Cold-water immersion (CWI) has become a widely used recovery method in sports performance in an attempt to enhance recovery after strenuous exercise (21). Despite its widespread use, evidence that CWI accelerates functional recovery is currently equivocal (21,27,28). By contrast, CWI improves perceptions of fatigue and muscle soreness (10,21) and reduces clinical signs of inflammation such as swelling/edema (11,38) after strenuous exercise in humans. Indeed, a logic model proposed by Costello et al. (2013) suggests that beneficial physiological, neuromuscular, and perceptual effects after exposure to cryotherapy may interact to improve the recovery of performance (6).
One proposed physiological mechanism of cryotherapy is decreases in tissue temperature that mediate reductions in limb (23,27) and deep muscle (20,32) blood flow. It has been proposed that cooling-induced reductions in limb blood flow are beneficial in limiting the inflammatory response to exercise in animal models (20,30,34). However, a recent study in humans has challenged this view by showing that CWI (10 min in 10°C water) had no effect on the muscle inflammatory or cellular stress response compared with active recovery (25). It is possible therefore that CWI-induced reductions in muscle blood flow may benefit recovery from strenuous exercise by attenuating clinical signs of inflammation including edema and swelling per se (11,38) and the associated pain (e.g., soreness) upon movement (10,21).
Although the majority of the research literature investigating cryotherapy during recovery from exercise has used CWI (18,23,27,28,33), the recent commercial availability of whole body cooling (WBC) facilities, which expose the body to very cold air (−110°C to −140°C) for short durations (2–4 min) (2), has led to further interest in the role of cryotherapy in exercise recovery (4). Various studies have reported potential beneficial effects of WBC on hematological profiles (22), inflammatory biomarkers (26,40), muscle damage (13,40), autonomic nervous system (29), body temperature (8), and tissue oxyhemoglobin and oxygenation (31). Despite these apparent favorable effects of WBC, there is equivocal evidence for a positive effect of WBC on functional recovery (7,13,14). Furthermore, the comparative physiological, especially vascular, effects of WBC relative to CWI remain to be elucidated. Costello et al. (8) have previously shown that 4 min of exposure to either CWI or WBC similarly decreased rectal and muscle temperatures for up to 60 min postexposure, despite lower thigh skin temperatures after CWI. However, the CWI duration used in that study was not typical of protocols used for recovery; that is, ≥10 min (21,36), the cryotherapy modalities were applied under resting conditions and the vascular (blood flow), and hemodynamic responses were not measured. It is therefore currently unknown if the changes in blood flow of previously exercised limb(s) are different between ecologically valid CWI and WBC protocols. This is important given that reducing blood flow may represent an important mechanism through which cooling influences postexercise muscle recovery.
The aim of the present study was to, therefore, examine the effects of ecologically valid CWI and WBC protocols on femoral artery and cutaneous blood flow and thermoregulatory responses after cycling exercise. We hypothesized that a longer duration of CWI would decrease femoral artery and lower limb skin blood flow to a greater extent, compared with WBC, and lead to a greater reduction in leg muscle temperature.
MATERIALS AND METHODS
Ten recreationally active men (mean ± SD: age = 22.3 ± 3.4 yr, height = 1.8 ± 0.1 m, mass = 81.1 ± 8.3 kg, V˙O2max = 45.0 ± 9.0 mL·kg−1·min−1, peak power output = 258 ± 31 W) free from cardiovascular, metabolic, and respiratory disease were studied. The experiment conformed to the Declaration of Helsinki and was approved by the Institutional Ethics Committee. After written informed consent, participants were familiarized with the experimental procedures and interventions. On the day of the experimental trials, participants arrived at the laboratory at least 3 h postprandial, having refrained from exercise, alcohol, tobacco, and caffeine during the previous 24 h. Nutritional and fluid intake was recorded across this period and returned to the participant so that they could repeat their preparation at the subsequent trial. They also consumed 5 mL·kg−1 of water 2 h before arriving at the laboratory.
