The increased physiological load and reduced performances noted during prolonged exercise in the heat are well documented (9,11). Further, the ergogenic benefits of precooling before exercising in hot conditions are also well established (17,28). Despite these findings, not all precooling studies have demonstrated an improvement in exercise performance, particularly during prolonged intermittent-sprint exercise (7,8), and as yet, the mechanisms relating to the ergogenic qualities of precooling remain equivocal (17,25). In addition, with the relatively more recent use of self-paced exercise protocols (14,26), the proposed mechanisms relating to performance improvements from precooling have been hypothesized to include alterations in muscle recruitment and the pacing strategies adopted rather than a direct response to the reduction in cardiovascular or thermoregulatory load per se (14,26).
Precooling procedures can be loosely classified as those designed to reduce skin temperature (ice vests, cold towels, sprays) or to reduce skin and muscle/core temperature (cold-water immersion, cold rooms, cold showers) (17). It is proposed that a longer and larger cooling stimulus will result in larger physiological perturbations and greater performance improvements (26), although the two are not necessarily directly linked (6,12,14). Traditionally, the ergogenic benefits of precooling were highlighted as a reduction in cardiovascular load, improved oxygen supply, and reduced accumulation of anaerobic metabolic products (16,24). However, the use of constant-intensity exercise protocols somewhat skewed these conclusions and also lack the ecological validity for the application to athletic environments. Research incorporating self-paced intermittent and continuous protocols has reported improved performances, without significant differences in HR, V˙O2, anaerobic metabolic markers, or end-exercise body temperatures (2,10,26). Accordingly, the mechanisms relating to improved exercise performance after precooling have been postulated to include the prevention of the heat-induced down-regulation of muscle recruitment (8,14,17), the prevention of the reduction in peak evoked torque and fiber recovery time (17,31), or the prevention of contractile force inhibition due to thermal sensory feedback (1,25). However, despite these proposed mechanisms, to date no research has provided evidence to show how precooling may be ergogenic for exercise in the heat.
Recent research has proposed that exercise in the heat results in the self-selection of lower exercise intensities (pacing), possibly resulting from a reduction in muscle recruitment or contractile function (18,21). Accordingly, the suppression of preexercise core temperatures via precooling may promote the ensuing selection of higher exercise intensities (2,14). Despite this proposition relating to pacing strategies, there is little evidence to substantiate whether and when pacing strategies are altered and, further, whether these alterations result from postcooling changes in contractile function. Accordingly, the aim of this study was to investigate the effects of precooling on pacing strategies during self-paced endurance exercise and, further, to determine the effect of precooling on voluntary and evoked contractile function and the ensuing effect on exercise performance.
Eight male, moderate- to well-trained cyclists (age = 24.8 ± 3.3 yr, height = 178.3 ± 8.0 cm, body mass = 76.1 ± 2.7 kg, sum of seven skinfolds = 54.4 ± 10.9 mm, and lactate threshold (LT) = 221 ± 42 W) volunteered to participate in this study. Participants were club and regional standard cyclists who trained multiple times a week, competing in regional competitions, and were familiar with the physical demands of set distance or duration time trials. All participants gave verbal and written consent to engage in all testing procedures, and human ethics clearance was granted by the institutional ethics committee.
Subjects performed three testing sessions, including an initial session to measure anthropometric characteristics and LT and to ensure familiarity with all equipment, procedures, measures, and the exercise protocol. The two following sessions involved the completion of either a precooling intervention or a control condition (no cooling) before a 40-min cycling time trial in hot conditions (33 ± 0.8°C and 50% ± 3% relative humidity) in an environmental chamber (WatFlow control system; TISS, Hampshire, UK) without any additional convective airflow (fan). The two time trial conditions were performed in a randomized, crossover design and involved identical procedures apart from the implementation or lack of a precooling intervention. Most subjects had prior familiarity with the time trial, having completed similar testing sessions previously. However, those subjects who had not recently undergone a 40-min time trial test performed a familiarization session of the trial before any testing. All testing sessions were performed at the same time of day, separated by at least 4 d of recovery. Participants were required to abstain from strenuous physical activity and the ingestion of alcohol for 24 h before testing and all caffeine and food substances 3 h before testing. In addition, participants recorded all food consumed and activity performed in the 48 h before the first testing session and were required to replicate these for the ensuing session.
