Am J Physiol Regul Integr Comp Physiol 309: R389–R398, 2015.

First published June 15, 2015; doi:10.1152/ajpregu.00151.2015.

Effects of cold water immersion and active recovery on hemodynamics and

recovery of muscle strength following resistance exercise
Llion A. Roberts,1,2 Makii Muthalib,3 Jamie Stanley,1,2,4 Glen Lichtwark,1 Kazunori Nosaka,5
Jeff S. Coombes,1 and Jonathan M. Peake2,6
1
The University of Queensland, School of Human Movement and Nutrition Sciences, Brisbane, Australia; 2Centre of
Excellence for Applied Sport Science Research, Queensland Academy of Sport, Brisbane, Australia; 3Movement to Health
Laboratory, Montpellier University, Montpellier, France; 4Physiology Department, South Australian Sports Institute,
Adelaide, Australia; 5School of Exercise and Health Sciences, Centre for Exercise and Sports Science Research, Edith Cowan
University, Joondalup, Australia; and 6School of Biomedical Sciences and Institute of Health and Biomedical Innovation,
Queensland University of Technology, Brisbane, Australia
Submitted 14 April 2015; accepted in final form 8 June 2015

Roberts LA, Muthalib M, Stanley J, Lichtwark G, Nosaka K,
Coombes JS, Peake JM. Effects of cold water immersion and
active recovery on hemodynamics and recovery of muscle strength
following resistance exercise. Am J Physiol Regul Integr Comp
Physiol 309: R389 –R398, 2015. First published June 15, 2015;
doi:10.1152/ajpregu.00151.2015.—Cold water immersion (CWI)
and active recovery (ACT) are frequently used as postexercise recov-
ery strategies. However, the physiological effects of CWI and ACT
after resistance exercise are not well characterized. We examined the
effects of CWI and ACT on cardiac output (Q̇), muscle oxygenation
(SmO2), blood volume (tHb), muscle temperature (Tmuscle), and
isometric strength after resistance exercise. On separate days, 10 men
performed resistance exercise, followed by 10 min CWI at 10°C or 10
min ACT (low-intensity cycling). Q̇ (7.9 ⫾ 2.7 l) and Tmuscle (2.2 ⫾
0.8°C) increased, whereas SmO2 (⫺21.5 ⫾ 8.8%) and tHb (⫺10.1 ⫾
7.7 ␮M) decreased after exercise (P ⬍ 0.05). During CWI, Q̇ (⫺1.1 ⫾ 0.7
l) and Tmuscle (⫺6.6 ⫾ 5.3°C) decreased, while tHb (121 ⫾ 77 ␮M)
increased (P ⬍ 0.05). In the hour after CWI, Q̇ and Tmuscle remained
low, while tHb also decreased (P ⬍ 0.05). By contrast, during ACT,
Q̇ (3.9 ⫾ 2.3 l), Tmuscle (2.2 ⫾ 0.5°C), SmO2 (17.1 ⫾ 5.7%), and tHb
(91 ⫾ 66 ␮M) all increased (P ⬍ 0.05). In the hour after ACT,
Tmuscle, and tHb remained high (P ⬍ 0.05). Peak isometric strength
during 10-s maximum voluntary contractions (MVCs) did not change
significantly after CWI, whereas it decreased after ACT (⫺30 to ⫺45
Nm; P ⬍ 0.05). Muscle deoxygenation time during MVCs increased
after ACT (P ⬍ 0.05), but not after CWI. Muscle reoxygenation time
after MVCs tended to increase after CWI (P ⫽ 0.052). These findings
suggest first that hemodynamics and muscle temperature after resis-
tance exercise are dependent on ambient temperature and metabolic
demands with skeletal muscle, and second, that recovery of strength
after resistance exercise is independent of changes in hemodynamics
and muscle temperature.
cryotherapy; muscle oxygenation; blood flow; recovery
CRYOTHERAPY TREATMENTS SUCH as cold water immersion, ice
baths, and ice massage are frequently used as an aid to
recovery from exercise. The use of this method is based partly
on the psychological benefits of these treatments, such as lower
ratings of muscle fatigue and soreness (51). Some studies have
also reported benefits of cold water immersion treatments on
muscle function and various aspects of exercise performance
[for review, see Ref. (51)]. Despite its popularity and anecdotal
Address for reprint requests and other correspondence: J. Peake, Queensland
University of Technology, Kelvin Grove, QLD 4059, Brisbane, Australia
(e-mail: jonathan.peake@qut.edu.au).
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support, the physiological mechanisms underlying the effects
of cold water immersion during the postexercise period are not
well established.
Various studies have examined changes in central hemody-
namics (e.g., cardiac output, blood pressure, and total periph-
eral resistance), and limb blood flow following immersion in
cold water (i.e., ⱕ15°C) under resting conditions (4, 13, 20, 28,
41, 42). Other studies have investigated the effects of cold
water immersion on central and peripheral hemodynamics
during recovery from endurance exercise (18, 26, 44, 48).
However, the findings from these studies are not necessarily
applicable to recovery from resistance exercise, because auto-
nomic regulation of the cardiovascular system differs between
recovery from endurance exercise and recovery from resistance
exercise (15). Cold water immersion may, therefore, induce
different cardiovascular responses following resistance exer-
cise compared with endurance exercise.
Previous research has used near-infrared spectroscopy (NIRS) to
measure changes in peripheral hemodynamics, including mus-
cle tissue oxygenation (oxyhemoglobin concentration [O2Hb]
or muscle oxygen saturation [SmO2]) and muscle blood vol-
ume (total hemoglobin concentration [tHb]) in response to cold
water immersion after endurance exercise (18, 44) or to icing
after eccentric contractions of the elbow flexors (46). Some of
these studies have produced variable findings in relation to
changes in SmO2 and have only included “passive” measure-
ments of SmO2 and tHb at rest after exercise (18, 46). Mea-
suring changes in SmO2 and tHb in response to maximal
muscle contractions arguably provides a better indication of
muscle O2 consumption (rate and level of SmO2) compared
with passive measurements (29). Considering the inconsisten-
cies and limitations of previous research (18, 46), more re-
search is needed to enhance our understanding of how cold
water immersion affects muscle hemodynamics, particularly
after traditional resistance exercise.
A number of studies have evaluated the effects of cold water
immersion or ice packs on recovery of strength after eccentric
exercise (17, 47), plyometrics (12, 19), resistance exercise (34,
38), intermittent sprint exercise (35), and exhaustive cycling
(31, 32). However, many of these studies only measured
strength after 24 h of recovery from previous exercise. Less is
known about short-term recovery of strength after exercise.
