This study examined the effects of precooling on performance and pacing during 30-km cycling exercise in hot and temperate environments. 8 trained male cyclists performed 4 trials involving either cooling (PREC and PREC) or no-cooling interventions (TEMP and HOT) prior to a 30-km self-paced cycling exercise in either a hot (35°C, 68% relative humidity) or temperate environment (24°C, 68% relative humidity). Exercise time was longer in HOT (60.62±3.47 min) than in TEMP (58.28±3.30 min; <0.001), and precooling attenuated this thermal strain performance impairment (PREC 58.28±3.30 min; =0.048), but it was still impaired compared with TEMP (=0.02). Exercise performance in PREC (54.58±4.35 min) was no different from TEMP. Initial power output was sustained until the end of the exercise in both TEMP and PREC, but was reduced from the 12 km until the end of the trial in HOT (P<0.05). This reduction was delayed by precooling because power output was reduced only after the 20 km during PREC (P<0.05). Heart rate was similar in all conditions throughout almost the entire exercise, suggesting the maintenance of similar relative intensities. In conclusion, precooling was effective in attenuating, but not completely reversing thermal strain performance impairment and offered no ergogenic effect in the temperate environment.

Exhaustive exercise in a hot environment can impair performance. Higher epinephrine plasma levels occur during exercise in heat, indicating greater sympathetic activity. This study examined the influence of exercise in the heat on stress levels. Nine young healthy men performed a maximal progressive test on a cycle ergometer at two different environmental conditions: hot (40°C) and normal (22°C), both between 40% and 50% relative humidity. Venous blood and saliva samples were collected pre-test and post-test. Before exercise there were no significant changes in salivary biomarkers (salivary IgA: p = 0.12; α-amylase: p = 0.66; cortisol: p = 0.95; nitric oxide: p = 0.13; total proteins: p = 0.07) or blood lactate (p = 0.14) between the two thermal environments. Following exercise, there were significant increases in all variables (salivary IgA 22°C: p = 0.04, 40°C: p = 0.0002; α-amylase 22°C: p = 0.0002, 40°C: p = 0.0002; cortisol 22°C: p = 0.02, 40°C: p = 0.0002; nitric oxide 22°C: p = 0.0005, 40°C: p = 0.0003, total proteins 22°C: p<0.0001, 40°C: p<0.0001 and; blood lactate 22°C: p<0.0001, 40°C: p<0.0001) both at 22°C and 40°C. There was no significant adjustment regarding IgA levels between the two thermal environments (p = 0.74), however the levels of α-amylase (p = 0.02), cortisol (p<0.0001), nitric oxide (p = 0.02) and total proteins (p = 0.01) in saliva were higher in the hotter conditions. Blood lactate was lower under the hot environment (p = 0.01). In conclusion, enduring hot temperature intensified stressful responses elicited by exercise. This study advocates that hot temperature deteriorates exercise performance under exhaustive stress and effort conditions.

The purpose of this study was to investigate the effects of a 6-week aerobic training period on the time to fatigue (t lim) during exercise performed at the maximal lactate steady state (MLSS). Thirteen untrained male subjects (TG; age 22.5 ± 2.4 years, body mass 72.9 ± 6.7 kg and VO2max 44.9 ± 4.8 mL kg(-1) min(-1)) performed a cycle ergometer test until fatigue at the MLSS power output before and after 6 weeks of aerobic training. A group of eight control subjects (CG; age 25.1 ± 2.4 years, body mass 70.1 ± 9.8 kg and VO2max 45.2 ± 4.1 mL kg(-1) min(-1)) also performed the two tests but did not train during the 6-week period. There were no differences between the groups with respect to the VO2max or MLSS power output (MLSSw) before the treatment period. The VO2max and the MLSSw of the TG increased by 11.2 ± 7.2 % (pre-treatment = 44.9 ± 4.8 vs. post-treatment = 49.8 ± 4.5 mL kg(-1) min(-1)) and 14.7 ± 8.9 % (pre-treatment = 150 ± 27 vs. post-treatment = 171 ± 26 W), respectively, after 6 weeks of training. The results of the CG were unchanged. There were no differences in t lim between the groups or within groups before and after training. Six weeks of aerobic training increases MLSSw and VO2max, but it does not alter the t lim at the MLSS.

The aim of this study was to compare the maximal lactate steady state (MLSS) and ventilatory threshold (VT) under different environments (TEMP: 22°C; and HOT: 40°C; 50% RH). 8 male subjects (age 23.9±2.4 years, body mass 75.9±7.3 kg and VO2(max) 47.8±4.9 mL·kg(-1)·min(-1)) performed a series of tests to determine the peak workload (W(peak)), VT and MLSS on a cycle ergometer. W(peak) was higher in the TEMP as compared to the HOT condition (225±9 W vs. 195±8 W, respectively; p<0.05). The workload at MLSS was higher at 22°C (180±11 W) than 40°C (148±11 W; p<0.05), as well as VT at 22°C (156±9 W) was higher than 40°C (128±6 W). Likewise, the blood lactate concentration at MLSS was higher at 22°C (5.60±0.26 mM) than 40°C (4.22±0.48 mM; p<0.05). The mean of heart rate (HR) was not statistically different between TEMP (168±3 bpm) and HOT (173±3 bpm) at MLSS, despite being different at trials between the 25(th) and the 30(th) min of exercise. The HR at VT was significantly higher in HOT (153±4 bpm) as compared to the TEMP (145±2 bpm). Our results suggest that environmental conditions may influence the determination of MLSS and VT. Moreover, VT was appropriate for estimation of the workload at MLSS in the HOT.