A proper heat-acclimatization plan in secondary school athletic programs is essential to minimize the risk of exertional heat illness during the preseason practice period. Gradually increasing athletes' exposure to the duration and intensity of physical activity and to the environment minimizes exertional heat-illness risk while improving athletic performance. Progressive acclimatization is especially important during the initial 3 to 5 days of summer practices. When an athlete undergoes a proper heat-acclimatization program, physiologic function, exercise heat tolerance, and exercise performance are all enhanced.1–6 In contrast, athletes who are not exposed to a proper heat-acclimatization program face measurable increased risks for exertional heat illness.For these reasons, the Inter-Association Task Force for Preseason Secondary School Athletics, in conjunction with the National Athletic Trainers' Association's Secondary School Athletic Trainers' Committee, recommends that these "Preseason Heat-Acclimatization Guidelines for Secondary School Athletics" be implemented by all secondary school athletic programs. These guidelines should be used for all preseason conditioning, training, and practice activities in a warm or hot environment, whether these activities are conducted indoors or outdoors. When athletic programs implement these guidelines, the health and safety of the athletes are primary. However, the recommendations outlined here are only minimum standards, based on the best heat-acclimatization evidence available. Following these guidelines provides all secondary school athletes an opportunity to train safely and effectively during the preseason practice period.Before participating in the preseason practice period, all student-athletes should undergo a preparticipation medical examination administered by a physician (MD or DO) or as required/approved by state law. The examination can identify predisposing factors related to a number of safety concerns, including the identification of youths at particular risk for exertional heat illness.The heat-acclimatization period is defined as the initial 14 consecutive days of preseason practice for all student-athletes. The goal of the acclimatization period is to enhance exercise heat tolerance and the ability to exercise safely and effectively in warm to hot conditions. This period should begin on the first day of practice or conditioning before the regular season. Any practices or conditioning conducted before this time should not be considered a part of the heat-acclimatization period. Regardless of the conditioning program and conditioning status leading up to the first formal practice, all student-athletes (including those who arrive at preseason practice after the first day of practice) should follow the 14-day heat-acclimatization plan. During the preseason heat-acclimatization period, if practice occurs on 6 consecutive days, student-athletes should have 1 day of complete rest (no conditioning, walk-throughs, practices, etc).Days on which athletes do not practice due to a scheduled rest day, injury, or illness do not count toward the heat-acclimatization period. For example, an athlete who sits out the third and fourth days of practice during this time (eg, Wednesday and Thursday) will resume practice as if on day 3 of the heat-acclimatization period when returning to play on Friday.A practice is defined as the period of time a participant engages in a coach-supervised, school-approved, sport- or conditioning-related physical activity. Each individual practice should last no more than 3 hours. Warm-up, stretching, and cool-down activities are included as part of the 3-hour practice time. Regardless of ambient temperature conditions, all conditioning and weight-room activities should be considered part of practice.A walk-through is defined as a teaching opportunity with the athletes not wearing protective equipment (eg, helmets, shoulder pads, catcher's gear, shin guards) or using other sport-related equipment (eg, footballs, lacrosse sticks, blocking sleds, pitching machines, soccer balls, marker cones). The walk-through is not part of the 3-hour practice period, can last no more than 1 hour per day, and does not include conditioning or weight-room activities.A recovery period is defined as the time between the end of 1 practice or walk-through and the beginning of the next practice or walk-through. During this time, athletes should rest in a cool environment, with no sport- or conditioning-related activity permitted (eg, speed or agility drills, strength training, conditioning, or walk-through). Treatment with the athletic trainer is permissible.The National Athletic Trainers' Association (NATA) and the Inter-Association Task Force for Preseason Secondary School Athletics advise individuals, schools, athletic training facilities, and institutions to carefully and independently consider each of the recommendations. The information contained in the statement is neither exhaustive nor exclusive to all circumstances or individuals. Variables such as institutional human resource guidelines, state or federal statutes, rules, or regulations, as well as regional environmental conditions, may impact the relevance and implementation of these recommendations. The NATA and the Inter-Association Task Force advise their members and others to carefully and independently consider each of the recommendations (including the applicability of same to any particular circumstance or individual). The foregoing statement should not be relied upon as an independent basis for care but rather as a resource available to NATA members or others. Moreover, no opinion is expressed herein regarding the quality of care that adheres to or differs from any of NATA's other statements. The NATA and the Inter-Association Task Force reserve the right to rescind or modify their statements at any time.