Familiarization Session and Graded Exercise Test
On arrival, anthropometric data were collected, including age, height (Detecto® Physicians Scales; Cranlea & Co., Birmingham, UK), body mass (SECA 778; Seca GmbH & Co., Hamburg, Germany), and sum of seven skinfold thickness (biceps, triceps, subscapular, abdominal, suprailiac, quadricep, and calf; Harpenden Skinfold Callipers; British Indicators, West Sussex, UK). After collection of anthropometric data, a graded exercise test was performed to determine LT using an SRM cycle ergometer (SRM, Welldorf, Germany) and an associated software (SRM Training Software, version 6.40.07). The SRM ergometer hertz offset was corrected at zero load before each testing session according to the manufacturer's recommendations. The exercise protocol consisted of 3-min stages commencing at 95 W and increasing by 25 W each stage. In the last 30 s of each stage, a capillary blood sample was obtained from a finger tip to measure lactate ([La−], YSI 2300 Stat Plus; Analox, Sheffield, UK). The test was complete once blood [La−] concentration showed a sudden, sustained increase of at least 1.0 mmol·L−1, with LT calculated as the power output associated with a 1.0-mmol·L−1 increase above resting values (13). Testing procedures to determine LT were conducted under normothermic laboratory conditions (22.0 ± 1.0°C). As most subjects had prior and recent familiarity with the time trial procedures, after a sufficient recovery from the graded exercise test (GXT), only those who had not recently performed the 40-min trial completed a familiarization of the time trial.
During both testing sessions, participants performed a 5-min warm-up and a 40-min self-paced cycling time trial on a customized cycle ergometer (620 Ergomedic; Monark, Varberg, Sweden) fitted with power measuring cranks (Pro Track, 8; SRM) connected to an SRM recording device (SRM Power Control V) that continuously recorded power and cadence at a frequency of 1 Hz. The warm-up was performed in the climate chamber and consisted of unweighted cycling at a standardized cadence of 60 RPM. During the trial, participants were blind to performance measures (power or cadence); however, they were aware of elapsed time because of the recording of measures every 5 min. Exercise intensity during the respective trials was regulated by the adjustment of cadence to alter power output. Performance was determined from both overall mean and minute-by-minute power outputs completed over the 40-min trial. Further, total distance was estimated on the basis of the second-by-second power output, cadence, and flywheel circumference. Standard cycling apparel was worn by all subjects, with the clothing worn standardized between respective conditions.
To standardize hydration status, participants ingested 500 mL of water 60 min before arrival at the laboratory. On arrival for each testing session, participants voided their bladder to provide a urine sample for measurement of urine specific gravity (URICON-NE 2722; Atago Co., Ltd., Tokyo, Japan) and osmolality (Osmocheck™; Vitech Scientific Ltd., West Sussex, UK) as measures of preexercise hydration status. Further, towel-dried nude mass was measured before and after the 40-min time trial on a set of calibrated weigh scales as a measure of nonurine fluid loss. No fluid was consumed by participants during either condition.
Core, skin, muscle, and body temperature.
After measurement of nude mass, participants inserted a rectal thermometer (Henley single use temperature probe, 4491H; Henleys Medical Supplies Ltd., Herts, UK) 10 cm past the anal sphincter to measure core temperature. Skin thermistors (EUS-U-VS5; Wessex Power Technology, Poole, UK) were attached under cycling apparel to the midpoint of the right pectoralis major and exposed skin of the midpoint of the right triceps brachii lateral head, right rectus femoris, and right gastrocnemius lateral head and connected to a 1000 series, 8-bit squirrel meter logger (Grant Instruments Ltd., Cambridge, UK) to record skin temperature. Core and skin temperature measures were recorded before cooling, every 5 min during the preexercise intervention, after the warm-up, and every 5 min during the time trial. Mean skin temperature (MST) was calculated on the basis of the equation of Ramanathan (27), MST = 0.3Tch + 0.3Ta + 0.2Tt + 0.2Tl, where Tch is the chest temperature, Ta is the arm temperature, Tt is the thigh temperature, and Tl is the calf temperature. In addition, mean body temperature (Tb) was calculated on the basis of the equation Tb = (0.87 × core temperature) + (0.13 MST) (5). A 2-g sample of an anesthetic cream (EMLA™ Cream 5%; AstraZeneca Ltd., Bedfordshire, UK) was applied to the right vastus lateralis muscle 30 min before measurement of resting muscle temperature. With participants seated with the lower leg supported at 90°, a needle (18 G 1.5 inches; BD Microlance 3, Drogheda, Ireland) and a sterile, flexible muscle temperature probe (medical precision thermometer; Ellab, Copenhagen, Denmark) were inserted 4 cm into the belly of the vastus lateralis until a constant temperature was recorded. After removal of the needle, pressure and small adhesive bandage were applied to the entry site to prevent bleeding. Muscle temperature was recorded before and after both preexercise intervention and time trial.
