Nielsen. Influence of body temperature on the development of fatigue during prolonged exercise in the heat. J. Appl. Physiol. 86(3): 1032-1039, 1999.-We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (T es ) ϭ 35.9 Ϯ 0.2, 37.4 Ϯ 0.1, or 38.2 Ϯ 0.1 (SE)°C induced by 30 min of water immersion], seven cyclists (maximal O 2 uptake ϭ 5.1 Ϯ 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O 2 uptake) in the heat (40°C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05°C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with T es of 37.0°C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (T es ϭ 40.1-40.2°C, muscle temperature ϭ 40.7-40.9°C, skin temperature ϭ 37.0-37.2°C) and cardiovascular strain (heart rate ϭ 196-198 beats/min, cardiac output ϭ 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 Ϯ 3, 46 Ϯ 3, and 28 Ϯ 2 min with initial T es of ϳ36, 37, and 38°C, respectively (all P Ͻ 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar T es and muscle temperature (40.1-40.3 and 40.7-40.9°C, respectively), but with significantly different skin temperature (38.4 Ϯ 0.4 vs. 35.6 Ϯ 0.2°C during high vs. low rate of heat storage, respectively, P Ͻ 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 Ϯ 4 vs. 56 Ϯ 11 min, respectively, P Ͻ 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40°C), with skin blood flow plateauing at T es of ϳ38°C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage. hyperthermia; skin blood flow; heart rate; stroke volume IT IS WELL DOCUMENTED that endurance can be impaired in hot compared with temperate climates (10,12,28) and that time to exhaustion is influenced by alterations of the initial body temperature (1,22,32,39). The attainment of a critically high level of body temperature has been proposed as the main factor limiting endurance performance in hot environments (7,28). The observation that trained subjects working at 60% of peak O 2 uptake (V O 2 peak ) in the heat [40°C, 10% relative humidity (RH)] for 9-12 consecutive days improved exercise performance from 48 to 80 min but fatigued at a core temperature of 39.7°C appears to support this notion (28). This large improvement in exercise time t...

SUMMARY1. Heat acclimation was induced in eight subjects by asking them to exercise until exhaustion at 60 % of maximum oxygen consumption rate (VO ) for 9-12 consecutive days at an ambient temperature of 40°C, with 10% relative humidity (RH). Five control subjects exercised similarly in a cool environment, 20 0C, for 90 min for 9-12 days; of these, three were exposed to exercise at 40°C on the first and last day.2. Acclimation had occurred as seen by the increased average endurance from 48 min to 80 min, the lower rate of rise in the heart rate (HR) and core temperature and the increased sweating.3. Cardiac output increased significantly from the first to the final heat exposure from 19 6 to 21V4 1 min-1; this was possibly due to an increased plasma volumne and stroke volume. 4. The mechanism for the increased plasma volume may be an isosmotic volume expansion caused by influx of protein to the vascular compartment, and a sodium retention induced by a significant increase in aldosterone.5. The exhaustion coincided with, or was elicited when, core temperature reached 39-7 + 0 15°C; with progressing acclimation processes it took progressively longer to reach this level. However, at this point we found no reduction in cardiac output, muscle (leg) blood flow, no changes in substrate utilization or availability, and no recognized accumulated 'fatigue' substances.6. It is concluded that the high core temperature per se, and not circulatory failure, is the critical factor for the exhaustion during exercise in heat stress.

The present study investigated the effects of hyperthermia on the contributions of central and peripheral factors to the development of neuromuscular fatigue. Fourteen men exercised at 60% maximal oxygen consumption on a cycle ergometer in hot (40 degrees C; hyperthermia) and thermoneutral (18 degrees C; control) environments. In hyperthermia, the core temperature increased throughout the exercise period and reached a peak value of 40.0 +/- 0.1 degrees C (mean +/- SE) at exhaustion after 50 +/- 3 min of exercise. In control, core temperature stabilized at approximately 38.0 +/- 0.1 degrees C, and exercise was maintained for 1 h without exhausting the subjects. Immediately after the cycle trials, subjects performed 2 min of sustained maximal voluntary contraction (MVC) either with the exercised legs (knee extension) or with a "nonexercised" muscle group (handgrip). The degree of voluntary activation during sustained maximal knee extensions was assessed by superimposing electrical stimulation (EL) to nervus femoralis. Voluntary knee extensor force was similar during the first 5 s of contraction in hyperthermia and control. Thereafter, force declined in both trials, but the reduction in maximal voluntary force was more pronounced in the hyperthermic trial, and, from 30 to 120 s, the force was significantly lower in hyperthermia compared with control. Calculation of the voluntary activation percentage (MVC/MVC + EL) revealed that the degree of central activation was significantly lower in hyperthermia (54 +/- 7%) compared with control (82 +/- 6%). In contrast, total force of the knee extensors (MVC + force from EL) was not different in the two trials. Force development during handgrip contraction followed the same pattern of response as was observed for the knee extensors. In conclusion, these data demonstrate that the ability to generate force during a prolonged MVC is attenuated with hyperthermia, and the impaired performance is associated with a reduction in the voluntary activation percentage.

