Effects of repeated whole-body cold stress on finger temperature responses to localized cooling
Effekter av upprepade helkropps
köldexponeringar på fingertemperatursvar vid lokal köldprovokation
PIT GÄNG
KTH ROYAL INSTITUTE OF TECHNOLOGY
SCHOOL OF ENGINEERING SCIENCES IN CHEMISTRY, BIOTECHNOLOGY AND HEALTH
whole-body cold stress on
finger temperature responses to localized cooling
PIT GÄNG
Master in Medical Engineering Date: June 16, 2020
Supervisor: Assist. Prof. Michail Keramidas, PhD Reviewer: Prof. Ola Eiken, MD, PhD
Examiner: Assoc. Prof. Matilda Larsson, PhD School of Chemistry, Biotechnology and Health
Swedish title: Effekter av upprepade helkropps köldexponeringar på fingertemperatursvar vid lokal köldprovokation
Abstract
The study aimed to assess whether a short-term, high-intensity cold acclimation pro- tocol would modulate finger vasomotor [i.e., finger temperature (TF), cold induced vasodilation (CIVD)] responses and regional thermo-perception to localized cool- ing. Six men performed a hand cold provocation (consisting of a 30-min immer- sion in 8◦C water), while being whole-body immersed, once, in 21◦C water (i.e., cold trial; HYPO), and, the following day, in 35.5◦C water (i.e., normothermic trial;
NORM). The local cold provocations were repeated, in the same order, after 10 days.
In the intervening period, the subjects undertook a whole-body cold acclimation pro- tocol, consisting of daily whole-body 14◦C-water immersions for 5 consecutive days, for a maximum of 2 h, while the skin temperature of the right hand was maintained at 35.6 (0.1)◦C. Thermal (rectal temperature, skin temperature, finger temperature) cardiorespiratory (mean arterial pressure (MAP), heart rate and oxygen uptake), and perceptual responses (thermal sensation and comfort, pain, affective valence) were monitored throughout the trials. The acclimation protocol resulted in hypothermic adaptation (i.e., habituation), which was characterized by a modest reduction in shiv- ering and an attenuation of whole-body thermal discomfort. The main finding of the study was that, regardless of subjects’ thermal status, the 5-day whole-body cold acclimation protocol did not alter TF (P > 0.1) and CIVD responses (P > 0.2) dur- ing local cold stress. Yet, after the acclimation, the cold-induced increase in MAP was reduced and tended to be reduced during the HYPO (P = 0.05) and NORM (P = 0.14) local cold provocation trials, respectively. Furthermore, the perceived thermal discomfort and pain in the immersed hand appeared to be alleviated in all post-acclimation trials.
Sammanfattning
Syftet var att utvärdera i vad mån en kortvarig anpassningsprocedur till sträng kyla inverkar på fingrarnas vasomotorsvar [d.v.s. fingertemperatur (TF), köld-inducerad vasodilatation (CIVD)] och på temperaturperception vid lokal nedkylning. Sex män genomgick köldprovokation av en hand (bestående i 30 minuters immersion i 8◦C vatten), under samtidig helkroppsimmersion, vid ett tillfälle i 21◦C vatten (hypo- term betingelse; HYPO) och, påföljande dag, i 35,5◦C vatten (normoterm betingelse;
NORM). De lokala köldprovokationerna upprepades i samma ordningsföljd efter 10 dagar. Under mellanperioden genomgick försökspersonerna en köldanpassningspro- cedur, bestående i helkroppsimmersioner i 14◦C vatten under 5 dagar i rad, där varje immersion varade i max 2 timmar och där hudtemperaturen i höger hand reglerades vid 35,6 (0,1)◦C under immersionerna. Temperatursvar (rektal-, hud- och fingertem- peratur) och kardiorespiratoriska svar (medelartärtryck (MAP), hjärtfrekvens och syreupptag) samt perceptionsvariabler (upplevd temperatur och temperaturobehag, smärta, affektvalens) mättes/uppskattades kontinuerligt under interventions- och för- sökstillfällena. Anpassningsproceduren framkallade en hypoterm adaptation (d.v.s.
habituering), bestående i måttlig reduktion av ”shivering thermogenesis” (huttring) och minskat generellt (helkropps) temperaturobehag. Undersökningens huvudresul- tat var att den 5-dagars helkropps-köldanpassningsproceduren inte påverkade TF(P
> 0,1) eller CIVD-svar (P > 0,2) vid lokal köldprovokation, oavsett om provokatio- nen genomfördes under HYPO eller NORM. Emellertid tenderade köldanpassnings- proceduren att dämpa den köldbetingade ökningen av MAP såväl under HYPO (P = 0,05) som under NORM (P = 0,14). Vidare var temperaturobehag och smärta i den köldexponerade handen mindre uttalade i bägge försöksbetingelserna efter köldan- passningsproceduren.
Acknowledgements
The present study was supported by a grant of the Swedish Armed Forces (Grant no.
9220918). The participation and effort of all subjects is greatfully acknowledged.
I would like to express my sincere gratitude to my supervisor Michail Keramidas for his unremitting support and guidance throughout this project. Also, I would like to thank everybody at the KTH Division of Environmental Physiology.
Abbreviations
AVA Arterio-venous anastomoses BL Baseline phase
B-WI Body water immersion phase B-RW Body rewarming phase
CIVD Cold induced vasodilation DAP Diastolic arterial pressure
H-CWI Hand cold water immersion phase HR Heart rate
HRV Heart rate variability H-RW Hand rewarming phase
HYPOPRE Hypothermic (pre acclimation) trial HYPOPOST Hypothermic (post acclimation) trial
kg Kilogram L Liter
MAP Mean arterial pressure mm Millimeter
mmHg Millimeter mercury N Number of CIVD events
n Number of subjects NE Norepinephrine NO Nitric oxide
NORMPRE Normothermic (pre acclimation) trial NORMPOST Normothermic (post acclimation) trial
rpm Revolutions per minute SAP Systolic arterial pressure
SCUBA Self-contained underwater breathing apparatus SD Standard deviation
TF Finger temperature
TF,avg Average finger temperature (of all right-hand fingers) TF,max Maximum finger temperature
TF,min Minimum finger temperature Trec Rectal temperature
Tsk Skin temperature TC Thermal comfort TS Thermal sensation
∆TF Temperature amplitude of CIVD event
∆tF Duration of CIVD event VAL Affective valence
VE Expired ventilation VO2 Oxygen uptake VO2peak Peak oxygen uptake
1 Introduction 1
1.1 Aims . . . 2
1.2 Hypotheses . . . 3
1.3 Significance of the study . . . 3
2 Methods 4 2.1 Ethics Approval . . . 4
2.2 Subjects . . . 4
2.3 Experimental Design . . . 5
2.4 Experimental Procedure . . . 6
2.5 Instrumentation . . . 8
2.6 Data Analysis . . . 10
2.7 Statistical Analysis . . . 10
3 Results 12 3.1 Acclimation sessions . . . 12
3.2 Local cold provocations . . . 12
3.2.1 Hypothermic trials . . . 13
3.2.2 Normothermic trials . . . 19
4 Discussion 24 4.1 Effect of acclimation on finger temperature responses to localized cooling . . . 25
4.2 Effect of acclimation on finger thermo-perceptual responses to lo- calized cooling . . . 27
4.3 Methodological considerations . . . 28
4.4 Practical perspectives . . . 29
4.5 Future studies . . . 29
5 Conclusions 30 A Background 36 A.1 Cutaneous responses to acute cold stress . . . 36
viii
A.1.1 Cold-induced vasoconstriction . . . 36 A.1.2 Cold-induced vasodilation (CIVD) . . . 37 A.2 Cutaneous responses to cold after long-term cold exposure . . . 41 A.2.1 Chronic adaptations to cold: evidence from population studies 42 A.2.2 Acclimatization to cold . . . 42 A.2.3 Acclimation to cold . . . 43
B Ethics approval 55
Introduction
During exposure to a cold environment, a sympathetically mediated increase in pe- ripheral vasomotor tone attenuates cutaneous blood flow, minimizing the skin-to- environment temperature gradient, and thus reducing the body’s heat loss. This initial autonomic thermo-effector response, via which thermal homeostasis is pre- served, occurs rapidly with declining ambient temperatures, and is regulated either centrally or locally [1]. Yet, sustained periods of peripheral vasoconstriction may lead to local pain, impaired manual dexterity, and freezing/non-freezing cold in- juries in the extremities (i.e., hands and feet) [2]. Notably, in cold-exposed extremi- ties, particularly in fingers and toes, the drive for peripheral vasoconstriction is often interrupted by transient fluctuations of cutaneous blood flow [3], which elevate the regional skin temperature. This vasomotor reaction, which has been termed cold- induced vasodilation (CIVD), mitigates the cold-induced pain and discomfort [4], and plausibly provides a cryoprotective function against local cold injury [5, 6], at least in conditions of normal body core temperature (i.e., normothermia). However, a high inter- and intra-individual variability exists; the incidence and magnitude of CIVD vary greatly between individuals [7], as well as between the digits of the same limb [8, 9].