Fluid intake during military training is prescribed based on the interactions among environmental conditions, uniform configurations and work rates. The efficacy of this guidance has not been empirically assessed for work bouts lasting >4 hours. PURPOSE: To determine the acceptability of the fluid intake guidance, sweat losses were measured in a variety of conditions and modern uniform/body armor configurations and were then compared to prescribed fluid intakes for each condition (clothing, environment, workload, duration). METHODS: Whole body sweat losses of 141 soldiers were measured over a variety of environmental conditions (White-Black flag), uniform configurations (including Battle Dress Uniform and body armor), exercise intensities (easy, moderate, heavy), and work durations (2,4, and 8 hr). Using the prescribed fluid intake guidance for each condition, the differences between the prescribed fluid intake and the total observed sweat loss were calculated. Differences were then expressed as a percent loss or gain of body weight using the following equation: [% body water flux= ((drinking volume- sweating volume)/body weight) x 100]. Values within a threshold of ±2% body water flux (BWF) were deemed acceptable. This threshold was considered the starting point for performance and health concerns. To simulate a worst-case scenario, it was assumed no urine was produced throughout testing. RESULTS: During short work durations (2 and 4hr), 0 of 75 Soldiers exceeded the +2% BWF. During longer work durations (8hr), 50 of 66 Soldiers exceeded the +2% BWF. In all conditions, 50 of 141 Soldiers (35%) exceeded the +2% BWF. In no condition did a Soldier exceed the -2% BWF. CONCLUSION: Current fluid intake guidance appears to be sufficient (no over- or under-drinking ±2% BWF) during work durations lasting ≤4 hours. However, for conditions beyond published guidance (>4hr), recommended drinking rates over-prescribe water needs in worst-case scenarios where no urine was produced. It is recommended that military fluid intake guidance be re-evaluated to include longer work durations of 8 hours. The views expressed in this abstract are those of the authors and do not reflect the official policy of the Department of Army, Department of Defense, or the U.S. Government.
Abstract : This chapter discusses the clinical manifestations, management, and prevention of heat-related illnesses. The spectrum of injury ranges from milder conditions such as heat cramps to fatal manifestations such as arrhythmias; it involves complications such as rhabdomyolysis and multiorgan dysfunction syndrome, and it may result in death from overwhelming cell necrosis caused by a lethal heat-shock exposure. Exertional heat stroke (EHS) is commonly characterized by development of mental status changes or collapse during physical activity in a warm environment. The severity of heat illness depends on the degree and duration of the elevation in core temperature (Tco). Heat stroke is an extreme medical emergency that can be fatal if it is not treated promptly with rapid cooling. To prevent and minimize complications and save lives, proper prevention, management, and clinical care are essential.
Changes in body water elicit reflex adjustments at the kidney, thus maintaining fluid volume homeostasis. These renal adjustments change the concentration and color of urine, variables that can, in turn, be used as biomarkers of hydration status. It has been suggested that vitamin supplementation alters urine color; it is unclear whether any such alteration would confound hydration assessment via colorimetric evaluation. We tested the hypothesis that overnight vitamin B2 and/or B12 supplementation alters urine color as a marker of hydration status. Thirty healthy volunteers were monitored during a 3-day euhydrated baseline, confirmed via first morning nude body mass, urine specific gravity, and urine osmolality. Volunteers then randomly received B2 (n = 10), B12 (n = 10), or B2 + B12 (n = 10) at ∼200 × recommended dietary allowance. Euhydration was verified on trial days (two of the following: body mass ± 1.0% of the mean of visits 1-3, urine specific gravity < 1.02, urine osmolality < 700 mmol/kg). Vitamin purity and urinary B2 concentration ([B2]) and [B12] were quantified via ultraperformance liquid chromatography. Two independent observers assessed urine color using an eight-point standardized color chart. Following supplementation, urinary [B2] was elevated; however, urine color was not different between nonsupplemented and supplemented trials. For example, in the B2 trial, urinary [B2] increased from 8.6 × 10(4) ± 7.7 × 10(4) to 5.7 × 10(6) ± 5.3 × 10(6) nmol/l (P < 0.05), and urine color went from 4 ± 1 to 5 ± 1 (P > 0.05). Both conditions met the euhydrated color classification. We conclude that a large overnight dose of vitamins B2 and B12 does not confound assessment of euhydrated status via urine color.
