Introduction Impairments in sudomotor function during passive whole-body heating have been reported in multiple sclerosis (MS), a demyelinating disease of the CNS that disrupts autonomic function. However, the capability of the thermoregulatory system to control body temperature during exercise has never been assessed in MS. Thus, the aim of the present study was to test the hypothesis that thermoregulatory function is impaired in MS patients compared with healthy controls (CON) exercising at similar rates of metabolic heat production. Methods Sweating and skin blood flow responses were compared between 12 individuals diagnosed with relapsing-remitting MS (9 females, 3 males) and 12 sex-, age-, mass-, and BSA-matched CON during a single bout of cycling exercise (rate of metabolic heat production: ∼4.5 W·kg−1) for 60 min in a climate-controlled room (25°C, 30% RH). Results Individuals with MS exhibited an attenuated increase in cumulative whole-body sweat loss after 30 min (MS, 72 ± 51 g; CON, 104 ± 37 g; P = 0.04) and 60 min (MS, 209 ± 94 g; CON, 285 ± 62 g; P = 0.02), as well as lower sweating thermosensitivity (MS, 0.49 ± 0.26 mg·cm−2·min−1·°C−1; CON, 0.86 ± 0.30 mg·cm−2·min−1·°C−1; P = 0.049). Despite evidence for thermoregulatory dysfunction, there were no differences between MS and CON in esophageal or rectal temperatures at 30- or 60-min time points (P > 0.05). Cutaneous vasculature responses were also not different in MS compared with CON (P > 0.05). Conclusion Taken together, MS blunts sweating responses during exercise while cutaneous vasculature responses are preserved. Altered mechanisms of body temperature regulation in persons with MS may lead to temporary worsening of disease symptoms and limit exercise tolerance under more thermally challenging conditions.

Huang M, Allen DR, Keller DM, Fadel PJ, Frohman EM, Davis SL. Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis. J Neurophysiol 116: 81-87, 2016. First published April 13, 2016 doi:10.1152/jn.00003.2016.-Multiple sclerosis (MS), a progressive neurological disease, can lead to impairments in the autonomic control of cardiovascular function. We tested the hypothesis that individuals with relapsing-remitting MS (n ϭ 10; 7 females, 3 males; 13 Ϯ 4 yr from diagnosis) exhibit impaired carotid baroreflex control of blood pressure and heart rate compared with sex, age, and body weight-matched healthy individuals (CON: n ϭ 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; ϩ40 Torr) and neck suction (NS; Ϫ60 Torr) were applied to simulate carotid hypotension and hypertension, respectively, while mean arterial pressure (MAP; finger photoplethysmography), heart rate (HR), cardiac output (CO; Modelflow), and total vascular conductance (TVC) were continuously measured. In response to NP, there was a blunted increase in peak MAP responses (MS: 5 Ϯ 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 Ϯ 3 mmHg; P ϭ 0.005), whereas peak HR responses were not different between groups. At the peak MAP response to NP, individuals with MS demonstrated an attenuated decrease in TVC (MS, Ϫ10 Ϯ 4% baseline vs. CON, Ϫ15 Ϯ 4% baseline, P ϭ 0.012), whereas changes in CO were similar between groups. Following NS, all cardiovascular responses (i.e., nadir MAP and HR and percent changes in CO and TVC) were not different between MS and CON groups. These data suggest that individuals with MS have impaired carotid baroreflex control of blood pressure via a blunted vascular conductance response resulting in a diminished ability to increase MAP in response to a hypotensive challenge.baroreceptors; heart rate; sympathetic nervous system; carotid hypotension; carotid hypertension MULTIPLE SCLEROSIS (MS), the most common disabling neurological disorder of young adults, is a progressive autoimmune disease affecting the central nervous system (Edmonds et al. 2010). This disease results in the demyelination of axons leading to slowed or blocked nerve conduction and ultimately axonal loss within the brain and spinal cord. Abnormal nerve conduction resulting from demyelination disrupts communication to, from, and within the central nervous system causing a constellation of neurological clinical signs and symptoms (Lubin 2005;Oger 2007).Because the underlying pathophysiology of MS becomes more severe as areas of disease progression get larger and involve more of the central nervous system, it is likely the autonomic nervous system is affected (Lubin 2005). Case in point, impaired autonomic control of cardiovascular function has been reported in up to two-thirds of individuals with MS (Acevedo et al. 2000;Nasseri et al. 1998). The most perilous health-related concern related to this autonomic cardiovascular dysfunction is the prevalence of orthostasis-related symptomology (i.e., orthostat...

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), disrupting autonomic function. PURPOSE: The aim of this study was to test the hypothesis that individuals with MS have blunted control of thermoregulatory reflex increases in sweat rate (SR) and cutaneous vasodilation compared to controls during a passive whole-body heat stress (WBH). METHODS: Eighteen individuals with relapsingremitting MS and 18 healthy controls (CON) participated in the study. Core temperature (Tcore), skin temperature, heart rate, arterial blood pressure (10 min intervals), skin blood flow (laser-Doppler flowmetry: LDF), and SR were continuously measured during normothermic baseline (34 °C water perfusing a tube-lined suit) and WBH (increased Tcore 0.8 °C via 48 °C water perfusing the suit). Following WBH, local heaters were warmed to 42 °C, inducing maximal cutaneous vasodilation at the site of LDF collection. Cutaneous vascular conductance (CVC) was calculated as the ratio of LDF to mean arterial pressure and expressed as a percentage of maximum. RESULTS: Individuals with MS had attenuated SR responses to WBH (∆SR from baseline: CON: 0.65±0.27; MS: 0.42±0.17 mg/cm 2 /min, p=0.003), while ∆%CVCmax from baseline was similar between groups (CON: 42±16%; MS: 38±12 %, p=0.39). SR responses were blunted as a function of Tcore in MS (interaction: group*Tcore, p=0.03), of which differences were evident at ∆Tcore 0.7 °C and 0.8 °C (p<0.05). No interaction was observed in ∆%CVCmax. CONCLUSION: Taken together, MS blunts sweating responses, while control of the cutaneous vasculature is preserved in response to WBH.