Brain temperature appears to be an important factor affecting motor activity, but it is not known to what extent brain temperature increases during prolonged exercise in humans. Cerebral heat exchange was therefore evaluated in seven males during exercise with and without hyperthermia. Middle cerebral artery mean blood velocity (MCA V(mean)) was continuously monitored while global cerebral blood flow (CBF) and cerebral energy turnover were determined at the end of the two exercise trials in three subjects. The arterial to venous temperature difference across the brain (v-aD(temp)) was determined via thermocouples placed in the internal jugular vein and in the aorta. The jugular venous blood temperature was always higher than that of the arterial blood, demonstrating that heat was released via the CBF during the normothermic as well as the hyperthermic exercise condition. However, heat removal via the jugular venous blood was 30 +/- 6 % lower during hyperthermia compared to the control trial. The reduced heat removal from the brain was mainly a result of a 20 +/- 6 % lower CBF (22 +/- 9 % reduction in MCA V(mean)), because the v-aD(temp) was not significantly different in the hyperthermic (0.20 +/- 0.05 degrees C) compared to the control trial (0.22 +/- 0.05 degrees C). During hyperthermia, the impaired heat removal via the blood was combined with a 7 +/- 2 % higher heat production in the brain and heat was consequently stored in the brain at a rate of 0.20 +/- 0.06 J g(-1) min(-1). The present results indicate that the average brain temperature is at least 0.2 degrees C higher than that of the body core during exercise with or without hyperthermia.

The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat. A secondary aim was to determine whether the upward drift in oxygen consumption (V̇O2) during prolonged exercise is confined to the active muscles. Seven euhydrated, endurance‐trained cyclists performed two bicycle exercise trials in the heat (35 °C; 40–50% relative humidity; 61 ± 2% of maximal V̇O2), separated by 1 week. During the first trial (dehydration trial, DE), they bicycled until volitional exhaustion (135 ± 4 min, mean ± s.e.m.), while developing progressive dehydration and hyperthermia (3.9 ± 0.3% body weight loss; 39.7 ± 0.2 °C oesophageal temperature, Toes). In the second trial (control trial), they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 ± 0.1 °C after 30 min exercise. In both trials, cardiac output, leg blood flow (LBF), vascular conductance and V̇O2 were similar after 20 min exercise. During the 20 min‐exhaustion period of DE, cardiac output, LBF and systemic vascular conductance declined significantly (8–14%; P < 0.05) yet muscle vascular conductance was unaltered. In contrast, during the same period of control, all these cardiovascular variables tended to increase. After 135 ± 4 min of DE, the 2.0 ± 0.6 l min−1 lower blood flow to the exercising legs accounted for approximately two‐thirds of the reduction in cardiac output. Blood flow to the skin also declined markedly as forearm blood flow was 39 ± 8% (P < 0.05) lower in DE vs. control after 135 ± 4 min. In both trials, whole body V̇O2 and leg V̇O2 increased in parallel and were similar throughout exercise. The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial‐venous O2 (a‐vO2) difference. It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction. Furthermore, the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles.