The exact underlying mechanisms of CIVD are not completely understood, and still remain hypothetical (see Appendix A.1.2.1). It has been shown, however, that the thermal state of the whole body constitutes an important determinant of the re- sponse. Specifically, CIVD is more pronounced when the body core temperature is elevated (i.e., hyperthermic state), and, conversely, is attenuated when the body core temperature is low (i.e., hypothermic state) [10, 11, 12].
A number of studies have provided evidence that prolonged, whole-body and/or local, cold exposure, encountered either continuously or intermittently, may lead to peripheral thermo-adaptive modifications to cold. However, hitherto, any informa- tion on the effects of whole-body cold adaptation on CIVD is limited to that derived from population and field (i.e., acclimatization) studies. For instance, population- based studies have shown that Arctic natives (e.g., Inuit and Sami), may exhibit higher CIVD amplitudes [13] and finger skin temperatures [14] than non-arctic na-
1
tives; responses that may reduce susceptibility to cold injuries in these groups. More- over, individuals that are exposed to low-temperature environments in a long-term repeated manner (e.g., fishermen or military personnel), appear to have enhanced skin blood flow and warmer extremities during local cold provocations [15, 16, 17].
However, in these field studies, it has not been possible to deduce whether the main driver of the adaptive response is the local surface, whole-body surface or body-core exposure to cold. Furthermore, several confounders (e.g., exercise, nutrition, sleep), that independently may influence the CIVD response (see Appendix A.1.2.2), have not been accounted for.
The majority of the laboratory (i.e., acclimation) studies, on the other hand, have investigated the effects of repeated local cold exposures (i.e., by immersing one limb or one digit in cold water) on the peripheral thermoregulatory responses. These acclimation studies have provided contradictory findings; some have observed an enhanced CIVD response (i.e., earlier onset and higher amplitude) [18, 19], while others have found either an impairment [20, 21] or no change [8, 22] in the CIVD response. It is also noteworthy that only O’Brien et al. [21] have examined the effect of a whole-body cold acclimation protocol (5 weeks of daily 1-h immersions in 20◦C water) on the finger CIVD response. They have found that the repeated whole-body exposures to cold water resulted in an enhanced finger vasoconstrictive response to local cooling, and the attenuation of CIVD [21]. Yet, this study was not designed to specifically test the CIVD; for instance, both hands were immersed to cold water during the acclimation protocol. Therefore, information regarding the effects of repeated whole-body cold stress on peripheral vasoreactivity is scarce.
1.1 Aims
The purpose of the present study was to examine whether, and to what extent, whole- body cold stress, encountered repeatedly over a 5-day period, would modulate fin- ger temperature responses to localized cooling. This question was addressed by monitoring, before and after a whole-body cold acclimation protocol, the thermal, cardiorespiratory, and perceptual responses to a hand cold-water provocation trial, while subjects were either mildly hypothermic or normothermic.
To isolate any confounding influences derived from local thermal stress during the adaptation process, a closed-loop acclimation protocol was employed, during which the subjects’ body core temperature was manipulated daily for a maximum of 2 h by whole-body cold water immersions, whereas the skin temperature of the region of interest (i.e., the right hand) was maintained at ∼35.5◦C.
1.2 Hypotheses
It was hypothesized that the repeated exposures to whole-body cold stress would enhance finger temperature and CIVD response to localized cooling, both in the mild hypothermic and normothermic body states. Furthermore, it was hypothesized, that the regional thermo-perceptual responses would be improved after the short-term protocol.
1.3 Significance of the study
The present study aimed to enhance the understanding of how humans can adapt to cold, and in particular, to clarify the contribution of whole-body cold adaptation on the CIVD response. Furthermore, the study evaluated the efficacy of a short- term cold acclimation protocol on finger temperature responses. Such a feasible cold acclimation protocol may be applied by individuals that are frequently exposed to cold environments (e.g., military personnel, hikers, arctic explorers), in order to minimize the risk for developing cold injuries.
Methods
2.1 Ethics Approval
The experimental protocol was approved by the Human Ethics Committee of Stock- holm (2019-05729; see Appendix B) and complied with the standards of the Decla- ration of Helsinki. All subjects were informed in detail about the experimental pro- cedures before giving their oral and written consent to participate, and were aware that they could terminate their participation at any time of the study.
2.2 Subjects
Six healthy men participated; their physical characteristics are presented in Table 2.1. Five subjects were non-smokers, and one subject was a light smoker (approx. 1- 2 cigarettes per day). The subjects had no history of cold injuries, were not suffering from Raynaud’s syndrome and were not taking medication. All subjects were aero- bically fit, which was verified by an exhaustive test on a cycle ergometer conducted prior to the main experimental sessions.
Table 2.1. Physical characteristics of the subjects.
Variable [unit] Mean (SD)
Age [y] 26 (1)
Body mass [kg] 82 (9.3)
Height [cm] 186 (5)
Body surface area [cm2] 2.06 (0.13)
Total skinfold thickness [mm] 92 (33)
Body fat [%] 12.8 (4.9)
Right hand volume [mL] 431 (46)
VO2peak [L/min] 3.3 (0.8)
SD: standard deviation. VO2peak: peak oxygen uptake.
4
2.3 Experimental Design
The study was performed between December 2019 and March 2020 in a laboratory of the Division of Environmental Physiology at the KTH Royal Institute of Tech- nology in Stockholm, Sweden. A week prior to the main sessions, subjects were thoroughly familiarized with the equipment and experimental procedures. Anthro- pometric measurements (i.e., body mass, height, body fat, and volume of the right hand), and an exhaustive trial on a cycle ergometer to determine their VO2peak were also performed.
A schematic representation of the overall study design is depicted in Figure 2.1.
During the main sessions, all subjects performed a hand cold provocation (consisting of a 30-min immersion in 8◦C water), while being whole-body immersed, once, in 21◦C water (i.e., cold trial; HYPOPRE), and, the following day, in 35.5◦C water (i.e., normothermic trial; NORMPRE). The local cold provocations were repeated, in the same order, after 10 days (i.e., HYPOPOST and NORMPOST, respectively).
In the intervening period, the subjects undertook a whole-body cold acclimation protocol, consisting of daily whole-body 14◦C-water immersions for 5 consecutive days. During all trials and acclimation sessions the subjects were clad in swim pants.
Figure 2.1. Schematic representation of the overall experimental design.
The subjects performed the pre- and post-trials at the same time of the day (ei- ther in the morning or in the afternoon), to avoid any circadian-related confounding influences on body temperature regulation. Subjects were asked to refrain from caf- feine, nicotine, alcohol and strenuous exercise 12 hours before each trial. No fluid intake was allowed during the trials and subjects were asked not to eat the 3 hours preceding each trial. The environmental conditions in the laboratory were kept con- stant at 27.1 (0.2)◦C room temperature, 752 (7) mmHg barometric pressure and 26 (3)% humidity.
