Sport-related concussions have been a major clinical concern for sports medicine professionals for many years. Though it is estimated that 1.6 to 3.8 million concussions occur each year (26), there is a surprising lack of understanding in how concussions can be prevented or reduced. Second to motor vehicle crashes, sports are the leading cause of concussion among teenagers and young adults (33). The recognition and management of concussions has been widely studied and strongly established. Notwithstanding the improved understanding of the potentially serious effects of concussion, there remains a dearth of scientific evidence specifically addressing injury prevention strategies and other causative factors contributing to concussion incidence. These include, but are not limited to, studying the intersection of concussion mechanics and environmental factors.
Athletes may experience exertional heat illness, such as heat stroke, heat exhaustion, and heat cramps during sports participation. Of particular concern is exertional heat stroke, because it accounts for approximately 2% of all sport-related deaths (28) and approximately 15% of all football deaths annually (6). Athletes suffering from exertional heat stroke will often present with central nervous system dysfunction symptoms similar to those observed in concussed individuals, such as disorientation, confusion, emotional instability, and/or unconsciousness (1). In addition to heat illnesses, hypohydration is a constant obstacle athletes face throughout sport and physical activity. As many as 54% (34) to 75% (15) of collegiate and youth athletes are hypohydrated when they arrive to practice. A state of hypohydration, alone or in conjunction with an exertional heat illness, may manifest in symptoms similar to those reported by concussed athletes. Research has identified hypohydrated individuals report symptoms including headache, dizziness, feeling slowed down, difficulty concentrating, difficulty remembering, anger, depression, and disorientation (17,32), with the majority of these consistent with concussion symptom inventories.
Collegiate football begins in early August and can continue through early January. It has been speculated that football players tend to suffer more concussions during the early part of the season (hot periods) as compared with the end (cooler periods). The increased number of concussions during the early months may be due to education, skill acquisition, practice parameters, physiological state (heat acclimatization, hydration, illness, and so on), environmental conditions, or healthy athlete bias. Hot and humid environmental conditions (37,38) as well as hypohydration (12,29) can influence an athlete’s heat dissipation mechanisms. It has been theorized that hot environmental exposures and corresponding elevated gastrointestinal temperatures impact the central nervous system. Cell membrane structures incur changes during these environmental exposures, and warm-sensitive neurons are activated (4). Temperature-sensitive neurons compose approximately 40% of the anterior hypothalamus with 30% of those defined as “warm-sensitive.” Warm-sensitive neurons are responsible for increasing their firing rate when the brain receives afferent signals of warming from the periphery or central locations (7,8). Decreases in cerebral blood flow due to the shunting of blood to the periphery in attempts to cool the body occur during exercise (31). These changes could be construed as positive or negative depending on the reason for heat exposure and may lead to an unstable neuronal environment.
Research has identified that hypohydration reduces cerebral blood flow velocity and volume after heat exposure (9,31,36). The decrease in fluid could result in a diminished ability to absorb head impacts, a clinical concern when combined with severe head impact forces. However, research has not endeavored to better understand how head impact severity could be affected by environmental conditions, hypohydration, and gastrointestinal temperature in the early months of the season. Therefore, the twofold purpose of this study was 1) to understand if environmental conditions and physiological factors, such as hypohydration and gastrointestinal temperature, affect head impact biomechanics; and 2) to determine if an in-helmet thermistor could validly measure gastrointestinal temperature.
We used a prospective within-subjects cohort design to assess whether head impact biomechanics were affected by environmental conditions (i.e., ambient temperature) and physiologic status (i.e., body temperature, hydration) during football practice. Eighteen Division I male collegiate football players participated in our study (Table 1). Our sample included subjects from each playing position category. Quarterbacks and kickers were excluded from the study due to their lack of contact during practice. Because temperature sensors were to be ingested, participants were excluded if a known gastrointestinal tract disease, impairment or disorders of the gag reflex, or any previous gastrointestinal surgery were present. Participants were excluded if they reported a history of concussion or bout of exertional heat illness in the 12 months preceding study enrollment. Subjects signed appropriate consent forms approved by our institutional review board before participating in this study.