After familiarization, each participant attended the laboratory on two occasions during which they completed an identical submaximal cycle ergometer protocol, followed by exposure to either WBC or CWI (Fig. 1). The conditions were conducted in a randomized and counterbalanced order, at least 1 wk apart and at the same time of day. The CWI exposure consisted of 10 min of immersion to the iliac crest in 8°C water in a temperature-controlled bath; dimensions = 1.34 m width × 1.64 m length × 1.20 m length (ECB Ltd., Gloucester, UK). The WBC exposure consisted of 2 min exposure at a temperature of −110°C in a specialized mobile cryotherapy unit: approximate dimensions = 2.40 m width × 2.90 m height × 1.20 m length (KrioSystem, Wroclaw, Poland). Entry to the main chamber was preceded by a 30-s adaptation period in a prechamber at a temperature of −60°C. The CWI and WBC protocols were based on methods and durations frequently reported in the literature and commonly used in applied sports science practice (16,23).
Before any experimental trials, each participant completed a maximal incremental cycling protocol on a cycle ergometer (Lode, Corival, Netherlands) while simultaneous breath-by-breath (V˙O2) measurements were recorded (Oxycon Pro, Jaeger, Germany). The cycling protocol commenced at 75 W and was increased 25 W every 2 min until volitional exhaustion was reached. Peak power output was derived as the highest power output attained at this point. Maximal oxygen uptake (V˙O2max) (mL·kg−1·min−1) was recorded as the highest 30-s average recorded before volitional exhaustion.
On arrival at the laboratory for each experimental trial, the participant's nude body mass (kg) was obtained using digital scales (Seca, Hamburg, Germany). A rectal probe was self-inserted, and a heart rate monitor was positioned across the chest. Participants were then placed in a supine position for 30 min on a bed for the attachment of instrumentation and to stabilize physiological status, wearing shorts where the ambient temperature was maintained at 22°C–24°C (~40% relative humidity) throughout the protocol. After baseline measurements, participants cycled at 70% V˙O2max until a rectal temperature of 38°C was attained. Participants were not allowed to consume any food or fluid during or after exercise. Participants then returned to a supine position for 10 min to enable precooling measurements to be taken. This protocol was selected in line with our previous study (23) to minimize muscle damage compared with other forms of exercise such as resistance training or other specific muscle damaging protocols, which may have confounded postexercise femoral artery blood flow measurements because of the protective effect of performing a single bout of muscle damaging exercise (24).
In the CWI condition, participants were subsequently raised from the bed in a semirecumbent posture, using an electronic hoist (Bianca; Arjo Ltd., Gloucester, UK), and lowered into the water bath (in the same position) until the thighs were fully submerged for 10 min. In the WBC condition, body sweat was lightly dabbed dry with a towel, and equipment was removed from the body (skin temperature probes and heart rate monitor) for entering the WBC chamber. Skin blood flow and rectal probes remained in situ, with connections covered and tucked inside the participant's shorts and socks. Next, with the help of the researchers, the participants donned the clothing to be worn inside the chamber (face mask, ear band, gloves, socks, and shoes) and were then transferred to, and pushed, in a chair to undergo WBC exposure inside the chamber (seated on the chair). At the end of each separate cooling trial, participants were returned to the bed either using the electronic hoist or via the chair and remained in a supine position for a period of 40 min under the temperature-controlled laboratory. A period of 10 min was permitted, before any postexposure measurements, for the reattachment of the skin temperature probes and heart rate monitor equipment and removing clothing required in the chamber. The use of the hoist to raise and lower the participants, and the chair to transfer the participants to and from the chamber, was important to avoid the effect of muscle activation on blood flow and hemodynamic measures (15,23).
Thermoregulatory variables were measured at baseline, precooling, and during postcooling period. Perceived thermal comfort, rated using a nine-point scale (0 = unbearably cold, 1 = very cold, 2 = cold, 3 = cool, 4 = slightly cool, 5 = neutral, 6 = slightly warm, 7 = warm, 8 = hot, and 9 = very hot) (39), and shivering, rated using a four-point scale (1 = no shivering, 2 = slight shivering, 3 = moderate shivering, and 4 = heavy shivering) (35), were also recorded. All pre- and postcooling measurements were made in a supine position. A schematic illustration of the experimental design is shown in Figure 1.
