complete surrogate to HH . ” 7 Although possibly providing minimal benefits for reduction in acute mountain sickness symptoms or ventilatory acclimatization, 8 it seems that NH preacclimatization strategy (eg, by using hypoxic tents) is less effective than HH. 8 Therefore, disentangling hypoxia and
Grégoire P. Millet and Kilian Jornet
Christopher Byrne and Jason K.W. Lee
proposition, as this would provide useful data on heat strain during training and competition, heat acclimatization status, and the effectiveness of interventions aimed at mitigating heat strain. A potential candidate is the physiological strain index (PSI) introduced by Moran et al 2 in 1998 as a novel and
Philo U. Saunders, Laura A. Garvican-Lewis, Robert F. Chapman and Julien D. Périard
that the environments of heat/humidity and altitude have on track-and-field performance and how athletes and coaches can utilize altered environmental conditions to acclimatize and best prepare. With that background in hand, we will share recommendations on specific nutritional interventions that can
Raphael Faiss, Claudia von Orelli, Olivier Dériaz and Grégoire P. Millet
Hypoxia is known to reduce maximal oxygen uptake (VO2max) more in trained than in untrained subjects in several lowland sports. Ski mountaineering is practiced mainly at altitude, so elite ski mountaineers spend significantly longer training duration at altitude than their lower-level counterparts. Since acclimatization in hypobaric hypoxia is effective, the authors hypothesized that elite ski mountaineers would exhibit a VO2max decrement in hypoxia similar to that of recreational ski mountaineers.
Eleven elite (E, Swiss national team) and 12 recreational (R) ski mountaineers completed an incremental treadmill test to exhaustion in normobaric hypoxia (H, 3000 m, FIO2 14.6% ± 0.1%) and in normoxia (N, 485 m, FIO2 20.9% ± 0.0%). Pulse oxygen saturation in blood (SpO2), VO2max, minute ventilation, and heart rate were recorded.
At rest, hypoxic ventilatory response was higher (P < .05) in E than in R (1.4 ± 1.9 vs 0.3 ± 0.6 L · min−1 · kg−1). At maximal intensity, SpO2 was significantly lower (P < .01) in E than in R, both in N (91.1% ± 3.3% vs 94.3% ± 2.3%) and in H (76.4% ± 5.4% vs 82.3% ± 3.5%). In both groups, SpO2 was lower (P < .01) in H. Between N and H, VO2max decreased to a greater extent (P < .05) in E than in R (–18% and –12%, P < .01). In E only, the VO2max decrement was significantly correlated with the SpO2 decrement (r = .74, P < .01) but also with VO2max measured in N (r = .64, P < .05).
Despite a probable better acclimatization to altitude, VO2max was more reduced in E than in R ski mountaineers, confirming previous results observed in lowlander E athletes.
Sebastien Racinais, Martin Buchheit, Johann Bilsborough, Pitre C. Bourdon, Justin Cordy and Aaron J. Coutts
To examine the physiological and performance responses to a heat-acclimatization camp in highly trained professional team-sport athletes.
Eighteen male Australian Rules Football players trained for 2 wk in hot ambient conditions (31–33°C, humidity 34–50%). Players performed a laboratory-based heat-response test (24-min walk + 24 min seated; 44°C), a YoYo Intermittent Recovery Level 2 Test (YoYoIR2; indoor, temperate environment, 23°C) and standardized training drills (STD; outdoor, hot environment, 32°C) at the beginning and end of the camp.
The heat-response test showed partial heat acclimatization (eg, a decrease in skin temperature, heart rate, and sweat sodium concentration, P < .05). In addition, plasma volume (PV, CO rebreathing, +2.68 [0.83; 4.53] mL/kg) and distance covered during both the YoYoIR2 (+311 [260; 361] m) and the STD (+45.6 [13.9; 77.4] m) increased postcamp (P < .01). None of the performance changes showed clear correlations with PV changes (r < .24), but the improvements in running STD distance in hot environment were correlated with changes in hematocrit during the heat-response test (r = –.52, 90%CI [–.77; –.12]). There was no clear correlation between the performance improvements in temperate and hot ambient conditions (r < .26).