Our previous work has documented that drivers are thermoregulatory challenged during competitive racing; however, the degree of fluid loss that occurs has not been quantified.
Aim
To quantify the degree of fluid losses that occurs during a competitive event under hot (summer) conditions.
Methods
Nine male stock car drivers (30 ± 9 yr, 178 ± 3 cm, 83 ± 19 kg) participated in the Pro Series Division of the NASCAR Whelen All-American Series race in August in the Northeastern United States. Seven drivers completed 40 laps with an average speed of ∼73 km/h, totaling ∼18 min in duration. Ambient track temperature was 22.3°C, 90 % rh and average cockpit temperatures were ∼31°C, 61% rh prior to the start of the race, and ∼41°C, 45 % rh upon completion. Sweat rate and percent dehydration was determined via nude body weight (BW) pre- and post-race. Due to race logistics, pre-race BWs were taken approximately one hour before the start of the race, and post-race BWs were taken immediately after the driver exited the car. Urine loss was considered fluid loss, and BWs were corrected for fluid and food intake. Intestinal core (Tc) and skin (Tsk) temperatures, and heart rate (HR) were also assessed.
Results
Pre-race BW was 81.5 ± 18.5 kg and decreased to 81.1 ± 18.5 kg immediately post-race (p = 0.001). Average sweat rate was 0.63 ± 0.4 L per hour; as pre-race BWs were taken approximately one hour prior to completion of the race, and this sweat rate incorporated approximately 40 min of pre-race activity which included ∼12 laps ( ∼ 3 min of driving) to establish starting position, 10 min of resting in the vehicle in full uniform, and 30 min of light activity (i.e., making car adjustments), in addition to the race itself. Percent BW loss following the race was 0.77 ± 0.3%. Pre-race Tc was 38.0 ± 0.4°C which increased to 38.5 ± 0.4°C post-race (p = 0.001). Tsk increased from 35.8 ± 0.8°C pre-race to 36.9 ± 0.8°C post-race (p = 0.001) whereas the core-to-skin temperature gradient decreased from a pre-race value of 2.2 ± 0.9°C to 1.6 ± 0.9°C post-race (p = 0.001). HRs post-race were 89 ± 0.0% of the drivers' age-predicted maximum HR.
Conclusions
This is the first study attempting to quantify fluid loss during a competitive stock car race. As this was a short race, sweat rate and% losses in BW were extrapolated to three hours (sweat rate: 1.90 ± 1.2 L per hour; 2.3 ± 1.0% BW loss) and four hours (sweat rate: 2.53 ± 1.5 L per hour; 3.1 ± 1.4% BW loss). As we included 40 minutes of pre-race activity into our sweat rate calculations, the extrapolated sweat rate and% losses in BWs are likely lower than those measured during continuous racing of 3 or 4 hours. These results suggest that fluid losses during competitive racing can be significant. Without a fluid replacement strategy, fluid losses for these drivers may exceed 3% BW and could negatively impact driving performance.