Cold exposure can impair muscle function, possibly by altering
neuromuscular properties during muscle contractions (7, 30,
52). These effects could have important implications for ath-
R389
R390 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE
letes who use cold water immersion to recover quickly between
training sessions or competitive events.
The aim of this study was to examine the effects of cold
water immersion on cardiac dynamics (cardiac output, heart
rate, cardiac parasympathetic activity), muscle hemodynamics
(SmO2 and tHb), thermoregulation (intramuscular and skin
temperature), and muscle strength following resistance exer-
cise. We also investigated changes in these variables in re-
sponse to light-intensity exercise or “active recovery” follow-
ing resistance exercise, because this method is used frequently
as a recovery therapy for athletes (37). These two recovery
therapies are very different and are difficult to compare di-
rectly. Nevertheless, contrasting physiological effects of these
two modalities are a valid reflection of current practices in the
training of high-performance athletes. We hypothesized that
cold water immersion would reduce tissue temperature and
cardiac and peripheral hemodynamics, and delay recovery of
strength after resistance exercise, whereas active recovery
would have the opposite effect.
METHODS
Subjects
Ten physically active men (mean ⫾ SD; age: 21.4 ⫾ 2.0 yr, height:
1.8 ⫾ 0.1 m, body mass: 83.7 ⫾ 14.8 kg), who were familiar with
knee extension exercise and who had been resistance training 2 to 3
times a week for the previous 12 mo, volunteered to participate.
Experimental procedures and risks were explained to the participants
before they provided their informed consent to take part in the study.
The study was approved by the Human Research Ethics Committee of
The University of Queensland.
Experimental Design
The participants completed a familiarization trial and baseline
testing 7 days before the first of two experimental trials. Each
experimental trial involved unilateral knee extensor exercise with the
dominant leg, followed by a 10-min period of cold water immersion
or active recovery, and a 70-min recovery period. Both experimental
trials were performed 7 days apart, in a randomized and counter-
balanced manner. Familiarization, baseline testing, and the experi-
mental trials were all performed in a temperature-controlled labora-
tory (means ⫾ SD: temperature 24.4 ⫾ 0.2°C, humidity 43.5 ⫾
1.6%).
Familiarization and Baseline Testing
The familiarization session allowed the participants to practice the
unilateral leg exercise that they would perform in the experimental
PRE measures
Unilateral exercise
bout
Trial time (min) 0 5
Recovery period (min)
Cardiac dynamics
Temperature
NIRS
rMSSD
Fig. 1. Experimental overview.
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trials, and familiarize themselves with the requirements of the phys-
iological measurements. Baseline testing was conducted ⬃60 min
following familiarization and involved recording isokinetic torque
during 50 maximal knee extensions (details below). The data recorded
for isokinetic torque during this testing were used for comparison with
postexercise values after each of the experimental trials. These data
were also used to calculate the coefficient of variation of measuring
the physiological variables that would be recorded during the exper-
imental trials. We did not measure isokinetic torque before exercise on
the day of each experimental trial because the 50 maximal knee
extensions would have caused fatigue prior to the unilateral resistance
exercise.
Experimental Trials
An overview of the experimental trials is shown in Fig. 1. All trials
started at 9 AM. The participants were asked to eat similar food and
drink 10 ml/kg body mass of water in the 2 h prior to each trial. They
were asked to avoid consuming stimulants, alcohol, tobacco, antiox-
idants, and nutritional supplementation for 24 h preceding all trials
and not to undertake any lower body strength exercise for 48 h prior
to each trial. Otherwise, they were allowed to exercise between the
trials, but physical activity before each trial was not monitored.
Trials commenced with a 15-min rest period, while the apparatus
for recording muscle and skin temperature, cardiac dynamics, and
muscle hemodynamics was inserted and/or attached. After the appa-
ratus was set up, preexercise data for muscle and skin temperature,
cardiac dynamics, heart rate variability, muscle hemodynamics, and
isometric strength were collected. The participants then rested for
another 5 min before they started the unilateral knee extension
exercise (see exercise and performance testing). Over the first 10 min
after exercise, heart rate variability was measured again (0 –5 min),
and the participants moved to the recovery room (5–10 min). At 10
min after exercise, the participants started one of the recovery inter-
ventions (cold water immersion or active recovery). Over 5 min after
completing the recovery interventions, the participants moved back to
the laboratory, where they began the 70-min recovery period. During
this recovery period, muscle and skin temperature, cardiac dynamics,
muscle hemodynamics, and isometric strength were measured. Rest-
ing heart rate variability and resting muscle hemodynamics were
measured immediately prior to testing isometric strength at 5, 20, and
40 min during the recovery period. Isokinetic torque was measured at
60 min. We chose this monitoring period based on previous reports of
greater macrovascular and microvascular blood flow in response to
cold water immersion at rest (13) and following exercise (26).
To minimize the influence of movement, shivering, and posture on
cardiac dynamics and muscle hemodynamics, all trials were per-
formed at ambient room temperature of ⬃24°C. Participants kept their
torso and exercising leg as still as possible, while measurements were
undertaken (accounting for muscle hemodynamic measurements
20 min measures
40 min measures
5 min measures
Isokinetic task
Transition from
recovery room
recovery room
Transition to
Recovery
intervention
40 45 50 60 65 70 90 110 120 130
0 5 20 40 60 70
 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE
taken during, and in response to exercise). The same upright posture
(hip-torso angle of ⬃90°) was maintained throughout each trial, other
than walking to/from the recovery room. During this period, the
