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Performance and Pacing during Cycle Exercise in Hyperthermic and Hypoxic Conditions


Medicine & Science in Sports & Exercise: May 2016 - Volume 48 - Issue 5 - p 845–853
doi: 10.1249/MSS.0000000000000839

Introduction This study examined the influence of alterations in maximal oxygen uptake (V˙O2max) in mediating performance and pacing during prolonged self-paced exercise.

Methods Twelve well-trained cyclists completed a 750-kJ time trial in temperate (COOL, 18°C), hot (HOT, 35°C), and hypoxic (HYP, 18°C; FiO2, 0.145) conditions, creating models with a stable, progressively decreasing, and acutely decreased V˙O2max, respectively.

Results Trial completion was faster in COOL (48.2 ± 5.7 min) compared with HOT (55.4 ± 5.0 min) and HYP (60.1 ± 6.5 min) (P < 0.001), with HOT being faster than HYP (P = 0.028). Core temperature reached 39.0°C ± 0.6°C (COOL), 39.8°C ± 0.5°C (HOT), and 38.5°C ± 0.4°C (HYP; P < 0.01). Power output during COOL was higher than HOT from 40% of work completed onward (P < 0.05) and for the entirety of HYP (P < 0.001), in which it was lower than HOT at 20%–30% (P < 0.05). Normalized power output during COOL and HYP varied by ∼13% and ∼16%, respectively, whereas a ∼27% variation occurred in HOT. V˙O2 in COOL was higher than HOT from 70% onward (P < 0.01) and higher than HYP throughout exercise (P < 0.001). Relative to baseline V˙O2max (%V˙O2max) in normoxia (COOL and HOT) and hypoxia (HYP), %V˙O2max during HOT (78% ± 8%) was lower than COOL (84% ± 7%; P = 0.005) and HYP (87% ± 5%; P = 0.003).

Conclusions Despite an acutely reduced V˙O2max and power output in HYP, pacing and %V˙O2max were similar to COOL. In contrast, the progressive decrease in V˙O2max and power output in HOT resulted in a more variable pacing pattern with %V˙O2max decreasing throughout exercise. These data support the premise that pacing is associated with maintaining an optimal performance intensity, in conjunction with acute and progressive alterations in V˙O2max.

Athlete Health and Performance Research Centre, Aspetar Orthopaedic and Sports Medicine Hospital, Doha, QATAR

Address for correspondence: Julien Périard, Ph.D., Aspetar Orthopaedic and Sports Medicine Hospital, Athlete Health and Performance Research Centre, PO Box 29222, Doha, Qatar; E-mail:

Submitted for publication October 2015.

Accepted for publication December 2015.

The regulation of prolonged self-paced (i.e., time trial) exercise has received considerable interest over the last decade owing to its relevance to real-world athletic competition. Various models of regulation have been proposed to modulate performance during such efforts based on independent and integrative mechanisms (1,16,46,47,51,55). Although contention remains, it is generally accepted that pacing—the distribution of work or energy expenditure throughout an exercise task—is a conscious process informed by the balance between effort (i.e., central motor command) and exertion (i.e., afferent feedback), which provokes behavioral adjustments in work rate (2,15).

When conducted under heat stress, performance (i.e., power output) during 30- to 60-min time trials has been shown to be progressively impaired (19,39,41,44,52). This impairment has been suggested to stem from a thermal strain-mediated increase in the cardiovascular response (10,39,42), whereby a thermoregulatory redistribution of blood toward the periphery and a temperature-mediated increase in intrinsic heart rate (HR) compromise central blood volume and the maintenance of cardiac output (13,23,27,48). These adjustments have been shown to decrease maximal oxygen uptake (V˙O2max) during exhaustive incremental and supramaximal exercise (3,37,43), as well as reduce peak oxygen uptake (V˙O2peak) during the end spurt of prolonged time trial efforts (39,41). The reduction in V˙O2peak under heat stress is typically ∼12% greater than that in temperate conditions, in which a ∼5% reduction can occur (39,41,42), primarily in response to the development of peripheral fatigue (40). Interestingly, it was recently demonstrated that the reduction in V˙O2peak occurs progressively during time trial efforts in the heat, but that relative exercise intensity (i.e., fractional utilization of V˙O2peak: %V˙O2peak) is maintained within a relatively narrow range, similar to that of a time trial performed in cool conditions (42).

Conversely, V˙O2max and aerobic performance are acutely decreased at altitude. This occurs in response to a reduction in the partial pressure of O2 in the inspired air at terrestrial altitude (21,25,59), and a reduction in the fraction of inspired O2 (FiO2) during simulated normobaric hypoxia. It is purported that V˙O2max decreases linearly at a rate of ∼7.7% per 1000 m in elevation (59); however, the reduction may actually be curvilinear, with altitude and baseline V˙O2max being factors of influence in determining individual reductions at altitude (34). Despite a dose–response effect of hypoxia reducing V˙O2peak and mean power output at altitude (i.e., 200, 1200, 2200 and 3200 m), pacing during a 5-min cycling time trial has been shown to remain unaffected (11). However, the %V˙O2peak sustained during more prolonged efforts has not been evaluated. Consequently, the acute reduction in V˙O2max at altitude, along with the progressive decrease in V˙O2peak under heat stress appears to provide ideal comparative models to examine the influence of alterations in aerobic capacity in mediating performance and pacing during prolonged self-paced efforts.