Rectal, thigh skin, and muscle temperature
A rectal probe (Rectal temperature probe, adult; ELLAB, Rodovre, Denmark) was inserted 15 cm beyond the anal sphincter for the assessment of rectal temperature. A skin thermistor (Surface temperature probe, stationary, ELLAB) was attached to the upper thigh for the assessment of skin temperature. Muscle temperature was assessed using a needle thermistor inserted into the vastus lateralis (multipurpose needle probe, ELLAB) as previously described (8,23). Briefly, thigh skinfold thickness was measured using Harpenden skinfold calipers (HSK BI; Baty International, West Sussex, UK) and divided by 2 to determine the thickness of the thigh subcutaneous fat layer over each participant's vastus lateralis. The needle thermistor was then placed at a depth of 3 cm plus one-half the skinfold measurement for the determination of deep muscle temperature (3 cm). The thermistor was then withdrawn at 1-cm increments for the determination of muscle temperature at 2 and 1 cm below the subcutaneous layer. Rectal, skin, and muscle temperatures were recorded using an electronic measuring system (CTF 9004, ELAB).
Heart rate and blood pressure
Heart rate was continuously measured using a heart rate monitor (S610; Polar Electro Oy, Kempele, Finland). Blood pressure was measured noninvasively via automated brachial auscultation (Dinamap, GE Pro 300V2, Tampa, FL).
Femoral artery blood flow
A 15-MHz linear array transducer attached to a high-resolution ultrasound machine (Acuson P50, Siemens, Germany) was used to measure superficial femoral artery diameter and velocity (3 cm distal to the bifurcation) as previously described (23). This position was marked on the skin such that the ultrasound head could be accurately repositioning during subsequent measures. Analysis of diameter and velocity was performed using custom designed edge detection and wall-tracking software (37), which is considerably more repeatable than manual methods and associated with less observer error (37). Resting diameter, blood velocity, and blood flow were calculated as the mean of the data collected during a 20-s period of each 2-min recoding for statistical analysis. Femoral vascular conductance was calculated as the ratio of blood flow/mean arterial pressure.
Cutaneous blood flow
Red blood cell flux was used as an index of skin blood flow via laser Doppler flowmetry (Periflux System 5001; Perimed Instruments, Jarfalla, Sweden). A laser Doppler probe (455, Perimed, Suffolk, UK) was attached to the mid-anterior thigh, midline, halfway between the inguinal line and the patella, and on the calf, left of the midline, in the region of the largest circumference. Once affixed, the probes were not removed until the completion of each trial. Cutaneous vascular conductance was calculated as the ratio of laser Doppler flux to mean arterial blood pressure (cutaneous vascular conductance = laser Doppler flux/mean arterial blood pressure × 100) and expressed as a percentage change from preimmersion values. When expressed as a percentage change from baseline to maximum, cutaneous blood flow has a coefficient variation of 4% in our laboratory with a coefficient of variation of 10% observed for resting cutaneous blood flow. Thigh and calf skin conductance was expressed as percentage change from preimmersion (zero).
Using our previous data (23), 8°C water immersion mediates a reduction from preexercise baseline in femoral artery blood flow of 60 mL·min−1. To replicate this reduction in femoral artery blood flow with 80% power and an α of 0.05, a sample size of nine participants is required. Similarly, we used a previous study (8) to estimate a minimum clinically important difference in thigh skin temperature of 3.4°C ± 2.4°C immediately after CWI compared with WBC. To detect this difference with 80% power and an α of 0.05, a sample size of seven participants is required.
A two-factor [condition (CWI and WBC) × time (baseline, postexercise/precooling, postcooling 10, 20, 30, and 40 min)] general linear model was used to evaluate treatment differences between the CWI and the WBC conditions. A three-way general linear model (condition–depth–time) was used to analyze muscle temperature. Where a significant interaction between condition and time was observed, differences were followed up with Newman–Keuls multiple contrasts.
