Cardiac function during heat stress: impact of short-term passive heat acclimation.

A lower heart rate (HR) during heat exposure is a classic marker of heat acclimation (HA), although it remains unclear whether this adaptation occurs secondary to reduced thermal strain and/or improvements in cardiac function. We evaluated the hypothesis that short-term passive HA reduces HR and improves cardiac function during passive heating. Echocardiography was performed under thermoneutral and hyperthermic conditions in 10 healthy adults (9 men/1 woman, 29 ± 6 yr old), pre and post 7 days of controlled hyperthermia. HR (P = 0.61), stroke volume (P = 0.99), and cardiac output (P = 0.99), were similar on days 1 and 7 of HA. Core (pre: 38.17 ± 0.42, post: 38.15 ± 0.27°C, P = 0.95) and mean skin (pre: 38.24 ± 0.41, post: 38.51 ± 0.29°C, P = 0.17) temperatures were similar during hyperthermic echocardiographic assessments. Cardiac systolic function was unaffected by HA (P ≥ 0.10). HA attenuated the decrease in end-diastolic volume (pre: -18 ± 18, post: -12 ± 19 mL, P = 0.05), accentuated the greater atrial contribution to diastolic filling (pre: +11 ± 5, post: +14 ± 5%, P = 0.02), and attenuated the increase in left atrial reservoir strain rate (pre: +1.5 ± 1.2, post: +0.8 ± 0.8 1/s, P = 0.02) during heating. Nonetheless, there were no differences in HR (pre: 106 ± 12, post: 104 ± 12 beats/min, P = 0.50), stroke volume (pre: 65 ± 15, post: 68 ± 13 mL, P = 0.55), or cardiac output (pre: 6.9 ± 2.0, post: 7.1 ± 1.7 L/min, P = 0.70) during passive heating. Short-term controlled hyperthermia HA results in limited adaptations of cardiac function during passive heating.NEW & NOTEWORTHY A lower heart rate during heat exposure is a classic marker of heat acclimation (HA). It remains unknown if improved cardiac function contributes to this response. A 7-day passive HA protocol did not alter cardiac systolic function during passive heating, whereas it improved some indexes of diastolic function in young adults. Nonetheless, heart rate during heating was unaffected by HA. These results suggest that passive HA induces limited adaptations in cardiac function during passive heating.

Evaluation of physiological strain in hot work areas using thermal imagery.

BACKGROUND: Monitoring core body temperature to identify heat strain in workers engaged in hot work in heat stress environments is intrusive and expensive. Nonintrusive, inexpensive methods are needed to calculate individual Physiological Strain Index (PSI). OBJECTIVE: Thermal imaging and heart rate monitoring were used in this study to calculate Physiological Strain Index (PSI) from thermal imaging temperatures of human subjects wearing thermal protective garments during recovery from hot work. METHODS: Ten male subjects were evaluated for physiological strain while participating in hot work. Thermal images of the head and neck were captured with a high-resolution thermal imaging camera concomitant with measures of gastrointestinal and skin temperature. Lin's concordance correlation coefficient (rho_c), Pearson's coefficient (r) and bias correction factor (C-b) were calculated to compare thermal imaging based temperatures to gastrointestinal temperatures. Calculations of PSI based thermal imaging recorded temperatures were compared to gastrointestinal based PSI. RESULTS: Participants reached a peak PSI of 5.2, indicating moderate heat strain. Sagittal measurements showed low correlation (rho_c=0.133), moderate precision (r=0.496) and low accuracy (C_b=0.269) with gastrointestinal temperature. Bland-Altman plots of imaging measurements showed increasing agreement as gastrointestinal temperature rose; however, the Limits of Agreement (LoA) fell outside the ±0.25C range of clinical significance. Bland-Altman plots of PSI calculated from imaging measurements showed increasing agreement as gastrointestinal temperature rose; however, the LoA fell outside the ±0.5 range of clinical significance. CONCLUSION: Results of this study confirmed previous research showing thermal imagery is not highly correlated to body core temperature during recovery from moderate heat strain in mild ambient conditions. Measurements display a trend toward increasing correlation at higher body core temperatures. Accuracy was not sufficient at mild to moderate heat strain to allow calculation of individual physiological stress.

Cerebral vasoreactivity: impact of heat stress and lower body negative pressure.