Figure 2.2. A subject immersed in the whole-body tank, which was filled with either 21◦C (HYPOPREand HYPOPOST), or 35.5◦C (NORMPREand NORMPOST) water in the local cold provocation trials, or with 14◦C water in the acclimation sessions. H-CWI: the 30-min hand cold water immersion phase.
2.4 Experimental Procedure
Preliminary session. Approximately one week prior to the first session, the subjects were invited to the laboratory, where the anthropometric measurements (i.e., body weight, height, skinfold thickness and right-hand volume) were conducted. VO2peak
was determined by a graded exercise to exhaustion on a cycle ergometer; after a 2- min warm-up at 60 W, the load was increased by 25 W/min until exhaustion (i.e., a minimum cadence of 60 rpm could not be sustained for >5 s).
Local cold provocations trials. The protocol of the local cold provocation trials is depicted in Figure 2.3. Before each immersion, subjects were accustomed to the ambient conditions of the laboratory for approximately 30 minutes. Each trial began with a baseline (BL) phase of 20 minutes, during which subjects rested on a gurney next to the water tank in a semi-reclined position. Following this, subjects entered the tank, which was filled with stirred water maintained either at 21◦C in the HYPOPREand HYPOPOST trials, or at 35.5◦C in the NORMPRE and NORMPOST
trials. The subjects were immersed to the level of the xiphoid process, while both arms were supported, at the heart level, above the water surface (Figure 2.2). During the HYPOPRE and HYPOPOST trials, the subjects rested idle in this position until their rectal temperature (Trec) dropped 0.5◦C from the baseline value (B-WI phase).
Throughout the trial, the left hand was exposed to ambient room temperature [27.1
(0.2)◦C], whereas, during the B-WI phase, the skin temperature of the right hand was maintained at 35.9 (0.4)◦C by means of a custom-made temperature controllable glove. At the end of each B-WI phase, the right hand was removed from the glove, covered with a thin plastic bag and immersed up to the ulnar and radial styloids for 30 min in a different tank filled with 8.0◦C water (H-CWI phase). After the completion of the H-CWI phase, the hand was removed from the water, dried with a towel, and a 15-min spontaneous hand rewarming period ensued (H-RW phase), during which the subjects remained in the tank with both hands resting on the arm supports.
Thereafter, the subjects were removed from the tank, and placed in a well-insulated sleeping bag on the gurney, and were monitored for a further 30-minute rewarming period (B-RW phase). The NORMPREand NORMPOSTtrials were conducted in the same manner, but the duration of the B-WI phase was similar to the B-WI phase of the HYPOPREtrial.
Figure 2.3. Experimental protocol of the hand cold provocation trial, while subjects were mildly hypothermic (i.e., HYPOPRE and HYPOPOST; A) and normothermic (i.e., NORMPREand NORMPOST; B). BL: baseline phase. B-WI: body water immersion phase.
H-CWI: hand cold-water immersion phase. H-RW: hand rewarming phase. B-RW: body rewarming phase.
Acclimation protocol. The protocol of each acclimation session is depicted in Figure 2.4. The acclimation protocol consisted of daily whole-body immersions in 14◦C water for 5 consecutive days, each lasting a maximum of 2 h. Specifically, subjects rested adjacent to the immersion tank in a thermoneutral air environment [27.0 (0.2)◦C] for 20 min, during which baseline values were recorded. Thereafter, subjects entered the tank, which was filled with stirred water maintained at 14◦C, and rested in a semi-upright sitting position (as described in the previous section).
Subjects were immersed to the level of the xiphoid process. The duration of the immersion was 120 min, but it was terminated earlier, if Trec dropped below 35◦C.
During the immersion, the subjects’ hands were supported, at heart level, above the water surface; the left hand was exposed to ambient room temperature, whereas the skin temperature of the right hand was maintained at 35.6 (0.1)◦C by means of the
aforementioned temperature controllable glove. After completing the immersion, the subjects were removed from the tank to a warm shower.
Figure 2.4. Experimental protocol of the acclimation sessions. BL: baseline phase. B-WI:
body water immersion phase.
2.5 Instrumentation
Anthropometry and peak oxygen uptake. Body mass was measured (accuracy 0.01 kg) with an electronic scale (Vetek, Väddö, Sweden). The skinfold thickness was as- sessed with a caliper (Harpenden, UK) at the triceps, subscapular, chest, suprailiac, abdomen, anterior thigh, and midaxillary (all on the right side of the body). Body fat percentage was then calculated according to an equation provided by Jackson and Pollock [23]. Right hand volume was estimated by the water displacement method.
VO2peak was determined by a graded exhaustive exercise, which was performed on a cycle ergometer (Daum Electronic GmbH, Furth, Germany).
Temperature measurements. Trec was recorded during the local cold provoca- tions and the acclimation sessions with a rectal thermistor probe (Yellow Springs Instruments, Yellow Springs, OH, USA) covered in a protective sheath, and in- serted to a depth of 10 cm beyond the anal sphincter. Finger skin temperature of the right (immersed) hand was recorded with copper-constantan (T-type) thermo- couple probes (Physitemp Instruments Inc., Clifton, NJ, USA), which were attached to the middle palmar skin of the distal phalanx of each right-hand finger. Ten addi- tional thermocouples were placed on the left side of the forehead, upper arm, upper back, chest, low back, abdomen, thigh, calf, foot and big toe. Using the unweighted average of these skin temperatures, the mean skin temperature (Tsk) was calculated.
A thermocouple consists of two wires made from different conductors (i.e., met- als, alloys, semiconductors) that are welded together at one end. A temperature difference between this junction causes small electric currents to flow in a closed circuit, thereby allowing electrical energy to be used as a means of temperature mea- surement [24]. Each conductor was 0.2 mm in diameter, and the primary insulation of the thermocouples was polytetrafluorethylene. The non-insulated welded ther- mocouple junctions were attached directly to the skin covered with air-permeable transparent film dressing (3M Health Care, St. Paul, MN, USA). All temperatures were sampled every second with a data acquisition system NI USB-6215 (National
Instruments, Austin, TX, USA). All temperature probes were calibrated with a cer- tified reference thermometer (Ellab, Copenhagen, Denmark) before each trial.
Temperature controllable glove. The skin temperature of the right hand was ma- nipulated by means of a custom-made temperature controllable glove. It was com- posed of a spiral of a garden-hose through which heated water (water temperature could be adjusted; accuracy 0.1◦C) was constantly circulating in a closed circuit. The subjects placed their right hand in the spiral, which was covered with an insulative textile winter glove.
Respiratory measurements. During the local cold provocations and acclimation sessions, the subjects were breathing through a facemask. Oxygen uptake (VO2) and expired ventilation (VE) were measured continuously using the metabolic unit Quark PFT (Cosmed, Rome, Italy). The Quark PFT, which uses a paramagnetic oxygen sensor to analyze exhaled gases, is based on the principle that O2, as a para- magnetic gas, is attracted to a magnetic field. In this way, an electromagnetic field is formed, generating a pressure differential between the exhaled gas of the subject and a reference sample. The pressure fluctuations are detected by a transducer, and converted into electrical current, which is directly proportional to the O2 concen- tration [25, 26]. According to the manufacturer instructions, the pneumotachograph and gas analyzers were calibrated, before each trial, with a 3-liter syringe and two different gas mixtures, respectively.
Arterial pressures and heart rate. During the local cold provocations and the acclimation sessions, beat-to-beat systolic (SAP), diastolic (DAP) and mean arte- rial pressures (MAP) were continuously measured on the middle phalanx of the left (non-immersed) middle finger by finger photoplethysmography (Finometer; Fi- napres Medical Systems BV, Enschede, the Netherlands). The Finometer employs the volume-clamp technique to measure finger arterial pressure using an inflatable bladder (in the finger cuff) in combination with an infrared photoplethysmograph, that consists of an infrared light source and detector. The blood absorbs the infrared light, and the pulsation of arterial diameter during a heartbeat causes a variation in the light detector signal [27, 28]. Thus, the cuff pressure provides an indirect mea- surement of the finger intra-arterial pressure. The reference pressure transducer was placed at heart level. Calibration was performed before each trial according to man- ufacturer instructions with a brachial arm cuff attached to the same arm. Heart rate (HR) was derived as the inverse of the inter-beat interval from the arterial pressure curves.