participants adopted a regular upright walking position. Finally, the
participants dried their legs with a towel following cold water immer-
sion and covered their torso with a towel for 5 min following both
recovery therapies.
Unilateral Resistance Exercise, Isometric Strength, and Isokinetic
Performance
All exercise was performed unilaterally with the dominant leg on
an isokinetic dynamometer (Cybex 6000; Computer Sports Medicine,
Stoughton, MA). Unilateral exercise was implemented to isolate the
quadriceps muscles, in particular, the vastus lateralis muscle for
temperature and muscle hemodynamic measurements. The dynamom-
eter position was modified to align the lateral condyle of the femur
with the fulcrum, and the seat angle was fixed at 90°. The unilateral
exercise bout consisted of 10 sets of 20 maximal isokinetic knee
extensions in a range from 0 to 90° at a velocity of 90°/s. The
participants rested in the seat of the dynamometer for 2 min between
sets. Repetition tempo was set at 0.5 Hz by an audio signal, and knee
flexion velocity was set at 250°/s to allow passive flexion following
each knee extension.
Isometric MVC knee extension strength was measured at a knee
flexion joint angle of 70° (full knee extension ⫽ 0°). For each
contraction, the participants were instructed to extend their knee as
forcefully as possible at 70° and continue pushing against the stop
point for the required duration. The participants performed two
warm-up contractions, each lasting 5 s and separated by 90 s. They
then rested for another 90 s before they performed a sustained MVC
contraction for 10 s. Maximum and mean isometric torques were
recorded from this 10-s contraction. This procedure was repeated
before the exercise bout, and 5, 20, and 40 min into the recovery
period. The isokinetic performance task was performed during base-
line testing (see previous details) and at 60 min during the recovery
period. It consisted of 50 sequential maximal isokinetic knee exten-
sions, using the same range, velocity, and tempo as the exercise bout.
All data from the dynamometer were collected at 1,000 Hz using a
custom-designed LabVIEW script (LabVIEW, National Instruments,
Austin, TX), and stored on a personal computer for offline analysis.
Test-retest coefficients of variation were determined from the muscle
function testing before both trials. The coefficient of variation for peak
torque from the 10-s isometric contraction was 2.5%. The coefficient
of variation for total work performed over the isokinetic task was
3.2%.
Recovery Interventions
Recovery interventions consisted of cold water immersion or active
recovery. For the cold water immersion therapy, the participants
adopted a seated position with a hip angle of ⬃90°, with their legs
outstretched and fully relaxed. This helped to minimize any confound-
ing effects of muscle contractions on the NIRS signals during the
immersion period. The participants were immersed up to the level of
the umbilicus continuously for 10 min in an inflatable bath (iBody,
iCool Australia, Miami, Australia) containing water at 10.0 ⫾ 0.2°C.
The participants only immersed their body to the level of their
umbilicus, because immersion up to the neck may have interfered with
the impedance cardiography electrodes placed on the torso (see
Cardiac Dynamics). Water temperature in the bath was continuously
maintained using a circulatory cooling unit (iCool Lite, iCool Aus-
tralia). For the active recovery therapy, the participants were in-
structed to exercise on a cycle ergometer (Wattbike, Wattbike, Not-
tingham, UK) for 10 min at a low, self-selected intensity, also
adopting a hip angle of ⬃90°. The participants cycled a distance of 3.4 ⫾
0.3 km, at an average power output of 41.1 ⫾ 10.3 W during active
recovery.
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R391
Cardiac Dynamics
Heart rate, stroke volume, and cardiac output were measured
continuously by impedance cardiography (Physioflow, Manatec Bio-
medical, Paris, France). This method detects changes in impedance of
alternating low-magnitude electrical current between electrodes
placed on the neck (above the supra-clavicular fossa) and the xiphoid
process. Calibration was completed at rest before exercise by collect-
ing data over 30 cardiac cycles and inputting data for diastolic and
systolic blood pressure measured from the brachial artery using an
automated sphygmomanometer (Digital blood pressure monitor,
UA-767;
ADInstruments, Oxford, UK) over the same period. Blood pressure
was recorded again and updated in the calibration 1 min before and 5
min after cold water immersion/active recovery. Data were sampled at
two-beat intervals and saved on a personal computer for offline
analysis. Test-retest coefficients of variation using the Physioflow at
rest were determined between the resting measures collected at the
start of each trial. The coefficient of variation at rest was 1.7% for
heart rate, 4.1% for stroke volume, and 2.9% for cardiac output.
Postexercise coefficients were calculated using data collected during
baseline testing and the first experimental trial. The coefficient of
variation postexercise was 5.4% for heart rate, 7.0% for stroke
volume, and 4.0% for cardiac output.
Heart rate variability was assessed from the time domain by
recording the natural logarithm of the square root mean of the sum of
the squared differences between adjacent normal sequential R-R
intervals (Ln rMSSD). This measurement provided a proxy estimate
of parasympathetic nervous activity of the heart (1). R-R intervals
were recorded while the participants were seated, using a heart rate
monitor (Suunto T6c, Suunto Oy, Vantaa, Finland) at a sampling
frequency of 1,000 Hz. Ln rMSSD was calculated for R-R intervals
recorded before exercise (PRE), immediately after the resistance
exercise (POST), during the recovery interventions (REC), between 0
and 5 min (5 min), 15 and 20 min (20 min), and 35 and 40 min (40
min) during the recovery period. Respiration rate was not controlled
during these measurement periods, because heart rate variability
indices of parasympathetic activity are similar during controlled or
spontaneous breathing (3), and do not influence Ln rMSSD (33). Data
files were transferred to a personal computer using Suunto Team
Manager Software (Suunto T6c, Suunto Oy, Vantaa, Finland). Offline