OBJECTIVE: Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). METHODS: Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS + 20 mmHg LBNP (HSLBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V mean). Cerebrovascular responses were calculated from the slope of the change in MCA V mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide ([Formula: see text]) during rebreathing. RESULTS: MCA V mean was similar in HS (55 ± 19 cm s(-1)) and HSLBNP (52 ± 16 cm s(-1)), and both values were reduced relative to NT (66 ± 20 cm s(-1)), yet the rise in MCA V mean per Torr increase in [Formula: see text] during rebreathing was similar in each condition (NT: 2.5 ± 0.6 cm s(-1) Torr(-1); HS: 2.4 ± 0.8 cm s(-1) Torr(-1); HSLBNP: 2.1 ± 1.1 cm s(-1) Torr(-1)). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1 ± 0.65 cm s(-1 )mmHg(-1)100 Torr(-1); HS: 2.4 ± 0.8 cm s(-1) mmHg(-1) 100 Torr(-1); HSLBNP: 2.0 ± 1.0 cm s(-1) mmHg(-1) 100 Torr(-1)). INTERPRETATIONS: These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.

Plasma hyperosmolality elevates the internal temperature threshold for active thermoregulatory vasodilation during heat stress in humans.

Plasma hyperosmolality delays the response in skin blood flow to heat stress by elevating the internal temperature threshold for cutaneous vasodilation. This elevation could be because of a delayed onset of cutaneous active vasodilation and/or to persistent cutaneous active vasoconstriction. Seven healthy men were infused with either hypertonic (3% NaCl) or isotonic (0.9% NaCl) saline and passively heated by immersing their lower legs in 42 degrees C water for 60 min (room temperature, 28 degrees C; relative humidity, 40%). Skin blood flow was monitored via laser-Doppler flowmetry at sites pretreated with bretylium tosylate (BT) to block sympathetic vasoconstriction selectively and at adjacent control sites. Plasma osmolality was increased by approximately 13 mosmol/kgH(2)O following hypertonic saline infusion and was unchanged following isotonic saline infusion. The esophageal temperature (T(es)) threshold for cutaneous vasodilation at untreated sites was significantly elevated in the hyperosmotic state (37.73 +/- 0.11 degrees C) relative to the isosmotic state (36.63 +/- 0.12 degrees C, P < 0.001). A similar elevation of the T(es) threshold for cutaneous vasodilation was observed between osmotic conditions at the BT-treated sites (37.74 +/- 0.18 vs. 36.67 +/- 0.07 degrees C, P < 0.001) as well as sweating. These results suggest that the hyperosmotically induced elevation of the internal temperature threshold for cutaneous vasodilation is due primarily to an elevation in the internal temperature threshold for the onset of active vasodilation, and not to an enhancement of vasoconstrictor activity.

Effects of self-contained breathing apparatus on ventricular function during strenuous exercise.

The purpose of this study was to investigate left-ventricular function during strenuous exercise with the self-contained breathing apparatus (SCBA). With the use of two-dimensional echocardiography, images of the left ventricle (LV) were acquired during sustained exercise (3 x 10 min) under two conditions: 1) SCBA, or 2) low resistance breathing valve. Twenty healthy men volunteered for the study, and in each condition subjects wore fire protective equipment. Heart rate, systolic blood pressure, cavity areas during systole and diastole (ESCA and EDCA, respectively), esophageal pressure, ventilation rate, oxygen consumption, perceived physical, thermal and respiratory distress, and core temperature were measured at regular intervals. Urine specific gravity (<1.020 g/ml) and hematological variables were used to infer hydration status. All subjects began both trials in a euhydrated state. No differences were found between conditions for heart rate, systolic blood pressure, ventilation rate, oxygen consumption, perceived distress, or any hematological variables. Peak expiratory esophageal pressure was always higher (P < 0.05), while EDCA and stroke area (SA) were significantly lower (P < 0.05) with the SCBA. ESCA, end-systolic transmural pressure (ESTMP), and LV contractility (ESTMP/ESCA) were similar between conditions. Sustained exercise with fire protective equipment resulted in significant reductions in EDCA, ESCA, and SA from the start of exercise, which was associated with a 6.3 +/- 0.8% reduction in plasma volume, an increase in core temperature (37.0 +/- 0.4 to 38.8 +/- 0.3 degrees C), and a significant increase in heart rate (146.9 +/- 2.1 to 181.7 +/- 2.4 beats/min) throughout exercise. The results from this study support research by others showing that increased intrathoracic pressure reduces LV preload (EDCA); however, the novelty of the present study is that when venous return is compromised by sustained exercise and heat stress, SA cannot be maintained.

Exercise-heat stress with and without water replacement alters brain structures and impairs visuomotor performance.

