistical differences between passive and active
recovery for muscle glycogen synthesis. Whatever the
outcome there are implications to the type of recovery
implemented in post training.
It appears that no further gains are elicited when
performing the intensity of the recovery period above
lactate threshold, as it may prolong the clearance of lactate
by accumulating more (Dodd et al., 1984; Gladden, 1989).
From isotope tracer studies, Brooks (2000) suggested that
lactate produced in fast twitch muscle fires can be
transported to other fast twitch or slow muscle fibres for
pyruvate conversion, which undergoes chemical reactions
for aerobic energy metabolism. This shuttling allows for
both production and removal of lactate. Signorile et al.
(1993) claimed that during recovery from low intensity
cycling, lactate clearance may be enhanced by active
muscles causing a pumping action and adjacent muscles
providing oxidative metabolism to removing metabolites.
Active recovery often requires additional energy that
further depletes precious energy stores therefore, if passive
recovery is proven to increase glycogen resynthesis contrast
hydrotherapy may be justified as a post training tool.
However, most athletes have the tendency to spend more
time in the warm water immersion thus off setting the
purported benefits as dehydration and neural fatigue are
accentuated.
Additionally, if competition is conducted at night
recovery could be compromised if other engagements
such as team debriefing, after match functions or press
conferences take priority. Conducting hot–cold contrast
training may not be any more beneficial than complete rest.
Sanders (1996) used a contrast-temperature protocol
involving hot–cold plunge pools to measure the recovery
of lactate levels in elite women hockey players after a
series of Wingate tests. A comparison of lactate clearances
following passive rest, light exercising (active recovery)
and the contrast immersion protocol was undertaken.
Results indicated that lactate levels were recovered equally
fast by using either the contrast water immersion or the
active recovery protocol. However, the lactate recovery
following passive rest was significantly slower. In sports
medicine contrast baths have been used to treat subacute
soft tissue and joint injuries by alternating hot – cold, thus
promoting vasodilation/vasoconstriction causing a ‘pump-
ing’ action to reduce swelling of the injured site
(Rivenburgh, 1992; Prentice, 1999). This ‘pumping’ action
may explain the possible anecdotal reports of reduced post
exercise stiffness and the accelerated return to basal and
metabolic resting levels. However, the removal of
metabolites and reduced swelling from the mechanical
force of alternating hot – cold immersion is unproven and
contentious. Myrer et al. (1997) suggested that
the significant skin temperature fluctuations from the
hot–cold contrast packs caused vasoconstriction and
vasodilation thereby initiating subcutaneous response
and mechanical shunting. Conversely, they argue that the
increase in local blood flow would not reduce oedema, as
swelling reduction requires the removal of debris and fluid
performed by the lymphatic system. Since the lymphatic
system requires muscle contraction or gravity to move fluid
contents, it is unlikely this mechanism can be substan-
tiated, as lymph flow is independent of circulatory
changes.Tomasik (1983) studied the effect of blood
electrolytes and lactic acid levels in participants that
underwent 30 min of hydromassage or control (no hydro-
massage) after 15 min of sub-maximal cycling. The
investigation found that the hydromassage intervention
was able to return haematocrit, plasma potassium and lactic
acid levels to resting levels faster than those who received
no hydromassage. However, the acquired effects of
hypergravity and proprioception from the underwater jets
to assist the clearance of waste products were not
discussed. Unfortunately the studies of Tomasik (1983)
and Sanders (1996) have relied on measurements of blood
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–3228

lactate to reflect muscle lactate clearance, which may
compromise conclusions on lactate removal (Tomlin and
Wenger, 2001). Further research is needed to establish
whether mechanical shunting from the hot – cold immersion
elicits a possible mechanism for metabolite removal to
accelerate post exercise recovery.