Accordingly, the purpose of this study was to examine performance and pacing during time trial exercise conducted in 1) cool normoxic conditions in which V˙O2max is relatively stable or deceases slightly, 2) hot normoxic conditions under which V˙O2max decreases progressively, and 3) cool normobaric hypoxic conditions under which V˙O2max is acutely decreased. To evaluate the %V˙O2max sustained during exercise, V˙O2 measures in the cool and hot conditions were referenced against a baseline V˙O2max value obtained in cool normoxic conditions, whereas %V˙O2max in the normobaric hypoxic condition was calculated with a V˙O2max test conducted in identical hypoxic conditions. It was hypothesized that pacing and %V˙O2max would be similar between the cool and hypoxic conditions due to the acute reduction in V˙O2max in the hypoxic condition, despite the maintenance of a lower power output. It was further hypothesized that pacing in the hot condition would follow a more pronounced positive profile, with %V˙O2max being similar to cool and hypoxic conditions at the start of exercise, and then progressively decreasing.

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Twelve well-trained (>250 km·wk−1) male cyclists not acclimatized to heat or altitude volunteered for this study, which took place in February–March in Qatar. The participants were experienced in self-paced efforts having participated in a series of time trials and/or triathlons in the months preceding the study. Their characteristics were (mean ± SD) age, 35 ± 4 yr; body mass, 77.3 ± 5.1 kg; and height, 177.3 ± 6.1 cm. Participants were fully informed of the experimental procedures, and potential risks before giving written informed consent. They were also required to complete a medical history questionnaire and physical activity readiness questionnaire before being admitted to the study. The protocol was approved by the Anti-Doping Lab Qatar Institutional Review Board. All procedures conformed to the standards of the Declaration of Helsinki.

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Preexperimental trial.

Two baseline testing sessions were undertaken in a counterbalanced order in normoxia (FiO2, 0.2093) and normobaric hypoxia (FiO2, 0.145; ∼3000 m) in an environment set to 18°C and 40% relative humidity with a 12.5 km·h−1 airflow. The participants were blinded to the FiO2. On arrival to the laboratory, height and nude body mass were measured using a precision stadiometer and balance (Seca 769, Hamburg, Germany). Participants then entered the environmental chamber and sat resting for 10 min before undertaking a V˙O2max test using an online breath-by-breath cardiopulmonary system (Oxycon Pro, CareFusion, Rolle, Switzerland), followed by a familiarization time trial. The V˙O2max protocol consisted of cycling on an electronically braked SRM (Schoberer Rad Meßtechnik, Jülich, Germany) cycle ergometer with a starting power output of 100 W and increasing by 25 W·min−1 until volitional fatigue. V˙O2max and maximum HR were obtained over a 60-s period during the classic plateau phase (24,53), with a respiratory exchange ratio greater than 1.10. Given that V˙O2max is not reduced in the heat during tests lasting less than 15 min (42,50), the V˙O2max value obtained in normoxia was used to calculate %V˙O2max in the COOL and HOT conditions, whereas the V˙O2max in normobaric hypoxia was used to calculate %V˙O2max in the HYP trial. After a 10-min rest period, the familiarization time trial was performed, which consisted of completing 350 kJ of work in the same conditions as the V˙O2max test. Saddle and handlebar positions were adjusted by the participants to their preferred cycling position and remained unchanged for all trials. During all tests, participants wore cycling shorts, socks, and cycling shoes.

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Experimental trial.

Participants arrived at the laboratory at the same time of day on three occasions separated by 4 to 6 d. On arrival (∼60 min before testing), they emptied their bladder and provided a urine sample for the measurement of urine specific gravity (Pal-10-S, Vitech Scientific Ltd. West Sussex, UK). They were then weighed nude before changing into cycling attire and inserting a rectal thermistor probe. Participants then rested in the seated position in temperate conditions (20°C–22°C; 50% relative humidity; FiO2, 0.2093) while being instrumented with HR and skin temperature sensors. After instrumentation, they mounted the cycle ergometer and rested in a cycling position for 5 min, after which time resting baseline data were collected for 1 min. Participants then performed a standard warm-up of 5 min at 150 W, which included 3 × 10 s spin-ups (i.e., high cadence accelerations) at 2, 3, and 4 min. Once the baseline and warm-up measurements in temperate conditions were completed, participants entered the climate chamber (Tescor, Warminster, PA) set to either cool (COOL, 18°C; 40% relative humidity; FiO2, 0.2093), hot (HOT, 35°C; 60% relative humidity; FiO2, 0.2093), or normobaric hypoxic (HYP, 18°C; 40% relative humidity, FiO2, 0.145; ∼3000 m) conditions with a 12.5 km·h−1 airflow. The experimental conditions were counterbalanced with participants blinded to the FiO2. The FiO2 in the HYP trial was chosen because it provides an acute reduction in V˙O2max similar to the progressive decrease in V˙O2peak (∼17%) that occurs on completion of a ∼60-min time trial in the heat (39,41,42). Upon entering the chamber, participants then sat resting on the ergometer for 5 min for the measurement of baseline values inside the chamber. A self-paced time trial was then performed with the aim of completing 750 kJ of work as quickly as possible. Participants were informed of every 10% work completed and upon reaching the final 3%, whereupon a kilojoule countdown was provided until completion of the time trial. This was the only form of feedback provided, along with the ability to change between gears (i.e., resistance).

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Cardiorespiratory and temperature measurements.