Head Impact Telemetry System
The Head Impact Telemetry (HIT) System is capable of measuring head impact biomechanics in real time, including resultant linear acceleration (in g, acceleration in terms of gravity), resultant rotational acceleration (rad·s−2), Head Impact Technology severity profile (HITsp), helmet impact location, and head impact frequency. The HIT System obtains data from units comprised of six spring-mounted single-axis accelerometers, a data storage device, and a battery pack housed within a waterproof plastic shell embedded within Riddell VSR-4, Revolution, or Revolution Speed football helmets (Riddell Corp., Elyria, OH). The HIT System accelerometer device is also equipped with a thermistor capable of measuring in-helmet temperatures at the time of each head impact. Temperature data were sent wirelessly with each impact data packet. The data were time stamped, encoded, stored locally, and then transmitted in real time to a sideline controller (antenna) incorporated within the Sideline Response System (Riddell; Elyria, OH) via a radiofrequency telemetry link. The HIT System has been validated in a laboratory setting using hybrid dummies that were equipped with football helmets (16). Even though other temperature devices placed on and around the head have been explored in previous research, the HIT System thermistor has not been validated compared with a criterion standard of body temperature (i.e., rectal, esophageal, or gastrointestinal).
CorTemp™ ingestible core body temperature sensor
The CorTemp™ Ingestible Core Body Temperature Sensor (model HT150002; HQ Inc., Palmetto, FL) provides a valid measure of gastrointestinal temperature as compared with rectal temperature (11,19). The temperature commonly is used as a representation of “core” or organ temperature. The sensor wirelessly transmits body temperature readings as it travels through the gastrointestinal system at a frequency of 262 kHz and is received by the Data Recorder (model HT150001). During data collection, the temperature readings were observed twice at each recording. The handwritten information was manually entered into data software for future analysis.
Wet bulb globe thermometer
The Kestrel 4600 (Kestrel Meters, Birmingham, MI), a digital wet bulb globe temperature (WBGT) device, was used during data collection. The WBGT index is derived using the following environmental readings in a weighted formula: dry bulb temperature (ambient air temperature), wet bulb temperature (humidity), and black globe temperature (radiant heat) (5,13). The National Athletic Trainers’ Association and the American College of Sports Medicine supports this index to modify activity during the American college football season (1,5).
A digital handheld refractometer (Misco Products Division, Cleveland, OH) was used for hydration status by measuring urine specific gravity for descriptive purposes. Specific gravity determines urine concentration and is defined as the ratio of the density of a given liquid to the density of water. Specific gravity levels less than or between 1.010 and 1.020 reflect a well hydrated condition; a reading of more than 1.020 reflects hypohydration on various levels of severity (5). We observed very strong instrument reliability and measurement precision during our internal testing (ICC3,1, 0.996; SEM, 0.0006).
We collected data during one control and three experimental sessions during the college football season. The first three sessions occurred in August on the 5th, 14th, and 15th days of preseason camp. Our fourth session consisted of an environmentally controlled practice session, which took place 7 wk after the third session. The control session occurred in an indoor facility, in which ambient temperature (22.4°C) and humidity were maintained for the duration of the practice session. The coaching staff informed us which days during camp were going to be the most physically challenging, and we chose those days to maximize the number of head impacts we would record under those heat conditions. This same approach was used for the control session, where we had confirmed ahead of time the nature of the indoor practice with the coaching staff. The frequency of head impacts remained consistent throughout our four test sessions, ensuring contact exposure during our indoor control session was commensurate with impacts sustained during the outdoor sessions.
Before the start of training camp, we recorded the following demographic data for each subject: age, height, mass, and football position. Height measurements were taken using a stadiometer after the athletes had removed their shoes. Mass was obtained with the athletes wearing only compression shorts on a standing weight scale (Wildcat Scale, Mettler-Toledo Scale & System Ltd.; Toledo, OH). It was during this time that the HIT System instrumentation was installed in the player helmets. Head impact biomechanics were captured all season as part of an ongoing research initiative in this area. The amount of fluid the subjects ingested was not monitored, and they were not given any specific directions pertaining to hydration for the purpose of this study. However, the subjects’ supervising athletic trainers encouraged proper hydration throughout the football season, with a special emphasis during the hot and humid periods related to preseason camp through typical resources (i.e., breaks, water bottles, and easy accessibility).
Before the start of each practice, subjects consumed the CorTemp™ sensors at least 4 to 5 h before practice to allow the pill time to fully enter the gastrointestinal tract and avoid food or fluid influences (11,37). The athletes’ gastrointestinal temperature, urine specific gravity, and body mass were recorded 1 h before the start of each practice session (21,37). Body mass was recorded at this time in the same manner we used during baseline. The subjects were required to provide a 2- to 4-oz sample of mainstream urine to evaluate their urine specific gravity levels (3).