Perceptual measurements. At specific time points during the local cold provoca- tions and the acclimation sessions, subjects were asked to provide ratings of thermal sensation on a 7-point scale (from 1: cold to 7: hot), thermal comfort on a 4-point scale (from 1: comfortable to 4: very uncomfortable), and pain on a 10-point scale (from 0: no pain to 10: unbearable pain) for the whole-body and the immersed hand.
Moreover, the subjects were asked to provide ratings for affective valence on a 10- point scale (from -5: very bad to +5: very good).
2.6 Data Analysis
The baseline values were calculated as averages of the last 10 min of the 20 min BL phase. Due to the inter- and intra-individual variability of the duration of the B-WI phase, only the last value prior to the H-CWI phase is reported in this study. During all phases, the minimum (TF,min), maximum (TF,max) and average (TF,avg) tempera- tures of each right-hand finger was calculated from the raw data of the thermocou- ples. CIVD events in the fingers (Figure 2.5), defined as a ≥1◦C local skin temper- ature increase that lasted for ≥3 min, were detected with a custom-made program in MATLAB (R2019b, MathWorks, Natick, MA, USA). Each result was manually reviewed to avoid any potential misinterpretations. For each detected CIVD event, the temperature amplitude (∆TF, i.e., the difference between the lowest temperature recorded just before the CIVD event, and the highest peak temperature during the CIVD event), as well as the duration of the CIVD event (∆tF) were determined.
Figure 2.5. Schematic representation of a typical finger CIVD response during a local cold provocation. ∆TF: temperature amplitude. TF,max: maximum temperature of the CIVD event. TF,min: minimum temperature of the CIVD event. Adapted from Cheung and Daanen [29], used with permission.
2.7 Statistical Analysis
To address the research questions posed by the present study, multiple, separate pairwise-comparisons (i.e, pre vs. post) within each condition (i.e., either hypother-
mia or normothermia) and phase (i.e., either BL, or B-WI, or H-CWI, or H-RW, or B-RW) were performed with paired sample Student’s t-test in Excel (Microsoft Corp., Redmond, WA, USA). The level of significance was set a priori at 0.05. All data are presented as mean (standard deviation; SD), unless otherwise stated.
Results
3.1 Acclimation sessions
All subjects participated in the five required acclimation sessions. Four of them com- pleted the 120-min immersion in all sessions. Two subjects, however, terminated the immersion prematurely (one subject in all five sessions, and the other subject in the last four sessions), because their Trecdropped below the critical temperature of 35◦C.
The mean (range) duration of the immersion was 110 (60 – 120) min in Session 1, 105 (63 – 120) min in Session 2, 109 (75 – 120) min in Session 3, 101 (59 – 120) min in Session 4, and 102 (36 – 120) min in Session 5. Table 3.1 summarizes the mean thermal and perceptual responses during each acclimation session. Overall, Trecdropped ∼1.5◦C from the BL; whereas TF,avgof all right-hand fingers was main- tained at 35.6 (0.1)◦C throughout. During the 14◦C-immersion, subjects consistently felt their right-hand slightly warm, thermally comfortable, and pain-free.
3.2 Local cold provocations
The whole-body temperatures, and the cardiovascular and whole-body perceptual responses obtained during all experimental trials are summarized in Table 3.2. BL Trecdid not differ between the trials [HYPOPRE= 37.2 (0.1)◦C, HYPOPOST= 37.1 (0.4)◦C; NORMPRE = 37.2 (0.3)◦C, NORMPOST = 37.1 (0.3)◦C; P > 0.10]. The duration of the B-WI phase was 81 (45) min before and 77 (45) min after the ac- climation protocol. In one subject, during the HYPOPOST, Trec dropped only 0.3◦C after 150 min of B-WI. During the H-CWI, H-RW and B-RW phases, ∆Trec did not differ between the HYPOPREand HYPOPOST, nor between the NORMPREand NORMPOST(P > 0.05). During the H-CWI phase, Tskwas slightly lower in NORMPOST
than in NORMPRE(P = 0.01).
Overall, during the hypothermic trials, subjects shivered, as it was indicated by the moderate elevations in VO2. However, the cold-induced increase in VO2 was somewhat attenuated during the HYPOPOST, especially in the H-CWI phase (P
12
Table 3.1. Thermal and perceptual responses obtained during the 5-day acclimation proto- col.
Session 1 Session 2 Session 3 Session 4 Session 5 Final ∆Trec [◦C] -1.4 (0.7) -1.5 (0.7) -1.4 (0.9) -1.4 (0.7) -1.4 (0.6)
Final Tsk[◦C] 22.2 (0.4) 22.2 (0.4) 21.9 (0.5) 22.2 (0.4) 22.3 (0.8)
TF,avg[◦C] 35.7 (0.1) 35.6 (0.2) 35.6 (0.2) 35.7 (0.1) 35.6 (0.1)
Body: TS (1 – 7) 1 (1 – 3) 1 (1 – 4) 1 (1 – 3) 1 (1 – 4) 2 (1 – 4)
Hand: TS (1 – 7) 5 (4 – 6) 5 (4 – 6) 5 (4 – 6) 5 (4 – 6) 5 (4 – 6)
Body: TC(1 – 4) 3 (1 – 4) 3 (1 – 4) 3 (1 – 4) 3 (1 – 4) 2 (1 – 4)
Hand: TC (1 – 4) 1 (1 – 1) 1 (1 – 1) 1 (1 – 1) 1 (1 – 1) 1 (1 – 1)
Body: Pain (0 – 10) 3 (0 – 7) 2 (0 – 8) 2 (0 – 8) 2 (0 – 7) 1 (0 – 6)
Hand: Pain (0 – 10) 0 (0 – 0) 0 (0 – 0) 0 (0 – 0) 0 (0 – 0) 0 (0 – 0)
Values are mean (SD) for the changes in rectal temperature relative to the respective baseline (∆Trec) and the skin temperature (Tsk) obtained during the final minute of immersion, as well as for the average skin temperature of the five right-hand fingers (TF,avg). Values are median (range) for the perceived thermal sensation (TS), comfort (TC) and pain in the whole body and the right hand.
= 0.07). Likewise, in comparison to the respected phases of HYPOPRE, subjects tended to hyperventilate by ∼1.5 L/min less during the HYPOPOST H-CWI phase (P = 0.15), and by ∼2 L/min less during the HYPOPOSTH-RW phase (P < 0.001).
During the hypothermic trials, subjects felt cold and thermally uncomfortable.
The acclimation protocol improved the ratings for the whole-body thermal sensa- tion during the B-RW phase in both the hypothermic (P = 0.03) and normothermic (P < 0.01) trials, as well as for the affective valence during the B-WI phase of the hypothermic trial (P = 0.03).
3.2.1 Hypothermic trials
Finger skin temperatures. The mean time series for TF,avg are shown in Figure 3.1. BL TF,avg did not differ between the trials [BL: HYPOPRE = 36.2 (0.4)◦C, HYPOPOST= 36.1 (0.2)◦C; P = 0.38]. TF,avg was similar throughout the two trials (Figures 3.1 and 3.2, and Table 3.3; P > 0.31). TF,avg, TF,min, TF,max, ∆TF, and
∆tFwere similar in the two trials (P > 0.20; Table 3.3). The total incidence of CIVD events was slightly lower during the HYPOPOST(Table 3.3), but the difference was not statistically significant (P = 0.19).
Table3.2.Thermal,respiratoryandwhole-bodyperceptualresponsesobtainedduringtheexperimentaltrials,whilesubjectswereimmersedin21 ◦C (HYPOtrials)andin35.5 ◦C(NORMtrials)water,beforeandafterthe5-dayacclimationprotocol.
