High Tsk Research Articles

Individualized monitoring of heat illness risk: novel adaptive physiological strain index to assess exercise-heat strain from athletes to fully encapsulated workers

Objective. Exercise-heat strain estimation approaches often involve combinations of body core temperature (Tcore), skin temperature (Tsk) and heart rate (HR). A successful existing measure is the ‘Physiological Strain Index’ (PSI), which combines HR and Tcore values to estimate strain. However, depending on variables such as aerobic fitness and clothing, the equation’s ‘maximal/critical’ Tcore must be changed to accurately represent the strain, in part because high Tsk (small Tcore−Tsk) can increase cardiovascular strain and thereby negatively affect performance. Here, an ‘adaptive PSI’ (aPSI) is presented where the original PSI Tcorecritical value is ‘adapted’ dynamically by the delta between Tcore and Tsk. Approach. PSI and aPSI were computed for athletes (ELITE, N = 11 male and 8 female, 8 km time-trial) and soldiers in fully encapsulating personal protective equipment (PPE, N = 8 male, 2 km approach-march). While these were dissimilar events, it was anticipated given that the clothing and work rates would elicit similar very-high exercise-heat strain values. Main results. Mean end HR values were similar (∼180 beats min−1) with higher Tcore = 40.1 ± 0.4 °C for ELITE versus PPE 38.4 ± 0.6 °C (P < 0.05). PSI end values were different between groups (P < 0.01) and appeared ‘too-high’ for ELITE (11.4 ± 0.8) and ‘too-low’ for PPE (7.6 ± 2.0). However, aPSI values were not different (9.9 ± 1.4 versus 9.0 ± 2.5 versus; p > 0.05) indicating a ‘very high’ level of exercise-heat strain for both conditions. Significance. A simple adaptation of the PSI equation, which accounts for differences in Tcore-to-Tsk gradients, provides a physiological approach to dynamically adapt PSI to provide a more accurate index of exercise-heat strain under very different working conditions.

Cardiovascular responses to exercise when increasing skin temperature with narrowing of the core-to-skin temperature gradient.

The decline in stroke volume (SV) during exercise in the heat has been attributed to either an increase in cutaneous blood flow (CBF) that reduces venous return or an increase in heart rate (HR) that reduces cardiac filling time. However, the evidence supporting each mechanism arises under experimental conditions with different skin temperatures (Tsk; e.g., ≥38°C vs. ≤36°C, respectively). We systematically studied cardiovascular responses to progressively increased Tsk (32°C-39°C) with narrowing of the core-to-skin gradient during moderate intensity exercise. Eight men cycled at 63 ± 1% peak oxygen consumption for 20-30 min. Tsk was manipulated by having subjects wear a water-perfused suit that covered most of the body and maintained Tsk that was significantly different between trials and averaged 32.4 ± 0.2, 35.5 ± 0.1, 37.5 ± 0.1, and 39.5 ± 0.1°C, respectively. The graded heating of Tsk ultimately produced a graded elevation of esophageal temperature (Tes) at the end of exercise. Incrementally increasing Tsk resulted in a graded increase in HR and a graded decrease in SV. CBF reached a similar average plateau value in all trials when Tes was above ~38°C, independent of Tsk. Tsk had no apparent effect on forearm venous volume (FVV). In conclusion, the CBF and FVV responses suggest no further pooling of blood in the skin when Tsk is increased from 32.4°C to 39.5°C. The decrease in SV during moderate intensity exercise when heating the skin to high levels appears related to an increase in HR and not an increase in CBF. NEW & NOTEWORTHY This study systematically investigated the effect of increasing skin temperature (Tsk) to high levels on cardiovascular responses during moderate intensity exercise. We conclude that the declines in stroke volume were related to the increases in heart rate but not the changes in cutaneous blood flow (CBF) and forearm venous volume (FVV) during moderate intensity exercise when Tsk increased from ~32°C to ~39°C. High Tsk (≥38°C) did not further elevate CBF and FVV compared with lower Tsk during moderate intensity exercise.

Increasing Skin Temperature During Exercise Lowers Stroke Volume Without Increasing Cutaneous Blood Flow.