Simple effect size (ES), estimated from the ratio of the mean difference to the pooled standard deviation (Hedges' g), was also calculated. The ES magnitude was classified as trivial (<0.2), small (>0.2–0.6), moderate (>0.6–1.2), large (>1.2–2.0), and very large (>2.0–4.0) (17). The Statistical Package for the Social Sciences version 20 was used for all statistical analysis (SPSS Inc., Chicago, IL). The statistical significance was set at P < 0.05. Data are presented as mean ± SD.
Baseline versus Postexercise/Precooling
All 10 participants completed the experiment, and no adverse events were recorded. The exercise time necessary to achieve a rectal temperature of 38°C was ~23 min for both trials. The cycling protocol elicited similar increases in heart rate, rectal and muscle temperatures, and thermal discomfort between CWI and WBC (Table 1). Thigh skin temperature also increased with exercise in both trials but was higher in the CWI trial (P = 0.01). Systolic blood pressure, diastolic blood pressure, and mean arterial pressure were unchanged after exercise and were similar between conditions (all P > 0.05). Exercise increased arterial blood flow and conductance by ~65%–70% (P < 0.001) with no difference between conditions (P > 0.05). Cutaneous vascular conductance increased after exercise and was similar between conditions at the thigh but was lower at the calf in WBC (Table 1).
Precooling versus Postcooling
Rectal temperature decreased during the postcooling recovery period (P < 0.001) and was similar between conditions (P = 0.98, ES = 0.3; Fig. 2). Thigh skin temperature was lower throughout the postcooling period in CWI compared with WBC (P < 0.001, ES = 3.6; Fig. 2) with the largest difference occurring 10 min postcooling (6.0°C ± 2.4°C, ES = 4.3).
Muscle temperature was reduced after cooling in both conditions at all depths (P < 0.001; Fig. 3). The reduction in muscle temperature at each depth was greater after CWI compared with WBC at 10 min (1 cm: 3.6°C ± 1.0°C, ES = 2.9; 2 cm: 2.8°C ± 1.0°C, ES = 2.5; 3 cm: 1.1°C ± 0.4°C, ES = 2.8) and 40 min time points (1 cm: 2.2°C ± 1.2°C, ES = 1.7; 2 cm: 2.2°C ± 1.1°C, ES = 1.9; 3 cm: 1.6°C ± 0.8°C, ES = 2.1). Decreases in thermal comfort were lower (1 ± 1 a.u., ES = 1.0) after CWI at 10 min and (1 ± 1 a.u., ES = 1.0) 20 min postcooling compared with WBC. There was no shivering observed throughout the postimmersion period in either experimental condition.
Heart rate, blood pressure, and arterial blood pressure
Heart rate decreased throughout the recovery period in both conditions (P < 0.001; see Table 2). There was a significant interaction of time and condition (P < 0.001). Heart rate returned to preexercise baseline during CWI at 10 min postcooling, whereas heart rate remained higher throughout postcooling recovery during WBC. Furthermore, relative to WBC, heart rate was higher at 10 and 20 min post-CWI. Systolic blood pressure was similar to preexercise throughout the recovery period with no difference between conditions (P > 0.05 for main effects of time and condition; see Table 2). There was a significant interaction effect of time and condition for diastolic blood pressure (P < 0.001) and mean arterial pressure (P = 0.002). Diastolic blood pressure and mean arterial pressure were similar to preexercise throughout the recovery period in WBC, whereas, during CWI, diastolic and mean arterial pressure were higher at 10 and 40 min postcooling during CWI relative to preexercise baseline.
Femoral artery and cutaneous blood flow responses.
The decrease in femoral artery blood flow (P < 0.001, ES ≥ 0.7) and femoral vascular conductance (P < 0.001, ES ≥ 1.0) was greater in the CWI condition throughout the postcooling period (Fig. 4). At 40 min postrecovery, femoral artery blood flow and femoral artery conductance were (~45%–50%) lower in CWI compared with WBC (Fig. 4). A greater skin vasoconstriction was observed after CWI at the thigh (~75% vs ~55%; P < 0.001, ES = 1.9) and calf (~70% vs ~45%; P < 0.001, ES = 1.6) throughout the recovery period (Fig. 4).