analysis was conducted from 2 to 5 min during each 5-min interval,
and from 2 to 9 min during REC.
Muscle Hemodynamics
Muscle hemodynamics were assessed using a portable NIRS sys-
tem (Portamon, Artinis Medical Systems, Elst, The Netherlands). The
NIRS device emits light at 760- and 850-nm wavelengths from three
optodes, with an average optode-detector distance of 35 mm. Pene-
tration depth of the light below the skin surface was estimated at 17.5
mm, or half the distance between the optode and the detector (29, 49).
The NIRS probe was placed on the midline of the vastus lateralis
muscle, one-third of the linear distance between the superior border of
the patella and the inguinal fold. Probe location measurements were
recorded and outlined with a marker for repositioning during the
second experimental trial. The NIRS probe was covered with a black
plastic cloth to protect it from ambient light. It was then placed in a
transparent sealed polyethylene bag for waterproofing and firmly
secured to the leg to prevent water leaking into the space between the
bag and the skin, which could potentially influence scattering of the
light (21). Pilot testing revealed no significant impact of the polyeth-
ylene bag upon SmO2 and tHb values. The combined adipose tissue
and skin thickness of the participants was measured by skinfold
calipers (Harpenden skinfold caliper, Baty International, West Sussex,
UK). Mean ⫾ SD adipose tissue and skin thickness was 6.5 ⫾ 3.4
mm, calculated as the skinfold thickness divided by two. Therefore,
the intramuscular NIRS penetration depth was estimated at 11.5 ⫾ 3.4
R392 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE
mm, calculated as 17.5 mm minus adipose tissue and skin thickness.
At this penetration depth, the NIRS signal mainly reflects the meta-
bolic and hemodynamic changes of the muscle (10). The NIRS
method is both reliable and valid for the measurement of muscle
oxidative metabolism (39). The coefficient of variation for test-retest
reliability of resting SmO2 was 2.3% in this investigation.
Data were recorded online at 10 Hz during all trials, using native
software (Oxysoft version 2.1.6; Artinis Medical Systems). The soft-
ware calculates changes in light absorption at the different wave-
lengths and converts them to relative concentrations of O2Hb and
deoxyhemoglobin (HHb) using the modified Lambert law to correct
for light scattering within the tissue. tHb was calculated as O2Hb ⫹
HHb and SmO2 was calculated as [O2Hb/tHb] ⫻ 100 using the
spatially resolved spectroscopy method. Off-line analysis was per-
formed using the same software.
SmO2 and tHb were measured before and after exercise and during
the recovery interventions. Changes in SmO2 and tHb were also
measured during the 10-s isometric MVCs, which the participants
performed before the exercise bout, and 5, 20, and 40 min into the
recovery period. These 10-s isometric MVCs were used in place of
arterial occlusions to obtain a measure of O2 consumption because O2
delivery is substantially occluded due to increased intramuscular
pressure of MVCs compressing blood vessels (40). Precontraction
SmO2 and tHb were calculated as the mean from ⫺4 to ⫺1 s prior to
the visually estimated onset of the MVCs and isokinetic task. The
exact onset of the MVCs and isokinetic task was identified as the time
at which tHb decreased below the mean from ⫺4 to ⫺1 s ⫹ 2 ⫻ SD
of the mean from ⫺4 to ⫺1 s. The following muscle hemodynamic
variables were calculated (11) (Fig. 2): 1) minimum ⌬SmO2 ampli-
tude (SmO2min), which corresponds to the difference between mini-
mum SmO2 during the contraction and mean SmO2 over ⫺4 to ⫺1 s
prior to the onset of the contraction. Larger ⌬ (i.e., more negative)
SmO2min values indicate greater O2 consumption relative to O2
delivery; 2) SmO2 ½ deoxygenation time (SmO2½DT), which corre-
sponds to the period of time between the start of the contraction until
SmO2 reaches 50% of the difference between baseline SmO2 and the
minimum SmO2 during the contraction. A shorter SmO2½DT (for a
similar SmO2min) represents a faster O2 consumption rate; 3) SmO2
maximum amplitude (SmO2max) was identified as the amplitude
corresponding to the maximum SmO2% within 120 s following the
end of the contraction; and 4) SmO2 ½ reoxygenation time
(SmO2½RT), which corresponds to the time required (from the end of
Fig. 2. An illustration of near-infrared spectrometry variables during and
following an isometric maximum voluntary contraction. Gray section
represents the 10-s contraction period. Note that the axes are not drawn to
scale.
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the contraction) for SmO2 to reach 50% of SmO2max. A lower value
(i.e., faster time) indicates greater O2 delivery relative to O2 consump-
tion.
Temperature Measurement
Intramuscular temperature was measured using a fine-wire implant-
able probe (T204E; Physitemp Instruments, Clifton, NJ), while skin
temperature was measured with a surface probe (SS-1; Physitemp
Instruments). Temperature was logged at a frequency of 1 Hz using a
portable data logger (SQ2020; Grant Instruments, Cambridge, UK),
and transferred to a portable computer for analysis. An 18-gauge
needle was used to insert the implantable probe to a depth of 18 mm
beneath the skin surface, 5 cm superior to the NIRS probe. To ensure
consistency in the depth of insertion, a piece of medical tape was
placed exactly 18 mm from the end of the probe. The probe was then
inserted into the muscle until the tape contacted the skin surface. This
depth was chosen because it was in the same region as the estimated
17.5 mm subcutaneous working depth of the NIRS probe. Taking into
account the thickness of the adipose tissue and skin at this site, the
temperature probe was inserted at a mean ⫾ SD intramuscular depth
of 11.5 ⫾ 3.4 mm. Once the intramuscular temperature probe was at
the required depth, the needle was removed, leaving the probe in
place. The skin temperature probe was placed on the quadriceps
immediately next to the medial border of the NIRS device. Data were
averaged at 1-min intervals before and after the exercise bout, during
the recovery interventions, and every 2 min for the recovery period.
Statistical Analysis
Statistical analysis was conducted using the Statistical Package for
Social Sciences program (version 21; IBM, New York). All data were
initially assessed for normality using the Shapiro-Wilk formula. All
