Reduced resting beat-to-beat blood pressure variability in females with relapsing-remitting multiple sclerosis.

BACKGROUND: Relapsing-remitting multiple sclerosis (RRMS) is a demyelinating disease of the central nervous system and cardiovascular autonomic dysfunction has been well documented in this population. The sympathetic nervous system contributes to beat-to-beat blood pressure regulation primarily by baroreflex control of the peripheral vasculature which may be impaired in females with RRMS. Even at rest, attenuated sympathetic control of vasomotor tone may result in large and frequent blood pressure excursions (i.e., greater blood pressure variability). Therefore, the primary purpose of this investigation was to test the following hypotheses; (1) females with RRMS have augmented beat-to-beat blood pressure variability compared to healthy controls and (2) reduced sympathetic baroreflex sensitivity in females with RRMS is related to augmented blood pressure variability. METHODS: Electrocardiogram and beat-to-beat blood pressure were continuously recorded during 8-10 min of supine rest in 26 females with clinically definite RRMS and 24 sex-, age- and BMI- matched healthy controls. Muscle sympathetic nerve activity (MSNA) was recorded in a subset of participants (MS, n = 15; CON, n = 14). Traditional statistical measurements of dispersions were used to index beat-to-beat blood pressure variability. Spontaneous sympathetic baroreflex sensitivity was quantified by sorting diastolic blood pressures into 3 mmHg bins and calculating MSNA burst incidence within each bin. Weighted linear regression was then used to account for the number of cardiac cycles in each bin and calculate slopes. Spontaneous cardiac baroreflex sensitivity was determined using the sequence method. RESULTS: Groups had similar resting mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), MSNA burst frequency and MSNA burst incidence (All P > 0.05). The standard deviation and interquartile range of MAP, SBP and DBP were less in females with RRMS compared to healthy controls (All P < 0.05). There were no between groups differences in sympathetic baroreflex sensitivity or cardiac baroreflex sensitivity (Both P > 0.05) and baroreflex sensitivity measures were not related to any indices of blood pressure variability (Both P > 0.05). CONCLUSION: These data suggest that females with RRMS have reduced beat-to-beat blood pressure variability. However, this does not appear to be related to changes in sympathetic or cardiac baroreflex sensitivity.

Heat stress and heat strain among outdoor workers in El Salvador and Nicaragua.

BACKGROUND: There is growing attention on occupational heat stress in Central America, as workers in this region are affected by a unique form of chronic kidney disease. Previous studies have examined wet bulb globe temperatures and estimated metabolic rates to assess heat stress, but there are limited data characterizing heat strain among these workers. OBJECTIVE: The aims were to characterize heat stress and heat strain and examine whether job task, break duration, hydration practices, and kidney function were associated with heat strain. METHODS: We used data from the MesoAmerican Nephropathy Occupational Study, a cohort of 569 outdoor workers in El Salvador and Nicaragua who underwent workplace exposure monitoring, including continuous measurement of core body temperature (Tc), heart rate (HR), physical activity, and wet bulb globe temperature (WBGT), over the course of three days in January 2018 - May 2018. Participants represented five industries: sugarcane, corn, plantain, brickmaking, and construction. RESULTS: Median WBGTs were relatively high (>27 °C) at most sites, particularly when work shifts spanned the afternoon hours (e.g., 29.2 °C among plantain workers). Sugarcane workers, especially cane cutters in both countries and Nicaraguan agrichemical applicators, had the highest estimated metabolic rates (medians: 299-318 kcal/hr). Most workers spent little time on break (<10% of the shift), as determined by physical activity data. Overall, sugarcane workers-particularly those in Nicaragua-experienced the highest Tc and HR values. However, a few workers in other industries reached high Tc (>39 °C) as well. Impaired kidney function (estimated glomerular filtration rate <90 mL/min/1.73 m2) was associated with higher Tc and HR values, even after adjustment. SIGNIFICANCE: This is the largest study to-date examining heat stress and strain among outdoor workers in Central America. Workers at sugar companies regularly experienced Tc > 38°C (76.9% of monitored person-days at Nicaraguan companies; 46.5% at Salvadoran companies). Workers with impaired kidney function had higher measures of Tc and HR. IMPACT STATEMENT: This study examined levels of occupational heat stress and heat strain experienced among outdoor workers in five industries in El Salvador and Nicaragua. We characterized heat stress using wet bulb globe temperatures and estimated metabolic rate and heat strain using core body temperature and heart rate. Sugarcane workers, particularly cane cutters and Nicaraguan agrichemical applicators, performed more strenuous work and experienced greater levels of heat strain. Impaired kidney function was associated with higher heart rates and core body temperatures.

