Lower-body Heating Research Articles

Age-Related Difference in Cognitive Performance under Severe Whole-Body Hyperthermia Parallels Cortisol and Physical Strain Responses.

Background and Objectives: To date, understanding age-related changes in cognitive processes during heat exposure still needs to be better-understood. Thus, the main aim of the current study was to evaluate the effects of whole-body hyperthermia (WBH), i.e., a ≈ 2.5 °C increase in rectal temperature (Tre) from overnight-fast baseline value, on cognitive functioning in old and young men and to explore factors, such as stress and thermophysiological strain, that could influence such changes. Materials and Methods: Ten young (19-21 years of age) and nine old (61-80 years of age) healthy men underwent an experimental trial with passive lower-body heating in hot water immersion (HWI) at 43 °C (HWI-43 °C) until Tre reached 39 °C in old adults and 39.5 °C in young adults. Cognitive performance and cortisol concentration were assessed before and after HWI, and the physiological strain index (PSI) was assessed during HWI-43 °C. Results: PSI was lower and cortisol concentration was greater after HWI-43 °C in the old group compared with the young group (p < 0.05). Surprisingly, hyperthermia improved cognitive flexibility only in old adults, whereas short-term and visual recognition memories were maintained in both age groups. Conclusions: A ≈ 2.5 °C increase in rectal temperature can improve executive function in old adults, and this increase parallels the increased cortisol concentration and the lower thermophysiological strain under severe WBH conditions.

Endothelial HSP72 is not reduced in type 2 diabetes nor is it a key determinant of endothelial insulin sensitivity.

Impaired endothelial insulin signaling and consequent blunting of insulin-induced vasodilation is a feature of type 2 diabetes (T2D) that contributes to vascular disease and glycemic dysregulation. However, the molecular mechanisms underlying endothelial insulin resistance remain poorly known. Herein, we tested the hypothesis that endothelial insulin resistance in T2D is attributed to reduced expression of heat shock protein 72 (HSP72). HSP72 is a cytoprotective chaperone protein that can be upregulated with heating and is reported to promote insulin sensitivity in metabolically active tissues, in part via inhibition of JNK activity. Accordingly, we further hypothesized that, in individuals with T2D, 7 days of passive heat treatment via hot water immersion to waist level would improve leg blood flow responses to an oral glucose load (i.e., endogenous insulin stimulation) via induction of endothelial HSP72. In contrast, we found that: 1) endothelial insulin resistance in T2D mice and humans was not associated with reduced HSP72 in aortas and venous endothelial cells, respectively; 2) after passive heat treatment, improved leg blood flow responses to an oral glucose load did not parallel with increased endothelial HSP72; and 3) downregulation of HSP72 (via small-interfering RNA) or upregulation of HSP72 (via heating) in cultured endothelial cells did not impair or enhance insulin signaling, respectively, nor was JNK activity altered. Collectively, these findings do not support the hypothesis that reduced HSP72 is a key driver of endothelial insulin resistance in T2D but provide novel evidence that lower-body heating may be an effective strategy for improving leg blood flow responses to glucose ingestion-induced hyperinsulinemia.

Attenuation of exaggerated blood pressure responses to exercise: a byproduct of improved vascular function with passive heat therapy?

Attenuation of exaggerated blood pressure responses to exercise: a byproduct of improved vascular function with passive heat therapy?

PSVII-3 Body temperature and movement patterns of Raramuri Criollo versus Angus-crossbred cows grazing Chihuahuan Desert rangeland in summer