During practice, the subjects’ gastrointestinal body temperatures were recorded as they entered that day’s practice facility. Temperature readings were obtained every 10 to 15 min, depending on the dynamics of practice, for the entirety of the practice (21). The WBGT was recorded before the start of practice and in 30-min increments throughout the practice session at the same location in the middle of the practice fields. Subjects were allowed to participate normally throughout practice during the data collection days.
Gastrointestinal temperature was recorded as the subjects left the field, and the WBGT was recorded in the same consistent location as previously described. Before the subjects showered, their mass was recorded and then a urine sample was obtained for specific gravity measurements. While obtaining mass measurements, the subjects wore only compression shorts, the same attire as prepractice measurements.
Outcome measures were obtained from the CorTemp™ ingestible sensors, which yielded gastrointestinal body temperature readings we entered into our data software and ultimately merged into our statistical software package. The raw head impact data were exported from the HIT System’s Sideline Response System into Matlab (The Mathwarks, Inc., Natick, MA) where data were reduced to include only the four data collection sessions during the fall season and only impacts registering above 10g (22). A custom export utility developed by Riddell was used to obtain the in-helmet temperature data captured along with head impact biomechanics for each head impact. To associate hydration status to impact magnitude, the prepractice body mass was matched to the beginning third of practice, the average between the prepractice and postpractice body mass to the middle third of practice, and postpractice mass matched to the final third of practice. The WBGT and pre–post practice mass were recorded and stored electronically, and later merged into the statistical analysis software.
We used random intercepts general linear mixed models for each of our following dependent variables: resultant linear acceleration, resultant rotational acceleration, and the HITsp. Player represented one level in each statistical model as a repeated factor. Gastrointestinal temperature, in-helmet temperature, WBGT, ambient temperature, and percent body mass loss served as independent variables of interest and were individually evaluated in separate models. Thus, a total of 15 separate analyses were used. The validity of the in-helmet thermistor was evaluated by comparing the difference between the in-helmet thermistor and gastrointestinal temperature, similar to previous research examining temperature device validity (11,19), against a theoretical test difference of 0 using a one-sample t test. An alpha level of P ≤ 0.05 was set before analysis, and data were analyzed using SAS (SAS Institute, Inc.; Cary, NC).
Eighteen football athletes were recruited to participate in this study. Due to injury attrition, only 17 individuals participated in the second and third practice sessions during training camp. On the last day of data collection, only 15 of these subjects participated in the fourth data collection period. Head impact biomechanics did not differ across our data collection sessions (Table 2) and, thus, we were able to control for our environmental and physiological factors on those days (linear acceleration: P = 0.57; rotational acceleration: P = 0.16; HITsp: P = 0.33). Environmental ambient temperatures during the fourth session were significantly lower than those in first three sessions (F3,1136 = 3409.19; P < 0.001). Overall, 1140 head impacts were recorded over the four test sessions. The offensive and defensive linemen accounted for 736 of the recorded head impacts. The defensive backs and wide receivers accounted for 187 head impacts, and the linebackers and running backs accounted for the remaining 217 head impacts. Table 3 depicts the mean and standard deviations for the impacts recorded by each position group. Consistent with previously published literature, defensive and offensive linemen sustained a disproportionately greater number of head impacts compared to the two other position groups we studied (χ2(2) = 207.04; P < 0.05).
Predictors of head impact biomechanics
Our environmental and physiological factors did not have an effect on resultant linear acceleration we observed during our study. Specifically, ambient temperature (F1,1119 = 1.90; P = 0.17), WBGT (F1,1038 = 1.12; P = 0.29), gastrointestinal temperature (F1,729 = 0.81; P = 0.37), in-helmet temperature (F1,1081 = 0.43; P = 0.51), and mild percent body mass loss (F1,992 = 0.49; P = 0.48) were not significant predictors of linear acceleration. Similar findings for rotational acceleration and HITsp were observed (P > 0.05 for all predictors). These results are provided in Table 4.