Skin tattooing impairs sweating during passive whole body heating.

Tattooing of the skin involves repeated needle insertions to deposit ink into the dermal layer of the skin, potentially damaging eccrine sweat glands and the cutaneous vasculature. This study tested the hypothesis that reflex increases in sweat rate (SR) and cutaneous vasodilation are blunted in tattooed skin (TAT) compared with adjacent healthy skin (CON) during a passive whole body heat stress (WBH). Ten individuals (5 males and 5 females) with a sufficient area of tattooed skin participated in the study. Intestinal temperature (Tint), skin temperature (Tskin), 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 Tint 1.0°C via 48°C water perfusing suit). SR throughout WBH was lower for TAT compared with CON (P = 0.033). Accumulated sweating responses during WBH (area under curve) were attenuated in TAT relative to CON (23.1 ± 12.9, 26.9 ± 14.5 mg/cm2, P = 0.043). Sweating threshold, expressed as the onset of sweating in time or Tint from the initiation of WBH, was not different between TAT and CON. Tattooing impeded the ability to obtain LDF measurements. These data suggest that tattooing functionally damages secretion mechanisms, affecting the reflex capacity of the gland to produce sweat, but does not appear to affect neural signaling to initiate sweating. Decreased sweating could impact heat dissipation especially when tattooing covers a higher percentage of body surface area and could be considered a potential long-term clinical side effect of tattooing.NEW & NOTEWORTHY This study is the first to assess the reflex control of sweating in tattooed skin. The novel findings are twofold. First, attenuated increases in sweat rate were observed in tattooed skin compared with adjacent healthy non-tattooed skin in response to a moderate increase (1.0°C) in internal temperature during a passive whole body heat stress. Second, reduced sweating in tattooed skin is likely related to functional damage to the secretory mechanisms of eccrine sweat glands, rendering it less responsive to cholinergic stimulation.

Impaired Thermoregulatory Function during Dynamic Exercise in Multiple Sclerosis.

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) 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·min·°C; CON, 0.86 ± 0.30 mg·cm·min·°C; 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.

Core temperature is not elevated at rest in people with relapsing-remitting multiple sclerosis.

PURPOSE: To reassess the notion that people with multiple sclerosis (MS) do not demonstrate an elevated resting core temperature when measured using best-practice precision thermometry. METHOD: Across two international data collection sites (Australia and USA), twenty-eight relapsing-remitting MS patients and 27 aged-matched controls (CON) were exposed to either 30 °C, 30% relative humidity (RH) (Sydney) or 25 °C, 30% RH (Dallas). Resting rectal (Tre) and esophageal (Teso) temperature and resting oxygen consumption (VO2) was measured in MS (n = 28) and CON (n = 27) groups who completed the 25 °C and 30 °C trials. Tympanic membrane (Ttym) temperature was measured in MS (n = 16) and CON (n = 15) groups in the 30 °C condition. A modified fatigue impact scale (MFIS) questionnaire was used to assess subjective measures of psychosocial, physical and cognitive fatigue in the 30 °C condition. RESULTS: Irrespective of ambient temperature, no group differences were observed for Tre (MS: 37.07 ±â€¯0.30 °C; CON: 37.18 ±â€¯0.30 °C; P = 0.29), Teso (MS: 36.84 ±â€¯0.42 °C; CON: 36.92 ±â€¯0.29 °C; P = 0.36) or resting VO2 (MS: 3.89 ±â€¯0.18 ml⋅kg-1⋅min-1; CON: 3.98 ±â€¯0.17 ml⋅kg-1⋅min-1; P = 0.67). Similarly, no group differences were observed for Ttym (MS: 36.52 ±â€¯0.38 °C; CON: 36.61 ±â€¯0.33 °C; P = 0.55) in the 30 °C condition. Resting Tre did not correlate with subjective measures of fatigue: physical: r = -0.11, P = 0.67; cognitive: r = -0.14, P = 0.60; and psychosocial: r = 0.05, P = 0.84. CONCLUSION: Contrary to recent reports, resting core temperature is not elevated in relapsing-remitting MS patients compared to healthy controls when measured using precision thermometry. Furthermore, no association was observed between resting Tre and any subjective measures of fatigue in a subset of participants 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.

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.

Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men.

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (-20, -40, -60, and -80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (-0.73 ± 0.11) compared with NT (-0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at -40, -60, and -80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

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.