4.2. Neural recovery
It is well established that during exercise there is a
decrease in parasympathetic and increase in sympathetic
activity. The sympathetic excitation causes a release of
noradrenaline and adrenaline that increases myocardial
contractility and accelerates heart rate (McArdle et al.,
2001). Additionally, vasodilation occurs in skeletal and
heart muscle, blood flow increases from vasoconstriction
of other organs and the airways become dilated. Post
exercise sympathetic activity remains high but with
adequate recovery it returns to resting levels. However,
if a high training load, volume or intensity is repeatedly
performed without the necessary rest, sympathetic activity
will become unceasingly high. This often leads to
overtraining/overreaching when the signs and symptoms
are not detected (Hahn, 1994).
Neurological recovery of the peripheral nervous system
may be augmented by contrast hydrotherapy, massage and
floatation by reducing the load of the sympathetic activity
(Hahn, 1994; Calder, 1996). Athletes who perform hot –
cold hydrotherapy after training or competition have
reported lighter and less tight muscles with a feeling of
mental freshness (Calder, 2001a). This may be associated
to central nervous system relief. However, little is known
on the effects that hot– cold water immersion has on the
nervous system. Research conducted by Gieremek (1990)
examined reaction time of simple reflex tasks, the tendon
reflex (T reflex) of the Achilles tendon, Hoffman reflex (H
reflex) of the soleus and conduction of the tibialis nerve
before and after 30 min of jet pressured spa water
immersion (34 – 36 8C) in judo fighters and healthy
untrained males. He found that for both groups, the
underwater jet spa improved the efficiency of both the
central and peripheral nervous system. He supported his
claim from the significant changes of simple reaction
time, T and H reflexes. Gieremek stated that the
underwater jets and lukewarm water activated the
proprioreceptors to increase the excitability to the brain,
which stimulated the neuromuscular system. Additionally,
he justified the periphery efficiency component from the
significant increases in neural transmission and the
induced M-response of the H reflex.
Gieremek claimed that the reflex and electrophysiologi-
cal responses elicited from the underwater jet immersion
may have improved the speed of the central spread of
electrical activation in the nerve, neuromuscular synapses
and the muscle thereby producing a positive post exercise
recovery effect.
Viitasalo et al. (1995) investigated the effect of exposure
and non-exposure of underwater jet massage (36 – 37 8C) on
junior track and field athletes. The experiment used a cross
over design where two groups of equal size under went a
week of non-exposure and exposure of underwater jet
massage. Three treatments of 20 min were performed over
five days after power, speed and strength conditioning
sessions. During the exposure week of underwater jet
massage vertical jumping power declined slightly, continu-
ous vertical jumping ground contact time increased, serum
creatine kinase and myoglobin levels were elevated
compared to no water jet treatment. The results indicated
that the combination of intense speed, power and strength
sessions with underwater jet massage increased blood
markers to release more protein from the muscle to the
blood thereby enhancing the neuromuscular system.
4.3. Muscle recovery
It has been confirmed that eccentric, intensive and
unfamiliar exercises are causes of muscle damage (Clarkson
and Sayers, 1999 McHugh et al., 1999; Armstrong, 1984).
Delayed onset of muscle soreness (DOMS) usually
transpires 24 – 48 h post exercise with symptoms consisting
of tender, stiff and sore muscles (Clarkson et al., 1992).
Several theories have been presented to explain the
physiological mechanism of DOMS but with little agree-
ment. They include muscle fibre damage, breakdown of
muscle proteins resulting in inflammation and cellular
degradation (Armstrong, 1984; Smith, 1991; Friden and
Lieber, 1992; Byrd, 1992; Clarkson and Sayers, 1999).
McHugh et al. (1999) has argued for a combined neural,
connective and cellular mechanism. Whatever the proposed
mechanism causing DOMS the recovery process is
important for regeneration. The symptoms of DOMS
normally develop within 24 h and peak between 24–72 h
(Cleak and Eston, 1992; Armstrong 1990).
