Enhanced heat loss responses induced by short‐term endurance training in exercising women

Ichinose, Tomoko; Inoue, Yoshimitsu; Hirata, Mari; Shamsuddin, A. K. M.; Kondo, Narihiko

doi:10.1113/expphysiol.2008.043810

Cited by 45 publications

(45 citation statements)

References 29 publications

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“…These adaptations likely include increases in the number of sweat expulsions per minute, sweat gland hypertrophy, increased NO availability, and/or enhanced sweat gland recruitment at a given internal temperature, or a combination of all of the above 47 . Importantly, these findings of improved thermoregulatory efficiency with exercise training support previous studies that suggest an improvement in VO 2peak in the range of ~15-20% mediates positive adaptations to thermoregulatory function in pre-menopausal females 20,48 . This is the first study to demonstrate that post-menopausal females can improve thermoregulatory function with exercise training, and, importantly, that this contributes to alleviating the frequency and severity of hot flushes with exercise training.…”

Section: Discussionsupporting

confidence: 78%

“…Furthermore, whether the positive effects of exercise on reducing hot flushes remain following cessation of exercise training is currently unknown; however it can be speculated that the positive effects may be transient in the absence of exercise training i.e. ~4 weeks, in line with the reductions observed in thermoregulatory function following the cessation of exercise training in young females 20 . Nevertheless, the findings of the present study suggest that improving thermoregulatory function in symptomatic postmenopausal females is beneficial for hot flushes.…”

Section: Discussionmentioning

confidence: 91%

“…It is well established that exercise training can improve the thermoregulatory control system by decreasing core body temperature, and by changing both the temperature threshold for the onset, and sensitivity of sweating and cutaneous vasodilation in pre-menopausal females 20 . Whilst HT reduces hot flushes it also affects thermoregulatory control mechanisms via lowering core body temperature and altering the threshold at which cutaneous vasodilation and sweating responses are initiated 21,22 .…”

Section: Introductionmentioning

confidence: 99%

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Exercise training reduces the frequency of menopausal hot flushes by improving thermoregulatory control

et al. 2016

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Objectives: Post-menopausal hot flushes occur due to a reduction in oestrogen production causing thermoregulatory and vascular dysfunction. Exercise training enhances thermoregulatory control of sweating, skin and brain blood flow. We aimed to determine if improving thermoregulatory control and vascular function with exercise training alleviated hot flushes.Methods: Twenty one symptomatic females completed a 7-day hot flush questionnaire and underwent brachial artery flow-mediated dilation and a cardiorespiratory fitness test. Sweat rate and skin blood flow temperature thresholds and sensitivities, and middle cerebral artery velocity (MCAv) was measured during passive heating. Females performed 16-weeks of supervised exercise training or control, and measurements were repeated. Conclusions: Exercise training that improves cardiorespiratory fitness reduces self-reported hot flushes. Improvements are likely mediated through greater thermoregulatory control in response to increases in core temperature and enhanced vascular function in the cutaneous and cerebral circulations. Results

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Exercise training reduces the frequency of menopausal hot flushes by improving thermoregulatory control

et al. 2016

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“…Aerobic exercise training alters central gain to initiate sweating at a lower body temperature (33,71) and also increases maximal sweating responses (12,90). Despite 15 wk of training, this group of MS patients improved neither sweat gland recruitment nor sweat output per gland.…”