Abstract Body temperature and movement patterns of Angus Hereford crossbred (AH) vs. Raramuri Criollo (RC) nursing cows were monitored in summer 2016 and 2017. AH and RC cows grazed separately in two adjacent Chihuahuan Desert pastures (1190ha, 1165ha) in a crossover design for 4 weeks each year. Body temperature (BodyT) was monitored at 10 min intervals by placing blank CIDRs containing a temperature logger in 10 cows per breed. Seven to 9 AH and RC cows were also fitted with GPS collars that recorded position and ambient temperature (CollarT) at 10 min intervals. A landscape thermal map (LandT) was developed for habitat analysis. Data were analyzed within four daytime segments: dawn (sunrise to 9AM); pre-noon (9AM to noon); post-noon (noon to 3PM); and dusk (3PM to sunset). ANOVA was used to determine whether BodyT, animal movement, CollarT, and mean LandT position within each day segment were different for AH vs. RC cows. Breed nested within Year*Pasture was treated as the experimental unit. BodyT increased as a day progressed and was higher (P &amp;lt; 0.05) in AH vs. RC during post-noon (38.83 vs. 38.42oC) and dusk (39.22 vs. 38.70oC). Compared to AH counterparts, RC cows traveled farther (4.7 vs. 2.7 km*daytime h-1, P &amp;lt; 0.05), at higher velocities (5.9 vs. 3.5 m*min-1, P &amp;lt; 0.05) and spent more time grazing (5.6 vs. 4.3 daytime h; P &amp;lt; 0.05) and traveling (0.7 vs. 0.3 daytime h; P &amp;lt; 0.05) during all four daytime segments. Largest breed differences were observed during the hottest segments of the day (post-noon and dusk). Increasing CollarT throughout a day was associated with selection of cooler landscape locations (LandT) in both breeds. Apparent lower body heat load in RC cows may reduce constraints on their movement patterns compared to AH cows grazing Chihuahuan Desert rangeland in summer.

The effects of lower body passive heating combined with mixed-method cooling during half-time on second-half intermittent sprint performance in the heat.

This study examined the effects of combined cooling and lower body heat maintenance during half-time on second-half intermittent sprint performances. In a repeated measures design, nine males completed four intermittent cycling trials (32.1 ± 0.3°C and 55.3 ± 3.7% relative humidity), with either one of the following half-time recovery interventions; mixed-method cooling (ice vest, ice slushy and hand cooling; COOL), lower body passive heating (HEAT), combined HEAT and COOL (COMB) and control (CON). Peak and mean power output (PPO and MPO), rectal (Tre), estimated muscle (Tes-Mus) and skin (TSK) temperatures were monitored throughout exercise. During half-time, the decrease in Tre was substantially greater in COOL and COMB compared with CON and HEAT, whereas declines in Tes-Mus within HEAT and COMB were substantially attenuated compared with CON and COOL. The decrease in TSK was most pronounced in COOL compared with CON, HEAT and COMB. During second-half, COMB and HEAT resulted in a larger decrease in PPO and MPO during the initial stages of the second-half when compared to CON. In addition, COOL resulted in an attenuated decrease in PPO and MPO compared to COMB in the latter stages of second-half. The maintenance of Tes-Mus following half-time was detrimental to prolonged intermittent sprint performance in the heat, even when used together with cooling.

Pre-Exercise Rehydration Attenuates Central Fatigability during 2-Min Maximum Voluntary Contraction in Hyperthermia.

Background and objectives: Hyperthermia with dehydration alters several brain structure volumes, mainly by changing plasma osmolality, thus strongly affecting neural functions (cognitive and motor). Here, we aimed to examine whether the prevention of significant dehydration caused by passively induced whole-body hyperthermia attenuates peripheral and/or central fatigability during a sustained 2-min isometric maximal voluntary contraction (MVC). Materials and Methods: Ten healthy and physically active adult men (21 ± 1 years of age) performed an isometric MVC of the knee extensors for 2 min (2-min MVC) under control (CON) conditions, after passive lower-body heating that induced severe whole-body hyperthermia (HT, Tre > 39 °C) with dehydration (HT-D) and after HT with rehydration (HT-RH). Results: In the HT-D trial, the subjects lost 0.94 ± 0.15 kg (1.33% ± 0.13%) of their body weight; in the HT-RH trial, their body weight increased by 0.1 ± 0.42 kg (0.1% ± 0.58%). After lower-body heating, the HT-RH trial (vs. HT-D trial) was accompanied by a significantly lower physiological stress index (6.77 ± 0.98 vs. 7.40 ± 1.46, respectively), heart rate (47.8 ± 9.8 vs. 60.8 ± 13.2 b min−1, respectively), and systolic blood pressure (−12.52 ± 5.1 vs. +2.3 ± 6.4, respectively). During 2-min MVC, hyperthermia (HT-D; HT-RH) resulted in greater central fatigability compared with the CON trial. The voluntary activation of exercising muscles was less depressed in the HT-RH trial compared with the HT-D trial. Over the exercise period, electrically (involuntary) induced torque decreased less in the HT-D trial than in the CON and HT-RH trials. Conclusions: Our results suggest that pre-exercise rehydration might have the immediate positive effect of reducing physiological thermal strain, thus attenuating central fatigability even when exercise is performed during severe (Tre > 39 °C) HT, induced by passive warming of the lower body.