PREacclimationPOSTacclimation
BLB-WIH-CWIH-RWB-RWBLB-WIH-CWIH-RWB-RWHYPOtrials∆Trec[ ◦C]0-0.5(0.1)-0.7(0.3)-0.9(0.5)-1.0(0.8)0-0.4(0.2)-0.6(0.2)-0.7(0.4)-0.9(0.7) Tsk[ ◦C]33.2(0.3)26.3(0.3)26.3(0.3)26.2(0.3)28.4(0.3)33.5(0.4)26.2(0.5)26.2(0.4)26.1(0.3)28.3(0.5) VO2[L/min]0.38(0.06)0.49(0.12)0.58(0.12)0.58(0.14)0.41(0.04)0.37(0.05)0.45(0.04)0.51(0.11)0.52(0.11)0.41(0.06)
VE[L/min]10.8(2.1)12.1(2.6)15.5(2.1)15.2(1.4)10.8(1.5)11(1.8)12.2(0.7)14.1(2.1)13.2(1.5)*10.8(1.3)
TS(1–7)6(4–6)2(1–4)3(1–4)3(2–4)4(3–5)6(4–6)2(2–4)3(2–4)3(1–4)4(4–6)*
TC(1–4)1(1–1)3(1–3)2(1–3)2(1–3)1(1–2)1(1–1)2(1–2)1(1–3)2(1–2)1(1–2)
VAL(-5–5)4(0–5)1(-3–3)-1(-4–3)-1(-2–3)3(-1–4)3(0–5)2(0–3)*1(-2–4)2(-2–4)3(0–4)NORMtrials∆Trec[ ◦C]00.1(0.3)0.1(0.3)0.1(0.3)0.0(0.3)00.1(0.2)0.1(0.2)0.0(0.3)0.1(0.2) Tsk[ ◦C]34.1(0.5)34.9(0.1)34.9(0.2)34.8(0.1)34.6(0.2)33.7(0.7)34.7(0.2)34.6(0.2)*34.6(0.3)34.6(0.3) VO2[L/min]0.38(0.07)0.41(0.09)0.39(0.07)0.38(0.07)0.38(0.05)0.37(0.05)0.38(0.04)0.38(0.04)0.37(0.04)0.36(0.04)
VE[L/min]10.5(2.3)11.3(2.8)10.6(2.5)10.5(2.4)10.7(2.1)11(1.4)10.5(1.3)10.7(1)10.4(1.1)9.8(1.4)
TS(1–7)5(4–6)5(4–6)5(4–6)5(4–7)5(4–6)6(4–6)6(5–6)5(5–6)5(4–6)5(5–6)*
TC(1–4)1(1–1)1(1–1)1(1–1)1(1–1)1(1–2)1(1–1)1(1–1)1(1–1)1(1–1)1(1–1)
VAL(-5–5)4(1–5)4(0–5)2(-2–4)3(0–5)3(0–5)2(0–5)3(0–5)3(-1–5)3(0–5)3(0–5)
Valuesaremean(SD)forthefinalchangesinrectaltemperaturerelativetotherespectivebaseline(∆Trec),skintemperature(Tsk),oxygenuptake(VO2)
andexpiredventilation(VE).Valuesaremedian(range)fortheperceivedwhole-bodythermalsensation(TS),thermalcomfort(TC),andaffectivevalence
(VAL).BL:baselinephase.B-WI:wholebodywaterimmersionphase.H-CWI:the30-minhandcold-waterimmersionphase.H-RW:the15-minhand
rewarmingphase.B-RW:the30-minwholebodyrewarmingphase.*Significantlydifferentfromthepre-acclimationtrial.
Figure 3.1. Mean (SD) skin temperature of all right-hand fingers (TF,avg) during the hy- pothermic local cold provocation trial performed before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol. H-CWI: the 30-min hand cold-water immersion phase. H- RW: the 15-min hand rewarming phase. B-RW: the 30-min body rewarming phase.
Figure 3.2. Mean (SD) and individual (grey, dotted lines) skin temperature (TF,avg) of all right-hand fingers during the 30-min hand cold water immersion phase (H-CWI), the 15- min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol.
Cardiovascular responses. Regarding the SAP, no differences (P > 0.10) were observed between HYPOPRE and HYPOPOST in the BL [HYPOPRE = 130 (12) mmHg, HYPOPOST= 128 (7) mmHg], in the B-WI [HYPOPRE= 133 (12) mmHg, HYPOPOST= 126 (11) mmHg], in the H-RW [HYPOPRE= 138 (8) mmHg, HYPOPOST
= 129 (11) mmHg] and in the B-RW [HYPOPRE= 139 (10) mmHg, HYPOPOST=
Table 3.3. Average (TF,avg), minimum (TF,min), and maximum temperature (TF,max), num- ber of CIVD events (N), and temperature amplitude (∆TF) and duration (∆tF) of CIVD on each right-hand finger obtained during the 30-min hand cold water immersion phase of the hypothermic trial before and after the 5-day acclimation protocol.
F1 F2 F3 F4 F5 Average
HYPOPRE
TF,avg[◦C] 9.8 (0.8) 9.0 (0.4) 9.9 (0.7) 9.5 (0.9) 9.5 (0.6) 9.6 (0.6) TF,min[◦C] 8.7 (0.9) 8.0 (0.3) 8.6 (0.8) 8.4 (0.7) 8.5 (0.7) 8.4 (0.6) TF,max[◦C] 14.0 (1.4) 12.8 (1.2) 15.4 (2.5) 14.3 (3.1) 13.4 (1.3) 14.0 (1.6)
N 0 (1) 0.5 (3) 0.5 (4) 0 (2) 0 (3) 0 (13)
∆TF[◦C] 0.2 (0.5) 0.6 (0.7) 0.8 (1.1) 0.5 (0.7) 0.4 (0.7) 0.5 (0.6)
∆tF[min] 1.9 (4.5) 4.2 (5.2) 5.5 (6.6) 2.3 (3.6) 3.0 (4.7) 3.4 (4.1)
HYPOPOST
TF,avg[◦C] 10.1 (0.6) 9.3 (0.4) 9.8 (0.7) 9.5 (0.5) 9.7 (0.5) 9.7 (0.4) TF,min[◦C] 8.8 (0.5) 8.2 (0.2) 8.6 (0.6) 8.5 (0.4) 8.6 (0.3) 8.5 (0.4) TF,max[◦C] 13.8 (1.4) 13.0 (0.9) 13.8 (1.2) 13.6 (2) 13.5 (2.5) 13.5 (0.9)
N 0 (1) 0 (1) 0 (1) 0 0 (2) 0 (5)
∆TF[◦C] 0.2 (0.5) 0.3 (0.6) 0.2 (0.4) 0 0.6 (1) 0.2 (0.2)
∆tF[min] 2.0 (4.9) 1.7 (4.2) 2.2 (5.4) 0 3.7 (6.2) 1.9 (1.9)
Values are mean (SD). Values for CIVD are median (total incidence). F1: Thumb; F2:
Index finger; F3: Middle finger; F4: Ring finger; F5: Small finger.
142 (12) mmHg] phases. However, SAP was lower in the HYPOPOSTH-CWI phase than in HYPOPREH-CWI phase [HYPOPRE= 143 (10) mmHg, HYPOPOST = 135 (8) mmHg; P < 0.01].
DAP did not differ between the trials in any phase [BL: HYPOPRE = 76 (11) mmHg, HYPOPOST= 76 (7) mmHg; B-WI: HYPOPRE= 76 (7) mmHg, HYPOPOST
= 76 (5) mmHg; H-CWI: HYPOPRE = 83 (7) mmHg, HYPOPOST= 82 (4) mmHg;
H-RW: HYPOPRE= 82 (5) mmHg, HYPOPOST= 80 (5) mmHg; B-RW: HYPOPRE
= 84 (8) mmHg, HYPOPOST= 87 (6) mmHg; P > 0.10].
