Physiological mechanisms impairing cardiovascular function and exercise capacity in the heat stressed human: role of skin versus body temperature.

Steven Trangmar; Scott T Chiesa; Kameljit Kalsi; Mark Rakobowchuk; Niels H. Secher; Jose Gonzalez-Alonso

Physiological mechanisms impairing cardiovascular function and exercise capacity in the heat stressed human: role of skin versus body temperature.

Steven Trangmar, Scott T Chiesa, Kameljit Kalsi, Mark Rakobowchuk, Niels H. Secher, Jose Gonzalez-Alonso

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

Abstract

Introduction: Cardiovascular strain and hyperthermia are thought to be important factors limiting exercise capacity in heat-stressed humans, but the contribution of elevations in skin (Tsk) versus body temperature remains unknown. Here we tested the hypothesis that an increased body temperature would accelerate the attenuation in leg, brain and systemic perfusion leading to impaired exercise performance, but the sole increase in Tsk would not. Methods: Nine cyclists completed 3 incremental cycling tests after (a) ~30 min whole-body heating (H30), (b) ~10 min whole-body heating (H10), and (c) in control conditions. Tsk and core temperature (Tc), heart rate (HR) and VO2 were measured continuously; whereas leg, brain and systemic haemodynamics and haematological parameters were assessed at the end of each exercise stage. To eliminate the effects of repeated exercise, the incremental tests were repeated, on a separate day, with each test performed in control conditions. Results: Prior to exercise in H30, Tsk, Tc and cardiac output were elevated by 6.2±0.2 °C, 0.9±0.1 °C and 4.8 L/min (P<0.05) compared to control, whereas only Tsk was elevated prior to exercise in H10 (6.0±0.2°C). During incremental exercise, Tsk was maintained, yet Tc rose gradually to a similar peak value in the 3 conditions (39.2±0.1 °C). Exercise capacity and VO2max were reduced in H30 by 13±1% and 6±2% (P<0.05), but remained unchanged in H10. On the transition from rest to sub-maximal exercise, VO2, cardiac output and leg blood flow increased at a similar rate across conditions. In contrast, mean arterial pressure and brain blood velocity increased but were lower, whereas HR and leg a-vO2 difference were higher in H30 vs. H10 and control. At exhaustion, HRmax (~186±3 beats/min) and leg a-vO2 difference (~182±5 ml/L) were similar in the 3 conditions, whereas mean arterial pressure (-14±1%), brain blood velocity (-16±6%), leg blood flow (-11±3%) and cardiac output (-9±3%; all P<0.05) were lower in H30 compared to H10 and control. In the 3 control incremental tests, exercise capacity, VO2max, HRmax and Tc were similar. Discussion: These findings demonstrate that skin hyperthermia per se does not compromise cardiovascular capacity or incremental exercise performance. Rather, combined skin and internal body hyperthermia reduces VO2max and exercise capacity through the early attenuation of leg, brain and systemic blood flow. Our findings have important implications for understanding why athletic performance in warm environments is not universally impaired across all sports and exercise modalities. Supported by the Gatorade Sports Science Institute, PepsiCo Inc., USA.

Original language	English
Title of host publication	Proceedings of the 19th annual Congress of the European College of Sport Science
Publication status	Published - Jul 2014

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http://www.ecss-congress.eu/2014/14/

Cite this

@inproceedings{fedf370a10654d759b2216493f524521,

title = "Physiological mechanisms impairing cardiovascular function and exercise capacity in the heat stressed human: role of skin versus body temperature.",