Effects of severe whole-body hyperthermia on ovarian hormone and extracellular Hsp72 responses in young adult women

Background: Although acute thermal stress appears to be one of the most effective stressors that increase the intra- and extracellular concentrations of heat shock protein 72 (Hsp72), 17β-estradiol has been shown to inhibit heat-induced Hsp72 expression.Materials and Methods: To determine whether severe whole-body hyperthermia (increase in rectal temperature up to 39.5 °C) induced by lower-body heating is a sufficient stimulus to modulate hormonal (17β-estradiol, progesterone, prolactin, epinephrine, and norepinephrine) and extracellular Hsp72 responses, we investigated young adult women (21 ± 1 yr).Results and Conclusions: In the present study, we show that a severe whole-body hyperthermia (increase in rectal temperature of approximately 2.6 °C and heart rate of approximately 80 bpm from baseline) was sufficient to increase 17β-estradiol, progesterone, and prolactin and catecholamine norepinephrine concentration. Moreover, we show that the concentration of extracellular Hsp72 and catecholamine epinephrine were not affected by severe whole-body hyperthermia in young adult women. From the functional point of view, expression of ovarian hormones induced by passive heat stress may have therapeutic potential for young adult women in, for example, estrogen treatment and overall women’s health.

Motor performance is preserved in healthy aged adults following severe whole-body hyperthermia

Healthy aging is associated with a progressive decline in motor performance and thermoregulatory efficiency. Functional consequences of severe whole-body hyperthermia on neurophysiological functions in healthy aged men have not been investigated. To determine whether severe whole-body hyperthermia (increase in rectal temperature of about 2.5 °C) induced by lower-body heating in older men (64–80 years, n = 9) would suppress excitability of reflexes, voluntarily and electrically induced ankle plantar flexor contractile properties were compared with those in young men (19–21 years, n = 11). Though no aging effect on hyperthermia-induced reflex amplitudes was observed, a decrease in maximal H-reflex and V-wave latencies was found to be greater in older than in young men. In older men, lower-body heating was accompanied by a significant increase in twitch and tetani test torque in parallel with a greater decrease in muscle contraction time. There was no temperature-depended aging effect on the voluntary activation and maximal voluntary torque production. Despite delayed and weakened thermoregulation and age-related decline in neuromuscular function, motor performance in whole-body severe hyperthermia is apparently preserved in healthy aging.

Differences in serum IL-6 response after 1 °C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress

Objectives: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6.Setting: A cross-sectional study.Methods: The study subjects were nine with CSCI, ten with thoracic and lumbar spinal cord injury (TLSCI) and eight able-bodied (AB) subjects. Time since injury was 16.1 ± 3.4 years in TLSCI and 16.4 ± 4.1 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1 °C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumour necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH.Results: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups.Conclusions: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline.

Fossilized skin reveals coevolution with feathers and metabolism in feathered dinosaurs and early birds

Feathers are remarkable evolutionary innovations that are associated with complex adaptations of the skin in modern birds. Fossilised feathers in non-avian dinosaurs and basal birds provide insights into feather evolution, but how associated integumentary adaptations evolved is unclear. Here we report the discovery of fossil skin, preserved with remarkable nanoscale fidelity, in three non-avian maniraptoran dinosaurs and a basal bird from the Cretaceous Jehol biota (China). The skin comprises patches of desquamating epidermal corneocytes that preserve a cytoskeletal array of helically coiled α-keratin tonofibrils. This structure confirms that basal birds and non-avian dinosaurs shed small epidermal flakes as in modern mammals and birds, but structural differences imply that these Cretaceous taxa had lower body heat production than modern birds. Feathered epidermis acquired many, but not all, anatomically modern attributes close to the base of the Maniraptora by the Middle Jurassic.