Validity of in-helmet thermistor
We computed change scores by subtracting the in-helmet temperature from gastrointestinal temperature. Theoretically, subtracting in-helmet temperature from gastrointestinal temperature would yield values close to zero if the in-helmet thermistor were truly representative of gastrointestinal temperature. Therefore, we compared this change score against a null test value of zero using a one-sample t test. A significant difference was found (t715 = −37.07; P < 0.01). The observed mean difference (−6.25° ± 4.51°) suggested the in-helmet thermistor significantly underestimated gastrointestinal temperature. Figure 1 depicts the comparison of gastrointestinal temperature averages to the in-helmet temperature averages during the four data collection sessions.
Our findings suggest that ambient temperature, WBGT, gastrointestinal temperature, in-helmet temperature and mild percent body mass loss are widely independent of head impact biomechanics.
Wet bulb globe temperature had no influence on impact magnitude. Ambient temperature, which is a component of WBGT, did not statistically affect linear acceleration, rotational acceleration or HITsp. However, rotational acceleration showed a significant decline in magnitude between session 1 and session 4 that may be worthy of further examination and discussion. The 15°C difference between experimental session 1 and the control session corresponded with a drastic drop of rotational acceleration. The sessions were similar with respect to the within-practice drill schedule, and any differences in rotational acceleration observed are not likely attributable to the effect of practice differences. It is apparent that as ambient temperature decreased, the mean rotational acceleration decreased, whereas linear acceleration and HITsp stayed relatively constant.
Rotational acceleration remained the same between the first three sessions (values ranged from 1598.3 to 1624.9 rad·s−2), contrasting the mean for the control session (1325.5 rad·s−2). It is plausible that the players were able to physiologically cope in a controlled environment (session 4) better than the experimental sessions. Heat acclimatization can be safely assumed at this point in the season and therefore we speculate that neuronal adaptive changes have already been made, and warm-sensitive neurons were not actively making changes within the brain (4). Thus, the lowered rotational acceleration measures observed in conjunction with a more stable neuronal environment promote a safer physiological environment for the athlete’s brain later in the season.
Other factors could explain why differences in rotational acceleration existed between experimental and control sessions. Subjects’ technique likely improved as the season progressed. Fatigue might have played a role in the experimental sessions resulting in higher impact magnitudes. The experimental sessions were held during training camp and the physical demand during this period can be very straining for athletes. The intensity of these practices may begin to wear on individuals, and it is possible that on-field performance may begin to degrade as a result. The potential for athletes to more easily fatigue as the season progresses due to repetitive cycling between practice weeks and weekend competitions is an important consideration when interpreting our results. This seasonal fatigue is not modifiable in the context of a research study as it would require altering entirely the nature of the college football season. Future studies should consider including regular fatigue assessments throughout the data collection period. Additionally, these practices occurred in a hot environment encouraging earlier fatigue of the player themselves (i.e., not protecting themselves when anticipating a hit) (18). It is also important to consider that hot environmental conditions, external and internal to the football helmet, encourage sweating and condensation at the head and neck, which can change helmet fit (2). Altering helmet fit may have minimally affected the coupling between the HIT System head impact accelerometers and the athlete’s head. Conversely, the control session took place in the middle of the season at a time when athletes had plenty of time to recover between practice sessions. This may explain why rotational accelerations measured during the control session were not comparable to the experimental sessions.
Hypohydration did not affect impact magnitude in our study; however, our methods of measuring hypohydration were limited to percent body mass loss. The average percent body mass loss across the four data collection days was 1.3%. Two percent or greater loss in total mass can be classified as mild hypohydration. This threshold of fluid loss has resulted in physiological and performance impairments (10). Of 67 athlete exposures, we observed only 10 instances in which subjects weighed in postpractice with a loss in body mass exceeding 2%. The low number of subjects who lost more than 2% of their mass can be attributed to the clinical practice used by the team’s athletic trainers in ensuring that athletes remained properly hydrated throughout heat-intensive practices.