Section: Thermoregulatory Effector Responses In Msmentioning

confidence: 86%

Thermoregulation in multiple sclerosis

Davis

Wilson

White

et al. 2010

Journal of Applied Physiology

149

147

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Davis SL, Wilson TE, White AT, Frohman EM. Thermoregulation in multiple sclerosis. J Appl Physiol 109: 1531-1537. First published July 29, 2010 doi:10.1152/japplphysiol.00460.2010.-Multiple sclerosis (MS) is a progressive neurological disorder that disrupts axonal myelin in the central nervous system. Demyelination produces alterations in saltatory conduction, slowed conduction velocity, and a predisposition to conduction block. An estimated 60 -80% of MS patients experience temporary worsening of clinical signs and neurological symptoms with heat exposure. Additionally, MS may produce impaired neural control of autonomic and endocrine functions. This review focuses on five main themes regarding the current understanding of thermoregulatory dysfunction in MS: 1) heat sensitivity; 2) central regulation of body temperature; 3) thermoregulatory effector responses; 4) heat-induced fatigue; and 5) countermeasures to improve or maintain function during thermal stress. Heat sensitivity in MS is related to the detrimental effects of increased temperature on action potential propagation in demyelinated axons, resulting in conduction slowing and/or block, which can be quantitatively characterized using precise measurements of ocular movements. MS lesions can also occur in areas of the brain responsible for the control and regulation of body temperature and thermoregulatory effector responses, resulting in impaired neural control of sudomotor pathways or neural-induced changes in eccrine sweat glands, as evidenced by observations of reduced sweating responses in MS patients. Fatigue during thermal stress is common in MS and results in decreased motor function and increased symptomatology likely due to impairments in central conduction. Although not comprehensive, some evidence exists concerning treatments (cooling, precooling, and pharmacological) for the MS patient to preserve function and decrease symptom worsening during heat stress. demyelination; core temperature; sweating; skin blood flow; fatigue MULTIPLE SCLEROSIS (MS) is a disabling progressive neurological disorder affecting ϳ400,000 individuals in the United States. The pathophysiology of MS results in a disruption or loss of axonal myelin in the central nervous system (CNS), leading to the formation of scar tissue (sclerosis). MS is thought to involve a number of autoimmune injury cascades that appear to be dependent on the interaction of complex epigenetic and environmental factors. Immune responses in individuals with MS are skewed toward a proinflammatory state, resulting in inflammation, demyelination, and ultimately loss of axons and disorganization of normal tissue architecture within the CNS (23). Demyelination is associated with corresponding changes in axonal physiology, including a loss of saltatory properties of electrical conduction, reduction in conduction velocity, and a predisposition to conduction block. These pathophysiological mechanisms underlie the myriad of symptoms (Table 1) in individuals with MS and are contingent on the neuroanatomic l...

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“…While long-term exercise training has consistently been related to an improved thermoregulatory function (Baum et al 1976; Buono and Sjoholm 1988;Fritzsche and Coyle 2000;Gisolfi and Robinson 1969;Piwonka et al 1965;Selkirk and McLellan 2001), shorttem exercise training has also been linked to improvements in the capacity to dissipate heat. Increases in maximal aerobic capacity _ VO 2 max À Á of 10-15% associated with short-term exercise training have consistently been shown to enhance thermoregulatory function as evidenced by reductions in the core temperature at which the onset of local sweating and skin vasodilation occurs during exercise (Henane et al 1977;Ichinose et al 2009;Johnson 1998;Okazaki et al 2002;Roberts et al 1977). While some studies report that these adaptations lead to increases in sweating and skin blood flow (SkBF) during exercise and/ or heat exposure (Gisolfi and Robinson 1969;Gisolfi 1973;Henane et al 1977;Ichinose et al 2009;Nadel et al 1974;Okazaki et al 2002;Shvartz et al 1974;Strydom et al 1966), these improvements in thermoregulatory function have not always resulted in greater local heat loss responses after exercise training (Gisolfi 1973;Nielsen et al 1993;Shields et al 2004;Shvartz et al 1973).…”

Section: Introductionmentioning

confidence: 99%

Short-term exercise training does not improve whole-body heat loss when rate of metabolic heat production is considered

2010

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We evaluated the effects of an 8-week exercise training program in previously sedentary individuals on whole-body heat balance during exercise at a constant rate of metabolic heat production. Prior to and after 8 weeks of training, ten participants performed 60-min of cycling exercise at a constant rate of heat production (approximately 450 W) followed by 60-min of recovery, at 30 degrees C and 15% relative humidity. Rate of total heat loss was measured directly by whole-body calorimetry, while rate of metabolic heat production was measured simultaneously by indirect calorimetry. Esophageal (T(es)), skin blood flow (SkBF) and local sweat rate (LSR) were also measured continuously. The 8-week exercise training program elicited a 10% increase in maximal aerobic capacity (P < 0.001). Furthermore, exercise training reduced (P

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Enhanced heat loss responses induced by short‐term endurance training in exercising women

Cited by 45 publications

References 29 publications

Exercise training reduces the frequency of menopausal hot flushes by improving thermoregulatory control

Exercise training reduces the frequency of menopausal hot flushes by improving thermoregulatory control

Thermoregulation in multiple sclerosis

Short-term exercise training does not improve whole-body heat loss when rate of metabolic heat production is considered

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