The effect of heat stress on blood flow and metabolism in an exercising leg was studied in seven subjects walking uphill (12-17%) at 5 km/h on a treadmill for 90 min or until exhaustion. The first 30 min of exercise were performed in a cool environment (18-21 degrees C); then subjects moved to an adjacent room at 40 degrees C and continued to exercise at the same speed and inclination for a further 60 min or to exhaustion, whichever occurred first. The rate of O2 consumption, 2.6 l/min (1.8-3.3) (average from cool and hot conditions), corresponded to 55-77% of their individual maximums. In the cool environment a steady state was reached at 30 min. When the subjects were shifted to the hot room, the core temperature and heart rate started to rise and reached values greater than 39 degrees C and near-maximal values, respectively, at the termination of the exercise. The leg blood flow (thermodilution method), femoral arteriovenous O2 difference, and consequently leg O2 consumption were unchanged in the hot compared with the cool condition. There was no increase in release of lactate and no reduction in glucose and free net fatty acid uptake in the exercising leg in the heat. Furthermore, the rate of glycogen utilization in the gastrocnemius muscle was not elevated in the hot environment. There was a tendency for cardiac output to increase in the heat (mean 15.2 to 18.4 l/min), which may have contributed to the increase in skin circulation, together with a possible further reduction in flow to other vascular beds, because muscle blood flow was not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present study we examined the effect of hyperthermia on the middle cerebral artery mean blood velocity (MCA Vmean) during prolonged exercise. We predicted that the cerebral circulation would be impaired when hyperthermia is present during exercise and assumed that this could be observed as a reduced MCA Vmean. Eight endurance trained men (maximum oxygen uptake (V̇O2,max) 70 ± 1 ml min−1 kg−1 (mean ±s.e.m.)) performed two exercise trials at 57 % of V̇O2,max on a cycle ergometer in a hot (40 °C; hyperthermic trial) and in a thermoneutral environment (18 °C; control trial). In the hyperthermic trial, the oesophageal temperature increased throughout the exercise period reaching a peak value of 40.0 ± 0.1 °C at exhaustion after 53 ± 4 min of exercise. In the control trial, exercise was maintained for 1 h without any signs of fatigue and with core temperature stabilised at 37.8 ± 0.1 °C after ≈15 min of exercise. Concomitant with the development of hyperthermia, MCA Vmean declined by 26 ± 3 % from 73 ± 4 cm s−1 at the beginning of exercise to 54 ± 4 cm s−1 at exhaustion (P < 0.001). In contrast, MCA Vmean remained unchanged at 70‐72 cm s−1 throughout the 1 h control trial. When individually determined regression lines for MCA Vmean and arterial carbon dioxide pressure (Pa,CO2) obtained during preliminary exercise tests were used to account for the differences in Pa,CO2 between the hyperthermic and control trial, it appeared that more than half of the reduction in MCA Vmean (56 ± 8 %) was related to a hyperventilation‐induced drop in Pa,CO2. Declining cardiac output and arterial blood pressure accounted for the remaining part of the hyperthermia‐induced reduction in MCA Vmean. The present results demonstrate that the development of hyperthermia during prolonged exercise is associated with a marked reduction in MCA Vmean.

We hypothesized that fatigue due to hyperthermia during prolonged exercise in the heat is in part related to alterations in frontal cortical brain activity. The electroencephalographic activity (EEG) of the frontal cortex of the brain was measured in seven cyclists [maximal O2 uptake (VO2max) 4.8 +/- 0.1 (SE) 1 min-1] cycling at 60% VO2max in a hot (H, 42 degrees C) and a cool (C, 19 degrees C) environment. Fast Fourier transformation of the EEG was used to obtain power spectrum areas in the alpha (8-13 Hz) and beta (13-30 Hz) frequencies. The ratio alpha/beta was calculated as an index of arousal level; an elevated alpha/beta index reflects suppressed arousal. In H, subjects fatigued after 34.4 +/- 1.4 min coinciding with an oesophageal temperature (Toes) of 39.8 +/- 0.1 degrees C, an almost maximal heart rate (HR 192 +/- 3 beats.min-1), a rating of perceived exertion (RPE) of 19.0 +/- 0.8 and significantly elevated alpha/beta index (188 +/- 71% of the value after 2 min of exercise; P < 0.05). In C, subjects cycled for a similar period while Toes was below 38 degrees C, HR and RPE were low, and the alpha/beta index was not significantly elevated (59 +/- 27% of 2 min value; P = NS). Increases in the alpha/beta index were strongly correlated to increases in Toes (r2 = 0.98; P = 0.0001).