“Normal” body temperature varies from person to person and also depends upon the place in the body at which the measurement is made, the time of day, as well as the activity level of the person. Nevertheless, commonly mentioned typical values are as follows: Oral (under the tongue): 36.8±0.4 °C (98.2±0.72 °F); Internal (rectal, vaginal): 37.0 °C (98.6 °F).
Different parts of the body have different temperatures. Rectal and vaginal measurements taken directly inside the body cavity are typically slightly higher than oral measurements, and oral measurements are somewhat higher than skin measurements. Other places, such as under the arm or in the ear, produce different typical temperatures. Although some people think of these averages as representing the normal or ideal temperature, a wide range of temperatures has been found in healthy people. The body temperature of a healthy person varies during the day by about 0.5 °C (0.9 °F) with lower temperatures in the morning and higher temperatures in the late afternoon and evening, as the body’s needs and activities change. Other circumstances also affect the body’s temperature. The core body temperature of an individual tends to have the lowest value in the second half of the sleep cycle; the lowest point, called the nadir, is one of the primary markers for circadian rhythms. The body temperature also changes when a person is hungry, sleepy, sick, or cold. Core temperature, also called core body temperature, is the operating temperature of an organism, specifically in deep structures of the body such as the liver, in comparison to temperatures of peripheral tissues. Core temperature is normally maintained within a narrow range so that essential enzymatic reactions can occur. Significant core temperature elevation (hyperthermia) or depression (hypothermia) that is prolonged for more than a brief period of time is incompatible with human life.
Temperature examination in the rectum is the traditional gold standard measurement used to estimate core temperature (oral temperature is affected by hot or cold drinks and mouth-breathing). Rectal temperature is expected to be approximately one Fahrenheit degree higher than an oral temperature taken on the same person at the same time. Ear thermometers measure eardrum temperature using infrared sensors. The blood supply to the tympanic membrane is shared with the brain. However, this method of measuring body temperature is not as accurate as rectal measurement and has a low sensitivity for fevers, missing three or four out of every ten fevers in children. Ear temperature measurement may be acceptable for observing trends in body temperature but is less useful in consistently identifying fevers.
Until recently, direct measurement of core body temperature required surgical insertion of a probe, so a variety of indirect methods have commonly been used. The rectal or vaginal temperature is generally considered to give the most accurate assessment of core body temperature, particularly in hypothermia. In the early 2000s, ingestible thermistors in capsule form were produced, allowing the temperature inside the digestive tract to be transmitted to an external receiver; one study found that these were comparable in accuracy to rectal temperature measurement.
The ability of humans to endure passive heat stress or the heat generated by active muscle during endurance exercise is limited by the maximum core temperature achieved during the exercise. Fatigue generally coincides with core temperatures ranging from 38 degrees C. to 40 degrees C. (104 degrees F.) This temperature range reflects a critical high body temperature that impairs muscle activation directly from a high brain temperature that decreases the central drive to continue exercising. Animal studies have determined, for example, that in exercising rats, exhaustion is reached at a core temperature of about 42°C. (107.6 degrees F.), regardless of the temperatures at the initiation of exercise. Published studies provide clear support for the concept that a critical internal temperature limits both moderate and strenuous exercise in the heat. A number of reports have linked internal temperature to impaired physical performance in the heat in humans and in animals. Caputa et al. reported that reduced running performance occurred when Thyp reached 42.0–42.9°C in exercising goats. Furthermore, cheetahs cease running when their core temperature reaches 40.5°C, whereas domestic dogs (beagles) reach exhaustion at Trec between 41.7 and 42.2°C. Endurance-trained humans exercising in the heat become exhausted at between 39.7 and 40.3°C. These studies have primarily used two different strategies to examine the question of whether a critical, exercise-limiting internal temperature exists. The first method is by altering the rate of heating during exercise by varying ambient temperature during exercise. The second method involves the use of heating (or cooling) before exercise to alter the initial temperature. When environmental heating is used as a preheating modality, the number of levels of preheating is limited. This is because the length of time required to induce a significant elevation in baseline temperature eventually leads to the introduction of confounding variables such as dehydration, electrolyte imbalances, and cardiovascular drift that hasten fatigue during exercise.
Human studies have also concluded that the physical endurance for exercise in hot, dry environments appears to be limited by the attainment of a critical level of core temperature…reducing motivation (Bruck & Olschewski, 1987). High core temperature, and not circulatory failure or metabolic depletion, is the critical factor in heat stress, both before and after acclimation (Nielsen, B., Hales, J.R., et al (1993); Fink, et. al (1975), Kozlowski, et. al. 1985)). Different aerobic fitness levels often result in slightly different core temperature at exhaustion tolerance levels, but experts believe this may result from the familiarization of regular aerobic training and exposure to higher body temperatures on a daily basis. (Selkirk, G. and McLellan, T., (2001).
