Thermoregulation là gì

Department of Applied earlsdaughter.com & Wellness, Southern Methodist University, Dallas, Texas;

Departments of Neurology and


Address for reprint requests và other correspondence: S. L. Davis, Dept. of Applied earlsdaughter.com & Wellness, Annette Caldwell Simmons School of Education và Human Development, Southern Methodist Univ., P..O. Box 750382 Dallas, TX 75275-0382 (e-mail: ).

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Departments of Biomedical Sciences và

Specialty Medicine, Ohio University College of Osteopathic Medicine, Athens, Ohio; và


Autonomic dysfunction involving the genitourinary, gastrointestinal, cardiovascular, và thermoregulatory systems is commonly observed in MS (29). In addition lớn autonomic dysfunction, the majority of MS patients experience transient và temporary worsening of clinical signs và neurological symptoms in response khổng lồ a number of factors, the most prominent of which are increased ambient or core body toàn thân temperature & exercise. However, the assessment & understanding of autonomic dysfunction in individuals with MS is problematic due to lớn the variability of early clinical symptoms & the heterogeneity in the clinical course over time (Fig. 1). With these limitations in mind, this nhận xét will focus on our current understanding of the thermoregulatory dysfunction in MS while characterizing five main topical themes: 1) heat sensitivity; 2) central regulation of body temperature; 3) thermoregulatory effector responses; 4) heat-induced fatigue; & 5) countermeasures to lớn improve function in MS patients during a thermal găng tay.

Fig. 1.Clinical courses of multiple sclerosis (MS). Adapted from Confavreux và Vukusic (11) with permission from Lippincott Williams and Wilkins/Wolters Kluwer Health.


HEAT SENSITIVITY IN MS

The earliest medical reports of thermal sensitivity in MS are derived from Charles Prosper Ollivier d"Angers who noted in 1824 that a hot bath induced numbness in the right leg and reduced feeling and dexterity in the hands of a patient with MS (56). However, Wilhelm Uhthoff"s mô tả tìm kiếm of this phenomenon occurring after a hot bath or with exercise in MS patients with a history of optic neuritis has most commonly been cited as the landmark observation of the pathophysiological principle of temperature-induced conduction block in demyelinated axonal segments (Uhthoff"s phenomenon) (77). It is estimated that 60–80% of the MS population experience transient & temporary worsening of clinical signs and neurological symptoms as a result of elevated body toàn thân temperature by immersion in warm water (41–43°C) or exposure khổng lồ infrared heating lamps (27, 46, 50, 51).

Symptom worsening can result from passive sầu heat exposure, exercise (increase in metabolism), or a combination of heat exposure & increases in metabolism (exercise-heat stress). Both physical (walking, running, driving, writing, etc.) và cognitive sầu (memory retrieval, processing tốc độ, multitasking, etc.) functions can be impaired by heat exposure, greatly impacting overall patient safety as well as the ability of individuals with MS khổng lồ persize routine activities of daily living, even in mildly affected individuals (57, 59). Symptom worsening has been reported with exercise (78), hot shower (81), và sunbathing (2). Even fluctuations in circadian body toàn thân temperature from the morning khổng lồ the afternoon can elicit changes in symptoms (62).

In the past, physicians & health care providers instructed MS patients khổng lồ minimize their exposure lớn high ambient temperatures và lớn avoid exercise or intense physical work in order lớn avoid symptom worsening. However, laông xã of exercise often results in deconditioning, reduced functional capabilities, increased risk of injury, và less weight-bearing movement, which has consequences on bone và mineral metabolism (59, 88). Evidence now indicates that exercise is beneficial khổng lồ individuals with MS by improving fitness and sense of well being, reducing fatigue, and increasing strength and safety of walking và should be incorporated into lớn their overall disease management plan (57).

Typically, deficits caused by increases in temperature are reversible by removing heat stressors & allowing subsequent cooling. Davis et al. (15) quantified Uhthoff"s phenomenon during indirect whole body toàn thân heating và its reversibility with the subsequent application of active sầu cooling by objectively measuring horizontal eye movement velocities in a group of MS patients with internuclear ophthalmoparesis, an abnormality characterized by the slowing of the eye moving toward the nose (adduction) during horizontal eye movements. The tốc độ of horizontal eye movements in MS patients with internuclear ophthalmoparesis was slowed from baseline when core toàn thân temperature was raised ∼0.8°C with whole toàn thân heating & returned to lớn baseline following 1 h of whole body toàn thân cooling (Fig. 2) (15).

Fig. 2.

