Mu Huang

Autonomic dysfunction in multiple sclerosis: implications for exercise.

Multiple sclerosis (MS), a progressive neurological disease, can result in autonomic dysfunction. Impairments in the autonomic control of cardiovascular and thermoregulatory function during exercise have been observed in MS. Attenuated elevations in blood pressure during exercise in MS patients can negatively impact blood flow to skeletal muscle. Diminished sweating during exercise may impair heat dissipation likely limiting the exercise intensity that can be performed before detrimental core temperatures are reached. Further understanding the physiologic mechanisms of autonomic dysfunction during exercise in MS may lead to the development of novel therapeutic strategies targeted at improving quality of life in individuals with this disease.

Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis.

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 = 10; 7 females, 3 males; 13 ± 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 = 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; +40 Torr) and neck suction (NS; -60 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 ± 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 ± 3 mmHg; P = 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, -10 ± 4% baseline vs. CON, -15 ± 4% baseline, P = 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.

Increased postural sway in persons with multiple sclerosis during short-term exposure to warm ambient temperatures

BACKGROUND Multiple sclerosis (MS) is a neurological disease marked by demyelination and axonal loss. Individuals with MS experience increases in clinical signs and symptoms during heat exposure. OBJECTIVE To test the hypothesis that moderate heat exposure adversely affects postural sway in individuals with MS. METHODS Ten individuals with relapsing-remitting MS (50±8y) and nine controls (47±10y) were examined under a Thermal and a Time Control trial. Following a 30min thermoneutral baseline (25°C, 30% relative humidity (RH)), stand tests randomized with eyes open and closed, were performed. For Thermal, subjects were first exposed to 60min of heating (40°C, 30%RH) followed by 60min of cooling (20°C, 30%RH). For Time Control, subjects remained in a thermoneutral environment throughout. Stand tests were repeated at consistent times in both trials. RESULTS No difference in skin and core temperatures between groups were observed for any trial (P>0.05). During heating, postural sway was higher in MS relative to control subjects (eyes open, P=0.03; eyes closed, P=0.011). No differences in postural sway, regardless of eye status, were observed during the Time Control trial for either group (P>0.05). CONCLUSION These data demonstrate that exposure to a moderate heating environment increases postural sway in patients with MS.

Impaired sweating responses to a passive whole body heat stress in individuals with multiple sclerosis

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), disrupting autonomic function. 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 with controls during a passive whole body heat stress (WBH). Eighteen individuals with relapsing-remitting 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 flux, 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 peak 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 peak achieved during local heating. Individuals with MS had attenuated SR responses to WBH (ΔSR from baseline: Con, 0.65 ± 0.27; MS, 0.42 ± 0.17 mg·cm-2·min-1, P = 0.003), whereas Δ%CVC42C 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 ΔTcore 0.7°C and 0.8°C (P < 0.05). No interaction was observed in Δ%CVC42C Taken together, the findings show MS blunts sweating responses, whereas control of the cutaneous vasculature is preserved, in response to WBH.NEW & NOTEWORTHY This study is the first to assess the reflex control of the thermoregulatory system in individuals living with multiple sclerosis (MS). The novel findings are twofold. First, attenuated increases in sweat rate in subjects with MS compared with healthy controls were observed in response to a moderate increase (0.8°C) in core temperature via passive whole body heat stress. Second, it appears the reflex control of the cutaneous vasculature is preserved in MS.

Tolerance to a haemorrhagic challenge during heat stress is improved with inspiratory resistance breathing

What is the central question of this study? Does inspiratory resistance breathing improve tolerance to simulated haemorrhage in individuals with elevated internal temperatures? What is the main finding and its importance? The main finding of this study is that inspiratory resistance breathing modestly improves tolerance to a simulated progressive haemorrhagic challenge during heat stress. These findings demonstrate a scenario in which exploitation of the respiratory pump can ameliorate serious conditions related to systemic hypotension.