Running performance in both hot and temperate environments was improved after a football training camp in hot ambient conditions that stimulated heat acclimatization. However, physiological and performance responses were highly individual, and the absence of correlations between physical-performance improvements in hot and temperate environments suggests that their physiological basis might differ.
Michael J. Zurawlew, Jessica A. Mee and Neil P. Walsh
.1152/japplphysiol.00495.2010 10.1152/japplphysiol.00495.2010 20724560 3. Gonzalez RR , Gagge AP . Warm discomfort and associated thermoregulatory changes during dry, and humid-heat acclimatization . Isr J Med Sci . 1976 ; 12 ( 8 ): 804 – 807 . PubMed ID: 977289 977289 4. Frank A , Belokopytov M
Thomas Reeve, Ralph Gordon, Paul B. Laursen, Jason K.W. Lee and Christopher J. Tyler
Exercise performance in the heat is often impaired due to the greater physiological strain experienced, 1 – 3 but heat acclimation/acclimatization (HA) can reduce this impairment by inducing a number of beneficial physiological (eg, reduction in cardiovascular strain, lower core body temperature
Scott J. Montain, Ronald J. Maughan and Michael N. Sawka
Michelle Cleary, Daniel Ruiz, Lindsey Eberman, Israel Mitchell and Helen Binkley
We present a case of severe dehydration, muscle cramping, and rhabdomyolysis in a high school football player followed by a suggested program for gradual return to play.
A 16-year-old male football player (body mass = 69.1 kg, height = 175.3 cm) reported to the ATC after the morning session on the second day of two-a-days complaining of severe muscle cramping.
The initial assessment included severe dehydration and exercise-induced muscle cramps. The differential diagnosis was severe dehydration, exertional rhabdomyolysis, or myositis. CK testing revealed elevated levels indicating mild rhabdomyolysis.
The emergency department administered 8 L of intravenous (IV) fluid within the 48-hr hospitalization period, followed by gradual return to activity.
To our knowledge, no reports of exertional rhabdomyolysis in an adolescent football player exist. In this case, a high school quarterback with a previous history of heat-related cramping succumbed to severe dehydration and exertional rhabdomyolysis during noncontact preseason practice. We provide suggestions for return to activity following exertional rhabdomyolysis.
Simone D. Henkin, Paulo L. Sehl and Flavia Meyer
Because swimmers train in an aquatic environment, they probably do not need to sweat as much as runners who train on land and, therefore, should not develop the same magnitude of sweating adaptations.
To compare sweat rate and electrolyte concentration in swimmers, runners and nonathletes.
Ten swimmers (22.9 ± 3.1 years old), 10 runners (25 ± 2.9 y) and 10 nonathletes (26.5 ± 2.2 y) cycled in the heat (32°C and 40% relative humidity) for 30 min at similar intensity relative to their maximal cycle test. Sweat volume was calculated from the difference of their body mass before and after cycling, since they were not allowed to drink. Sweat was collected from the scapula using absorbent patch placed on the skin that was cleaned with distilled water. After cycling, the patch was transferred to syringe and the sample was obtained when squeezing it to a tube. Concentration of sodium ([Na+]), chloride ([Cl–]) and potassium ([K+]) were analyzed using an ion selector analyzer.
The sweat volume, in liters, of swimmers (0.9 ± 0.3) was lower (P < .05) than that of runners (1.5 ± 0.2) and similar to that of nonathletes (0.6 ± 0.2). [Na+] and [Cl-], in mmolL-1, of swimmers (65.4 ± 5.5 and 61.2 ± 81), and nonathletes (67.3 ± 8.5 and 58.3 ± 9.6) were higher (P < .05) than those of runners (45.2 ± 7.5 and 38.9 ± 8.3). [K+] was similar among groups.
The lower sweat volume and higher sweat [Na+] and [Cl-] of swimmers, as compared with runners, indicate that training in the water does not cause the same magnitude of sweating adaptations.