We hypothesized that muscle sympathetic nerve activity (MSNA) during head-up tilt (HUT) would be augmented during exercise-induced (hyperosmotic) dehydration but not isoosmotic dehydration via an oral diuretic. We studied 26 young healthy subjects (7 female, 19 male) divided into three groups: euhydrated (EUH, n = 7), previously exercised in 40°C while maintaining hydration; dehydrated (DEH, n = 10), previously exercised in 40°C during which ~3% of body weight was lost via sweat loss; and diuretic (DIUR, n = 9), a group that did not exercise but lost ~3% of body weight via diuresis (furosemide, 80 mg by mouth). We measured MSNA, heart rate (HR), and blood pressure (BP) during supine rest and 30° and 45° HUT. Plasma volume (PV) decreased similarly in DEH (-8.5 ± 3.3%) and DIUR (-11.4 ± 5.7%) (P > 0.05). Plasma osmolality was similar between DIUR and EUH (288 ± 4 vs. 284 ± 5 mmol/kg, respectively) but was significantly higher in DEH (299 ± 5 mmol/kg) (P < 0.05). Mixed-model ANOVA was used with repeated measures on position (HUT) and between-group analysis on condition. HR and MSNA increased in all subjects during HUT (main effect of position; P < 0.05). There was also a significant main effect of group, such that MSNA and HR were higher in DEH compared with DIUR (P < 0.05). Changes in HR with HUT were larger in both hypovolemic groups compared with EUH (P < 0.05). The differential HUT response "strategies" in each group suggest a greater role for hypovolemia per se in controlling HR responses during dehydration, and a stronger role for osmolality in control of SNA.NEW & NOTEWORTHY Interactions of volume regulation with control of vascular sympathetic nerve activity (SNA) have important implications for blood pressure regulation. Here, we demonstrate that SNA and heart rate (HR) during hyperosmotic hypovolemia (exercise-induced) were augmented during supine and tilt compared with isoosmotic hypovolemia (diuretic), which primarily augmented the HR response. Our data suggest that hypovolemia per se had a larger role in controlling HR responses, whereas osmolality had a stronger role in control of SNA.
Identifying global alterations in genomic factors as a result of various exercise stimuli has the potential to afford a better understanding of adaptive responses to exercise. To date, only a limited number of gene transcripts related to the immune and inflammatory processes have been examined. PURPOSE: The present study utilized an acute bout of resistance exercise to examine the effects on the immune- and inflammatory-related genes in peripheral blood mononuclear cells (PBMCs). METHODS: Ten resistance-trained men (20-24 yrs), with at least 2 yrs resistance exercise training (RET) experience performed an acute bout of RET for ∼30 min following a 12 hr fast. Venous blood was sampled at rest, immediately following exercise, and at 2 hr post-exercise and analyzed for total and differential leukocytes and global gene expression using Affymetrix Genechips. RESULTS: Using a conservative false discovery rate (FDR) of p<0.05 and a two-fold change of or higher threshold, 167 genes were differentially detected between baseline and 2 hr post-exercise, 259 genes between 2 hr post-exercise and immediately post-exercise, and six genes between immediately post-exercise and baseline indicating the greatest gene response was seen at the 2 hour post-exercise. At the 2 hr recovery time point, matrix metalloproteinase 9 (MMP 9), orosomucoid 1 (ORM 1) and arginase 1 (ARG 1) all showed significant up regulation, while the gene CD160 was down regulated. CONCLUSION: Initial microarray results indicate that gene expression signatures are highly correlated with peripheral blood mononuclear counts and that differentially expressed genes supported the immunophenotyping results. These results demonstrate that an acute bout of RET disrupts cellular homeostasis, induces a transient redistribution of certain leukocytes, and results in a transcriptional change in blood samples consistent with phenotyping results that differs from aerobic exercise. Support made possible by the Vermont Genetics Network through Grant Number P20 RR16462 from the INBRE Program of the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NCRR or NIH.
This paper reviews the roles of hot skin (>35°C) and body water deficits (>2% body mass; hypohydration) in impairing submaximal aerobic performance. Hot skin is associated with high skin blood flow requirements and hypohydration is associated with reduced cardiac filling, both of which act to reduce aerobic reserve. In euhydrated subjects, hot skin alone (with a modest core temperature elevation) impairs submaximal aerobic performance. Conversely, aerobic performance is sustained with core temperatures >40°C if skin temperatures are cool-warm when euhydrated. No study has demonstrated that high core temperature (∼40°C) alone, without coexisting hot skin, will impair aerobic performance. In hypohydrated subjects, aerobic performance begins to be impaired when skin temperatures exceed 27°C, and even warmer skin exacerbates the aerobic performance impairment (–1.5% for each 1°C skin temperature). We conclude that hot skin (high skin blood flow requirements from narrow skin temperature to core temperature gradients), not high core temperature, is the 'primary' factor impairing aerobic exercise performance when euhydrated and that hypohydration exacerbates this effect.