Both skin (Tsk) and core temperature (Tc) are elevated in most studies of heat stress during exercise and this is accompanied by increased heart rate (HR) and decreased stroke volume (SV). However, only a few studies have systemically investigated the effect of progressively increasing Tsk on cardiovascular responses during exercise. PURPOSE:To systemically investigate how progressive increases in Tsk (32 to 40°C) affects cardiovascular responses and Tc during moderate exercise. METHODS: Subjects (n=8, active men 25±1 y) cycled at 60% VO2peak for 20-30 min. Tsk was manipulated by wearing a water perfused suit that covered the whole body, except head, hands, and feet and maintained a perfused water temperature of 20, 30, 40, and 50°C. Subjects performed all four trials separated by at least 72 h. Esophageal temperature (Tes), Tsk, VO2, Q, HR, mean arterial pressure (MAP), cutaneous blood flow (CBF), and forearm venous volume (FVV) were measured during exercise. RESULTS: Tsk was significantly different between all trials (P < 0.01) and averaged 32.4 ± 0.2, 35.5 ± 0.1, 37.5 ± 0.1, and 39.5°C ± 0.1°C, respectively. Tes was significantly different between each trial after 16 min of exercise (p < 0.05) and at the end of exercise were 37.6 ± 0.2, 38.3 ± 0.1, 39.2 ± 0.1, and 39.2 ± 0.2°C, respectively. The graded heating of Tsk resulted in a graded increase of HR and decrease of SV. However, CBF during exercise reached a similar average plateau value in all trials when Tes was above 38°C independent of Tsk. There was no apparent effect of Tsk on FVV, VO2, Q, and MAP. CONCLUSIONS: Graded increases of Tsk from 32 to 40°C progressively increased Tes and HR and decreased SV during moderate exercise. Tsk had no effect on CBF when Tes was above 38°C. High Tsk (39.5 ± 0.1°C) did not elicit higher CBF and FVV compared to low Tsk during moderate exercise. CBF and FVV responses suggest no further blood pooling in the forearm skin when Tsk is increased from 32.4 to 39.5°C. The decrease of SV during exercise when heating the skin is related to an increase of HR but not an increase in CBF.

Mild cooling of the feet does not aid night-time vigilance

Vigilance is related to core temperature (TC) and skin temperature (Tsk). Biological day reflects a high TC, alertness and modest Tsk; night reflects vice versa [1,2]. At rest, TC is regulated largely via controlling blood flow in extremities (and thus Tsk); vasodilation strongly predicts reduced vigilance [3] and faster sleep onset[4]. In narcolepsy, high daytime extremity temperatures and a smaller distal-to-proximal gradient (DPG) indicates higher sleep propensity [5]. Cool extremities have been linked observationally to delayed sleep onset in the elderly, and experimentally shown to reduce sleep propensity in narcolepsy [6]. Therefore, the aim of this study was to test the hypothesis that cooling the feet would maintain vigilance during extended wakefulness in healthy adults.

Warm skin alters cardiovascular responses to cycling after preheating and precooling.

Exercise in hot conditions increases core (TC) and skin temperature (TSK) and can lead to a progressive rise in HR and decline in stroke volume (SV) during prolonged exercise. Thermoregulatory-driven elevations in skin blood flow (SkBF) adds complexity to cardiovascular regulation during exercise in these conditions. Presently, the dominant, although debated, view is that raising TSK increases SkBF and reduces SV through diminished venous return; however, this scenario has not been rigorously investigated across core and skin temperatures. We tested the hypothesis that high TSK would raise HR and reduce SV during exercise after precooling (cold water bath) and preheating (hot water bath) and that no relationship would exist between SkBF and SV during exercise. Non-endurance-trained individuals cycled for 20 min at 69% ± 1% VO₂peak on four occasions: cool skin-cool core (SkCCC), warm skin-cool core (SkWCC), cool skin-warm core (SkCCW), and warm skin-warm core (SkWCW) on separate days. After precooling of TC, the rise in HR was greater in SkWCC than in SkCCC (P < 0.001), yet SV was similar (P = 0.26), which resulted in higher QC at min 20 in SkWCC (P < 0.01). Throughout exercise after preheating of TC, HR was higher (P < 0.001), SV was reduced (P < 0.01), and QC was similar (P = 0.40) in SkWCW versus SkCCW. When all trials were compared, there was no relationship between SkBF and SV (r = -0.08, P = 0.70); however, there was an inverse relationship between HR and SV (r = -0.75, P < 0.001). These data suggest that when TSK is elevated during exercise, HR and TC will rise but SV will only be reduced when TC is also elevated above 38°C. Furthermore, changes in SV are not related to changes in SkBF.