The symptom of exercise-induced muscle damage (pain,
spasm and inflammation) is similar to that of injured muscle
therefore cryotherapy has been the primary treatment
modality. Kuligowski et al. (1998) studied the effectiveness
of warm, cold whirl pool and contrast therapy for treating
delayed-onset muscle soreness 24, 48, and 72 h post
exercise. The elbow flexors were eccentrically trained to
elicit DOMS. Resting elbow flexion, active elbow flexion
and extension, perceived soreness and maximal isometric
contraction were the criteria used to assess what effect the
different treatments had on DOMS. They found that
perceived soreness and resting elbow flexion returned to
baseline levels when cold whirlpool and contrast therapy
were administered, propagating that these treatments were
more effective than warm whirlpool and passive resting.
Contrary, Miller (1992) found that a warm whirlpool was
sufficient enough to decrease the perceived pain of DOMS
in down hill treadmill running. However, the efficacy of
control and warm whirlpool produced no significant
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–32 29

difference on quadriceps flexibility or strength. Likewise
Easton and Peters (1999) concluded that following exhaus-
tive eccentric exercise the cold-water immersion appeared
to reduce muscle damage and stiffness but had no effect on
the perception of muscle tenderness and strength loss.
It can be concluded that the research is contradictory to
alleviating the symptoms of DOMS due to variations in the
type, frequency and duration of treatments.
4.4. Water temperature and ratio of cold to hot
for hydrotherapy recovery
The common practised ratio of warm to cold bath
duration for injury treatment is normally 3:1 or 4:1, with hot
baths ranging from 37 to 43 8C alternating with cold baths
temperature ranging from 12 to15 8C(Bell and Horton,
1987; Myrer et al., 1994; Brukner and Khan, 2001;
Halvorson, 1990). The duration of the treatment is normally
20–30 min repeated twice daily (Higgins and Kaminski,
1998). It is also well documented that the treatment should
finish on the cold treatment to encourage vasoconstriction
for the injured athlete (Bell and Horton, 1987; Prentice,
1999; Zuluaga et al., 1995; Brukner and Khan, 2001).
Calder (1996) has documented guidelines (water tempera-
ture, repetitions and durations) for post exercise contrast
water recovery that are similar to injury management.
However, the duration for hot–cold shower (1 –2 min hot,
10–30 s cold) differs to that of a spa/bath (3–4 min hot, 30 –
60 s cold) with little justification. Higgins and Kaminski
(1998) and Myrer et al. (1997) found cold exposure of
approximately 1 min was not sufficient enough to signifi-
cantly decrease muscle temperature following warm water
immersion, thus nullifying the required physiologic effects.
There is a lack of evidence to support the post exercise
recovery guidelines especially in the light of injury contrast
treatment. Further research is required to investigate the
different hot to cold time ratios. The appropriate mode of
contrast treatment, the duration and the optimum water
temperature need to be examined to verify its effectiveness
as a recovery modality.
5. Holistic approach
Training and competition creates an overload to stress
the body, which in turn produces fatigue followed by
improved performance (Calder, 1996). Depending on the
nature of the training or activities; nutritional, physiologi-
cal, neurological and psychological components are
stressed in different ways that result in fatigue. Calder
(1995) devised a ranking system to help coaches identify
which of the four fatigue components are the most
stressed. For endurance training the ranking from the
most to the least fatigued was nutritional, physiological,
neurological, and psychological. However, for speed
training the order was neurological, physiological,
nutritional and psychological fatigue. According to Calder
(1995) the site of fatigue for the neurological component is
the peripheral nervous system; physiological (muscle cell);
nutritional (fluid and fuel stores); and psychological
(central nervous system). From the ranking system the
athlete and coach can then identify the appropriate
recovery techniques needed to accelerate the recovery,
which are rehydration and carbohydrate intake for fluid
and fuel stores; hydrotherapy, ‘warm down’ and massage
for increasing blood flow to fatigued muscles; visualisa-
tion, progressive muscular relaxation, meditation, flotation
and massage for psychological fatigue; passive rest,
massage, hydrotherapy, and ‘warm down’ for neurological
fatigue. The holistic approach for recovery training may
give better responses rather than using isolated recovery
techniques. Flanagan et al. (1998) simulated a soccer
tournament to examine the effects of recovery strategies
on young male soccer players. They found those in the
recovery group did not show any significant decline in 10
and 20 m speed times until the sixth day of competition
compared to the control group. However, there was no
change in vertical jump for both groups during the
tournament. The recovery techniques that were employed
included; massage, active pool sessions, hot – cold
showers, stretching, hydration and nutritional plans. The
consequences of the combined recovery techniques pre-
vented physical drop off, lowered the occurrence of
influenza symptoms and produced a higher rating
of overall wellness.