MAP did not differ between the trials during the BL [HYPOPRE= 95 (11) mmHg, HYPOPOST= 94 (7) mmHg; P = 0.73] and the B-WI [HYPOPRE = 99 (9) mmHg, HYPOPOST= 96 (8) mmHg; P = 0.28] phases. However, the cold-induced increase in MAP was less in the HYPOPOST H-CWI phase than in the HYPOPRE H-CWI phase (P = 0.05; Figure 3.3). MAP did not differ between the trials in the H-RW and B-RW phases (P > 0.10; Figure 3.3).
Regarding the HR, no differences were observed between the trials in the BL [HYPOPRE= 68 (6) mmHg, HYPOPOST= 66 (6) mmHg; P = 0.14], B-WI [HYPOPRE
= 62 (8) mmHg, HYPOPOST= 60 (7) mmHg; P = 0.47], H-CWI (P = 0.11), H-RW (P = 0.43) and B-RW (P = 0.63) phases (Figure 3.4).
Figure 3.3. Mean (SD) and individual (grey, dotted lines) mean arterial pressure (MAP) during the 30-min hand cold water immersion phase (H-CWI), the 15-min hand rewarm- ing phase (H-RW), and the 30-min body rewarming phase (B-RW) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol. *Significantly different from the pre- acclimation trial.
Figure 3.4. Mean (SD) and individual (grey, dotted lines) heart rate (HR) during the 30-min hand cold water immersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol.
Perceptions. During the B-WI phase of both trials, the right hand was per- ceived slightly warm [5 (4 – 6)], thermally comfortable [1 (1 – 1)], and pain-free (0). Throughout the cold provocation, the sensation of coldness was similar in the two trials (P > 0.05; Figure 3.5). The cold-induced thermal discomfort in the right hand was not altered in the HYPOPOSTH-CWI and B-RW phases (P > 0.26), but it was attenuated in the HYPOPOSTH-RW phase (P = 0.04; Figure 3.6). Moreover, during the HYPOPOSTH-CWI phase, the cold-evoked hand pain was decreased in 5 out of 6 subjects (P = 0.08; Figure 3.7).
Figure 3.5. Median (range) hand thermal sensation during the 30-min hand cold water immersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol.
Figure 3.6. Median (range) hand thermal comfort during the 30-min hand cold water im- mersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol. *Significantly different from the pre-acclimation trial.
Figure 3.7. Median (range) hand pain during the 30-min hand cold water immersion phase (H-CWI) before (HYPOPRE) and after (HYPOPOST) the 5-day acclimation protocol.
3.2.2 Normothermic trials
Finger skin temperatures. The mean time series for TF,avgare shown in Figure 3.8.
BL TF,avgwas similar in the two trials [BL: NORMPRE= 36.3 (0.2)◦C, NORMPOST
= 36.1 (0.3)◦C; P > 0.10]. Also, TF,avgdid not differ between the two trials through- out (Figures 3.8 and 3.9, and Table 3.4; P > 0.10). No differences (P > 0.25) re- garding the TF,min, TF,max, N, ∆TF, and ∆tF were observed between the two trials (Table 3.4).
Figure 3.8. Mean (SD) skin temperature of all right-hand fingers (TF,avg) during the normothermic local cold provocation trial performed before (NORMPRE) and after (NORMPOST) the 5-day acclimation protocol. H-CWI: the 30-min hand cold-water immer- sion phase. H-RW: the 15-min hand rewarming phase. B-RW: the 30-min body rewarming phase.
Figure 3.9. Mean (SD) and individual (grey, dotted lines) skin temperature (TF,avg) of all right-hand fingers during the 30-min hand cold water immersion phase (H-CWI), the 15- min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (NORMPRE) and after (NORMPOST) the 5-day acclimation protocol.
Table 3.4. Average (TF,avg), minimum (TF,min), and maximum temperature (TF,max), num- ber of CIVD events (N), and temperature amplitude (∆TF) and duration (∆tF) of CIVD on each right-hand finger obtained during the 30-min hand cold water immersion phase of the hypothermic trial before and after the 5-day acclimation protocol.
F1 F2 F3 F4 F5 Average
NORMPRE
TF,avg[◦C] 10.4 (1) 11.2 (1.2) 12.0 (1.5) 11.4 (1.9) 11.0 (1.3) 11.4 (1.2) TF,min[◦C] 9.4 (0.8) 8.8 (0.6) 9.4 (0.6) 9.0 (0.6) 8.9 (0.4) 9.1 (0.5) TF,max[◦C] 17.3 (2.8) 16.0 (1.4) 17.5 (1.7) 16.1 (2.5) 16.5 (1.6) 16.7 (1)
N 1.5 (11) 1 (9) 1.5 (10) 1 (9) 1.5 (9) 1 (48)
∆TF [◦C] 2.1 (1.1) 3.4 (1.9) 3.6 (3.3) 3.1 (2.7) 2.6 (2.4) 3.0 (2)
∆tF[min] 6.6 (1.5) 8.8 (3.2) 7.6 (5.5) 6.2 (3.8) 4.5 (3.6) 6.7 (3)
NORMPOST
TF,avg[◦C] 12.0 (1.1) 10.7 (1.4) 11.8 (1.7) 11.3 (1.4) 11.0 (1.1) 11.4 (1.2) TF,min[◦C] 10.1 (0.8) 8.9 (0.9) 9.5 (0.9) 9.2 (0.6) 9.0 (0.3) 9.3 (0.6) TF,max[◦C] 17.1 (3.4) 15.6 (3.8) 16.8 (3.1) 16.0 (2.3) 14.8 (2.2) 16.1 (2.7)
N 1 (8) 1 (7) 1 (9) 2.5 (14) 2 (13) 1 (51)
∆TF [◦C] 1.8 (1.5) 2.7 (2) 3.0 (2.9) 2.6 (2.1) 3.0 (1.5) 2.6 (1.8)
∆tF[min] 4.8 (4.1) 6.6 (4.7) 7.2 (5.1) 6.8 (3.4) 5.9 (2.1) 6.3 (3.5)
Values are mean (SD). Values for CIVD are median (total incidence). F1: Thumb; F2: Index finger; F3: Middle finger; F4: Ring finger; F5: Small finger.
Cardiovascular responses. Both SAP [BL: NORMPRE= 123 (9) mmHg, NORMPOST
= 121 (10) mmHg; B-WI: NORMPRE = 114 (9) mmHg, NORMPOST = 108 (14) mmHg; H-CWI: NORMPRE= 116 (8) mmHg, NORMPOST = 111 (12) mmHg; H- RW: NORMPRE= 113 (7) mmHg, NORMPOST= 110 (10) mmHg; B-RW: NORMPRE
= 121 (9) mmHg, NORMPOST = 120 (14) mmHg] and DAP [BL: NORMPRE = 74 (7) mmHg, NORMPOST = 72 (10) mmHg; B-WI: NORMPRE= 63 (7) mmHg, NORMPOST = 59 (9) mmHg; H-CWI: NORMPRE = 64 (7) mmHg, NORMPOST = 60 (8) mmHg; H-RW: NORMPRE= 62 (6) mmHg, NORMPOST= 60 (7) mmHg; B- RW: NORMPRE= 70 (8) mmHg, NORMPOST= 68 (10) mmHg] were similar across the two trials (P > 0.10).
MAP did not differ between the trials during the BL [NORMPRE= 91 (8) mmHg, NORMPOST= 89 (10) mmHg; P = 0.49] and the B-WI [NORMPRE= 81 (7) mmHg, NORMPOST = 75 (12) mmHg; P = 0.12] phases. However, during the H-CWI phase, the cold-induced increase in MAP was diminished in 5 out of 6 subjects in the NORMPOSTtrial (P = 0.14; Figure 3.10).