Pulmonary V˙O2, carbon dioxide elimination (V˙CO2), ventilation (V˙E), respiratory frequency (Rf), end-tidal partial pressure of O2 (PETO2) and end-tidal partial pressure of CO2 (PETCO2) were measured with the breath-by-breath cardiopulmonary system at 10%, 30%, 50%, 70%, 90%, and 100% of work completed. Percent oxyhemoglobin saturation (SpO2) was measured via pulse oximetry (8000SL; Nonin Medical Inc, Plymouth, MN) on the right middle finger at the same intervals. Measurements were conducted over 1 min and averaged to represent the percent of work completed. HR was monitored telemetrically via a chest-strap transmitter (T-31 Polar Electro, Lake Success, NY) and recorded continuously for each 10% work interval. Results for HR and power output represent the mean of each 10% segment (i.e., 75 kJ).

Body core temperature was continuously monitored with a rectal temperature probe (MRB rectal probe; Ellab, Hilleroed, Denmark) inserted 12 cm beyond the anal sphincter. Skin temperatures were monitored with iButton™ temperature sensors/data loggers (Maxim Integrated Products, Sunnyvale, CA) and used to calculate mean skin temperature with the weighted coefficient proposed by Ramanathan (45): chest, 30%; upper arm, 30%; thigh, 20%; and lower leg, 20%. Ethical cutoff points for terminating the trials were attaining a rectal temperature of 40.5°C or maintaining an SpO2 below 75% for 15 min.

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Hydration and perceptual measurements.

Participants were instructed to drink 6 mL of water per kg of body mass every 2.5 h on the day before each experimental session to ensure euhydration at the start of exercise. During the time trial, they were permitted to drink ad libitum. Body mass changes were evaluated at the conclusion of each trial (nude with dry skin) to determine sweat production with corrections for fluid ingested and sweat trapped in clothing. The participants were also asked to keep a 24-h food diary before testing and to replicate their diet before the second and third trials. Rating of perceived exertion (RPE) using the Borg 6–20 scale (7) and thermal comfort using the Bedford Thermal Comfort Scale (5) were recorded at 10%, 30%, 50%, 70%, 90%, and 100% work intervals. Participants were familiarized with the scales before testing.

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Statistical analysis.

All statistical calculations were performed using predictive analytics software (PASW) version 21.0 (SPSS, Chicago, IL). Two-way (condition × time) repeated-measures ANOVA were performed to test significance between and within treatments. ANOVA assumptions were verified preceding all statistical procedures; however, none of the data violated the assumption of sphericity. Where significant effects were established, pairwise differences were identified using the Bonferroni post hoc analysis procedure adjusted for multiple comparisons. Preexperimental values between COOL, HOT, and HYP, as well as hydration and time values between conditions, were evaluated using a one-way ANOVA. P values less than 0.05 were considered statistically significant. Effect size was measured using partial eta-squared (η2) values with η2 > 0.06 representing a moderate effect and η2 ≥ 0.14 a large effect. All values are expressed as means ± SD.

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Preexperimental V˙O2max assessment responses.

Participants attained a significantly higher V˙O2max in normoxia (4.6 ± 0.3 L·min−1) compared with normobaric hypoxia (3.9 ± 0.2 L·min−1; P < 0.001). Peak power output (378 ± 28 vs 328 ± 31 W; P < 0.001) and HR (182 ± 8 bpm vs 178 ± 8 bpm; P = 0.002) at V˙O2max were also higher in normoxia, as was SpO2 (89% ± 4% vs 78% ± 4%; P < 0.001).

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Time trial responses.

The time required to complete 750 kJ was shorter in COOL (48.2 ± 5.7 min) compared with HOT (55.4 ± 5.0 min) and HYP (60.1 ± 6.5 min) (P < 0.001), with HOT being shorter than HYP (P = 0.028). A significant condition effect (P < 0.001, η2 = 0.83) was observed for power output whereby it was higher in COOL relative to HOT (P < 0.001) and HYP (P < 0.001) (Fig. 1). A trend toward power output being higher in HOT compared with HYP was also noted (P = 0.08). Significant time (P < 0.001, η2 = 0.60) and interaction (P < 0.001, η2 = 0.31) effects were observed for power output with an increase from 90% to 100% of work completed (P < 0.046). In COOL and HYP, power output remained stable during the first 90% of the trial, whereas in HOT, a decrease occurred from 10% to 90% of work completed (P < 0.05). When expressed as a function of the average power sustained in each respective condition (Fig. 1), pacing remained even during COOL, with normalized power output varying only by ∼13%. In HOT a ∼27% variation in normalized power output was observed, which resulted in a significant decrease from 10% to 90% of work completed (P < 0.05). In HYP, normalized power output followed a similar pattern to COOL, varying by ∼16%, but decreasing from 20% to 90% (P < 0.05).



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Cardiorespiratory responses.

A significant condition effect (P < 0.001, η2 = 0.70) was observed for V˙O2, which was higher in COOL than HOT (P = 0.006) and HYP (P < 0.01) (Fig. 2). Time (P < 0.001, η2 = 0.46) and interaction (P = 0.003, η2 = 0.21) effects were noted with V˙O2 increasing at 100% of work completed relative to 70% and 90% values (P < 0.05). When expressed as a percentage of baseline V˙O2max in normoxia (COOL and HOT trials) and hypoxia (HYP trial), a significant condition effect (P < 0.001, η2 = 0.53) was observed with mean %V˙O2max in HOT (78% ± 8%) being lower than COOL (84% ± 7%; P = 0.005) and HYP (87% ± 5%; P = 0.003) (Fig. 2). An interaction effect (P = 0.004, η2 = 0.20) revealed that %V˙O2max in COOL increased at 100% of work completed relative to 50%, 70%, and 90% (P < 0.05), whereas in HOT and HYP, the increase at 100% was greater than that sustained at 70% and 90% (P < 0.05). %V˙O2max during the final 3% of the time trial was higher in COOL (91% ± 8%) and HYP (94% ± 6%) compared with HOT (83% ± 9%; P < 0.001).