HR and perceived exertion and thermal stress.
HR was measured with a chest monitor and telemetric receiver (Accurex Plus; Polar Electro Oy, Kempele, Finland). RPE and rating from the thermal sensation scale (TSS) were obtained on the basis of a 10-point CR-10 Borg scale (4) and an eight-point (32) Likert scale, respectively. HR, RPE, and TSS measures were recorded before cooling, every 5 min during the preexercise intervention, after the warm-up, and every 5 min during the time trial.
Capillary blood measures.
A sample of capillary blood was obtained from a fingertip with a sterilized lancet to measure [La−] and glucose (Glu) concentrations (YSI 2300 Stat Plus; Analox). Blood samples for the measurement of [La−] and Glu were obtained at rest before cooling, postcooling, after warm-up, and postexercise.
Voluntary and evoked twitch contractile properties.
Voluntary and evoked twitch properties of the right knee extensors were assessed using repeated isometric contractions against a stable tension load cell (Model 616, RS Components; Tedea Huntleigh, Cardiff, UK) linked to a host computer and data acquisition and analysis system (Spike2 v3.21; Cambridge Electronic, Cambridge Design, Cambridge, UK). During testing, participants were seated upright with the knee flexed at 90° (0° being full extension) and secured to the dynamometer via waist and shoulder straps. Muscle activation was achieved by stimulation of the quadriceps using two 110 × 80-mm reusable electrodes positioned on the anterior surface of the right thigh, 2 cm above the superior border of the patella and 1 cm below the inguinal fold. The current was delivered by a Digitimer DS7AH stimulator (Digitimer, Welwyn Garden City, England) using a single square-wave pulse with a width of 200 μs (400 V with a current of 150-800 mA). Initially, the current was applied in incremental steps until peak twitch force (Pf) was attained. After this, stimulus intensity was increased by a further 10% to ensure that supramaximal stimulation was achieved. Four pulses each separated by 10 s were delivered at a current of 500-600 mA in a resting state. For analysis, twitch force was averaged over all four evoked contractions with the mean used to determine Pf, defined as the highest isometric force value achieved during the evoked contraction. After evoked twitch assessment, maximal voluntary contraction (MVC) performance testing consisted of 10 × 5 s of maximal isometric trials, where participants were instructed to exert maximal effort throughout each contraction, with a recovery of 5 s between efforts. MVC was defined as the highest isometric force value achieved during the voluntary contraction. Further, on the first three contractions, a superimposed twitch was delivered after the initial plateau of MVC (after 2 s) to measure superimposed force (SIF). SIF was determined as the mean of the highest isometric force values achieved during all superimposed contractions. Voluntary and evoked measures were obtained before the cooling intervention, after cooling and postexercise.
After recording of all resting measures, participants performed either the precooling or the control interventions. The precooling procedure involved immersing the lower body to the level of the greater trochanter in 14 ± 0.3°C water for 20 min. This procedure was achieved by participants standing in an environmental tank filled with cool water located outside the chamber in ambient laboratory conditions of 22 ± 1.0°C. In addition, after postcooling MVC measures, cooling of the quadriceps and hamstrings were maintained during the warm-up via the application of thin, gel-based cold packs (3M; Boots, Nottingham, UK), weighing no more than 800 g in total per leg, and were held in place with tubular bandaging (Boots). The packs were removed from a −16°C freezer and placed between layers of the bandaging around the thigh, with three packs on the quadriceps and three packs on the hamstrings for each leg. The ice packs and the bandages were removed before recording of post-warm-up measures. During the control condition, participants stood in the environmental chamber for 20 min and received no cooling during the warm-up. The duration between the completion of the intervention and the warm-up was 8-10 min, whereas the duration between the cessation of the warm-up and the start of the time trial was less than 5 min.