BL HR was similar between the trials [NORMPRE= 70 (6) mmHg, NORMPOST
= 65 (6) mmHg; P = 0.10]. During the NORMPOST, HR was reduced in the B-WI [NORMPRE= 73 (5) mmHg, NORMPOST= 67 (5) mmHg; P = 0.04] and the B-RW phases (P = 0.02; Figure 3.11), and tended to be reduced in the H-CWI phase (P = 0.09; Figure 3.11).
Figure 3.10. Mean (SD) and individual (grey, dotted lines) mean arterial pressure (MAP) during the 30-min hand cold water immersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (NORMPRE) and after (NORMPOST) the 5-day acclimation protocol.
Figure 3.11. Mean (SD) and individual (grey, dotted lines) heart rate (HR) during the 30- min hand cold water immersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (NORMPRE) and after (NORMPOST) the 5-day acclimation protocol. *Significantly different from the pre-acclimation trial.
Perceptions. During the B-WI phase of both trials, the right hand was perceived somewhat warm [NORMPRE= 5 (4 – 6), NORMPOST = 6 (4 – 6); P = 0.61], ther- mally comfortable [1 (1 – 1)], and pain-free (0). During the H-CWI, H-RW and B-RW phases, the thermal sensation in the hand was not altered in NORMPOST(P >
0.20; Figure 3.12). The cold-induced thermal discomfort was somewhat attenuated during the NORMPOST H-CWI phase (P = 0.11; Figure 3.13). The cold-evoked pain during the H-CWI phase did not change (P = 0.25; Figure 3.14).
Figure 3.12. Median (range) hand thermal sensation during the 30-min hand cold water im- mersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (NORMPRE) and after (NORMPOST) the 5-day acclima- tion protocol.
Figure 3.13. Median (range) hand thermal comfort during the 30-min hand cold water im- mersion phase (H-CWI), the 15-min hand rewarming phase (H-RW), and the 30-min body rewarming phase (B-RW) before (NORMPRE) and after (NORMPOST) the 5-day acclima- tion protocol.
Figure 3.14. Median (range) hand pain during the 30-min hand cold water immersion phase (H-CWI) before (NORMPRE) and after (NORMPOST) the 5-day acclimation protocol.
Discussion
The present study aimed to assess whether a short-term, high-intensity cold accli- mation protocol would modulate finger vasomotor (i.e., TF, CIVD) and thermo- perceptual responses to localized cooling. To address this question, six healthy men completed, within a week, five daily 2-h static, whole-body immersions in 14◦C wa- ter. To isolate any confounding influences derived from local thermal stress during the adaptation process, the area of interest (i.e., the right hand) was consistently kept at TF of 35.6◦C with a temperature-controllable glove; this was also confirmed by the regional thermo-perceptual responses of the subjects – despite being immersed in 14◦C-water, they perceived their right hand slightly warm, thermally comfort- able, and pain-free in all five sessions. Before and after the acclimation protocol, the subjects’ right hand was exposed to a cold stimulus (hand immersion in 8◦C wa- ter), while they were rendered either mildly hypothermic (whole-body immersion in 21◦C water) or normothermic (whole-body immersion in 35.5◦C water). Thermal, cardiorespiratory, and perceptual responses were monitored throughout the trials.
The 5-day acclimation protocol resulted in hypothermic adaptation (i.e., habit- uation; [2, 30, 31, 32]), which was characterized by a modest reduction in shiver- ing and an attenuation of whole-body thermal discomfort. The main finding of the present work, however, was that the 5-day whole-body cold acclimation protocol did not alter finger temperature and CIVD responses during local cold stress, regardless of subjects’ thermal status. Yet, after the acclimation, the cold-induced increase in MAP was reduced during both the HYPO and NORM H-CWI phases. Furthermore, the perceived thermal discomfort and pain in the immersed hand appeared to be al- leviated in the post-acclimation HYPO and NORM trials, even though the thermal status of the finger was not influenced by the acclimation protocol. Due to the rel- atively small sample size (n = 6), present data are discussed with some liberty, and are based not only on the detected statistical significances (P ≤ 0.05), but also on the observed statistical tendencies (0.05 < P < 0.09).
24
4.1 Effect of acclimation on finger temperature responses to localized cooling
It is evident that the incidence and magnitude of the CIVD response was largely determined by the whole-body thermal status of the subjects. CIVD was more pro- nounced in the NORM than in the HYPO trials; the total incidence of CIVDs was
∼550% higher in NORM than in HYPO. This finding is in line with the results from previous studies, demonstrating that the CIVD response is greater when the body core temperature is elevated (i.e., hyperthermic state), and, conversely, is attenu- ated when the body core temperature is low (i.e., hypothermic state) [10, 11, 12, 33]. Additionally, and in accordance with previous studies [7, 8, 9], a high inter- and intra-individual variability in the CIVD response was observed, given that its incidence and magnitude varied between individuals and amongst the fingers of the hand: for instance, the total incidence of CIVDs ranged from 7 in subject 3 to 43 in subject 4, and it ranged from 20 in finger 2 to 27 in finger 5.
Findings regarding the effect of whole-body acclimation on CIVD are limited to those derived from population and field (i.e., acclimatization) studies. Population studies (see Appendix A.2.1) have indicated that individuals residing in cold envi- ronments, such as Arctic residents (e.g., Inuit and Sami), may exhibit an enhanced CIVD amplitude [13], an earlier CIVD onset [16] and an increased finger skin tem- perature [14] than individuals residing in temperate conditions. On the other hand, acclimatization studies (see Appendix A.2.2) have provided more equivocal findings.
Some studies have observed that individuals that are exposed to low-temperature en- vironments in a long-term repeated manner (e.g., fishermen or military personnel), often have enhanced skin blood flow and warmer extremities during local cold provo- cations [15, 16, 17], while others have failed to detect any differences [34, 35], or have found that CIVD might be diminished [36, 37]. These ambiguous findings can be explained, to a large extent, by the methodological limitations of those studies.
For instance, the ratio between whole-body and local cold exposure, the intensity of cold stress employed, and the contribution of several confounders (e.g., exercise, nu- trition, sleep) had not been controlled. For these reasons, the present study applied a closed-loop protocol, in which the right hand was isolated and kept warm during the cold acclimation sessions, while the body core temperature was manipulated in a controlled environment (i.e., fixed water and room temperatures).
Previously, O’Brien et al. [21] have reported that the finger CIVD response was suppressed after a 5-week whole-body cold acclimation protocol, during which sub- jects were immersed into 20◦C water for 1 h per day. Apparently, their findings are not supported by those derived from the present study, given that the employed 5- day acclimation protocol failed to alter the CIVD response. The total incidence of CIVD events decreased from 13 in HYPOPREto 5 in HYPOPOST, but the difference was not statistically significant (P = 0.19); whereas no changes in the total number of CIVDs were observed in the NORM trials. However, the discrepancy between the
two studies might be explained by the different methodologies applied. Namely, in this study, subjects immersed their whole hand (to the radial styloids) in 8◦C water, while, in the study of O’Brien et al. [21], subjects immersed only the middle fin- ger (to the middle phalanx) into 4◦C water. In addition to the differences regarding the local cold provocation trials, the employed acclimation protocols also differed between the two studies. The present study used 14◦C water immersions for five consecutive days, whereas O’Brien et al. [21], used 20◦C water immersions for 5 consecutive weeks. Thus, although the cold stimulus was higher in the present study, the total duration of the intervention was seven times longer in the study by O’Brien et al. [21]. It is interesting that the authors observed an insulative whole-body adap- tation, described by an enhanced peripheral vasoconstriction, which was associated with an elevated sympathetic response [i.e., increased circulation of norepinephrine (NE)] to cold. In contrast, in this study, most likely due to the shorter overall du- ration of the intervention, a hypothermic whole-body adaptation was ensued from the 5 repeated cold exposures [2, 30, 31, 32, 38]. This adaptation was characterized by the reductions in the shivering response and the cardiovascular stress response to cold (judging from MAP and HR), but by an unaltered peripheral vasomotor reactiv- ity. Lastly, in the study by O’Brien et al. [21], the testing hand was also immersed in the 20◦C water during the acclimation sessions, which might have also contributed to the discrepancy between the studies.