The major finding of the present study is that, relative to WBC, CWI led to greater reductions in femoral artery and cutaneous blood flow, as well as deep and superficial muscle temperature, during the postexercise recovery period. Collectively, our novel data provide evidence that postexercise CWI may potentially reduce muscle blood flow to a greater extent than WBC. These findings provide important insights into the relative efficacy of, and the possible mechanisms that underpin, distinct cryotherapy recovery modalities commonly used in clinical and sporting environments.
To our knowledge, only one study has previously attempted to document the limb blood flow response to WBC cooling, using near-infrared spectroscopy (31). On the morning after exercise (a rugby league match), reductions in tissue oxyhemoglobin and tissue oxygenation index of the vastus lateralis were evident immediately after 3 min of WBC, which caused a reduction in mean skin temperature of a maximum of ~9°C (31). The near-infrared spectroscopy method provides indirect estimates of relative changes in blood volume within the muscle microcirculation, but is associated with several limitations (12), including that tissue oxygenation indices are confounded when marked changes in skin blood flow arise (e.g., exercise, heating, and cooling) (9). In the present investigation, we continuously measured changes in lower limb cutaneous blood flow using laser Doppler flowmetry while simultaneously measuring femoral artery blood flow via conduit artery high-resolution duplex ultrasound. Cutaneous blood flow was reduced throughout the recovery period relative to preimmersion in both CWI (~70%–75%) and WBC (~45%–55%) conditions, with a greater vasoconstriction observed after CWI (ES = 1.6–1.9).
Alongside the changes in cutaneous blood flow, there was a ~50% greater reduction in femoral artery conductance after CWI at the end of the recovery period, which may infer that CWI reduces muscle blood flow to a greater extent and has a superior effect upon reducing edema (32). Greater CWI-induced reductions in limb blood flow suggest that CWI may limit the inflammatory response after exercise to a greater extent compared with WBC based on previous animal (20,30) and human (26,40) studies that reported blunted increases in inflammatory markers after local/whole-body cryotherapy. The purported relationship of blood flow and inflammation after exercise has recently been challenged in a study that reported no effect of CWI (10 min at 10°C) on the muscle inflammatory or cellular stress response compared with an active recovery after lower body resistance exercise (25). A reduction in muscle blood flow may therefore provide benefits to the acute recovery from exercise by attenuating the clinical signs of inflammation such as edema and swelling per se (11,38) and associated pain (e.g., soreness) upon movement. Indeed, recent work reported that CWI was more effective than WBC in accelerating recovery kinetics and reducing muscle soreness postexercise (1).
The interpretation of the magnitude of change in postcooling limb blood flow with regard to the therapeutic benefit to recovery is difficult to ascertain. In practical terms, the difference of femoral artery blood flow of ~50 mL·min−1 between WBC and CWI conditions is of physiological relevance, particularly when it is evident during the entire 40 min and perhaps longer. To our knowledge, no study has directly addressed the cooling-induced minimally important clinical difference in limb/muscle blood flow required to influence muscle soreness and clinical signs of inflammation such as swelling/edema after exercise. Past studies have largely focused on the effects of cooling on functional/performance measures and/or markers of muscle damage but have not related the desired outcome measures with changes in limb blood flow. More work is required to relate changes in limb blood flow with the measured outcome variable of interest after postexercise cooling.
The reduction in femoral artery blood flow is mediated via activation of thermal nociceptors during skin cooling, which leads to a reflex increase in sympathetic nerve activity (19). The differences in arterial blood flow between CWI and WBC may therefore be related to the different thermal input; for example, core and local tissue temperatures, associated with skin cooling in both recovery modalities. To date, only one study (8) has compared the thermoregulatory responses (i.e., core, muscle, and skin temperatures) between CWI and WBC recovery modalities. In that study, the duration of exposures was matched to delineate the effect of the different modalities. However, the duration of the CWI (4 min) protocol was not representative of the CWI protocol typically used for recovery in various sporting environments; that is, ≥ 10 min (21,36), and neither modality was applied after exercise. In the current study, we observed no difference in recovery rectal temperatures between cooling modalities and noted a lower skin temperature after CWI throughout the recovery period in agreement with Costello et al. (8). By contrast, our findings of greater reductions in deep and superficial muscle temperatures after CWI are not consistent with the findings of Costello et al. (8). These findings are likely related to the greater conductance of tissue heat transfer/loss in water compared with air (4) and/or the greater duration of CWI cooling used after exercise in the current study.