measures were assessed by one-way ANOVA for each trial. When
significant time effects were evident, paired t-tests were used to
compare changes over time, and the false discovery rate was used to
correct P values for these multiple comparisons. To complement these
statistical comparisons, Cohen’s effect sizes (d) were calculated to
illustrate the magnitudes of differences in muscle function and phys-
iological variables over time. Effect sizes were assessed as 0.2 ⫽
small effect, 0.5 ⫽ moderate effect, and ⱖ0.8 ⫽ large effect. Data
collected before exercise and prior to the MVCs at 5, 20, and 40 min
after cold water immersion/active recovery were pooled to calculate
Pearson’s correlations between muscle temperature, skin temperature,
cardiac output, heart rate, stroke volume, SmO2, and tHb. Data for
SmO2 and tHb during cold water immersion/active recovery were
averaged over 10 min to calculate Pearson’s correlations with mean
arterial pressure measured 5 min after cold water immersion/active
recovery. All data are presented as means ⫾ SD. Significance was set
at a level of P ⬍ 0.05.
RESULTS
Resistance Exercise Bout
The total work completed during the unilateral knee exten-
sion exercise bout did not differ (P ⫽ 0.2) between the active
recovery (22.2 ⫾ 4.4 kJ) and cold water immersion (22.8 ⫾ 5.9
kJ) trials.
Cardiac Dynamics
After exercise and during recovery interventions. Systolic,
diastolic, and mean arterial pressures increased significantly
after exercise compared with before exercise (P ⬍ 0.05) and
did not differ significantly before the two recovery interven-
tions (Table 1). Systolic blood pressure remained higher after
cold water immersion than before exercise, whereas systolic,
 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE R393
Table 1. Systolic, diastolic, and mean arterial pressure but remained higher than the minute 1 value during cold water
(mmHg) measured before and after exercise, and 1 min after immersion (P ⬍ 0.05; d ⫽ 0.6 to 0.9). tHb increased above
the recovery therapies prerecovery value from minute 3 onward during active recov-
ery (P ⬍ 0.05; d ⫽ 0.4 to 1.2). Pooled data for SmO2 and tHb
Before Exercise After Exercise After Recovery
during cold water immersion and active recovery did not
Systolic pressure correlate with mean arterial pressure measured 5 min after
CWI 118 ⫾ 5 131 ⫾ 3* 125 ⫾ 8* these recovery interventions (SmO2: r ⫽ 0.10; P ⫽ 0.72 and
ACT 118 ⫾ 6 130 ⫾ 9* 126 ⫾ 8*
Diastolic pressure
tHb: r ⫽ ⫺0.16; P ⫽ 0.56).
CWI 71 ⫾ 9 74 ⫾ 9* 71 ⫾ 8† After the recovery interventions. SmO2 did not change
ACT 74 ⫾ 5 76 ⫾ 5* 78 ⫾ 6*† significantly compared with preexercise values after either trial
Mean arterial pressure (time effect: P ⫽ 0.093) (Fig. 4C). tHb was lower than
CWI 87 ⫾ 7 93 ⫾ 6* 89 ⫾ 7† preexercise values 5 min (P ⫽ 0.003; d ⫽ 2.1) and 20 min (P ⫽
ACT 88 ⫾ 4 94 ⫾ 4* 94 ⫾ 4*
0.033; d ⫽ 1.7) after cold water immersion, whereas it was
Values are expressed as means ⫾ SD. *Significantly different vs. preexer- higher than before exercise 40 min after active recovery (P ⫽
cise, P ⬍ 0.05. †Significantly different vs. postexercise, P ⬍ 0.05. 0.037; d ⫽ 1.3) (Fig. 4D). Pooled data for resting SmO2 before
exercise and before the MVCs at 5, 20, and 40 min after cold
diastolic, and mean arterial blood pressure remained higher water immersion and active recovery correlated with muscle
after active recovery than before exercise (P ⬍ 0.05). temperature (r ⫽ 0.59; P ⬍ 0.01) and tHb (r ⫽ 0.34; P ⫽
Heart rate (Fig. 3A), stroke volume (Fig. 3B), and cardiac 0.002). Pooled data for tHb at the same time points correlated
output (Fig. 3C) increased significantly during exercise in both with muscle temperature (r ⫽ 0.62; P ⬍ 0.001), skin temper-
trials (P ⬍ 0.05). Heart rate (P ⫽ 0.84), stroke volume (P ⫽ ature (r ⫽ 0.59; P ⬍ 0.001), and cardiac output (r ⫽ 0.38;
0.89), and cardiac output (P ⫽ 0.78) did not differ before the P ⬍ 0.001).
two recovery interventions. Heart rate remained higher during
cold water immersion than before exercise (P ⬍ 0.05) over the A
first 2 min and returned to preexercise values after 5 min.
Stroke volume decreased gradually during cold water immer-
sion and tended to be lower than before exercise at 7–10 min
(P ⫽ 0.1 to 0.06; d ⫽ ⫺0.3 to ⫺0.5). Consistent with the
decrease in stroke volume, cardiac output also decreased dur-
ing cold water immersion and was lower than before exercise
at 8 –10 min (P ⬍ 0.05). During active recovery, heart rate was
higher than before exercise and remained elevated (P ⫽ 0.001;
d ⫽ 1.3 to 4.1). Stroke volume (P ⫽ 0.08 to 0.03; d ⫽ 0.4 to
0.6) tended to remain above the preexercise value, and cardiac
output (P ⫽ ⬍0.0001 to 0.001; d ⫽ 2.1 to 2.4) remained above B
the preexercise value throughout the recovery therapy.
After the recovery interventions. Heart rate was lower than
before exercise at 50 –70 min after cold water immersion (P ⬍
0.05; d ⫽ 0.7 to 1.0) but remained higher than before exercise
during the entire period following active recovery. Cardiac
output also decreased below the preexercise rate at 30 – 60 min
after cold water immersion (P ⬍ 0.05; d ⫽ 0.7 to 1.4), whereas
it remained above the preexercise value until 20 min after
active recovery.
C
Heart Rate Variability
Ln rMSSD was used as a marker of cardiac parasympathetic
activity. Ln rMSSD was lower after the exercise bout in both
trials (P ⬍ 0.01; d ⫽ ⫺2.4) (data not shown). It rapidly
returned toward the preexercise value during cold water im-
mersion (P ⫽ 0.003; d ⫽ 1.8), whereas it remained lower than
the preexercise value at 5 min after active recovery.
Muscle Hemodynamics
During the recovery interventions. During cold water im-
mersion, SmO2 did not change from minute 1 values (P ⬎ 0.5), Fig. 3. Heart rate (A), stroke volume (B), and cardiac output (C) before (PRE)
whereas it decreased progressively during active recovery (P ⫽ and after (POST) resistance exercise, during the recovery interventions (gray
section), during the recovery period, and following the dynamic task (PD).
0.065 to 0.004) (Fig. 4A). During cold water immersion, tHb Vertical dashed lines represent the beginning of the recovery period (0 min) in
increased above the prerecovery value during the first 4 min the cold water immersion (CWI) and active recovery (ACT) trials. Data are
(Fig. 4B). It then decreased slightly over the remaining 6 min, expressed as means ⫾ SD. *P ⬍ 0.05 vs. preexercise.