Data are reported as mean ± SD. Respective paired-samples t-tests were used to compare between conditions for mean power output, percentage of LT, distance covered, and body mass. For all other performance and physiological measures, a two-way (condition × time) repeated-measures ANOVA was used to determine the main effects between the two conditions (cooling vs control). Post hoc paired t-test analyses with Bonferroni corrections were performed to determine the location of significant differences. Significance was set at P ≤ 0.05.
Precooling resulted in a significantly greater mean power during the 40-min time trial (198 ± 25 vs 178 ± 26 W for precooling and control, respectively; P = 0.05). There was no significant main effect present (P = 0.25) for minute-by-minute power output; however, differences in minute power output between conditions were present during the last 10 min of the time trial, specifically the 29th-33rd and the 37th-40th min, when a significantly increased power output was produced in the cooling condition (P < 0.02; Fig. 1). Further, the overall mean power output represented the maintenance of a higher percentage of LT during the cooling condition (88% ± 9% vs 78% ± 9% for precooling and control, respectively; P = 0.05). Finally, a significantly greater distance was estimated for the precooling condition (19.3 ± 1.3 vs 18.0 ± 1.4 km for precooling and control, respectively; P = 0.05).
Physiological and perceptual.
Preexercise hydration status was not significantly different between conditions for either urine specific gravity (1.025 ± 0.022 vs 1.015 ± 0.008; P = 0.30) or urine osmolality (611 ± 217 vs 595 ± 290 mOsm·L−1; P = 0.40) for cooling and control conditions, respectively. The change in body mass after the time trial, representing nonurine fluid loss, was significantly smaller (by 300 mL) in the precooling condition (0.8 ± 0.2 vs 1.1 ± 0.2 kg for precooling and control, respectively; P = 0.05).
Core, skin, muscle, and mean body temperature data are presented in Figure 2. Significant main effects were present for a reduction in core (P = 0.04), mean skin (P = 0.01), mean body (P = 0.01), and muscle (P = 0.01) temperatures, respectively. The lower-body precooling intervention did not reduce core temperature at the start of exercise (P = 0.25); however, it did suppress core temperature until the 20th minute of the time trial (0.2 ± 0.1°C; P < 0.05). Despite a blunted initial rise in core temperature after precooling, there were no differences between conditions after the 20th minute of exercise (P > 0.05). Both skin and mean body temperatures were significantly reduced in the precooling condition during the intervention and the warm-up and until the 20th minute of the time trial (1.0-3.0°C; P < 0.05). Muscle temperature was also significantly reduced after the cooling intervention and before exercise in the cooling condition (10 ± 2.0°C; P < 0.01).
Results for HR, RPE, TSS, and capillary blood measures are presented in Table 1. No significant main effects were present for HR (P = 0.61) or RPE (P = 0.81) measures. HR was not significantly different between conditions during the intervention, warm-up, or time trial (P > 0.05). Similarly, RPE was also not different between conditions during the exercise protocol (P > 0.05). However, a main effect was present for TSS (P < 0.01), with significantly lower values in the precooling condition during the intervention and until the 20th minute of the time trial (P < 0.05). Capillary blood measures of [La−] and Glu were not significantly different preintervention (P > 0.05); however, postintervention and preexercise [La−] values were significantly lower (P = 0.04) in the cooling condition. Finally, there were no differences (P > 0.05) between conditions in preexercise or postexercise Glu or postexercise [La−] values.
Voluntary and evoked muscle properties.
No significant main effects were present for MVC (P = 0.65), SIF (P = 0.60), or Pf (P = 0.42). MVC and SIF were significantly reduced postexercise in both conditions (P = 0.03-0.05; Fig. 3); however, there were no significant differences between the respective conditions preexercise or postexercise (P > 0.05; Fig. 3). In contrast, Pf was not significantly reduced postexercise in either condition (P > 0.05; Fig. 3); however, again there were no significant differences between the respective conditions preexercise or postexercise (P > 0.05; Fig. 3). Interestingly, neither preexercise intervention significantly affected (P > 0.05) postintervention voluntary or evoked force production; however, nonsignificant tendencies (P = 0.20-0.80) were noted in reduced Pf after exposure to cooling and in smaller MVC and SIF after exposure to hot environments.