Short-term Electricity Price Forecasting Using Optimal Tsk Fuzzy Systems

Since all financial transactions in restructured power markets are based on electricity prices, it is necessary that the price of electric power be predicted precisely. Some particular features such as: nonlinearity, non-stationary behaviors, as well as volatility of electricity prices make such a prediction a very challenging task. In this paper, a new structure of TSK fuzzy systems is presented that provides high order TSK fuzzy systems from lower orders which have capability of modeling and forecasting chaotic time series. The method used for optimization of fuzzy systems is the Interior point method. Using this method for forecasting electricity price is useful because of its chaotic behavior. The results are compared with RBF neural network and TSK fuzzy system presents better results.

Impact of skin temperature and hydration on plasma volume responses during exercise.

Heat stress and hydration may both alter plasma volume (PV) responses during acute exercise; potential interactions have not been fully studied. The purpose of this study was to determine the effect of graded elevations in skin temperature (Tsk) on PV changes during steady-state exercise under conditions of euhydration (EU) and hypohydration (HYPO, -4% of body mass). Thirty-two men (22 ± 4 yr) were divided into four cohorts (n = 8 each) and completed EU and HYPO trials in one environment [ambient temperature (Ta) 10, 20, 30, and 40°C]. Thirty minutes of cycle ergometry (50% V̇o2peak) was performed. Core (Tre) and mean skin (Tsk) temperatures were measured; changes in PV, total circulating protein (TCP), and mean arterial pressure (MAP) were calculated; and skin blood flow (SkBF) was estimated. Hypohydration decreased (P < 0.05) PV by 200 ml (-5.7%) but did not alter TCP. Plasma loss was not different between EU and HYPO during exercise at any Ta. Plasma losses were greater (P < 0.05) with elevated Ta with an average -130, -174, -294, and -445 ml losses during the 10, 20, 30, and 40°C trials, respectively. Significant (P < 0.05) correlations (r = 0.50 to 0.84) were found between ΔTCP and ΔPV during exercise when Tsk was cool/warm (<33°C; Ta 10, 20, and 30°C), but not at 40°C (high Tsk). We conclude that 1) graded skin warming proportionally accentuated plasma loss; 2) plasma loss was associated with plasma protein efflux at lower Tsk and SkBF; 3) at high Tsk, additional plasma loss likely results from increased net filtration at the capillaries; and 4) HYPO did not alter vascular fluid loss during exercise in any environment.

Central and Peripheral Fatigue during Passive and Exercise-Induced Hyperthermia

Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined. On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC. Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05). The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

Mechanisms of aerobic performance impairment with heat stress and dehydration

Environmental heat stress can challenge the limits of human cardiovascular and temperature regulation, body fluid balance, and thus aerobic performance. This minireview proposes that the cardiovascular adjustments accompanying high skin temperatures (T(sk)), alone or in combination with high core body temperatures (T(c)), provide a primary explanation for impaired aerobic exercise performance in warm-hot environments. The independent (T(sk)) and combined (T(sk) + T(c)) effects of hyperthermia reduce maximal oxygen uptake (Vo(2max)), which leads to higher relative exercise intensity and an exponential decline in aerobic performance at any given exercise workload. Greater relative exercise intensity increases cardiovascular strain, which is a prominent mediator of rated perceived exertion. As a consequence, incremental or constant-rate exercise is more difficult to sustain (earlier fatigue) or requires a slowing of self-paced exercise to achieve a similar sensation of effort. It is proposed that high T(sk) and T(c) impair aerobic performance in tandem primarily through elevated cardiovascular strain, rather than a deterioration in central nervous system (CNS) function or skeletal muscle metabolism. Evaporative sweating is the principal means of heat loss in warm-hot environments where sweat losses frequently exceed fluid intakes. When dehydration exceeds 3% of total body water (2% of body mass) then aerobic performance is consistently impaired independent and additive to heat stress. Dehydration augments hyperthermia and plasma volume reductions, which combine to accentuate cardiovascular strain and reduce Vo(2max). Importantly, the negative performance consequences of dehydration worsen as T(sk) increases.