There were significant condition (P ≤ 0.05, η2 > 0.24) and time (P < 0.001, η2 > 0.53) effects for V˙CO2, Rf, V˙E, PETO2, and PETCO2 (Table 1). Moreover, V˙E, PETO2, and PETCO2 showed a significant interaction effect (P < 0.005, η2 > 0.20), whereas only a trend was noted for V˙CO2 and Rf (P ≤ 0.162, η2 ≥ 0.12). A significant condition effect (P < 0.001, η2 = 0.98) was observed for SpO2 with HYP being lower than both COOL and HOT (P < 0.001; Table 1). Time (P < 0.001, η2 = 0.82) and interaction (P < 0.001, η2 = 0.62) effects indicated a significant decrease in SpO2 from rest to exercise onset (P < 0.001), remaining stable thereafter. Baseline SpO2 inside the environmental chamber was higher in COOL (99% ± 1%) than HOT (97% ± 1%) and HYP (93% ± 2%) (P < 0.001), with HOT also being higher than HYP (P < 0.001).



A significant condition effect (P < 0.001, η2 = 0.55) was observed for HR, which was higher in HOT compared with HYP (P < 0.001; Fig. 3). A trend toward HR being higher in HOT compared with COOL was also noted (P = 0.063). A time effect (P < 0.001, η2 = 0.71) indicated that HR increased from 10% to 20% and then remained stable (P < 0.001). An interaction effect (P < 0.001, η2 = 0.32) revealed an increase in each condition from 10% to 20% of work completed (P < 0.001) and then a stabilization in COOL and HYP, whereas an increase was observed at 50%, 60%, and 70% in HOT (P < 0.05). Peak HR during the final 3% of the time trials reached 98% ± 3% (COOL), 98% ± 5% (HOT), and 95% ± 5% (HYP) of that observed in the pre-experimental V˙O2max assessment in normoxia and normobaric hypoxia, respectively.



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Temperature responses.

A significant condition effect (P = 0.002, η2 = 0.42) was noted for core temperature whereby it was higher in HOT compared with HYP (P = 0.005), with a trend toward being significantly higher than COOL (P = 0.096; Fig. 4). A time effect (P < 0.001, η2 = 0.92) was also noted indicating a progressive increase in core temperature for resting values. An interaction effect (P < 0.001, η2 = 0.86) further indicated that in COOL the increase levelled off after 50% of work completed, whereas in HOT, it continued until time trial completion, and in HYP, a levelling off occurred from 30% onward. A significant condition effect (P < 0.001, η2 = 0.97) was noted for skin temperature with HOT being higher than both COOL and HYP (P < 0.001; Fig. 4). Time (P < 0.001, η2 = 0.53) and interaction (P < 0.001, η2 = 0.84) effects were also observed with skin temperature decreasing in COOL (P < 0.05) and then levelling off from 30% onward. In HOT, an increase occurred up to 20% of work completed (P < 0.05), remaining stable thereafter. In HYP, a biphasic decrease occurred from preexercise baseline outside the climate chamber to 60% (P < 0.05) and then from 70% onward (P < 0.05).



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Hydration and perceptual responses.

Preexercise body mass in COOL (77.0 ± 4.9 kg), HOT (77.1 ± 4.9 kg), and HYP (77.3 ± 4.8 kg) were similar (P = 0.081), as was urine specific gravity (1.015 ± 0.008, 1.014 ± 0.007 and 1.016 ± 0.008, respectively, for COOL, HOT, and HYP, P = 0.592). Fluid consumption during exercise was greater in HOT (1.2 ± 0.3 L·h−1) compared with COOL (0.6 ± 0.2 L·h−1) and HYP (0.6 ± 0.3 L·h−1) (P < 0.001). The greater fluid intake compensated for the greater sweat rate observed in HOT (2.1 ± 0.4 L·h−1) compared with COOL (1.3 ± 0.2 L·h−1) and HYP (1.1 ± 0.2 L·h−1) (P < 0.001). Sweat rate was also slightly greater in COOL compared with HYP (P = 0.047). Percent body mass loss in COOL, HOT, and HYP were 0.7% ± 0.2%, 1.2% ± 0.4%, and 0.7% ± 0.7%, respectively, with a trend toward HOT being greater than COOL (P = 0.065).

A condition effect (P = 0.028, η2 = 0.28) was noted for RPE with HOT being higher than HYP (P = 0.029; Table 2). A time effect (P < 0.001, η2 = 0.82) was also observed with a progressive increase in RPE, whereas only a trend toward and interaction effect was indicated (P = 0.082, η2 = 0.14). A main effect of condition (P < 0.001, η2 = 0.88) was observed for thermal discomfort with HOT being higher than both COOL and HYP (P < 0.001; Table 2). Preexercise thermal discomfort inside the climate chamber was greater in HOT (5.0 ± 0.6) than COOL (2.0 ± 0.9) and HYP (2.0 ± 0.9) (P < 0.001). A time effect (P < 0.001, η2 = 0.85) revealed an increase from preexercise baseline inside the climate chamber to 10% of work completed (P < 0.001) with values stabilizing from 50% onward. An interaction effect (P < 0.001, η2 = 0.36) further indicated that in COOL and HYP thermal discomfort increased from rest to 10% (P < 0.001) and then remained relatively stable. In HOT, thermal discomfort increased from rest to 30% (P = 0.046) and thereafter at 100% (P = 0.006).