The decreases in deep muscle temperature after CWI likely contributed to the larger reduction in femoral artery conductance after CWI (3). The temporal pattern in femoral artery conductance mirrored that of deep muscle temperature in that the differences between CWI and WBC became larger as the postcooling recovery period progressed. Previous work from our laboratory (23) has shown that relatively small changes in deep muscle temperature (~0.5°C) do not influence femoral artery conductance. Our findings indicate that relative to WBC, lower deep muscle temperature is evident during CWI recovery, which may suggest deep muscle temperature differences of >1.0°C likely modulated limb, and perhaps muscle, blood flow.
Cold stress can also induce pain via noxious stimulation (19). Immersing the hands in 28°C, 21°C, and 14°C water temperatures decreased hand skin temperature to 20°C–24°C and pain sensations ranged from not painful to somewhat painful, but muscle sympathetic nerve activity was unchanged (19). During 7°C and 0°C water hand immersion, which decreased skin temperature below 15°C, perceived pain was rated as intensively painful and muscle sympathetic nerve activity greatly increased. It is therefore possible that CWI could induce pain and elevations in sympathetic nerve activity, independent of the thermal stimulus, depending on the magnitude of reduction in skin temperature. In the present study, the lowest skin temperatures were approximately 24°C after CWI. Therefore, despite a likely minor increase in pain sensation after CWI in the present study, sympathetic nerve activity directed to the musculature was likely not increased above that caused by the cold thermal stimulus alone.
Although there are no definitive guidelines regarding the effective and safe use of WBC (6), it is common that individuals continuously move their arms and legs and/or walk around the inside of the cryotherapy chamber during relatively short exposure durations (5,8). Methodologically, this is problematic in the assessment of limb blood flow because of muscle activation confounding measurements. We were therefore cautious to select a less severe WBC temperature and duration to limit the prospect of any adverse skin reactions/cold burn injury whilst seated inside the cryotherapy chamber (no adverse skin reactions were noted in the present study) and to match typical durations of WBC protocols. Previous research suggests that colder temperatures (e.g., −135°C) may be better for recovery (31); therefore, colder WBC temperatures and/or longer exposure durations may have a greater effect on deep tissue temperature, which may lead to greater reductions in limb blood flow than presently observed. Further work is required to explore the potential benefits of lower WBC temperatures and/or increased durations on the limb blood flow response after exercise. Nevertheless, despite a greater thermal gradient between colder air temperatures and skin during WBC exposure, the greater thermal conductance and/or duration of CWI promoted greater changes in tissue temperature and limb blood flow in the present study. In light of the current findings, the physiological rationale for using WBC instead of CWI, in addition to the associated logistical and cost implications, is questionable.
It is also important to acknowledge that CWI will result in increased hydrostatic pressure and potentially increased central blood volume, which could affect vascular responses independent of the water temperature. More specifically, baroreceptor-mediated peripheral vasodilation could occur. Nevertheless, previous research has reported no change in total peripheral resistance during hip-level (the same level used for CWI in the present study) thermoneutral water immersion (36). Moreover, any baroreflex-mediated vasodilation from immersion per se would have blunted the sympathetic peripheral vasoconstriction from cold-water stimulation rather than contributed to/exacerbated the clear differences in vascular responses between CWI and WBC observed in the present study. Finally, the aim of the present practically oriented study was to compare the thermoregulatory and vascular responses to two commonly used/ecologically valid but very different recovery methods, rather than investigate the effects of each intervention independently. Because of the repeated-measures design of the present study, moderate-intensity cycling was used as the exercise stimulus before the cooling interventions, which would likely have not induced significant muscle damage. It would be logical to further investigate the vascular and thermoregulatory responses to CWI versus WBC after high-intensity endurance exercise that results in pronounced muscle damage.