It has been proposed that a critical sublethal temperature exists beyond which physical activity is not possible; such a mechanism is hypothesized to protect animals from reaching a lethal level of hyperthermia. Studies designed to assess lethality of exertional heat stress have demonstrated that rats will run to the point of heatstroke leading to death. However, it is not temperature alone that determines the lethality of heat stress, but rather the thermal load, which is determined by the level of hyperthermia and the duration for which it is sustained. The thermal load encountered by rats during exercise has been calculated by the method of Fruth and Gisolfi and found similar values (37.4–43.8°C · min) after all treatments. This range of values is below the lethal thermal load reported for untrained rats by Fruth and Gisolfi. Thus our rats became fatigued before they reached a lethal thermal load. In the present study, as well as in a previous investigation, we found that rats always became too fatigued to run before lethal thermal loads were encountered. Studies that have exercised rats to lethality have intentionally designed the exercise protocol to maximize the thermal load encountered by the animals. This has been accomplished by either running rats under a work-rest paradigm at a low level of exercise or by ramping up exercise intensity and environmental temperature during the course of the session. Interestingly, in this last study (4), fatigue occurred at a Trec (42.4°C) similar to the one we report. In contrast to our study, however, Fruth and Gisolfi reported 100% mortality. The difference between the studies relates to the thermal load. Although exhaustion was reached at the same temperature in both studies, Fruth and Gisolfi used ramped-up temperature and TM speed to produce a thermal load threefold greater than that achieved in our investigation. This is important because it suggests that, although there may be a critical temperature beyond which exercise cannot continue in the heat, it is not sensitive to thermal load and thus cannot protect against thermal damage or lethality under all circumstances. Another condition in which the critical temperature cannot protect against lethality can occur during low-level exercise in the heat. Under these conditions, a lethal thermal load can occur before the critical temperature for cessation of exercise is reached .
Although this investigation provides evidence for the existence of a limiting body temperature during exercise in the heat, it is not clear how these limits are controlled. Exercise ceased at a similar Thyp and Trec independent of the level of preheating; thus it cannot be determined from the present study whether fatigue is related to elevated brain or core temperature. It was not possible to measure metabolic indicators associated with fatigue (e.g., blood glucose, lactate, or muscle glycogen concentrations) because of the repeated-measures design of the study. If these factors were involved, however, it is unlikely that their influence would coincide with the same internal temperatures across treatments. In addition, exercise after medium and high was only 19.4 and 10.7 min, respectively, which is too short a time period in which to expect significant substrate depletion. Furthermore, it has been demonstrated in humans exercising in the heat that exhaustion occurs before significant decline in muscle glycogen and blood glucose concentrations or increases in muscle and blood lactate concentrations. A recent investigation in humans has linked accumulation of IMP and NH3 with fatigue in the heat. Studies in racehorses have led to the postulation that fatigue in the heat may also be due to metabolic dysfunction precipitated by oxidative stress . Although we cannot rule out these possibilities in the present investigation, they appear unlikely because of the fact that fatigue occurred at nearly the identical temperature after all treatments. Dehydration was also not a factor, given that the amount of weight lost during exercise does not reflect a level of dehydration associated with fatigue.
It has been suggested that fatigue during exercise in the heat is related to a diminished central drive. The hypothalamus has been shown to be involved in a myriad of themoregulatory responses and behaviors . It would thus appear to be a likely candidate for limiting exercise in the heat. Caputa et al. used intravascular heat exchangers to selectively heat and cool the brain and trunk independently in exercising goats. The results of these experiments have demonstrated that exhaustion is reached when Thyp reaches 42.0–42.9°C if trunk temperature is maintained at 40.0°C. In contrast, a trunk temperature of over 43.5°C was required before exercise performance was affected. This suggests central involvement in mediating fatigue. The postural extension response, used by Fuller et al. as their operational definition of fatigue, has been clearly demonstrated to occur in response to warming of the preoptic area of the anterior hypothalamus. Thus fatigue during volitional exercise in rats is most likely controlled by the hypothalamus. However, it is not clear whether the hypothalamus mediates fatigue under the more stringent criteria used in the present study. Although this study provides strong evidence for the existence of a critical temperature that limits exercise in the heat, additional investigations are required to determine where the locus of control resides. In addition, it remains to be determined whether temperature per se is the critical variable or whether the temperature just coincides with the limiting variable.
In summary, this study clearly demonstrates that exhaustion during exercise in the heat in rats occurs at a critical internal temperature level regardless of the initial levels of temperature. By using MW technology, we were able to set initial temperature at various levels rapidly, thereby avoiding confounding factors inherent to more familiar modalities of pre-exercise heating. Because the temperatures at exhaustion were virtually identical, whereas the run times to exhaustion were correlated with the initial temperatures, this study provides strong evidence that exercise is limited by the attainment of a critical internal temperature.
APL (American Performance Labs) is a research group dedicated to the collection, analysis, and dissemination of published research and articles on the science of hyperthermia and the various applications, technologies and protocols for the use of hyperthermic conditioning.