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The purpose of this study was to examine performance and pacing during prolonged self-paced exercise in response to acute (HYP) and progressive (HOT) reductions in V˙O2max. The novel findings of the study are that despite an acutely reduced V˙O2max and average power output in HYP, pacing was similar to that of the COOL condition, as was the %V˙O2max sustained. In contrast, the progressive decrease in power output in the HOT condition resulted in a more pronounced positive or parabolic (i.e., reversed J-shaped) pacing pattern, with %V˙O2max decreasing throughout the time trial. Based on previous findings, however, it would appear that the decrease in %V˙O2max in the heat occurred in response to a progressive reduction in V˙O2max/peak, which allowed for maintaining a similar %V˙O2max/peak to that of cooler conditions (42). Taken together, these results reinforce the premise that self-paced exercise in experienced and motivated individuals is mediated by the maintenance of relative exercise intensity within a narrow range, or optimal performance intensity, in conjunction with both acute and progressive reductions in maximal aerobic capacity.

Our data indicate that the pacing pattern adopted during protracted time trials (50–60 min) in COOL and HYP was similar, despite significantly different mean power outputs (Fig. 1). This observation is supported by a previous study examining short time trials (5 min) at altitudes ranging from 200 to 3200 m (11). Interestingly, the authors also reported that hypoxia did not affect gross mechanical efficiency during time trials efforts, likely because cadence was self-selected (31,32), as it was in the current study. Hence, the similar pacing pattern observed in the present study appears to result from the maintenance of an analogous %V˙O2max. The acute reduction in V˙O2max induced by moderate hypoxia occurs in response to a decrease in the fraction of O2 in the inspired air (21,25,59). Accordingly, a ∼15% lower V˙O2max was noted in normobaric hypoxia during the preexperimental V˙O2max assessment, relative to measures taken in normoxia. During the time trial in HYP, SpO2 and V˙O2 were ∼12% lower than in COOL, yet the %V˙O2max maintained was comparable (Fig. 2). This is attributable to a similar relative reduction in V˙O2peak during the final 3% of the time trial in the COOL and HYP conditions. Moreover, maximum HR during the V˙O2max assessment was ∼2.6% lower in HYP than in COOL, whereas HR throughout the time trials was ∼2.8% lower (Fig. 3). The magnitude of decrease in maximum HR during acute hypoxia is related to the severity of the hypoxic challenge and suggested to stem from an increase in parasympathetic activity (6,8,33). The maintenance of a similar %V˙O2max in the COOL and HYP conditions is also evidenced by a comparable ventilatory response (i.e., Rf and V˙E, Table 1), which is modulated by changes in relative exercise intensity (4,58). The RPE values in Table 2 lend further support to the notion that participants were exercising at similar relative exercise intensities while maintaining very dissimilar power outputs.

In the HOT condition, pacing followed a similar pattern to several previous studies in which power output was matched to that of exercise in cooler conditions at the onset of exercise (∼10–15 min), but then decreased significantly as exercise progressed (Fig. 1) (19,38,39,41,42,44,52,56). This response has been described previously and stems from V˙O2max/peak remaining unaffected during exercise in the heat over short periods when thermal strain is minimal (i.e., when skin temperature is elevated and core temperature remains <38°C) (42,49,50). When thermal strain develops, however, it significantly impacts upon the circulatory response inducing a decrease in V˙O2max (3,37,39,41,43). The decrement in power output in the current study can therefore be attributed to the influence of increasing thermal strain (Fig. 4) on the cardiovascular response (e.g., HR; Fig. 3). Indeed, the development of thermal strain beyond core and skin temperatures of 38°C and 34°C, respectively (30) induces systemic cardiovascular adjustments during exercise in the heat that are characterized by an elevated HR and declines in arterial blood pressure, stroke volume, and cardiac output (48,49). These adjustments stem from a narrowing of the core-to-skin temperature gradient reflexively increasing cutaneous blood flow (10,49) and from a rise in HR mediated by high core temperatures and sympathetic nervous activity (13,28). The thermoregulatory redistribution of blood toward peripheral vascular beds, in combination with the exacerbated HR response, contributes to a reduced central blood volume that ultimately compromises the maintenance of cardiac output (17,48). As a result, V˙O2max is decreased in hot environments, which causes an increase in %V˙O2max when exercising at a given absolute workload. Recently, our laboratory demonstrated that despite differences in power output and pacing profiles, prolonged self-paced exercise performance was associated with the maintenance of %V˙O2peak within a relatively narrow range (80%–85% V˙O2peak) in both HOT and COOL conditions (42). The novelty of this latter study was in describing the time course and extent of decrease in V˙O2peak during prolonged self-paced exercise in the heat, and in demonstrating that the regulation of time trial efforts is associated with the maintenance of an optimal performance intensity. The results of the current study (e.g., V˙O2, HR and RPE) further support this observation, with changes in exercise intensity (relative to preexperimental baseline V˙O2max) similar to those of previous studies with comparable time trial durations (39,41).