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R394 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE

100 ACT CWI 20

ACT CWI
90 A C
10

SmO2 change (%)

80
0
SmO2 (%)

70
60
-10 *
* -20
50
40 -30

30 -40
*
300 20
250 B D
* 10
*

tHb change (µM)

200
*
tHb (µM)

150 0
100
*
50 -10
0
-20
-50 * * * *
-30
POST

POST
PRE

PRE
PRE REC

PRE REC
0 1 2 3 4 5 6 7 8 9 10 5 20 40

Fig. 4. Quadriceps muscle oxygenation (SmO2) and blood volume (tHb) during (minutes 1–10; A and B) and following (minutes 5– 40; C and D) the CWI and
ACT interventions. PRE, preexercise; POST, post-exercise; PRE REC, prerecovery therapy. Data are expressed as means ⫾ SD. *P ⬍ 0.05 vs. preexercise.

Skin and Muscle Temperature
After exercise and during the recovery interventions. Muscle
and skin temperatures were higher than preexercise tempera-
tures immediately after resistance exercise and before the
recovery interventions in both trials (P ⬍ 0.001) (Fig. 5). There
were no differences in muscle temperature (P ⫽ 0.32) or skin
temperature (P ⫽ 0.38) before the recovery interventions.
Muscle (d ⫽ 0.3 to 2.1) and skin (d ⫽ 0.3 to 3.3) temperature
decreased below preexercise values during cold water immer-
sion (P ⬍ 0.05), whereas muscle (d ⫽ 4.0 to 4.8) and skin
(d ⫽ 2.1 to 3.7) temperature remained elevated above preex-
ercise throughout the active recovery exercise (P ⬍ 0.001).
After the recovery interventions. Muscle temperature re-
mained below the preexercise value for 40 min following cold
water immersion (P ⬍ 0.05; d ⫽ 1.4 to 4.5), whereas skin
temperature remained below the preexercise value for the
entire period (P ⬍ 0.05; d ⫽ 0.7 to 6.0) (Fig. 5). Muscle (d ⫽
2.7 to 3.8) and skin (d ⫽ 3.3 to 4.7) temperatures remained
above preexercise values for the entire period after active
recovery (P ⬍ 0.001). Both muscle (r ⫽ 0.26; P ⫽ 0.019) and
skin temperature (r ⫽ 0.38; P ⬍ 0.001) correlated with cardiac
output.
Recovery of Muscle Strength
Peak isometric torque did not change after cold water im-
mersion (P ⫽ 0.24 to 0.62), whereas it was lower than before
exercise at 5, 20, and 40 min (P ⬍ 0.05; d ⫽ 0.4 to 0.7) after
the active recovery trial (Fig. 6). The total amount of work
completed during the 50 isokinetic contractions was similar at
baseline (i.e., preexercise) compared with when the same
contractions were performed ⬃70 min after exercise (Table 3).
During the 50 contractions performed ⬃70 min postexercise,
isokinetic torque decreased progressively over time (time ef-
fect P ⬍ 0.001) in both the cold water immersion and active
recovery trials.
Muscle Hemodynamics in Response to Muscle Contractions
Compared with preexercise, the SmO2min change during the
10 s MVC was smaller (P ⬍ 0.05) at 5 min (d ⫽ 1 and 1.3) and
20 min (d ⫽ 0.6 and 1.4) after both cold water immersion and
active recovery, respectively (Fig. 7A) and remained lower at
40 min (d ⫽ 1.4) after active recovery. Compared with preex-
ercise, SmO2½DT during the MVCs did not change significantly
at any time after cold water immersion (P ⫽ 0.155 to 0.631).
SmO2½DT was longer compared with preexercise values at 20
min (P ⫽ 0.001; d ⫽ 1.3) and 40 min (P ⫽ 0.003; d ⫽ 1.2)
after active recovery (Fig. 7B). Compared with preexercise
values, SmO2½RT after the MVCs tended to be longer at 20 min
(P ⫽ 0.1; d ⫽ 0.4) and 40 min (P ⫽ 0.052; d ⫽ 0.5) after cold
water immersion (Fig. 7B). SmO2½RT was not significantly
different to preexercise values at any time (P ⬎ 0.05) after
active recovery. SmO2min was lower than baseline (preexer-
cise) values after the isokinetic contractions in the active
recovery trial (P ⬍ 0.05; d ⫽ 3.2) but not in the cold water
immersion trial (Table 3). There were no significant changes in
SmO2½DT during the isokinetic contractions or SmO2½RT after
the isokinetic contractions in either trial (Table 3).
DISCUSSION
The aim of this study was to examine the effects of cold
water immersion and active recovery on cardiac dynamics,

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 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE R395

A Muscle temperature (°C) 40 * A 0

*

Amplitude (%)
35
* -5

30
ACT
*
-10
CWI *
25 *
CWI ACT
-15
20 * PRE 5 min 20 min 40 min

B 40
* B 15
ACT CWI
30
*
Skin temperature (°C)

35
*
30 10 * * 20

Time (s)
Time (s)
25
5 10
20

15 * 0 0
POST
POST
PRE

10 20 30 40 50 60
REC

in

in

in

in

in

in
E

E
PR

PR
m

m
m

m
Time (min)

5
20

40

20

Fig. 5. Muscle (A) and skin (B) temperatures before (PRE) and after (POST)
the exercise bout, during the recovery interventions (gray section), after the
recovery intervention (POST REC), and during the recovery period in the CWI
and ACT trials. Vertical dashed line represents the beginning of the recovery
period (0 min). Data are expressed as means ⫾ SD. *P ⬍ 0.05 vs. preexercise.
muscle hemodynamics, tissue temperature, and strength fol-
lowing resistance exercise. Cold water immersion reduced
hemodynamics and tissue temperature and helped to maintain
muscle strength after resistance exercise. By contrast, active
recovery maintained hemodynamics and tissue temperature
and reduced muscle strength after resistance exercise. Collec-
tively, these findings suggest that 1) hemodynamics and mus-
cle temperature after resistance exercise are dependent on
ambient temperature and metabolic demands of skeletal mus-
cle, and 2) recovery of strength after resistance exercise is
independent of changes in hemodynamics and muscle temper-
ature. Although some of these findings were somewhat pre-
400 ACT
CWI
350
Peak torque (Nm)
40
1/2 DT 1/2 RT
Fig. 7. Quadriceps muscle oxygenation (SmO2) amplitude (A) and kinetics (B)
during isometric contractions. SmO2½DT, half deoxygenation time; SmO2½RT,
half reoxygenation time in the CWI, and ACT trials. Note that data to the left
of the dotted line are plotted on the left y-axis; data to the right of the dotted
line are plotted on the right y-axis. Data are expressed as means ⫾ SD. *P ⬍
0.05 vs. preexercise.
dictable, they are nevertheless interesting and valuable, be-
cause they represent the first systematic comparison of the
physiological effects of these two frequently used recovery
therapies.
This is the first study to investigate the effects of cold water
immersion on stroke volume and cardiac output during recov-
ery from resistance exercise. Cardiac output and stroke volume
decreased rapidly after exercise in response to cold water
immersion, whereas they remained moderately elevated in
response to active recovery (Fig. 3). The decrease in cardiac
output during cold water immersion probably reduced blood
flow to peripheral regions of the body to protect and maintain
core temperature. By contrast, the maintenance of cardiac