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Data from healthy controls (Control; n = 8), MS patients without internuclear opthalmoparesis (MS-Control; n = 8), & MS patients diagnosed with internuclear ophthalmoparesis (MS-INO; n = 8) showing ocular function responses during whole toàn thân heat bao tay (increase internal temperature ∼0.8°C) and subsequent whole body toàn thân cooling (return khổng lồ normothermic baseline). A significant slowing (P 15) with permission from Lippincott Williams và Wilkins/Wolters Kluwer Health.


THERMOREGULATORY EFFECTOR RESPONSES IN MS

Increases in skin blood flow và sweating are the primary heat dissipation mechanisms in humans. Without these dissipation mechanisms, internal temperature would reach the upper “safe” limit within 10 min of moderate exercise (36). Based on the severe consequences that may occur with elevated body toàn thân temperature in MS, control of skin blood flow & sweating are crucial for patient safety (81).

Lesions affecting conduction within the CNS of MS patients can potentially impair thermoregulatory effector responses khổng lồ eccrine sweat glands. This is evidenced by previous studies that report reduced sweating responses in MS patients (10, 53, 79). In the aforementioned studies, abnormal sweating responses were identified by using quinizarin powder placed on the skin of individuals followed by exposure to lớn a heat căng thẳng. Quinizarin powder, normally gray in color, changes to a deep blue when exposed lớn sweat. The intensity of the change in color provides a visual estimate of sweating (19, 41). However, this technique cannot quantitatively identify differences in sweating or determine whether diminished sweating is due khổng lồ a decreased number of active sweat glands, altered innervation of the glands, and/or reduced output from activated glands. Using a more quantitative sầu approach, Davis et al. (17) transdermally delivered a cholinergic agonist (pilocarpine) to activate eccrine sweat glands independent of the CNS. Diminished sweat function was identified in individuals with MS, và this reduction was not caused by reduced sweat gl& recruitment but was due khổng lồ reduced sweat glvà output per gl& (Fig. 3). Even though sweating was induced locally by an agonist, it is possible that CNS impairments or even neuronal loss within the descending sudomotor pathways due to lớn the disease process contributed to lớn the observations of diminished sweat function in these patients (1, 79). Impaired sweat function appears to occur more frequently in MS patients with more severe cases of disease (10).

Fig. 3.Data from control & MS patients showing decreased sweat gland output per glvà (P A). No differences were observed in the number of sweat glands recruited between healthy controls and MS patients (B). Data are expressed as means ± SD. Modified from Davis et al. (17).


COUNTERMEASURES TO IMPROVE FUNCTION IN MS PATIENTS DURING THERMAL STRESS

To reduce the potentially detrimental effects of heat sensitivity, several treatment strategies have been employed lớn allow individuals with MS to lớn participate in activities of daily living, including exercise. Simple behavioral strategies are used to lớn minimize heat exposure, such as performing work or exercise outside during the early morning or late evening when temperatures are cooler. A small number of studies have reported potential benefits using cooling strategies that are convenient methods available khổng lồ most MS patients such as cold showers, applying ice packs, the use of regional cooling devices, and drinking cold beverages (3, 7, 26, 67, 80).

Precooling (cooling before heat exposure) presents another practical & strategic treatment option for minimizing the consequences of heat áp lực in MS patients. Immersing the lower limbs in cool water (i.e., cold tap water in a bath tub) creates negative sầu heat storage before thermal găng tay or the initiation of exercise. White et al. (86) demonstrated that water immersion precooling (cooling the lower limbs in 20°C water for 30 min before physical activity) was effective sầu in preventing gains in core temperature during physical work and may minimize heat-induced conduction difficulties in MS patients (Fig. 4). Precooling allows the lower limbs khổng lồ effectively serve as heat “sinks” in order khổng lồ blunt internal temperature increases and decrease reliance on eccrine sweating, which may be compromised in MS patients (89). Precooling allows heat-sensitive individuals with MS khổng lồ persize exercise with greater physical comfort & fewer side effects (86). The heat load induced via increases in metabolism during exercise appears to lớn be reduced most effectively by cooling the greakiểm tra body mass while minimizing thermogenic responses (i.e., shivering) (85). This cooling (or temperature-blunting effect) can last for several hours, depending on the intensity of the activities performed by the individual with MS.

Fig. 4.

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Core body temperatures responses during 30 min of aerobic exercise & subsequent recovery following a noncooled trial (open circles) và a precooled trial (closed circles). Chip Core body temperature during the precooled trial remained below baseline values during exercise và recovery whereas core temperature during the noncooled trial exceeded a critical threshold (0.5°C) for potential increases in symptom worsening. Data are expressed as means ± SD. Modified from White et al. (86) with permission from Sage Publication Ltd., UK.


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