When comparing the HOT and HYP conditions, differences between a progressively and acutely decreased V˙O2max are observed. For example, pacing during HYP followed that of the COOL condition with normalized power output varying by ∼16%, whereas a more variable pace (∼27%) occurred in the HOT condition (Fig. 1). The larger variation in power output in the heat was accompanied by higher core and skin temperatures (Fig. 4), along with greater HR, SpO2, PETCO2, and PETO2 values (Table 1). Accordingly, variations in power output under heat stress have previously been reported with trial duration and thermal strain seemingly influencing the extent of variation. Ely et al. (18) reported a variation of 19% in the work performed during a 15-min time trial with modest hyperthermia (peak core and skin temperatures of 38.2°C and ∼36°C, respectively), whereas a >30% variation in normalized power output was noted during a simulated 60-min time trial with severe hyperthermia (core and skin temperatures reaching 39.4°C and ∼35°C, respectively) (42). Interestingly, the progressive increase in thermal and cardiovascular strain resulted in a decrease in power output in the HOT condition, which yielded a similar power output to that of the HYP condition from 40% of work completed onward. Notwithstanding, mean power output was ∼8% greater in the HOT condition (35°C), resulting in a faster time trial than that in HYP (∼3000 m). Interestingly, RPE remained similar between conditions, which is indicative of maintaining similar relative exercise intensities (Table 2). Based on these findings, it may be surmised that a time trial performed in combined hot and hypoxic conditions would be initiated at a power output comparable to that of the HYP time trial. Thereafter, power output would gradually decrease in conjunction with the development of thermal and cardiovascular strain. The extent of the decrement, however, would likely not be as pronounced as during the heat stress condition, given the lower power output sustained and concomitantly lesser overall metabolic heat production (26). This is supported by the observation that despite maintaining a similar %V˙O2max during the COOL and HYP conditions, core and skin temperatures (Fig. 4) were lower in the HYP time trial, where average power output was lower. Interestingly, three recent studies have combined warm/hot and hypoxic environments to investigate their influence on exercise performance (22,29,57). Girard and Racinais (22) showed that relative to control conditions (22°C), exercise capacity was reduced by ∼35% when cycling to exhaustion at 66% V˙O2max in hot (35°C) or hypoxic (FiO2, 0.15) conditions, and by ∼51% when combining the two stressors. Correspondingly, Lee et al. (29) concluded that the combination of heat stress (40°C) and hypoxia (FiO2, 0.14) induced greater physiological strain than either stress independently during 90 min of cycling at 50% V˙O2max. In one study using self-paced exercise (30 min), it was shown that total work (kJ) was reduced by ∼34% in hypoxia (FiO2: 0.13) and ∼3% when ambient temperature was increased by 10°C, with the combination of both stressors being additive and reducing performance by ∼38% (57). This latter protocol, however, only compared ambient temperatures of 15°C and 25°C with a relative humidity of ∼35%, conditions which are compensable. In the current study, time trial performance was reduced by ∼12% in the HOT condition and by ∼21% in HYP (Fig. 1).

Data from this study, in conjunction with recent observations (42), propose that self-paced exercise performance is modulated by the maintenance of an optimal performance intensity. The intensity that can be sustained is dependent on several factors, including prior experience, fitness, task knowledge, and motivation. Accordingly, interindividual differences and slight intraindividual (i.e., day-to-day) variations exist in the %V˙O2max that can be sustained (12,14). The exercise task itself should also be considered as a factor of influence. For example, time trials of ∼60 min have been shown to be conducted around 85% V˙O2max, whereas during shorter efforts, a greater fraction of V˙O2max is used (35,36,39,41,42,54). Interestingly, the range in which %V˙O2max is sustained widens under heat stress when exercise becomes protracted and a disassociation develops between %V˙O2peak and HR and RPE (42). In the current study, HR tended to be higher in the HOT relative to COOL condition, as did RPE from 50% of work completed onward (Table 2). Consequently, pacing appears to involve the conscious interpretation of effort (i.e., amount of mental and physical energy allocated toward completing a task) and exertion (i.e., level of strain experienced during a task) (2,7). More specifically, it is an integrative process during which a balance is stricken between an efferent copy of central motor command (i.e., corollary discharge) and afferent sensory input (i.e., physiological signals) originating from the periphery (9,15,20). The comparative balance between effort and exertion, or the predicted and actual sensory feedback, may therefore allow for sustaining an optimal performance intensity.

In summary, data from the current study support the premise that pacing and performance during prolonged time trial efforts are associated with acute and progressive alterations in V˙O2max/peak. Although V˙O2max was acutely reduced in HYP, a pacing pattern similar to that adopted in the COOL conditions was observed. This occurred in conjunction with the maintenance of a similar %V˙O2max throughout the time trials, despite a reduced power output. Conversely, pacing in the HOT condition followed a positive or parabolic (i.e., reversed J-shaped) pattern. This occurred in response to a progressive decrease in V˙O2max/peak, mediated by the rise in thermal strain. Accordingly, power output at the onset of exercise in the heat was similar to that of the cooler environment, and as V˙O2max decreased, power output was reduced in conjunction with the maintenance of a similar %V˙O2max (42). In conclusion, self-paced exercise in experienced and motivated individuals appears to be associated with the maintenance of relative exercise intensity within a narrow range, or optimal performance intensity, in conjunction with acute and progressive alterations in maximal oxygen uptake, which influence the perception of effort and exertion.

The authors thank the participants for their time and effort. The results of the present study do not constitute endorsement by ACSM.

This project was funded by the Qatar National Research Fund Junior Scientists Research Experience Program (3-004-3-002).

The authors have no conflicts of interest to disclose.

J. D. P. conceived and designed the experiments. J. D. P. and S. R. collected, analyzed and interpreted the data. J. D. P. drafted and revised the article. S. R. revised the article. J. D. P. and S. R. approved the final version of the article.