Hypohydration decreases the amount of blood volume; therefore, it decreases the stroke volume and cardiac output (1). Giza and Hovda (20) state cerebral blood flow is coupled with neuronal activity in normal conditions, and a concussive episode can result in a 50% decrease in cerebral blood flow. Compounding a concussive mechanism of injury, heat stressors and hypohydration also play a role in reducing cerebral blood flow. One study identified an 18% decrease in cerebral blood flow in participants who were physically exerted in a dehydrated state during hyperthermia trials compared with normothermic trials (31). Another study identified a reduction of cerebral blood flow velocity by 28% in hypohydrated individuals after heat exposure (9). Preliminary research of mildly hypohydrated individuals after exercise noted that brain volume was protected, but that cerebral spinal fluid was reduced (35). Reductions in cerebral spinal fluid could speculatively allow more brain “slosh” within the skull (30). If hypohydration would have been more prevalent during the practice sessions, we could hypothesize that a concussion would be more likely. In 2% and 4% hypohydration test trials, work performance can decrease 18% to 44% when compared with euhydrated test trials (14). Hypohydration has little effect on single maximal effort strength and power test, but may limit the muscular endurance of trained athletes (25). It was assumed, as athletes became more hypohydrated, that the severity of impact magnitude would increase due to a decrease in performance and ability to defend themselves from oncoming collisions. Our findings suggest that mild hypohydration (less than 2%) does not play a role in impact magnitude; however, additional studies need to be conducted with a larger sample of individuals who meet the 2% and greater hypohydration criteria.
Gastrointestinal temperature did not appear to influence impact magnitude. As gastrointestinal temperature elevates, there is a decrease in cerebral blood flow due to the shunting of blood to the periphery in attempts to cool the body (31). The measurement of cerebral blood flow is limited to laboratory studies and cannot be obtained during football practice. The underlying premise of our study was that as a player’s gastrointestinal temperature increased, there would be a resultant decrease in the amount of cerebral blood in the cranium. The decrease of fluid could result in a decreased ability to absorb head impacts when greater head impact magnitudes are experienced. Additionally, gastrointestinal temperature increases would activate warm-sensitive neurons causing a non-homeostatic environment at the neuronal level, which may also allow for disruption of the central nervous system from head impacts. However, players in the current study achieved a mean gastrointestinal temperature of 38.3°C in practice, which would be considered a normal elevation in temperature associated with exercise. Had players reached higher gastrointestinal temperatures (e.g. ≥40°C), an influence of elevated gastrointestinal temperatures on impact magnitude may have been observed. Once again, individuals who are approaching critical threshold temperatures (~40.5°C), or considered hyperthermic, will fatigue quickly (31), possibly resulting in more frequent impacts.
It is important to note the HIT System has been validated in laboratory studies to measure head acceleration and not helmet acceleration (27). Head acceleration is of interest when dealing with a decrease of fluid within the cranium; however, no known study has determined if decreases in intracranial fluid affects head impact biomechanics. Our study was a first step in determining if physiological effects of elevated gastrointestinal temperature would affect head impact biomechanics. Higher ambient temperatures result in increased body temperatures, which can result in hypohydration due to the body’s attempt to maintain a homeostatic core temperature through sweat evaporation (5,10,37). As core temperature is elevated, the body must shunt blood to the periphery to help dissipate heat (24). As blood is diverted to the periphery, cerebral blood flow can decrease up to 18% resulting in a loss of fluid volume within the cranium (31). The higher rotational accelerations during the experimental sessions should be strongly considered if the buoyancy effect of the cerebrospinal fluid after the decrease in fluid volume within the cranium is decreased. A reduction has also been noted with cerebral blood flow velocity in hypohydrated individuals, which may be linked to orthostatic intolerance (9,36). Syncope commonly occurs with orthostatic changes. This is particularly true when cerebral blood flow falls below normal value, which results from plasma volume decreases after fluid losses. During syncope events, the appendicular and axial skeleton proprioceptive responses are affected, and a fall or balance disturbance occurs (23). It could be that this impacts not only axial and appendicular musculoskeletal balance but also cranial positioning as well.
In-helmet thermistor validity
The in-helmet thermistor housed in all HIT System accelerometers is not a valid device for measuring gastrointestinal temperature. Clinicians should never use the device for interpreting a player’s gastrointestinal temperature. The in-helmet thermistor reported temperatures lower than gastrointestinal temperature readings during the four data collection days. An overview of in-helmet temperature and gastrointestinal temperature readings during the four data collection sessions are illustrated in Figure 1. The in-helmet temperature was not only consistently below gastrointestinal temperature but also did not follow the same trend as gastrointestinal temperature. Gastrointestinal temperature readings gradually increased as practice progressed as expected; however, the in-helmet temperature did not provide the same pattern as gastrointestinal temperature. The in-helmet readings were sporadic and seem to be influenced more by ambient temperature and radiant energy rather than gastrointestinal temperature.