The implementation of a 20-min lower-body precooling intervention improved 40-min cycling time trial performance compared with the control condition. The precooling intervention reduced muscle, skin, and mean body temperature at the start of the time trial and blunted the rise in core temperature during the first 15 min of exercise. Further, a reduction of nonurine fluid loss was evident in the precooling condition, indicating the potential maintenance of a larger blood volume. Despite a reduced thermal load in the precooling condition, the intervention had no effect on voluntary or evoked force production at the start of exercise. Further, although core and muscle temperature were initially reduced after precooling, MVC was maintained, and the early selection of exercise intensity was similar between conditions. However, performance was improved in the cooling condition during the later stages of the time trial, and of the physiological measures recorded, only nonurine fluid loss differed between conditions.
The present study supports previous findings on the ergogenic benefits of precooling for endurance exercise (3,12,26). Previous studies have reported similar results in self-paced exercise, with a 900-m improvement in performance for a 30-min cycling time trial (14), a 12-W increase in mean power during the 20-min variable-intensity portion of a 40-min cycling trial (26), and a 13-s improvement for a 5-km (19 min) running trial (2). Further, as with the present study, these studies reported the blunting of core and skin temperatures, a reduction in sweat loss, and the reduction in perceived thermal stress. Moreover, as with the present data, most physiological differences between conditions had disappeared by the end of the respective protocols. Collectively, these data, in addition to studies using constant-intensity exercise (16,17,24), highlight the performance improvements after precooling for endurance exercise in the heat. Despite these ergogenic benefits of precooling, few studies have described the pacing or selection of exercise intensity throughout the exercise bout to locate where or how precooling improves exercise performance.
The performance improvements in the precooling condition were not evident until the final 10 min of the time trial, by which time all measured physiological changes (apart from fluid loss) induced by precooling had dissipated. However, it must be noted that rather than cycling performance in the precooling condition being improved per se, it seems that the reduction in performance observed in the control condition was prevented in the cooling condition (17). Previously, Tucker et al. (34) have reported that compared with cool conditions, reductions in power output during the 20-km self-paced cycling trials in the heat occurred during the final 20% of the trial, without an abnormally increased core temperature. Accordingly, it seems evident that precooling interventions of sufficient volume or duration may delay the self-regulated reduction in exercise intensity apparent in the control condition. As such, in agreement with previous studies (2,14,26), precooling can have ergogenic benefits for prolonged endurance exercise in the heat, although to date the mechanisms remain equivocal.
The reason for the earlier reduction of exercise intensity in hot conditions remains the topic of some debate (20). Recent research has highlighted the role of the selective and protective reduction in neuromuscular recruitment based on the endogenous thermal strain (20,21,33). Further, this reduction in voluntary recruitment that results in a diminished exercise intensity may develop from either a sensory feedback (11,22) or an anticipatory avoidance of developing cellular harm (19,33). Moreover, other physiological perturbations may also collaborate to invoke a reduced recruitment or be directly responsible for the reduction in exercise intensity (20). Factors potentially responsible for the heat-induced reduction in exercise intensity include a build up of branched chain amino acids in the cerebral blood (23), a reduction in neural transmission or neurochemicals such as dopamine (21), a reduced supply of metabolically active substrates to the cerebrum (21), or any number of peripheral responses (blood volume and core temperature) inducing altered afferent feedback (11,22). As the mechanisms for heat-induced reduction in performance may be intensity and duration specific, the present data indicated an inability of participants to maintain a power output corresponding to 80%-90% LT at a time when the physiological responses were similar to those present at the same stage in the cooling condition.
Given the debate regarding mechanisms regulating exercise performance in the heat, the present study sought to determine the influence of precooling on contractile function and ensuing exercise performance. The precooling intervention reduced muscle temperature at the commencement of the time trial, with minimal alterations to voluntary or evoked force or starting exercise intensity. Together, these data suggest that the ergogenic benefits from precooling were not due to an improvement or maintenance in contractile element function. Given that an improved performance was present in the precooling condition, without changes in muscle contractile force properties, it is assumed that the maintenance of power output after precooling resulted from the sustained recruitment of exercising musculature (15). Although EMG measures were not recorded, the self-paced nature of exercise would have made the interpretation and comparison of these data between conditions difficult. Further, the reduction in EMG alongside power output during exercise in the heat has been previously reported (33). Nonetheless, there was no difference in postexercise MVC, SIF, or Pf, although the cooling condition maintained a greater mean power output by ≈20 W. As such, this may highlight evidence for a selective reduction in voluntary force in the heat that is ameliorated by precooling. In addition, the reduction in SIF in both conditions indicates the presence of some fatigue of peripheral origin and may further highlight that precooling may not act as a protective agent against mechanisms of peripheral fatigue.