6. Conclusion
Despite the popularity of hot – cold water immersion as a
recovery modality, little research has been conducted. hot –
cold contrast therapy for acute injuries has been used to
explain the purported physiologic effects for post exercise
recovery. However, the conflict of literature makes it
difficult to give a conclusive mechanism. Additionally, the
guidelines of the duration spent in each water condition,
the repetitions, temperature, the use of underwater jets, the
learning and training effect of the body adapting to the hot–
cold contrast therapy all need to be vigorously investigated
before it can be claimed as an accelerant for aiding
recovery.
References
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.
Bahr, R., 1992. Excess postexercise oxygen consumption—magnitude,
mechanisms, and practical implications. Acta Physiologica Scandina-
vica 144 (Suppl. 605), 1–43.
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–3230

Bahr, R., Maehlum, S., 1986. Excess post-exercise oxygen consumption. A
short review. Acta Physiologica Scandinavica Suppl. 128 (556),
99–104.
Bell, A.T., Horton, P.G., 1987. The uses and abuse of hydrotherapy in
athletics: a review. Athletic Training 22 (2), 115 –119.
Beltisky, R.B., Odam, S.J., Hubley-Kozey, C., 1987. Evaluation of the
effectiveness of wet ice, dry ice and cryogen packs in reducing skin
temperature. Physical Therapy 67, 1080–1084.
Brooks, G.A., 2000. Intra- and extra-cellular lactate shuttles. Medicine and
Science in Sports and Exercise 32 (4), 790–799.
Brukner, P., Khan, K., 2001. Clinical Review of Sports Medicine, second
ed., McGraw-Hill, Roseville, NSW.
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 (5), 531–536.
Calder, A., 1995. Accelerating adaptation to training. Australian Strength
and Conditioning Association National Conference and Trade Show
(Gold Coast, Australia), 68–73.
Calder, A., 1996. Recovery training. In: Reaburn, P., Jenkins, D. (Eds.),
Training for Speed and Endurance, Allen and Unwin, Sydney.
Calder, A., 2001a. The science behind recovery: strategies for athletes.
SportsMed News August 2–3.
Calder, A., 2001b Personal Communication.
Choi, D., Cole, K.J., Goodpaster, B.H., Fink, W.J., Costill, D.L., 1994.
Effect of passive and active recovery on the resynthesis of muscle
glycogen. Medicine and Science in Sports and Exercise 26 (8),
992– 996.
Clarkson, P.M., Nosaka, K., Braun, B., 1992. Muscle function after
exercise-induced muscle damage and rapid adaptation. Medicine and
Science in Sports and Exercise 24 (5), 512–520.
Clarkson, P.P.M., Sayers, S.P., 1999. Etiology of exercise-induced muscle
damage. Canadian Journal of Applied Physiology 24 (3), 234 – 248.
Cleak, M.J., Eston, R.G., 1992. Delayed onset muscle soreness:
mechanisms and management. Journal of Sports Sciences 10, 325 –341.
Cortes, C.W., Kreider, R.B., Al-Mandaloui, S., Lamberth, J., Johnson,
K.D., Thompson, W.R., Anderson, H.N., 1989. Lactate clearance
during active and passive recovery. Annals of Sports Medicine 4 (1),
26–28.
de Jesus, P., Hausmanowa-Petrusewicz, I., Barchi, R., 1973. The effect of
cold on nerve conduction human slow and fast nerve fibres. Neurology
23, 1182–1189.