The consistent attenuation of the cold-induced increase in MAP observed during the post-acclimation H-CWI phases indicates a general reduction in sympathetic ac- tivation. This was also supported by the decline in HR, especially in the NORMPOST
trial, and perhaps by the lower degree of hyperventilation in the HYPOPOST trial.
These findings seem to be consistent with the responses associated with the hypother- mic mode of whole-body adaptation, and indeed suggest a reduction of sympathetic drive in response to localized cooling [39, 40].
It is noteworthy, however, that, despite the acclimation-related reduction in the general sympathetic discharge, the finger thermal responses (i.e., TFand the CIVD) to the localized cold stress remained unaffected. Thus, in both whole-body ther- mal states, the magnitude of finger vasoconstriction to cold appeared to be mediated primarily by local factors (see Appendix A.1.2.1), rather than by the amount of over- all sympathoactivation. Both animal [41] and human-clinical [42, 43] experiments have indicated that CIVD depends not solely on the general sympathetic activity, but also on local reflexes that modulate cutaneous vascular tone [44]. Moreover, it is well established that arterio-venous anastomoses (AVAs) play a key role in the incidence of CIVD [45, 46, 47]. AVAs are shunts with thick muscular walls, which, when they open, allow large amounts of blood to pass directly from the arterioles to the venules. AVAs, which are solely innervated by sympathetic vasoconstrictor nerves [48], appeared not to have allowed more blood to flow, despite the decrease in sympathetic tone; an observation that confirms that AVAs are autoregulated [49]
and probably their function had not been modulated by the current acclimation pro-
tocol. Thus, although the underlying mechanisms of CIVD response remain unclear by the present study, it is further confirmed that peripheral cutaneous blood flow and temperature during localized cold exposure is dependent on both local and central influences, and the relative contribution of each component may vary in different conditions (cf. [50]).
4.2 Effect of acclimation on finger thermo-perceptual responses to localized cooling
In agreement with previous studies, it appears that the perceptual responses to cold are indeed dependent on the whole-body thermal status [51, 52, 53]. Subjects felt more pain and regional discomfort during the hand cold provocation in the HYPO than in the NORM trials. However, whether these subjective thermo-perceptual re- sponses were mediated by independent changes in Tskand/or Trecremains unknown.
The thermal discomfort in response to the localized cooling decreased in both the HYPO and NORM trials. This is interesting, since even though no changes in TF were noted after the acclimation, the hand thermal discomfort was attenuated, and the pain was decreased in 5 out of 6 subjects during the local cold provocation.
These findings are in line with previous studies observing a reduction in thermal dis- comfort and pain after repeated local (e.g., hand) exposures to cold [54, 55]; which often are not associated with any coincident changes in the thermal status of the immersed region [20]. Previous studies have also observed that the habituation of thermal sensation to local cold stimuli can occur already after the first cold exposure [56], and can also be observed after repeated cold showers [57]. Still, as supported by the present study, these modifications can be induced in regions that are not di- rectly exposed to cold during the intervention process; the right hand was maintained at 35.6◦C, and subjects were free from any regional thermal discomfort or pain dur- ing the acclimation. Moreover, given that, during the post-acclimation local cold provocations, the peripheral sensory input was unchanged (i.e., similar TF), as well as the internal body temperature [29], the alleviated thermal discomfort and pain were attributable to a central adaptation induced by the repeated whole-body cold exposures.
Interestingly, after the acclimation, subjects perceived their whole body to be warmer, and the overall affective valence was enhanced, especially in the HYPO trial; observations that are in line with those typically detected in conditions of whole-body habituation (cf. [58]). Therefore, it might be argued that the enhanced overall perceptual ratings might have, to some extent, influenced the regional per- ceptual responses, and thus biased the subjects’ ratings to local cold.
4.3 Methodological considerations
Delimitations. In the present study, only men aged between 24 to 28 years were tested. All subjects were non-smokers, aerobically fit and healthy (i.e., no vascu- lar pathologies, no history of cold injuries, normotensive); delimitations that aimed to limit the influence of non-thermal factors on thermoregulation (see Appendix A.1.2.2) and to reduce the inter-individual variability. Furthermore, cold water was chosen as a cooling medium for both the acclimation protocol and the testing ses- sions. However, it remains unknown whether the responses would be similar during a cold-air acclimation protocol, or during a cold-air local cold provocation.
Limitations. First of all, the small sample size does not allow to draw any firm conclusions – this was also evident in the statistical analyses. The initial goal was to test 8 subjects, which would have powered the analyses; yet the experiments had to be stopped due to the COVID-19 pandemic. Furthermore, no diary was kept ensuring whether subjects followed the recommendations regarding sleep, fluid and food consumption prior to each session and trial. Moreover, one subject, who was a slight smoker, participated in the study. Although smoking might have influenced his vasomotor reactivity to cold [59, 60], his responses conformed to those obtained by the majority of the subjects.
It is also possible, that the employed acclimation protocol was too short to induce any autonomic adaptations. For a deeper understanding of this, additional important variables, such as the heart rate variability (HRV) or NE levels could have been mon- itored and analyzed. Furthermore, it is possible that the 8◦C water during the local provocation was a too strong cold stimulus overriding any adaptive response. Other limitations arise from the instrumentation used. For instance, the thermocouples were attached to the skin with surgical tape, and thus, the measured temperature value might have been a combination of skin and water temperature rather than just the desired skin temperature. Also, the Finometer measures cardiovascular variables only indirectly, based on the unloaded diameter of the finger artery, which may be influenced by changes in hematocrit or stress, and thus negatively influence the accu- racy of the measurement [61, 62]. As mental stress, in general, is known to enhance vasoconstriction [18, 63], it might have influenced the subjects vasomotor tone as they were anticipating the cold stimulus before being exposed to it; this mental stress might have been lower in the second than in the first trial, since subjects knew what to expect. Furthermore, the rectal temperature, which was used as an index of the body core temperature, is a relatively slow indicator, and it might be affected by the body position and the abdominal blood flow [64]. The same holds for the finger skin temperature, which can also be considered a slow indicator of reactions on the tissue level; blood flow appears to precede finger skin temperature by more than a minute [11].
4.4 Practical perspectives
The present study indicates that a 5-day, high intensity cold acclimation protocol is unable to modulate finger temperature responses to localized cooling. Thus, it might be argued that this specific acclimation protocol is insufficient to minimize the risk for local cold injuries in the fingers. Yet, the employed protocol was able to alleviate the thermal discomfort induced by the local cold stimulus. However, such an adaptive response might be considered counterintuitive and possibly even dangerous; subjects might be persuaded to endure the localized cooling for a longer time, despite the low peripheral skin temperature, thereby increasing the risk for cold injuries. Nonetheless, due to the above stated methodological considerations of the study, these suggestions have to be interpreted with caution.
4.5 Future studies
Future research should examine the effects of different acclimation protocols with a more severe whole-body thermal stimulus (e.g., a lower water temperature) and/or a longer duration (e.g., for several weeks) on finger temperature responses. Further- more, the influence of non-thermal factors on CIVD (e.g., age, gender, ethnicity, and physical fitness; see Appendix A.1.2.2), as well as any limb-related differences (i.e., between hand and feet, or between left and right limb) should be investigated. Ad- ditionally, more variables should be monitored, such as HRV, NE, and blood flow measurements. Lastly, a larger sample size, as well as a control (either a control group, or the contralateral (i.e., non-acclimated) hand [7]), may help clarifying any observed effects.
Conclusions
The present study demonstrated that a 5-day, whole-body cold acclimation protocol does not alter finger thermal responses to localized cooling, despite that the general sympathetic response to cold appeared to be attenuated after the acclimation. More- over, such a brief, high-intensity whole-body cold acclimation seems to mitigate the regional perception of thermal discomfort and pain induced by local cooling.
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