In summary, this study demonstrates that an ecologically valid CWI protocol decreases both femoral artery and cutaneous blood flow and muscle temperature to a greater extent compared with a typical WBC protocol after endurance exercise. CWI may therefore be a more effective cooling modality due, in part, to the hydrostatic pressure of water and the greater ability of water to conduct heat. These findings have practical implications in athletic and clinical settings where cryotherapy is used with the aim to accelerate recovery from exercise. Further studies are necessary to evaluate if, relative to WBC, CWI-induced greater decreases in conduit and microvascular blood flow and muscle temperature result in greater therapeutic benefits postexercise.
The authors express their gratitude to all who participated in this study. They also thank ECB Cold Spa Ltd. and Air Products Ltd. for providing the water tank and whole body cryotherapy chamber, respectively, and UK Sport for funding the present investigation.
WG has received funding from ECB Cold Spa Ltd. for the CWI facility and from UK Sport for part funding of a Ph.D. program. C. M., D. L., H. J., D. G., and J. C. have no conflicts of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.
Whole body cryotherapy is not yet approved by the FDA and is not labeled for the use under discussion.
1. Abaïdia AE, Lamblin J, Delecroix B, et al. Recovery
-induced muscle damage
: cold water immersion versus whole body cryotherapy. Int J Sports Physiol Perform
2. Banfi G, Lombardi G, Colombini A, Melegati G. Whole-body cryotherapy in athletes. Sports Med
3. Barcroft H, Edholm OG. The effect of temperature on blood flow and deep temperature in the human forearm. J Physiol
4. Bleakley CM, Bieuzen F, Davison GW, Costello JT. Whole-body cryotherapy: empirical evidence and theoretical perspectives. Open Access J Sports Med
5. Costello JT, Algar LA, Donnelly AE. Effects of whole-body cryotherapy (−110°C) on proprioception and indices of muscle damage
. Scand J Med Sci Sports
6. Costello JT, Baker PR, Minett GM, Bieuzen F, Stewart IB, Bleakley C. Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise
in adults (Protocol). Cochrane Database Syst Rev
7. Costello JT, Baker PR, Minett GM, Bieuzen F, Stewart IB, Bleakley C. Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise
in adults. Cochrane Database Syst Rev
8. Costello JT, Culligan K, Selfe J, Donnelly AE. Muscle, skin and core temperature after −110°C cold air and 8°C water treatment. PLoS One
9. Davis SL, Fadel PJ, Cui J, Thomas GD, Crandall CG. Skin blood flow influences near-infrared spectroscopy-derived measurements of tissue oxygenation during heat stress. J Appl Physiol
10. Diong J, Kamper SJ. Cold water immersion (cryotherapy) for preventing muscle soreness after exercise
. Br J Sports Med
11. Dolan MG, Thornton RM, Fish DR, Mendel FC. Effects of cold water immersion on edema formation after blunt injury to the hind limbs of rats. J Athl Train
12. Ferrari M, Mottola L, Quaresima V. Principles, techniques, and limitations of near infrared spectroscopy. Can J Appl Physiol
13. Ferreira-Junior JB, Bottaro M, Vieira A, et al. One session of partial-body cryotherapy (−110°C) improves muscle damage recovery
. Scand J Med Sci Sports
14. Fonda B, Sarabon N. Effects of whole-body cryotherapy on recovery
after hamstring damaging exercise
: a crossover study. Scand J Med Sci Sports
15. Gregson W, Black MA, Jones H, et al. Influence of cold water immersion on limb and cutaneous blood flow at rest. Am J Sports Med
16. Hausswirth C, Louis J, Bieuzen F, et al. Effects of whole-body cryotherapy vs. far-infrared vs. passive modalities on recovery
-induced muscle damage
in highly-trained runners. PLoS One
17. Hopkins WG, Marshall SW, Batterham AM, Hanin J. Progressive statistics for studies in sports medicine and exercise
