Central and peripheral fatigue during passive and exercise-induced hyperthermia

Julien D Périard, Corinne Caillaud, Martin W. Thompson

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

PURPOSE: Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined.

METHODS: On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC.

RESULTS: Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05).

CONCLUSIONS: The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

Original languageEnglish
Pages (from-to)1657-65
Number of pages9
JournalMedicine and Science in Sports and Exercise
Volume43
Issue number9
DOIs
Publication statusPublished - Sep 2011
Externally publishedYes

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Induced Hyperthermia
Heating
Fatigue
Isometric Contraction
Hot Temperature
Temperature
Tetanus
Humidity
Baths
Stroke Volume
Arterial Pressure
Fever
Oxygen
Water

Cite this

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title = "Central and peripheral fatigue during passive and exercise-induced hyperthermia",
abstract = "PURPOSE: Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined.METHODS: On separate days, eight males cycled to exhaustion at 60{\%} maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60{\%} relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC.RESULTS: Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90{\%} during both PaH and ExH MVC. This decline accounted for 41.5{\%} (PaH) and 33.1{\%} (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96{\%} of maximum) and a decline in stroke volume (25{\%}) and mean arterial pressure (10{\%}) (P < 0.05).CONCLUSIONS: The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.",
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Central and peripheral fatigue during passive and exercise-induced hyperthermia. / Périard, Julien D; Caillaud, Corinne; Thompson, Martin W.

In: Medicine and Science in Sports and Exercise, Vol. 43, No. 9, 09.2011, p. 1657-65.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Central and peripheral fatigue during passive and exercise-induced hyperthermia

AU - Périard, Julien D

AU - Caillaud, Corinne

AU - Thompson, Martin W.

PY - 2011/9

Y1 - 2011/9

N2 - PURPOSE: Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined.METHODS: On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC.RESULTS: Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05).CONCLUSIONS: The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

AB - PURPOSE: Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined.METHODS: On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC.RESULTS: Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05).CONCLUSIONS: The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

KW - Adult

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KW - Exercise Test

KW - Fever

KW - Heart Rate

KW - Humans

KW - Isometric Contraction

KW - Male

KW - Muscle Fatigue

KW - Muscle Strength

KW - Oxygen Consumption

KW - Quadriceps Muscle

KW - Journal Article

KW - Randomized Controlled Trial

KW - Research Support, Non-U.S. Gov't

U2 - 10.1249/MSS.0b013e3182148a9a

DO - 10.1249/MSS.0b013e3182148a9a

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JO - Medicine Science in Sports Exercise

JF - Medicine Science in Sports Exercise

SN - 0195-9131

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