The purpose of this investigation was to observe the effect of hypohydration (-4% body mass) on lactate threshold (LAT) in 14 collegiate athletes (8 men and 6 women; age, 20.9 ± 0.5 years; height, 171.1 ± 2.4 cm; weight, 64.8 ± 2.3 kg; Vo2max, 62.8 ± 1.9 ml.kg-1.min-1; percentage of fat, 11.4 ± 1.5%). Subjects performed 2 randomized, discontinuous treadmill bouts at a dry bulb temperature (Tdb) of 22° C to volitional exhaustion in 2 states of hydration, euhydrated and hypohydrated. The hypohydrated condition was achieved in a thermally neutral environment (Tdb, 22° C; humidity, 45%), with exercise conducted at a moderate intensity as defined by rating of perceived exertion (RPE, approximately 12) 12–16 hours before testing. On average, subjects decreased 3.9% of their body mass before the hypohydration test. Blood lactate, hematocrit, Vo2, minute ventilation (VE), R value, heart rate (HR), and RPE were measured during each 4-minute stage of testing. In the hypohydrated condition, LAT occurred significantly earlier during exercise and at a lower absolute Vo2, VE, respiratory exchange ratio, RPE, and blood lactate concentration. Also, the blood lactate concentration was significantly lower in the hypohydrated condition (6.7 ± 0.8 mmol) compared with the euhydrated condition (10.2 ± 0.9 mmol) at peak exercise. There were no differences in HR or percentage of maximum HR at LAT nor did plots of Vco2:Vo2 reveal differences in bicarbonate buffering during exercise between the 2 conditions. From these results, we speculate that hypohydration did not significantly alter cardiovascular function or buffering capacity but did cause LAT to occur at a lower absolute exercise intensity.
Exercise-heat acclimation (EHA) induces adaptations that improve tolerance to heat exposure. Whether adaptations from EHA can also alter responses to hypobaric hypoxia (HH) conditions remains unclear. This study assessed whether EHA can alter time-trial performance and/or incidence of acute mountain sickness (AMS) during HH exposure. Thirteen sea-level (SL) resident men [SL peak oxygen consumption (V̇o2peak) 3.19 ± 0.43 L/min] completed steady-state exercise, followed by a 15-min cycle time trial and assessment of AMS before (HH1; 3,500 m) and after (HH2) an 8-day EHA protocol [120 min; 5 km/h; 2% incline; 40°C and 40% relative humidity (RH)]. EHA induced lower heart rate (HR) and core temperature and plasma volume expansion. Time-trial performance was not different between HH1 and HH2 after 2 h (106.3 ± 23.8 vs. 101.4 ± 23.0 kJ, P = 0.71) or 24 h (107.3 ± 23.4 vs. 106.3 ± 20.8 kJ, P > 0.9). From HH1 to HH2, HR and oxygen saturation, at the end of steady-state exercise and time-trial tests at 2 h and 24 h, were not different (P > 0.05). Three of 13 volunteers developed AMS during HH1 but not during HH2, whereas a fourth volunteer only developed AMS during HH2. Heat shock protein 70 was not different from HH1 to HH2 at SL [1.9 ± 0.7 vs. 1.8 ± 0.6 normalized integrated intensities (NII), P = 0.97] or after 23 h (1.8 ± 0.4 vs. 1.7 ± 0.5 NII, P = 0.78) at HH. Our results indicate that this EHA protocol had little to no effect-neither beneficial nor detrimental-on exercise performance in HH. EHA may reduce AMS in those who initially developed AMS; however, studies at higher elevations, having higher incidence rates, are needed to confirm our findings.