science. Med Sci Sports Exerc
18. Ihsan M, Watson G, Lipski M, Abbiss CR. Influence of postexercise cooling
on muscle oxygenation and blood volume changes. Med Sci Sports Exerc
19. Kregel KC, Seals DR, Callister R. Sympathetic nervous system activity during skin cooling
in humans: relationship to stimulus intensity and pain sensation. J Physiol
20. Lee H, Natsui H, Akimoto T, Yanagi K, Ohshima N, Kono I. Effects of cryotherapy after contusion using real-time intravital microscopy. Med Sci Sports Exerc
21. Leeder J, Gissane C, van Someren K, Gregson W, Howatson G. Cold water immersion and recovery
from strenuous exercise
: a meta-analysis. Br J Sports Med
22. Lombardi G, Lanteri P, Porcelli S, et al. Hematological profile and martial status in rugby players during whole body cryostimulation. PLoS One
23. Mawhinney C, Jones H, Joo CH, Low DA, Green DJ, Gregson W. Influence of cold-water immersion on limb and cutaneous blood flow after exercise
. Med Sci Sports Exerc
24. McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage
from a single bout of eccentric exercise
. Scand J Med Sci Sports
25. Peake JM, Roberts LA, Figueiredo VC, et al. The effects of cold water immersion and active recovery
on inflammation and cell stress responses in human skeletal muscle after resistance exercise
. J Physiol
26. Pournot H, Bieuzen F, Louis J, et al. Time-course of changes in inflammatory response after whole-body cryotherapy multi exposures following severe exercise
. PLoS One
27. Roberts LA, Muthalib M, Stanley J, et al. 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
28. Roberts LA, Nosaka K, Coombes JS, Peake JM. Cold water immersion enhances recovery
of submaximal muscle function after resistance exercise
. Am J Physiol Regul Integr Comp Physiol
29. Schaal K, Le Meur Y, Bieuzen F, et al. Effect of recovery
mode on postexercise vagal reactivation in elite synchronized swimmers. Appl Physiol Nutr Metab
30. Schaser KD, Disch AC, Stover JF, Lauffer A, Bail HJ, Mittlmeier T. Prolonged superficial local cryotherapy attenuates microcirculatory impairment, regional inflammation, and muscle necrosis after closed soft tissue injury in rats. Am J Sports Med
31. Selfe J, Alexander J, Costello JT, et al. The effect of three different (−135°C) whole body cryotherapy exposure durations on elite rugby league players. PLoS One
32. Thorlacius H, Vollmar B, Westermann S, Törkvist L, Menger MD. Effects of local cooling
on microvascular hemodynamics and leukocyte adhesion in the striated muscle of hamsters. J Trauma
33. Vaile J, O'Hagan C, Stefanovic B, Walker M, Gill N, Askew CD. Effect of cold water immersion on repeated cycling performance and limb blood flow. Br J Sports Med
34. Vieira Ramos G, Pinheiro CM, Messa SP, et al. Cryotherapy reduces inflammatory response without altering muscle regeneration process and extracellular matrix remodeling of rat muscle. Sci Rep
35. Wakabayashi H, Hanai A, Yokoyama S, Nomura T. Thermal insulation and body temperature wearing a thermal swimsuit during water immersion. J Physiol Anthropol
36. Wilcock IM, Cronin JB, Hing WA. Physiological response to water immersion: a method for sport recovery
? Sports Med
37. Woodman RJ, Playford DA, Watts GF, et al. Improved analysis of brachial artery ultrasound using a novel edge-detection software system. J Appl Physiol
38. Yanagisawa O, Niitsu M, Yoshioka H, Goto K, Kudo H, Itai Y. The use of magnetic resonance imaging to evaluate the effects of cooling
on skeletal muscle after strenuous exercise
. Eur J Appl Physiol
39. Young AJ, Sawka MN, Epstein Y, Decristofano B, Pandolf KB. Cooling
different body surfaces during upper and lower body exercise
. J Appl Physiol
40. Ziemann E, Olek RA, Kujach S, et al. Five-day whole-body cryostimulation, blood inflammatory markers, and performance in high-ranking professional tennis players. J Athl Train