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1. Abbiss CR, Laursen PB. Describing and understanding pacing strategies during athletic competition. Sports Med. 2008; 38(3): 239–52.
2. Abbiss CR, Peiffer JJ, Meeusen R, Skorski S. Role of ratings of perceived exertion during self-paced exercise: what are we actually measuring? Sports Med. 2015; 45(9): 1235–43.
3. Arngrímsson SA, Stewart DJ, Borrani F, Skinner KA, Cureton KJ. Relation of heart rate to percent VO2 peak during submaximal exercise in the heat. J Appl Physiol (1985). 2003; 94(3): 1162–8.
4. Åstrand P-O, Rodahl K, Dahl HA, Stromme SB. Respiration. In: Åstrand P-O, Rodahl K, editors. Text Book of Worf Physiology: Physiological Bases of Exercise. Champaign, IL: McGraw-Hill; 2003. pp. 177–212.
5. Bedford T. The Warmth Factor In Comfort At Work: A Physiological Study Of Heating And Ventilation. London: HMSO; 1936. Available from: HMSO.
6. Benoit H, Busso T, Castells J, Geyssant A, Denis C. Decrease in peak heart rate with acute hypoxia in relation to sea level VO(2max). Eur J Appl Physiol. 2003; 905–6): 514–9.
7. Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc. 1982; 14(5): 377–81.
8. Boushel R, Calbet J-AL, Rådegran G, Sondergaard H, Wagner PD, Saltin B. Parasympathetic neural activity accounts for the lowering of exercise heart rate at high altitude. Circulation. 2001; 104(15): 1785–91.
9. Bubic A, von Cramon DY, Schubotz RI. Prediction, cognition and the brain. Front Hum Neurosci. 2010; 4: 25.
10. Cheuvront SN, Kenefick RW, Montain SJ, Sawka MN. Mechanisms of aerobic performance impairment with heat stress and dehydration. J Appl Physiol (1985). 2010; 109(6): 1989–95.
11. Clark SA, Bourdon PC, Schmidt W, et al. The effect of acute simulated moderate altitude on power, performance and pacing strategies in well-trained cyclists. Eur J Appl Physiol. 2007; 102(1): 45–55.
12. Coyle EF, Coggan AR, Hopper MK, Walters TJ. Determinants of endurance in well-trained cyclists. J Appl Physiol (1985). 1988; 64(6): 2622–30.
13. Coyle EF, Gonzalez-Alonso J. Cardiovascular drift during prolonged exercise: new perspectives. Exerc Sport Sci Rev. 2001; 29(2): 88–92.
14. Coyle EF, Holloszy JO. Integration of the physiological factors determining endurance performance ability. In: Holloszy JO, editor. Exercise and Sport Science Reviews. Baltimore, MD: Williams & Wilkins; 1995. pp. 25–63.
15. de Morree HM, Klein C, Marcora SM. Perception of effort reflects central motor command during movement execution. Psychophysiology. 2012; 49(9): 1242–53.
16. Edwards AM, Polman RC. Pacing and awareness: brain regulation of physical activity. Sports Med. 2013; 43(11): 1057–64.
17. Ekelund LG. Circulatory and respiratory adaptation during prolonged exercise of moderate intensity in the sitting position. Acta Physiol Scand. 1967; 69(4): 327–40.
18. Ely BR, Cheuvront SN, Kenefick RW, Sawka MN. Aerobic performance is degraded, despite modest hyperthermia, in hot environments. Med Sci Sports Exerc. 2010; 42(1): 135–41.
19. Ely BR, Ely MR, Cheuvront SN, Kenefick RW, Degroot DW, Montain SJ. Evidence against a 40 degrees C core temperature threshold for fatigue in humans. J Appl Physiol (1985). 2009; 107(5): 1519–25.
20. Fontes EB, Okano AH, De Guio F, et al. Brain activity and perceived exertion during cycling exercise: an fMRI study. Br J Sports Med. 2015; 49(8): 556–60.
21. Fulco CS, Rock PB, Cymerman A. Maximal and submaximal exercise performance at altitude. Aviat Space Environ Med. 1998; 69(8): 793–801.
22. Girard O, Racinais S. Combining heat stress and moderate hypoxia reduces cycling time to exhaustion without modifying neuromuscular fatigue characteristics. Eur J Appl Physiol. 2014; 114(7): 1521–32.
23. Gorman AJ, Proppe DW. Mechanisms producing tachycardia in conscious baboons during environmental heat stress. J Appl Physiol Respir Environ Exerc Physiol. 1984; 56(2): 441–6.
24. Hawkins MN, Raven PB, Snell PG, Stray-Gundersen J, Levine BD. Maximal oxygen uptake as a parametric measure of cardiorespiratory capacity. Med Sci Sports Exerc. 2007; 39(1): 103–7.
25. Jackson CG, Sharkey BJ. Altitude, training and human performance. Sports Med. 1988; 6(5): 279–84.
26. Jay O, Bain AR, Deren TM, Sacheli M, Cramer MN. Large differences in peak oxygen uptake do not independently alter changes in core temperature and sweating during exercise. Am J Physiol Regul Integr Comp Physiol. 2011; 301(3): R832–41.
27. Johnson JM, Rowell LB. Forearm skin and muscle vascular responses to prolonged leg exercise in man. J Appl Physiol. 1975; 39(6): 920–4.
28. Jose AD, Stitt F, Collison D. The effects of exercise and changes in body temperature on the intrinsic heart rate in man. Am Heart J. 1970; 79(4): 488–98.
29. Lee BJ, Emery-Sinclair EL, Mackenzie RW, et al. The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia. Extrem Physiol Med. 2014; 3: 15.
30. Lee JF, Christmas KM, Machin DR, McLean BD, Coyle EF. Warm skin alters cardiovascular responses to cycling after preheating and precooling. Med Sci Sports Exerc. 2015; 47(6): 1168–76.