Effects of exercise-heat stress with and without water replacement on brain structure and visuomotor performance were examined. Thirteen healthy adults (23.6 ± 4.2 years) completed counterbalanced 150 min trials of exercise-heat stress (45°C, 15% RH) with water replacement (EHS) or without (~3% body mass loss; EHS-DEH) compared to seated rest (CON). Anatomical scans and fMRI Blood-Oxygen-Level-Dependent responses during a visuomotor pacing task were evaluated. Accuracy decreased (P < 0.05) despite water replacement during EHS (-8.2 ± 6.8% vs. CON) but further degraded with EHS-DEH (-8.3 ± 6.4% vs. EHS and -16.5 ± 10.2% vs. CON). Relative to CON, EHS elicited opposing volumetric changes (P < 0.05) in brain ventricles (-5.3 ± 1.7%) and periventricular structures (cerebellum: 1.5 ± 0.8%) compared to EHS-DEH (ventricles: 6.8 ± 3.4, cerebellum: -0.7 ± 0.7; thalamus: -2.7 ± 1.3%). Changes in plasma osmolality (EHS: -3.0 ± 2.1; EHS-DEH: 9.3 ± 2.1 mOsm/kg) were related (P < 0.05) to thalamus (r = -0.45) and cerebellum volume (r = -0.61) which, in turn, were related (P < 0.05) to lateral (r = -0.41) and fourth ventricle volume (r = -0.67) changes, respectively; but, there were no associations (P > 0.50) between structural changes and visuomotor accuracy. EHS-DEH increased neural activation (P < 0.05) within motor and visual areas versus EHS and CON. Brain structural changes are related to bidirectional plasma osmolality perturbations resulting from exercise-heat stress (with and without water replacement), but do not explain visuomotor impairments. Negative impacts of exercise-heat stress on visuomotor tasks are further exacerbated by dehydration.

Regional and long-range neural synchronization abnormality during passive hyperthermia.

Passive hyperthermia would impair wide-domain cognitive performances (e.g. attention, working memory), which may involve abnormal regional and long-range neural activity. Combining the regional homogeneity (ReHo) and seed-based functional connectivity analysis, this study investigated the regional and long-range neural synchronization abnormality during passive hyperthermia. We acquired the resting-state blood oxygenation level dependent (BOLD) data from twenty-three healthy male participants in two simulated thermal conditions: normothermic condition (NC) with temperature at 25°C for 1 h and hyperthermic condition (HC) with temperature at 50°C for 1 h. After scanning, participants were asked to perform an attention network test (ANT). Relative to NC participants, the participants in HC group exhibited decreased regional neural synchronization in the frontal-occipital cortex, specifically in the left opercular part of inferior frontal gyrus/insula, bilateral middle occipital gyrus, and posterior cingulate cortex/precuneus, but increased one in the left dorsal superior/middle frontal gyrus. Using these significantly differed ReHo clusters as seeds, we further performed functional connectivity analysis and found aberrant long-range neural synchronization in the orbital medial frontal cortex, temporal-parietal junction areas. Further neurobehavioral correlation analysis showed significant positive correlation between the regional ReHo alteration in left dorsolateral superior/middle frontal gyrus and executive control effect. Additionally, the functional connectivity of the orbital medial frontal cortex with the seeds "left superior/middle frontal gyrus" and "posterior cingulate cortex/precuneus" were negatively correlated with the increase of rectal temperature. In current study, the participants showed hyperthermia-induced brain activity disruptions, appearing as altered local ReHo and long-range functional connectivity, which might help understand the relationship between neuronal and circuit activities and physiological thermal sensation and regulation as well as behavioral changes.

Delayed vestibulopathy after heat exposure.

Even though dizziness is a common symptom of heat illness, comprehensive evaluation of the vestibular function has not been available in this potentially life-threatening disorder. Three patients developed vertigo about a week after heat exposure. Evaluation showed bilateral impairments of the vestibulo-ocular reflex during head impulses and the signs of vestibulocerebellar dysfunction that included spontaneous downbeat nystagmus, gaze-evoked nystagmus, and positional downbeat nystagmus. Exposure to excessive heat may give rise to delayed vestibulopathy by damaging the vestibulocerebellum.

Immunohistochemical and radiological characterization of wound healing in porcine liver after radiofrequency ablation.

BACKGROUND: Radiofrequency ablation (RFA) is a minimal invasive therapeutic option for patients with hepatocellular carcinoma or liver metastases. We investigated RFA-induced cellular changes in the liver of pigs. MATERIAL AND METHODS: Healthy pigs (n=18) were sacrificed between day 0 and 3 months after RFA. The wound healing process was evaluated by computed tomography (CT), chromotrope anilinblue (CAB) staining of large-scale and standard tissue sections. Immunohistochemistry (IHC) for heat shock protein 70, Caspase-3, Ki67, Reelin, Vinculin, Vimentin and α-SMA was perfomed. RESULTS: One day after RFA, CAB staining showed cell damage and massive hyperaemia. All IHC markers were predominantly expressed at the outer borders of the lesion, except Reelin, which was mainly detected in untreated liver regions. By staining for Hsp70, the heat stress during RFA was monitored, which was most distinct 1-2 days after RFA. CT revealed decreased lesion size after one week. Development of a Vimentin and α-SMA positive fibrotic capsule was observed. CONCLUSION: In the early phase signs of cell damage, apoptosis and proliferation are dominant. Reduced expression of Reelin suggests a minor role of hepatic stellate cells in the RFA zone. After one week myofibroblasts become prominent and contribute to the development of the fibrotic capsule. This elucidates the pathophysiology of RFA and could contribute to the future optimization of RFA procedures.