abstract = "Introduction: Cardiovascular strain and hyperthermia are thought to be important factors limiting exercise capacity in heat-stressed humans, but the contribution of elevations in skin (Tsk) versus body temperature remains unknown. Here we tested the hypothesis that an increased body temperature would accelerate the attenuation in leg, brain and systemic perfusion leading to impaired exercise performance, but the sole increase in Tsk would not. Methods: Nine cyclists completed 3 incremental cycling tests after (a) ~30 min whole-body heating (H30), (b) ~10 min whole-body heating (H10), and (c) in control conditions. Tsk and core temperature (Tc), heart rate (HR) and VO2 were measured continuously; whereas leg, brain and systemic haemodynamics and haematological parameters were assessed at the end of each exercise stage. To eliminate the effects of repeated exercise, the incremental tests were repeated, on a separate day, with each test performed in control conditions. Results: Prior to exercise in H30, Tsk, Tc and cardiac output were elevated by 6.2±0.2 °C, 0.9±0.1 °C and 4.8 L/min (P<0.05) compared to control, whereas only Tsk was elevated prior to exercise in H10 (6.0±0.2°C). During incremental exercise, Tsk was maintained, yet Tc rose gradually to a similar peak value in the 3 conditions (39.2±0.1 °C). Exercise capacity and VO2max were reduced in H30 by 13±1% and 6±2% (P<0.05), but remained unchanged in H10. On the transition from rest to sub-maximal exercise, VO2, cardiac output and leg blood flow increased at a similar rate across conditions. In contrast, mean arterial pressure and brain blood velocity increased but were lower, whereas HR and leg a-vO2 difference were higher in H30 vs. H10 and control. At exhaustion, HRmax (~186±3 beats/min) and leg a-vO2 difference (~182±5 ml/L) were similar in the 3 conditions, whereas mean arterial pressure (-14±1%), brain blood velocity (-16±6%), leg blood flow (-11±3%) and cardiac output (-9±3%; all P<0.05) were lower in H30 compared to H10 and control. In the 3 control incremental tests, exercise capacity, VO2max, HRmax and Tc were similar. Discussion: These findings demonstrate that skin hyperthermia per se does not compromise cardiovascular capacity or incremental exercise performance. Rather, combined skin and internal body hyperthermia reduces VO2max and exercise capacity through the early attenuation of leg, brain and systemic blood flow. Our findings have important implications for understanding why athletic performance in warm environments is not universally impaired across all sports and exercise modalities. Supported by the Gatorade Sports Science Institute, PepsiCo Inc., USA. ",

author = "Steven Trangmar and Chiesa, {Scott T} and Kameljit Kalsi and Mark Rakobowchuk and Secher, {Niels H.} and Jose Gonzalez-Alonso",

year = "2014",

month = jul,

language = "English",

booktitle = "Proceedings of the 19th annual Congress of the European College of Sport Science",

}

Physiological mechanisms impairing cardiovascular function and exercise capacity in the heat stressed human: role of skin versus body temperature. / Trangmar, Steven; Chiesa, Scott T; Kalsi, Kameljit et al.
Proceedings of the 19th annual Congress of the European College of Sport Science. 2014.

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

TY - GEN

T1 - Physiological mechanisms impairing cardiovascular function and exercise capacity in the heat stressed human: role of skin versus body temperature.

AU - Trangmar, Steven

AU - Chiesa, Scott T

AU - Kalsi, Kameljit

AU - Rakobowchuk, Mark

AU - Secher, Niels H.