31. Lucia A, Hoyos J, Chicharro JL. Preferred pedalling cadence in professional cycling. Med Sci Sports Exerc. 2001; 33(8): 1361–6.
32. Lućia A, San Juan AF, Montilla M, et al. In professional road cyclists, low pedaling cadences are less efficient. Med Sci Sports Exerc. 2004; 36(6): 1048–54.
33. Lundby C, Mauricio A, van Hall G. Peak heart rate decreases with increasing severity of acute hypoxia. High Alt Med Biol. 2001; 2(3): 369–76.
34. MacInnis MJ, Nugent SF, MacLeod KE, Lohse KR. Methods to estimate V˙O2max upon acute hypoxia exposure. Med Sci Sports Exerc. 2015; 47(9): 1869–76.
35. Mattern CO, Kenefick RW, Kertzer R, Quinn TJ. Impact of starting strategy on cycling performance. Int J Sports Med. 2001; 22(5): 350–5.
36. Neary JP, Hall K, Bhambhani YN. Vastus medialis muscle oxygenation trends during a simulated 20-km cycle time trial. Eur J Appl Physiol. 2001; 85(5): 427–33.
37. Nybo L, Jensen T, Nielsen B, González-Alonso J. Effects of marked hyperthermia with and without dehydration on VO(2) kinetics during intense exercise. J Appl Physiol (1985). 2001; 90(3): 1057–64.
38. Peiffer JJ, Abbiss CR. Influence of environmental temperature on 40 km cycling time-trial performance. Int J Sports Physiol Perform. 2011; 6(2): 208–20.
39. Périard JD, Cramer MN, Chapman PG, Caillaud C, Thompson MW. Cardiovascular strain impairs prolonged self-paced exercise in the heat. Exp Physiol. 2011; 96(2): 134–44.
40. Périard JD, Cramer MN, Chapman PG, Caillaud C, Thompson MW. Neuromuscular function following prolonged intense self-paced exercise in hot climatic conditions. Eur J Appl Physiol. 2011; 111(8): 1561–9.
41. Périard JD, Racinais S. Heat stress exacerbates the reduction in middle cerebral artery blood velocity during prolonged self-paced exercise. Scand J Med Sci Sports. 2015; 25(1 Suppl): 135–44.
42. Périard JD, Racinais S. Self-paced exercise in hot and cool conditions is associated with the maintenance of %V˙O2peak within a narrow range. J Appl Physiol (1985). 2015; 118(10): 1258–65.
43. Pirnay F, Deroanne R, Petit JM. Maximal oxygen consumption in a hot environment. J Appl Physiol. 1970; 28(5): 642–5.
44. Racinais S, Périard JD, Karlsen A, Nybo L. Effect of heat and heat-acclimatization on cycling time-trial performance and pacing. Med Sci Sports Exerc. 2015; 47(3): 601–6.
45. Ramanathan NL. A new weighting system for mean surface temperature of the human body. J Appl Physiol. 1964; 19: 531–3.
46. Renfree A, Martin L, Micklewright D, St Clair Gibson A. Application of decision-making theory to the regulation of muscular work rate during self-paced competitive endurance activity. Sports Med. 2014; 44(2): 147–58.
47. Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R. Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing. Sports Med. 2013; 43(5): 301–11.
48. Rowell LB. Human cardiovascular adjustments to exercise and thermal stress. Physiol Rev. 1974; 54(1): 75–159.
49. Rowell LB. Circulatory adjustments to dynamic exercise and heat stress: competing controls. In: Human Circulation: Regulation during Physical Stress. New York: Oxford University Press; 1986. pp. 363–406.
50. Schlader ZJ, Stannard SR, Mündel T. Is peak oxygen uptake a determinant of moderate-duration self-paced exercise performance in the heat? Appl Physiol Nutr Metab. 2011; 36(6): 863–72.
51. St Clair Gibson A, Lambert EV, Rauch LH, et al. The role of information processing between the brain and peripheral physiological systems in pacing and perception of effort. Sports Med. 2006; 36(8): 705–22.
52. Tatterson AJ, Hahn AG, Martin DT, Febbraio MA. Effects of heat stress on physiological responses and exercise performance in elite cyclists. J Sci Med Sport. 2000; 3(2): 186–93.
53. Taylor HL, Buskirk E, Henschel A. Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Appl Physiol. 1955; 8(1): 73–80.
54. Thomas K, Goodall S, Stone M, Howatson G, Gibson AS, Ansley L. Central and peripheral fatigue in male cyclists after 4-, 20-, and 40-km time trials. Med Sci Sports Exerc. 2015; 47(3): 537–46.
55. Tucker R. The anticipatory regulation of performance: the physiological basis for pacing strategies and the development of a perception-based model for exercise performance. Br J Sports Med. 2009; 43(6): 392–400.
56. Tucker R, Rauch L, Harley YX, Noakes TD. Impaired exercise performance in the heat is associated with an anticipatory reduction in skeletal muscle recruitment. Pflugers Arch. 2004; 448(4): 422–30.
57. Van Cutsem J, Pattyn N, Vissenaeken D, et al. The influence of a mild thermal challenge and severe hypoxia on exercise performance and serum BDNF. Eur J Appl Physiol. 2015; 115(10): 2135–48.
58. Wasserman K, Whipp BJ, Koyal SN, Beaver WL. Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol. 1973; 35(2): 236–43.
59. Wehrlin JP, Hallén J. Linear decrease in .VO2max and performance with increasing altitude in endurance athletes. Eur J Appl Physiol. 2006; 96(4): 404–12.


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