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow.

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g⁻¹·min⁻¹ (P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g⁻¹·min⁻¹ (P < 0.01). While whole body heat stress increased intestinal temperature by ∼1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g⁻¹·min⁻¹; heat stress: 1.7 ± 0.3 ml·100 g⁻¹·min⁻¹; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g⁻¹·min⁻¹) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.

Aerobic fitness does not influence the biventricular response to whole body passive heat stress.

We examined biventricular function during passive heat stress in endurance trained (ET) and untrained (UT) men to evaluate whether aerobic fitness alters the volumetric response. Body temperature was elevated ~0.8°C above baseline in 20 healthy men (10 ET, 64.4 ± 3.0 ml·kg(-1)·min(-1); and 10 UT, 46.3 ± 6.2 ml·kg(-1)·min(-1)) by circulating warm water (50°C) throughout a tube-lined suit. Cardiac magnetic resonance imaging was used to measure biventricular volumes, function, filling velocities, volumetric flow rates, and left ventricular (LV) twist and circumferential strain at baseline (BL) and after 45 min of heat stress. In both groups, passive heat stress reduced biventricular end-diastolic (ET, -19.5 ± 24.0 ml; UT, -25.1 ± 23.8 ml) and end-systolic (ET, -15.9 ± 8.8 ml; UT, -17.6 ± 7.9 ml) volumes and left atrial volume (ET, -19.2 ± 11.6 ml; UT, -15.0 ± 12.7 ml) and significantly increased heart rate (ET, 29.3 ± 9.0 beats/min; UT, 31.7 ± 10.4 beats/min) and cardiac output (ET, 3.8 ± 2.2 l/min; UT, 3.2 ± 1.4 l/min) similarly, while biventricular stroke volume was unchanged. There were no between-group differences in any parameter. Heat stress increased (P < 0.05), as a percentage of baseline values, biventricular ejection fraction (ET, 3.4 ± 5.3%; UT, 4.4 ± 3.7%), annular systolic tissue velocities (ET, 32.5 ± 34.9%; UT, 44.0 ± 38.1%), and peak LV twist (ET, 51.6 ± 59.7%; UT, 59.7 ± 54.2%) and untwisting rates (ET, 45.5 ± 42.3%; UT, 51.8 ± 55.0%) similarly in both groups. Early LV diastolic tissue and blood velocities, volumetric flow rates, and strain rates (diastole) were unchanged with heat stress in both groups. The present findings indicate that aerobic fitness does not influence the biventricular response to passive heat stress.

Methodological assessment of skin and limb blood flows in the human forearm during thermal and baroreceptor provocations.

Skin blood flow responses in the human forearm, assessed by three commonly used technologies-single-point laser-Doppler flowmetry, integrated laser-Doppler flowmetry, and laser-Doppler imaging-were compared in eight subjects during normothermic baseline, acute skin-surface cooling, and whole body heat stress (Δ internal temperature=1.0±0.2 degrees C; P<0.001). In addition, while normothermic and heat stressed, subjects were exposed to 30-mmHg lower-body negative pressure (LBNP). Skin blood flow was normalized to the maximum value obtained at each site during local heating to 42 degrees C for at least 30 min. Furthermore, comparisons of forearm blood flow (FBF) measures obtained using venous occlusion plethysmography and Doppler ultrasound were made during the aforementioned perturbations. Relative to normothermic baseline, skin blood flow decreased during normothermia+LBNP (P<0.05) and skin-surface cooling (P<0.01) and increased during whole body heating (P<0.001). Subsequent LBNP during whole body heating significantly decreased skin blood flow relative to control heat stress (P<0.05). Importantly, for each of the aforementioned conditions, skin blood flow was similar between the three measurement devices (main effect of device: P>0.05 for all conditions). Similarly, no differences were identified across all perturbations between FBF measures using plethysmography and Doppler ultrasound (P>0.05 for all perturbations). These data indicate that when normalized to maximum, assessment of skin blood flow in response to vasoconstrictor and dilator perturbations are similar regardless of methodology. Likewise, FBF responses to these perturbations are similar between two commonly used methodologies of limb blood flow assessment.