output during active recovery most likely conserved oxygen

300 delivery to contracting muscle. These differences in cardiac
dynamics between cold water immersion and active recovery
250
probably reflect divergent activity of the parasympathetic and
200 sympathetic nervous systems (1, 43). As a proxy measure of
parasympathetic nervous activity, ln rMSSD increased after
150 cold water immersion (data not shown), which provides tenta-
tive evidence that cardiac output decreased as a result of
100 * greater parasympathetic nervous activity. By contrast, ln
PRE 5 20 40
rMSSD remained low after active recovery, which suggests
Fig. 6. Peak isometric torque preexercise (PRE) and at 5, 20, and 40 min in to that cardiac output remained elevated as a result of lower
the recovery period (corresponding to 25, 40, and 65 min after the resistance
exercise bout) in the CWI and ACT trials. Gray shaded area indicates the
parasympathetic nervous activity.
period of CWI or ACT. Note that the x-axis is not drawn to scale. Data are We used NIRS to examine changes in muscle oxygenation
expressed as means ⫾ SD. *P ⬍ 0.05 vs. preexercise. and blood volume during and after cold water immersion and

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R396 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE

Table 2. Peak isokinetic torque (Nm) during the fatigue task at baseline, and during the cold water immersion and active
recovery trials
Contraction Number

Condition 1–5 6–10 11–15 16–20 21–25 26–30 31–35 36–40 41–45 46–50

Baseline 137 ⫾ 30 152 ⫾ 23 147 ⫾ 20 135 ⫾ 25 123 ⫾ 23* 111 ⫾ 24* 99 ⫾ 24* 86 ⫾ 22* 79 ⫾ 19* 75 ⫾ 17*
CWI 135 ⫾ 29 156 ⫾ 30 141 ⫾ 31 133 ⫾ 26 115 ⫾ 25* 102 ⫾ 20* 93 ⫾ 18* 86 ⫾ 18* 82 ⫾ 14* 81 ⫾ 18*
ACT 140 ⫾ 29 150 ⫾ 36 144 ⫾ 39 128 ⫾ 42 116 ⫾ 34* 101 ⫾ 32* 91 ⫾ 32* 82 ⫾ 30* 79 ⫾ 26* 78 ⫾ 26*
Values are expressed as means ⫾ SD. Baseline performance was measured 7 days prior to the first trial and was used as a “preexercise” comparison for both
experimental trials; see MATERIALS AND METHODS. CWI, cold water immersion; ACT, active recovery. *Significant difference from contractions 1–5 (P ⬍ 0.05).

active recovery. SmO2 did not change significantly during cold
water immersion but decreased during active recovery. This
difference reflects the greater demand for oxygen in contract-
ing muscle during active recovery. tHb increased during cold
water immersion (Fig. 4B), indicating an increase in muscle
blood volume similar to the cold-induced vasodilation ob-
served by Gregson et al. (13). This is the first study to combine
measurements of central and peripheral hemodynamics after
exercise. It is intriguing that muscle blood volume (tHb)
increased during cold water immersion, whereas cardiac output
decreased. This suggests that changes in central blood flow do
not necessarily influence local perfusion within skeletal mus-
cle. In contrast to the increase during cold water immersion,
tHb decreased for at least 20 min thereafter (Fig. 4D), which
may reflect microvascular adaptation to the cold.
Previous research has used NIRS only to examine resting
muscle oxygenation and blood volume after cold water immer-
sion (18, 46). We have extended current knowledge of the
effects of cold water immersion by evaluating changes in
muscle oxygenation in response to occlusion and hyperemia
associated with MVCs. SmO2 amplitude (SmO2min) and deox-
ygenation time (SmO2½DT) derived from NIRS measurements
indicate the demand for oxygen in contracting muscle (11, 29).
We are confident that occlusion was maintained during the
MVCs because 1) full blood flow occlusion occurs at or above
50 – 60% maximum isometric torque (32), and 2) torque did not
decrease substantially during the MVCs (data not shown).
SmO2min during MVCs decreased (relative to preexercise val-
ues) after both cold water immersion and active recovery (Fig.
7A), indicating a reduction in total O2 consumption. This
Table 3. Total work and changes in muscle oxygenation and
blood volume during and for 2 min after 50 isokinetic
contractions
Trials
Isokinetic Task Variable Baseline CWI
Total work, kJ
Contractions 1–25 3.5 ⫾ 0.7 3.5 ⫾ 0.8 3.6 ⫾ 0.9
Contractions 26–50 2.2 ⫾ 0.6 2.2 ⫾ 0.5 2.2 ⫾ 0.8
tHb minimum amplitude, ␮M 1.1 ⫾ 3.3 ⫺1.3 ⫾ 2.0* ⫺0.2 ⫾ 3.5
tHb maximum amplitude, ␮M 10.0 ⫾ 5.7 6.9 ⫾ 3.7* 7.0 ⫾ 5.4
SmO2 min, % ⫺14.7 ⫾ 8.4 ⫺17.3 ⫾ 8.0 ⫺14.2 ⫾ 6.5
SmO2½DT, s 11.7 ⫾ 8.3 10.9 ⫾ 3.4 11.8 ⫾ 6.6
SmO2½RT, s 22.5 ⫾ 29.4 19.0 ⫾ 9.6 19.6 ⫾ 8.0
Values are expressed as means ⫾ SD. CWI, cold water immersion; ACT,
active recovery trials; SmO2), muscle oxygenation; tHb, blood volume. Base-
line performance was measured 7 days prior to the first trial and was used as
a “preexercise” comparison for both experimental trials; see MATERIALS AND
METHODS. *Significantly different from baseline, P ⬍ 0.05.
response may reflect temporary muscle fatigue following re-
sistance exercise. SmO2½DT during MVCs did not change
significantly after cold water immersion, whereas it was longer
after active recovery (Fig. 7B). This finding indicates that the
rate of O2 consumption in muscle during MVCs slowed after
active recovery but not after cold water immersion. SmO2
reoxygenation time (SmO2½RT) after MVCs tended to be lon-
ger (P ⫽ 0.052 vs. preexercise values) 40 min after cold water
immersion (Fig. 7B). This finding suggests that O2 consump-
tion mildly exceeded O2 delivery after MVCs following cold
water immersion. This mismatch possibly resulted from the
decrease in cardiac output (Fig. 3C) and/or muscle perfusion
(Fig. 4D) that occurred after cold water immersion (14, 25, 27).
Another new and important finding from this study is that
cold water immersion prevented any decrease in maximal
isometric strength after resistance exercise (Fig. 6). By con-
trast, strength remained below preexercise values for at least 40
min after active recovery. Previous research on the short-term
effects of cold water immersion on muscle function has pro-
duced inconsistent findings. Similar to our findings, Pointon et
al. (35) reported that cold water immersion helped to maintain
maximal isometric strength immediately after 30 min intermit-
tent sprint exercise. By contrast, other research has demon-
strated no effect of cold water immersion on maximal isometric
strength at rest (i.e., with no prior exercise) (52) or 1–2 h after
exhaustive cycling (31, 32) or resistance exercise (34, 38). This
variability may be due to differences in cold water immersion
protocols (temperature, duration, or body surface area im-
mersed) and the metabolic and neuromuscular demands of
exercise. In the present study, cold water immersion may have
helped to maintain strength after resistance exercise through
direct and indirect mechanisms involving group III and IV
afferents. Cold exposure inhibits the activity of group III and
IV afferents in skeletal muscle (24) and reduces the accumu-
lation of lactic acid during muscle contractions (8). Lactic acid
stimulates group III and IV afferents in skeletal muscle, result-
ACT
ing in perceptions of fatigue and pain (36). By inhibiting the
activity of group III and IV afferents and reducing lactic acid
accumulation in muscle after exercise (53), cold water immer-
sion may have minimized the perceptions of fatigue and pain.
In turn, this could have allowed the participants to produce
greater force during MVCs following cold water immersion.
Although cold water immersion reduced resting muscle blood
volume (Fig. 4D) and tended to slow the rate of SmO2
reoxygenation after MVCs (Fig. 7B), these effects did not seem
to influence muscle function. Active recovery could have
interfered with the restoration of sarcoplasmic reticulum func-
tion and Ca2⫹ signaling, which have been linked to prolonged
muscle fatigue after exercise (16, 50).