Session 1 illustrates how in-helmet temperature seemed to be influenced by ambient temperature and radiant energy rather than gastrointestinal temperature (Fig. 1). At the beginning of session 1, the lower in-helmet temperature readings could be attributed to players just beginning to wear their helmets. When the helmets are not being worn, they are not in direct sunlight and may not be influenced by radiant energy, but once the helmets are being worn they are directly exposed to sunlight. At the middle third of practice, during individual drills when the majority of the athletes were wearing their helmets, the in-helmet temperature increased to a point in which it closely resembled ambient temperature. The in-helmet temperature was still below gastrointestinal temperature readings during the middle third of practice. The decline of in-helmet temperature over the last 30 min of session 1 can be attributed to players removing their helmets. At the end of each practice, the team practices as a unit, and during this time, more individuals have the opportunity to remove their helmets and cool down.
Our finding that the in-helmet temperature recording device was not valid for measuring gastrointestinal temperature is supported through work performed by Casa et al. (11,19) who compared the reliability of temporal and sticker forehead devices to rectal temperature assessment. The HIT System thermistor is similar to these two methods as all recorded temperatures from the surface of the head. The inaccuracies of the temporal and sticker forehead devices were similar to our in-helmet thermistor. In Casa et al.’s study, the forehead temporal monitor consistently recorded temperatures lower than rectal temperature, and the forehead sticker recorded irregular readings above and below the rectal temperature. We strongly urge clinicians using in-helmet and skin surface devices that claim to measure gastrointestinal temperature to exercise extreme caution. These surface-level devices have been shown to be unreliable and will provide inaccurate information when assessing gastrointestinal temperature (11). Riddell has never made a claim that the HIT System accelerometer units (more specifically the in-helmet thermistors built into these devices) should be used as a valid device for measuring core body temperature; however, other manufacturers have developed similar technology (in-helmet temperature measurement devices) and marketed them as a reliable means of measuring core body temperature.
The number of sessions and subject attrition were the primary limitations to this study. The four data collection days were based on the fact they would be the most demanding and contact oriented practices. Including more session days into the study would have provided a better understanding of how differing environmental conditions might have affected impact magnitudes. Additionally, although the first three sessions all took place during times where exertional heat illness is greatest (i.e., preseason camp), the control session took place several weeks later. We acknowledge that this may have resulted in a number of factors changing between the experimental and control sessions. We submit that a perfect control may have been a preseason session in a controlled environment within the dates of the first three experimental sessions. Unfortunately, given a lack of inclement weather, our football program did not practice in the indoor facility during the preseason timeframe. We thus resorted to identifying a practice session that was considered by the coaching staff to be equally physical and to control for physicality of the practice. We believe that although this introduces a potential limitation to our study, it does little to adversely affect our results nor the ensuing discussion. Lastly, only 10 individuals were considered hypohydrated during the study due to their amount of mass loss. Including more participants into the study may have allowed us to capture a broader range of naturally occurring hydration statuses. Not knowing the exact hydration status of our subjects throughout practice limited us from making precise associations with recorded impact magnitudes.
Results indicate ambient temperature, WBGT, mild hypohydration, and elevated gastrointestinal temperatures (<40°C) did not influence head impact biomechanics. However, we feel that there is a theoretical framework to indicate a relationship to some degree. Even though we did not find any statistically significant or clinically meaningful predictors of impact magnitude, further research needs to be conducted to further elucidate rotational acceleration. We feel that the decline between our experimental and control sessions are worthy of further exploration. The in-helmet thermistor was not a valid measure of body temperature, and we do not recommend its use as a surrogate for gastrointestinal temperature.
The corresponding author was awarded a research grant from the Canadian Athletic Therapists Association (CATA; Calgary, Alberta, Canada) to support the completion of this project. Some of the data collection was funded in part by a grant from the National Operating Committee on Standards for Athletic Equipment (NOCSAE). The opinions expressed herein are those of the authors and do not necessarily reflect the opinions of the CATA or the NOCSAE. The authors would like to thank Douglas J. Casa, PhD, ATC, FACSM, FNATA (University of Connecticut, Storrs, CT), for his assistance with interpretation of the data, and HQ Inc. (Palmetto, FL) for providing materials upon request necessary to support the study. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. The results of the present study do not constitute endorsement by ACSM.
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