Despite performance improvements after precooling, specifically during the final 10 min of the time trial, the only difference between conditions in measured physiological variables after 40 min was a reduced fluid loss in the cooling condition. The possible maintenance of an increased central blood volume (300 mL) due to a reduction in nonurine fluid loss after cooling is a common finding in precooling studies (2,14). Although 300 mL is comparable to results from these studies (200-500 mL [2,14]), it is arguable whether this volume would be sufficient in euhydrated cyclists to elicit reductions in performance. However, these results may suggest that the reduced physiological responses present in the precooling time trial acted to reduce the afferent feedback that would invoke a centrally mediated reduction in muscle recruitment (20). Alternatively, precooling may have allowed these familiarized participants to select a higher-exercise intensity based on a prediction of the ensuing requirement based on the blunted physiologically demands after precooling (18,33). Of interest is that although subjects rated the thermal comfort as lower preexercise, this in itself did not mediate an increased power output at the commencement of the time trial. Previous research highlights either feedback (11,22) or feed-forward (18,29) models regulating exercise in the heat; however, there is the possibility of a mixed-model response, whereby based on both the response to afferent feedback, combined with the knowledge of the required workload to be completed, muscle recruitment is regulated to both tolerate the thermoregulatory load yet optimize power output for the external demands of prolonged performance (21).
The altered physiological and perceptual responses induced by cooling may have resulted in the maintenance of exercise intensity not observed in the control condition. The combination of a slower rise in core and muscle temperature and a larger blood volume (reduced sweat rate) along with a lowered perception of thermal stress may delay the reduction in voluntary force recruitment (21,31,33). To highlight this, although postexercise MVC and SIF do not differ between conditions in absolute values, the reduction in voluntary force based on the amount of work performed is greater in the noncooling condition. The notion of a reduction in voluntary force is supported by previous evidence indicating that passive elevation of core temperature can reduce voluntary activation (19,30). Further, voluntary activation is returned to normal when the endogenous thermal stress is ameliorated (19,30). In relation to the present study, blunting the rise in the thermoregulatory load via precooling may act to delay the reduction in voluntary force and maintain power output. In addition, the reduced physiological (blood volume and core/muscle temperature) and perceptual load (RPE and TSS) resulting from precooling may also assist the self-selection of higher exercise intensities. As such, it is possible that alterations to both feedback and feed-forward mechanisms result from precooling to ensure the maintenance of exercise intensity in the heat.
In conclusion, a 20-min lower-body precooling intervention improved the 40-min cycling time trial performance in the heat. Further, the precooling intervention reduced the thermoregulatory and perceptual strain of the hot conditions, in particular, until the 20th minute of the time trial. However, performance benefits were only evident during the final 10 min of the trial, whereby the reduction in exercise intensity noted in the control condition was not present during the precooling condition, although the measured cooling-induced physiological benefits had dissipated. As a result, given the comparable reduction in postexercise voluntary force for a greater distance covered, is it possible that the advantages of precooling result from the prevention of the down-regulation of exercise intensity present in the heat. However, whether the prevention of the heat-induced reduction in exercise intensity results from either feed-forward or feedback based regulation or a combination of the two remains speculative.
This study was partly funded by a Charles Sturt University Special Studies Program grant. The research team would also like to state that the results of the present study do not constitute endorsement by the American College of Sports Medicine.
