Passive hyperthermia reduces voluntary activation and isometric force production

Morrison, Shawnda A.; Sleivert, Gordon G.; Cheung, Stephen S.

doi:10.1007/s00421-004-1063-z

Cited by 202 publications

(250 citation statements)

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“…In addition, hyperthermia was achieved actively, altering peripheral metabolic characteristics that could further influence peak force. Still, other studies (16,33) have demonstrated progressive decreases in MVC and voluntary activation with increasing core temperatures in the range of the present study. It is possible that mechanisms of task failure for the small hand muscles used in the present study differ from those of the knee extensors and plantar flexors of those studies (7,16).…”

Section: Discussioncontrasting

confidence: 51%

“…passive hyperthermia; recruitment curve; transcranial magnetic stimulation HIGH INTERNAL TEMPERATURE, ranging from 38.6 to 40.3°C, is associated with voluntary exhaustion during aerobic exercise, despite variations in baseline core temperature, heat storage rates, and final skin temperature (4, 10). Similarly, hyperthermia has been shown to produce motor fatigue, evidenced by decreased voluntary activation during sustained maximal voluntary contractions (MVC) (16,34). Cardiovascular strain during thermal stress contributes to the development of fatigue; however, evidence also suggests that hyperthermia alters central nervous system (CNS) functions, resulting in alterations in voluntary activation of muscle, as well as changes in perception of effort (18,24,33).…”

mentioning

confidence: 99%

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Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls

White

VanHaitsma

Vener

et al. 2013

Journal of Applied Physiology

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White AT, VanHaitsma TA, Vener J, Davis SL. Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls. J Appl Physiol 114: 1697-1704, 2013. First published April 18, 2013 doi:10.1152/japplphysiol.01119.2012.-Heat stress is associated with increased fatigue perception and decrements in function for individuals with multiple sclerosis (MS). Similarly, healthy individuals experience decrements in exercise performance during hyperthermia. Alterations in central nervous system (CNS) function during hyperthermia include reduced voluntary activation of muscle and increased effort perception. The purpose of this investigation was to test the hypothesis that passive heat exposure in MS patients will produce increased subjective fatigue and impairments in physiological measures of central conduction and cortical excitability compared with healthy individuals. Eleven healthy individuals and 11 MS patients completed a series of transcranial magnetic stimulation studies to examine central conduction and cortical excitability under thermoneutral and heat-stressed (HS) conditions at rest and after a fatiguing thumb abduction task. Passive heat stress resulted in significantly greater fatigue perception and impairments in force production in MS patients. Central motor conduction time was significantly shorter during HS in controls; however, in MS patients normal increases in conduction velocity with increased temperature were not observed centrally. MS patients also exhibited decreased cortical excitability during HS, evidenced by significant increases in resting motor threshold, decreased MEP amplitude, and decreased recruitment curve slope. Both groups exhibited postexercise depression of MEP amplitude, but the magnitude of these decrements was amplified in MS patients during HS. Taken together, these results suggest that CNS pathology in MS patients played a substantial role in reducing cortical excitability during HS. passive hyperthermia; recruitment curve; transcranial magnetic stimulation HIGH INTERNAL TEMPERATURE, ranging from 38.6 to 40.3°C, is associated with voluntary exhaustion during aerobic exercise, despite variations in baseline core temperature, heat storage rates, and final skin temperature (4, 10). Similarly, hyperthermia has been shown to produce motor fatigue, evidenced by decreased voluntary activation during sustained maximal voluntary contractions (MVC) (16,34). Cardiovascular strain during thermal stress contributes to the development of fatigue; however, evidence also suggests that hyperthermia alters central nervous system (CNS) functions, resulting in alterations in voluntary activation of muscle, as well as changes in perception of effort (18,24,33). Little is known about the effects of moderate core temperature increases, in the range between 0.5 to 1.0°C, on CNS function in healthy individuals, although some evidence suggests that decrements in function may begin to appear when core temperatures exceed normal levels (1...

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Section: Discussioncontrasting

confidence: 51%

mentioning

confidence: 99%

Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls

White

VanHaitsma

Vener

et al. 2013

Journal of Applied Physiology

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“…Recent studies using passively induced hyperthermia have demonstrated that heat-related impairment of force development is attributable to both central and peripheral effects (35,54). Thus high body temperature itself can impair exercise tolerance independently of its effects in elevating cardiovascular, metabolic, and neuroendocrine strain.…”

Section: Discussionmentioning

confidence: 99%

Exercise can be pyrogenic in humans

Bradford¹,

Cotter²,

Thorburn³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise increases mean body temperature ( Tbody) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE2 can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T body in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), V O2 max: 53 ml⅐ kg Ϫ1 ⅐ min Ϫ1 (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running (ϳ75% V O2 max) followed by 45-min cycling and 60-min seated recovery (28°C, 50% relative humidity). Plasma cytokine (TNF-␣, IL-10) concentrations were measured at rest and 30-min recovery. T body was similar at rest in PLAC (35.59°C) and NSAID (35.53°C) and increased similarly during running, but became 0.33°C (SD 0.26) lower in NSAID during cycling (37.39°C vs. 37.07°C; P ϭ 0.03), and remained lower throughout recovery. Sweating was initiated at T body of ϳ35.6°C in both conditions but ceased at higher T body in PLAC than NSAID during recovery [36.66°C (SD 0.36) vs. 36.39°C (SD 0.27); P ϭ 0.03]. Cardiac frequency averaged 6 ⅐ min Ϫ1 higher in PLAC (P Ͻ 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W ⅐ m Ϫ2 ; P ϭ 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.

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“…This mechanism presupposes that approaching or achieving the higher brain and core temperature is a symptom of exhaustion development to keep the individual being knocked down. Morrison, Sleivert, and Cheung (2004) has shown a progressive central disruption associated with increased temperature. Therefore, it seems that during exercise under increased thermal pressure, high body temperature may directly or indirectly affect endurance performance.…”

Section: Temperature and Central Fatiguementioning

confidence: 99%

Role of Central Fatigue in Resistance and Endurance Exercises: An Emphasis on Mechanisms and Potential Sites

Sadri¹,

Khani²,

Sadri³

2014

sgia

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SUMMARYAn exercise-induced reduction in maximal force production, or the inability to continue an activity with enough force, is defined as fatigue. Although the etiology of fatigue is complex, it can be divided into two distinct components: central and peripheral. Central fatigue is the progressive exerciseinduced loss of the voluntary activation, or decrease in the neural stimulation, of the muscle, thereby reducing maximal force production. Considering the different mechanisms of strength and endurance activities as well as previous research, the authors suggest that there is peripheral fatigue in both kinds of activities. However, the mechanisms of fatigue and the rate of perceived exertion are distinct (mentally, endurance exercise is more difficult). An analysis of fatigue kinetics shows that peripheral fatigue occurs initially, and the central nervous system tries to prevent the disorder via output force through the perceptions of the metabolic condition of the muscle and the activation of additional motor units. Once peripheral fatigue surpasses a certain amount, the central nervous system reduces the number of activated motor units to prevent serious disorders in homeostasis and muscle damage, and protects the central governor. Still, in important and critical situations such as the final stages of running a marathon (when the last flight of runners is observed) and fight-or-flight situations in which someone faces a worse outcome if a task is abandoned, humans can choose one of worse or the worst alternatives to write their final destiny.

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Passive hyperthermia reduces voluntary activation and isometric force production

Cited by 202 publications

References 29 publications

Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls

Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls

Exercise can be pyrogenic in humans

Role of Central Fatigue in Resistance and Endurance Exercises: An Emphasis on Mechanisms and Potential Sites

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