Dodd, S.L., Powers, S.K., Callender, T., Brooks, E., 1984. Blood lactate
disappearance at various intensities of recovery exercise. Journal of
Applied Physiology 57, 1462– 1465.
Easton, R., Peters, D., 1999. Effects of cold water immersion on the
symptoms of exercise-induced muscle damage. Journal of Sports
Sciences 13 (7), 231–238.
Enwemeka, C.S., Allen, C., Avila, P., Bina, J., Konrade, J., Munns, S.,
2002. Soft tissue thermodynamics before, during, and after cold pack
therapy. Medicine and Science in Sports and Exercise 34 (1), 45– 50.
Flanagan, T.E., Pruscino, C., Pihan, J., Marshall, R., Healy, A., Baum, M.,
Merrick, M., 1998. Brisbane Tour 1998: achieving recovery during
major tournaments, In: Success in Sport and Life, Victorian Institute of
Sport, Melbourne.
Friden, J., Lieber, R., 1992. Structural and mechanical basis of exercise-
induced muscle injury. Medicine and Science in Sports and Exercise 24
(5), 521– 530.
Futre, E.M.P., Noakes, T.D., Raine, R.I., Terblanche, S.E., 1987. Muscle
glycogen repletion during active postexercise recovery. American
Journal of Physiology 253 (3), 305 –311.
Gaesser, G.A., Brooks, G.A., 1984. Metabolic bases of excess post-exercise
oxygen consumption: a review. Medicine and Science in Sports and
Exercise 16 (1), 29–43.
Gladden, L.B., 1989. Lactate uptake by skeletal muscle. Exercise Sport
Science Review 17, 115–155.
Gieremek, K., 1990. Effects of underwater massage on the responsiveness
of the motoric neural system. Biology of Sport (1), 53– 63.
Hahn, A.G., 1994. Training, recovery and overtraining—the role of the
autonomic nervous system. Sports Coach, 29–30.
Halvorson, G.A., 1990. Therapeutic heat and cold for athletic injuries.
Physician and Sportsmedicine 18 (5), 87 –92.See also page 94.
Hartvickson, K., 1962. Ice therapy is spasticity. Acta Neurologica
Scandinavica 38, 79–84.
Hermansen, L., Stensvold, I., 1972. Production and removal of lactate acid
in man. Acta Physiologica Scandinavica 86, 191 –201.
Higgins, D., Kaminski, T.W., 1998. Contrast therapy does not cause
fluctuations in human gastrocnemius intramuscular temperature.
Journal of Athletic Training 33 (4), 336–340.
Hocutt, J.E., Beebe, J.K., Jaffe, R., Rylander, C.R., 1982. Cryotherapy in
ankle sprains. American Journal of Sports Medicine 10 (5), 316 –319.
Hultman, E., Bergstrom, J., McLenan-Anderson, N., 1967. Breakdown and
resynthesis of phosphorylcreatine and adenosine triphosphate in
connection with muscular work in man. Scandinavica Journal Clinical
Investigation 19, 56– 66.
Johnson, D.J., Moore, S., Moore, J., Olive, R.A., 1979. Effect of cold
submersion on intramuscular temperature of the gastrocnemius muscle.
Physical Therapy 59, 1238–1242.
Kuligowski, L.A., Lephart, S.M., Giannantonio, F.P., Blanc, R.O., 1998.
Effect of whirpool therapy on the signs and symptoms of delayed-onset
muscle soreness. Journal of Athletic Training 33 (3), 222 –228.
Lehmann, J.F., Warren, C.G., Scham, S.M., 1974. Therapeutic heat and
cold. Clinical Orthopaedics 99, 207–245.
Lowden, B.J., Moore, R.J., 1975. Determinants and nature of intramuscular
temperature changes during cold therapy. American Journal of Sports
Medicine 54, 223–232.
McHugh, M.P., Connolly, D.A.J., Eston, R.G., Gleim, G.W., 1999.
Exercise-induced muscle damage and potential mechanisms for the
repeated bout effect. Sports Medicine 27 (3), 157– 170.