1. Amann M, Eldridge MW, Lovering AT, Stickland MK, Pegelow DF, Dempsey JA. Arterial oxygenation influences central motor output and exercise performance
via effects on peripheral locomotor muscle fatigue in humans. J Physiol
2. Arngrímsson SA, Petitt DS, Stueck MG, Jorgensen DK, Cureton KJ. Cooling vest worn during active warm-up improves 5-km run performance
in the heat. J Appl Physiol
3. Booth J, Marino F, Ward JJ. Improved running performance
in hot humid conditions following whole body precooling. Med Sci Sports Exerc
4. Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc
5. Burton AC. Human calorimetry. II. The average temperature of the tissues of the body. J Nutr
6. Castle PC, Macdonald AL, Philp A, Webborn N, Watt PW, Maxwell NS. Pre-cooling leg muscle improves intermittent sprint exercise performance
in hot, humid conditions. J Appl Physiol
7. Cheung SS, Robinson AM. The influence of upper-body pre-cooling on repeated sprint performance
in moderate ambient temperatures. J Sports Sci
8. Drust B, Cable NT, Reilly T. Investigation of the effects of the pre-cooling on the physiological responses to soccer-specific intermittent exercise. Eur J Appl Physiol
9. Drust B, Rasmussen P, Mohr M, Nielsen B, Nybo L. Elevations in core and muscle temperature impairs repeated sprint performance
. Acta Physiol Scand
10. Duffield R, Marino FE. Effects of pre-cooling procedures on intermittent-sprint exercise performance
in warm conditions. Eur J Appl Physiol
11. Gonzalez-Alonso J, Teller C, Anderson SL, Jensen FB, Hyldig T, Nielsen B. Influence of body temperature on the development of fatigue during prolonged exercise in the heat. J Appl Physiol
12. Hasegawa H, Takatori T, Komura T, Yamsaki M. Wearing a cooling jacket during exercise reduces thermal strain and improves endurance performance
in a warm environment. J Strength Cond Res
13. Jones AM, Doust JH. The validity of the lactate minimum test for determination of the maximal lactate steady state. Med Sci Sports Exerc
14. Kay D, Taafe DR, Marino FE. Whole-body pre-cooling and heat storage during self paced cycling performance
in warm humid conditions. J Sports Sci
15. Kay D, Marino FE, Cannon J, St Clair Gibson A, Lambert M, Noakes TD. Evidence for neuromuscular fatigue during high-intensity cycling in warm, humid conditions. Eur J Appl Physiol
16. Lee D, Haymes E. Exercise duration and thermoregulatory responses after whole body precooling. J Appl Physiol
17. Marino FE. Methods, advantages and limitations of body cooling for exercise performance
. Br J Sports Med
18. Marino FE. Anticipatory regulation and avoidance of catastrophe during exercise-induced hyperthermia. Comp Biochem Physiol B Biochem Mol Biol
19. Morrison S, Sleivert GC, Cheung SS. Passive hyperthermia reduces voluntary activation and isometric force production. Eur J Appl Physiol
20. Nybo L. Exercise and heat stress: cerebral challenges and consequences. Prog Brain Res
21. Nybo L. Hyperthermia and fatigue. J Appl Physiol
22. Nybo L, Nielsen B. Hyperthermia and central fatigue during prolonged exercise in humans. J Appl Physiol
23. Nybo L, Secher NH. Central perturbations provoked by prolonged exercise. Prog Neurobiol
24. Olschewski H, Bruck K. Thermoregulatory, cardiovascular, and muscular factors related to exercise after precooling. J Appl Physiol
25. Quod MJ, Martin DT, Laursen PB. Cooling athletes before competition in the heat. Comparison of techniques and practical considerations. Sports Med
26. Quod MJ, Martin DT, Laursen PB, et al. Practical precooling: effect on cycling time trial performance
in warm conditions. J Sports Sci
27. Ramanathan NLA. A new weighting system for mean surface temperature of the human body. J Appl Physiol
28. Reilly T, Drust B, Gregson W. Thermoregulation
in elite athletes. Curr Opin Clin Nutr Metab Care
29. St Clair Gibson A, Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med
30. Thomas MM, Cheung SS, Elder GC, Sleivert GG. Voluntary muscle activation is impaired by core temperature rather than local muscle temperature. J Appl Physiol
31. Todd G, Butler JE, Taylor JL, Gandevia SC. Hyperthermia: a failure of the motor cortex and the muscle. J Physiol
32. Toner MM, Sawka MN, Foley ME, Pandolf KB. Effects of body mass and morphology on thermal responses in water. J Appl Physiol
33. Tucker R, Rauch L, Harley YX, Noakes TD. Impaired exercise performance
in the heat is associated with an anticipatory reduction in skeletal muscle activation. Pflugers Arch
34. Tucker R, Marle T, Lambert EV, Noakes TD. The rate of heat storage mediates an anticipatory reduction in exercise intensity during cycling at a fixed rating of perceived exertion. J Physiol