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 PHYSIOLOGICAL EFFECTS OF RECOVERY THERAPIES AFTER EXERCISE
Perspectives and Significance
Several theoretical and technical issues relating to our mea-
surements of cardiac dynamics, muscle oxygenation, and blood
volume are worth considering. First, our findings are specific to
the context in which we applied cold water immersion and
active recovery. The physiological and functional effects of
these recovery treatments will most likely vary depending on
the situation. For example, these treatments may induce dif-
ferent effects when they are applied during other phases of
postexercise recovery or after other modes of exercise. The
alterations in muscle temperature and central and peripheral
hemodynamics in response to cold water immersion or active
recovery may also influence other aspects of muscle function/
exercise performance in different ways.
Second, impedance cardiography and NIRS offer advan-
tages over other more invasive, complicated, or costly methods
for assessing central and peripheral hemodynamics. However,
we acknowledge that these methods are not without limita-
tions. The main limitation of impedance cardiography is that it
is based only on estimates of stroke volume. Anecdotal evi-
dence suggests that impedance cardiography is also affected by
shivering (2). The participants in our study probably did shiver
to some degree while sitting in cold water, but we can only
speculate how much this may have influenced the impedance
cardiography data. Impedance cardiography also assumes that
central venous pressure remains constant, but it is unlikely that
it was constant during cold water immersion or active recov-
ery. Some studies have reported that tissue oxygenation mea-
sured using NIRS fluctuates with changes in skin blood flow,
which has raised doubts as to whether NIRS signals accurately
reflect tissue oxygenation within skeletal muscle (5, 6, 22, 45).
The accuracy of the NIRS signal depends on the depth at which
the light from the probe penetrates through skin and adipose
tissue into skeletal muscle (9). We estimate that our NIRS
probe penetrated to 11.5 ⫾ 3.4 mm within skeletal muscle. At
this penetration depth, we contend that the changes in SmO2
and tHb genuinely reflect differences in tissue oxygenation in
the muscle, rather than experimental artifacts arising from
changes in skin temperature and/or blood flow (23).
Third, the lack of any extended warm-up before the MVCs
could have influenced muscle function, particularly at 20 and
40 min after exercise. We did not allow the participants to
warm up their muscles for any extended period because this
probably would have confounded the effects of the prior
recovery interventions. We contend that the muscle function
tests are valid because 1) we explicitly set out to examine how
differences in muscle temperature after exercise influence re-
covery of muscle strength and 2) we followed the same
protocol in both experimental trials. Last, we were careful not
to suggest or imply any benefits of cold water immersion over
active recovery to the participants in this study. However, it
was impossible to blind the participants to the treatments that
they received. The participants may also have had some pre-
conceptions about the benefits of cold water immersion as a
recovery strategy that could have influenced how they per-
formed in the muscle function tests. Notwithstanding these
limitations, we believe our findings advance existing knowl-
edge of the physiological effects of cold water immersion after
exercise.
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R397
In summary, this is the first systematic investigation into the
effects of two frequently used postexercise recovery therapies
on cardiac dynamics, tissue temperature, muscle function,
muscle oxygenation, and blood volume. The strength of the
study lies in the simultaneous measurement of these physio-
logical variables during and after cold water immersion and
active recovery. It is difficult to compare directly the physio-
logical effects of cold water immersion and active recovery.
Nevertheless, knowledge of the contrasting effects of these
recovery therapies is important to enhance our understanding
of which modality to use in different circumstances. Future
research could compare the effects of different water temper-
ature on these physiological variables and examine in more
detail the hyperemic responses in skeletal muscle after cold
water immersion.
ACKNOWLEDGMENTS
The authors thank the subjects for their time and effort during this study.
We also thank Professor Stéphane Perrey at Montpellier University for feed-
back on this manuscript.
GRANTS
This study was supported by research grants from the Centre of Excellence
for Applied Sport Science Research at the Queensland Academy of Sport, and
the Sports Medicine Australia Research Foundation. L. A. Roberts was
supported by an International Postgraduate Research Scholarship from The
University of Queensland.
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the authors.
AUTHOR CONTRIBUTIONS
Author contributions: L.A.R., M.M., K.N., J.S.C., and J.M.P. conception
and design of research; L.A.R. and G.A.L. performed experiments; L.A.R.,
J.S., G.A.L., and J.M.P. analyzed data; L.A.R., M.M., J.S., K.N., and J.M.P.
interpreted results of experiments; L.A.R. and J.M.P. prepared figures; L.A.R.
and J.M.P. drafted manuscript; L.A.R., M.M., J.S., K.N., J.S.C., and J.M.P.
edited and revised manuscript; L.A.R., M.M., J.S., G.A.L., K.N., J.S.C., and
J.M.P. approved final version of manuscript.
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