McArdle, W.D., Katch, F.I., Katch, V.L., 2001. Exercise Physiology:
Energy, Nutrition, and Human Performance, fifth ed., Lippincott
Williams and Wilkins, Philadelphia.
Mackinnon, L.T. Hooper, S., 1991. Overtraining. National Sports Research
Program, State of the art review; no.26. Canberra: Australian Sports
Commission.
McMaster, W.C., Liddle, S., Waugh, T.R., 1979. Laboratory evaluations of
various cold therapy modalities. American Journal of Sports Medicine 6
(5), 291– 294.
Miller, M.K., 1992. The Effectiveness of Repeated Submaximal Concentric
Exercise and Heated Whirlpool in the Treatment of Delayed Onset
Muscular Soreness, Microform Publications, College of Human
Development and Performance, University of Oregon.
Myrer, J.W., Draper, D.O., Durrant, E., 1994. Contrast therapy and
intramuscular temperature in the human leg. Journal of Athletic
Training 29 (4), 318–322.
Myrer, J.W., Measom, G., Durrant, E., Fellingham, G.W., 1997. Cold- and
hot-pack contrast therapy: subcutaneous and intramuscular temperature
change. Journal of Athletic Training 32 (3), 238 –241.
Prentice, W.E., 1999. Therapeutic Modalities in Sports Medicine, fourth
ed., WCB/McGraw-Hill, Boston, USA.
Pugh, L., Edholm, R., Fox, R., 1960. A physiological study of channel
swimming. Clinical Science 19, 257–273.
Rivenburgh, D.W., 1992. Physical modalities in the treatment of tendon
injuries. Clinics in Sports Medicine 11 (3), 645 – 659.
Sahlin, K., Henriksson, J., 1984. Buffer capacity and lactate accumulation
in skeletal muscle of trained and untrained men. Acta Physiologica
Scandinavica 122 (3), 331–339.
Sahlin, K., 1992. Metabolic factors in fatigue. Sports Medicine 13 (9),
99–107.
Sanders, J. (1996). Effect of contrast-temperature immersion on recovery
from short-duration intense exercise, Unpublished thesis, Bachelor of
applied Science, University of Canberra.
Signorile, J.F., Ingalls, C., Tremblay, L., 1993. The effects of active and
passive recovery on short-term, high intensity power output. Canadian
Journal of Applied Physiology 18 (1), 31 – 42.
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–32 31

Smith, L.L., 1991. Acute inflammation: the underlying mechanism in
delayed onset muscle soreness? Medicine and Science in Sports and
Exercise 23 (5), 542–551.
Tomasik, M., 1983. Effect of hydromassage on changes in blood electrolyte
and lactic acid levels and haematocrit value after maximal effort. Acta
Physiologica Polonica 34 (2), 257–261.
Tomlin, D.L., Wenger, H.A., 2001. The relationship between aerobic
fitness and recovery from high intensity intermittent exercise. Sports
Medicine 31 (1), 1–11.
Viitasalo, J.T., Niemela, K., Kaappola, R., Korjus, T., Levola, M.,
Mononen, H.V., Rusko, H.K., Takala, T.E.S., 1995. Warm underwater
water-jet massage improves recovery from intense physical exercise.
European Journal of Applied Physiology and Occupational Physiology
71 (5), 431–438.
Weltman, K., Stamford, B.A., Fulco, C., 1979. Recovery from maximal
effort exercise: lactate disappearance and subsequent performance.
Journal of Applied Physiology 47, 677–682.
Wertz, A.S., 1998. Intramuscular and Subcutaneous Temperature Changes
in the Human Leg due to Contrast Hydrotherapy, University of Oregon
Eugene, Oregon.
Zuluaga, M., Briggs, C., Carlisle, J., McDonald, V., McMeeken, J.,
Nickson, W., Oddy, P., Wilson, D. (Eds.), 1995. Sports Physiother-
apy: Applied Science and Practice, Churchill Livingstone, Mel-
bourne.
D.J. Cochrane / Physical Therapy in Sport 5 (2004) 26–3232