AU - Gonzalez-Alonso, Jose

PY - 2014/7

Y1 - 2014/7

N2 - Introduction: Cardiovascular strain and hyperthermia are thought to be important factors limiting exercise capacity in heat-stressed humans, but the contribution of elevations in skin (Tsk) versus body temperature remains unknown. Here we tested the hypothesis that an increased body temperature would accelerate the attenuation in leg, brain and systemic perfusion leading to impaired exercise performance, but the sole increase in Tsk would not. Methods: Nine cyclists completed 3 incremental cycling tests after (a) ~30 min whole-body heating (H30), (b) ~10 min whole-body heating (H10), and (c) in control conditions. Tsk and core temperature (Tc), heart rate (HR) and VO2 were measured continuously; whereas leg, brain and systemic haemodynamics and haematological parameters were assessed at the end of each exercise stage. To eliminate the effects of repeated exercise, the incremental tests were repeated, on a separate day, with each test performed in control conditions. Results: Prior to exercise in H30, Tsk, Tc and cardiac output were elevated by 6.2±0.2 °C, 0.9±0.1 °C and 4.8 L/min (P<0.05) compared to control, whereas only Tsk was elevated prior to exercise in H10 (6.0±0.2°C). During incremental exercise, Tsk was maintained, yet Tc rose gradually to a similar peak value in the 3 conditions (39.2±0.1 °C). Exercise capacity and VO2max were reduced in H30 by 13±1% and 6±2% (P<0.05), but remained unchanged in H10. On the transition from rest to sub-maximal exercise, VO2, cardiac output and leg blood flow increased at a similar rate across conditions. In contrast, mean arterial pressure and brain blood velocity increased but were lower, whereas HR and leg a-vO2 difference were higher in H30 vs. H10 and control. At exhaustion, HRmax (~186±3 beats/min) and leg a-vO2 difference (~182±5 ml/L) were similar in the 3 conditions, whereas mean arterial pressure (-14±1%), brain blood velocity (-16±6%), leg blood flow (-11±3%) and cardiac output (-9±3%; all P<0.05) were lower in H30 compared to H10 and control. In the 3 control incremental tests, exercise capacity, VO2max, HRmax and Tc were similar. Discussion: These findings demonstrate that skin hyperthermia per se does not compromise cardiovascular capacity or incremental exercise performance. Rather, combined skin and internal body hyperthermia reduces VO2max and exercise capacity through the early attenuation of leg, brain and systemic blood flow. Our findings have important implications for understanding why athletic performance in warm environments is not universally impaired across all sports and exercise modalities. Supported by the Gatorade Sports Science Institute, PepsiCo Inc., USA.

AB - Introduction: Cardiovascular strain and hyperthermia are thought to be important factors limiting exercise capacity in heat-stressed humans, but the contribution of elevations in skin (Tsk) versus body temperature remains unknown. Here we tested the hypothesis that an increased body temperature would accelerate the attenuation in leg, brain and systemic perfusion leading to impaired exercise performance, but the sole increase in Tsk would not. Methods: Nine cyclists completed 3 incremental cycling tests after (a) ~30 min whole-body heating (H30), (b) ~10 min whole-body heating (H10), and (c) in control conditions. Tsk and core temperature (Tc), heart rate (HR) and VO2 were measured continuously; whereas leg, brain and systemic haemodynamics and haematological parameters were assessed at the end of each exercise stage. To eliminate the effects of repeated exercise, the incremental tests were repeated, on a separate day, with each test performed in control conditions. Results: Prior to exercise in H30, Tsk, Tc and cardiac output were elevated by 6.2±0.2 °C, 0.9±0.1 °C and 4.8 L/min (P<0.05) compared to control, whereas only Tsk was elevated prior to exercise in H10 (6.0±0.2°C). During incremental exercise, Tsk was maintained, yet Tc rose gradually to a similar peak value in the 3 conditions (39.2±0.1 °C). Exercise capacity and VO2max were reduced in H30 by 13±1% and 6±2% (P<0.05), but remained unchanged in H10. On the transition from rest to sub-maximal exercise, VO2, cardiac output and leg blood flow increased at a similar rate across conditions. In contrast, mean arterial pressure and brain blood velocity increased but were lower, whereas HR and leg a-vO2 difference were higher in H30 vs. H10 and control. At exhaustion, HRmax (~186±3 beats/min) and leg a-vO2 difference (~182±5 ml/L) were similar in the 3 conditions, whereas mean arterial pressure (-14±1%), brain blood velocity (-16±6%), leg blood flow (-11±3%) and cardiac output (-9±3%; all P<0.05) were lower in H30 compared to H10 and control. In the 3 control incremental tests, exercise capacity, VO2max, HRmax and Tc were similar. Discussion: These findings demonstrate that skin hyperthermia per se does not compromise cardiovascular capacity or incremental exercise performance. Rather, combined skin and internal body hyperthermia reduces VO2max and exercise capacity through the early attenuation of leg, brain and systemic blood flow. Our findings have important implications for understanding why athletic performance in warm environments is not universally impaired across all sports and exercise modalities. Supported by the Gatorade Sports Science Institute, PepsiCo Inc., USA.

M3 - Conference contribution

BT - Proceedings of the 19th annual Congress of the European College of Sport Science

ER -