MEASUREMENT OF MEAN SKIN TEMPERATURE: ???COVERED??? VS.???UNCOVERED??? CONTACT THERMISTORS

1620 The purpose of this study was to compare the mean skin temperature(Tsk) obtained using “covered” vs. “uncovered” contact thermistors in a variety of environmental conditions. Ten male subjects walked on a treadmill at 4 mph for 30 min in three different environments: temperate (23 °C/50% rH), hot-humid (35 °C/80%), and hot-dry (42 °C/20%). Tsk was measured using three“uncovered” contact thermistors, and three “covered” thermistors. The “uncovered” probes were attached using acrylic rings that allowed the outer surface of the thermistors to have free exchange with the environment. The “covered” probes were affixed to the skin using foam patches and tape. The latter procedure is commonly used in many research and clinical laboratories. The “covered” probes resulted in a significantly (p<0.05) higher Tsk under all three environmental conditions. The largest difference occurred in the temperate condition with the “covered” Tsk being 1.3 °C higher than the “uncovered” Tsk. Furthermore,“covered” vs. “uncovered” forearm Tsk was measured in a variety of ambient air temperatures ranging from 12 °C to 43°C. The results showed that ▵ (“covered” minus“un-covered”) forearm Tsk was inversely correlated (r=-0.97) with ambient air temperature. These results suggest that covering a contact skin thermistor hinders heat loss and results in an artificially high Tsk. The results of this study will hopefully encourage the adoption of using “uncovered” contact skin thermistors in the future.

Core threshold temperatures for sweating

To detect shifts in the threshold core temperature (Tc) for sweating caused by particular nonthermal stresses, it is necessary to stabilize or standardize all other environmental and physiological variables which cause such shifts. It is, however, difficult to cause progressive changes in Tc without also causing changes in skin temperature (Tsk). This study compares the technique of body warming by immersion in water at 40 degrees C, and subsequent body cooling in water at 28 degrees C, to determine the core threshold for sweating, with one by which Tc was raised by cycling exercise in air at 20 degrees C, and then lowered by immersion in water at 28 degrees C. The first of these procedures involved considerable shifts in Tsk upon immersion in water at 40 degrees C, and again upon transfer to water at 28 degrees C; the second procedure caused only small changes in Tsk. The onset of sweating at a lower esophageal temperature (Tes) during immersion in water at 40 degrees C (36.9 +/- 0.1 degrees C) than during exercise (37.4 +/- 0.3 degree C) is attributed to the high Tsk since Tes was then unchanged. Likewise, the rapid decline in the sweat rate during immersion at 28 degrees C had the same time course to extinction after the pretreatments. This related more to the Tsk, which was common, than to the levels or rates of change of Tes, which both differed between techniques. Tes fell most rapidly, and thus sweating was extinguished at a lower Tes, following 40 degrees C immersion than following exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of skin temperature on central thermoregulatory control of leg blood flow.

This study examined the influence of elevated skin temperature (Tsk) on the central thermoregulatory control of leg blood flow in five unanesthetized, chronically instrumented, resting baboons (Papio anubis and P. cynocephalus). In each experiment, mean iliac blood flow (MIBF), mean arterial blood pressure, arterial blood temperature (Tbl), and Tsk were measured, and iliac vascular conductance (IVC) was calculated. A heat exchanger was incorporated into a chronic arteriovenous femoral shunt to control Tbl. The protocol consisted of raising Tbl approximately 2.6 degrees C in thermoneutral environment (cool Tsk) an then again after Tsk had been elevated by environmental heating. A major influence of raising Tsk was the lowering of threshold Tbl at which the rise in MIBF and IVC commenced. This threshold Tbl was lowered at least 0.8 degrees C on the average. Also, over the whole range of Tbl studied (37.0-39.6 degrees C), MIBF and IVC were higher at high Tsk than at cool Tsk. Thus an elevation of Tsk significantly influences the control of skin blood flow by central thermoreceptors.

Control of forearm venous volume during exercise and body heating

Subjects ate ice to cool sufficiently to constrict the superficial forearm veins. After ice-eating, esophageal temperature (Tes) recovered from local cooling in 10-15 min, and thereafter reflected body core temperature. Eight skin temperatures (Tsk) were measured, and a weighted mean (Tsk) computed. The left wrist was suspended 5-6 in. above shoulder level, and left forearm skin temperature was maintained at 35 degrees C with a controlled-temperature air stream. Forearm venous volume (FVV) w-s the volume difference between the forearm drained by gravity and the forearm congested by a pneumatic cuff inflated to 32 Torr. Subjects were warmed either by storage of resting metabolic heat or by cycle exercise at 40-45% of maximal O2 consumption. Exercise experiments were conducted in ambient temperatures of 15, 25, and 35 degrees C, and resting experiments in 25 and 35 degrees C. FVV rose linearly with Tes, but during exercise FVV was lower than at the same Tes and Tsk during rest, and the difference was greater at high Tsk and FVV. Our data fit the equation FVV-FVV0 = (a1 Tes + a2 Tsk - b).[1 - phi (W).(Tsk - T-sk0)], where phi (W) is a function of exercise, and phi (W) = 0 at rest.