Heat transfer and loss by whole-body hyperthermia during severe lower-body heating are impaired in healthy older men

Most studies demonstrate that aging is associated with a weakened thermoregulation. However, it remains unclear whether heat transfer (for heat loss) from the lower (uncompensable) to the upper (compensable) body during passively-induced severe lower-body heating is delayed or attenuated with aging. Therefore, the main purpose of this study was to investigate heat transfer from uncompensable to compensable body areas in young men and healthy older men during passively-induced whole-body hyperthermia with a demonstrated post-heating change in core body (rectal; Tre) temperature. Nine healthy older men and eleven healthy young men (69±6 vs. 21±1 years old, mean±SD, P<0.05) participated in passively-induced severe lower-body heating in water at approximately 43°C. Despite a similar increment in Tre (approximately 2.5°C) in both groups, the heating rate was significantly lower in older men than in young men (1.69±0.12 vs. 2.47±0.29°C/h, respectively; P<0.05). The temperature increase in calf muscle and calf skin (uncompensable areas) was significantly higher in older men than in young men (5.10±0.18 vs. 3.99±0.14°C; P<0.05 and 9.92±0.22 vs. 7.65±0.33°C; P<0.05, respectively). However, the temperature increase in back skin and forearm skin (compensable areas) was significantly lower in older men than in young men (0.76±0.63 vs. 2.83±0.68°C; P<0.05 and 0.39±0.76 vs. 2.73±0.5°C; P<0.05, respectively). Furthermore, a post-warming increase in Tre of approximately 0.2°C was observed only in older men (P<0.05). In conclusion, older men whose lower extremities were immersed showed greater accumulation and storage of heat in the skin and deep muscles than young men, and this was associated with a greater heat-transfer delay and subsequent inertia in the increased core body (Tre) temperature.

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle.

Heat therapy has been shown to promote capillary growth in skeletal muscle and in the heart in several animal models, but the effects of this therapy on angiogenic signaling in humans are unknown. We evaluated the acute effect of lower body heating (LBH) and unilateral thigh heating (TH) on the expression of angiogenic regulators and heat shock proteins (HSPs) in healthy young individuals. Exposure to LBH (n = 18) increased core temperature (Tc) from 36.9 ± 0.1 to 37.4 ± 0.1°C (P < 0.01) and average leg skin temperature (Tleg) from 33.1 ± 0.1 to 39.6 ± 0.1°C (P < 0.01), but did not alter the levels of circulating angiogenic cytokines and bone marrow-derived proangiogenic cells (CD34(+)CD133(+)). In skeletal muscle, the change in mRNA expression from baseline of vascular endothelial growth factor (VEGF), angiopoietin 2 (ANGPT2), chemokines CCL2 and CX3CL1, platelet factor-4 (PF4), and several members of the HSP family was higher 30 min after the intervention in the individuals exposed to LBH (n = 11) compared with the control group (n = 12). LBH also reduced the expression of transcription factor FOXO1 (P = 0.03). Exposure to TH (n = 14) increased Tleg from 32.8 ± 0.2 to 40.3 ± 0.1°C (P < 0.05) but Tc remained unaltered (36.8 ± 0.1°C at baseline and 36.9 ± 0.1°C at 90 min). This intervention upregulated the expression of VEGF, ANGPT1, ANGPT2, CCL2, and HSPs in skeletal muscle but did not affect the levels of CX3CL1, FOXO-1, and PF4. These findings suggest that both LBH and TH increase the expression of factors associated with capillary growth in human skeletal muscle.

Influence of passive lower-body heating on muscle metabolic perturbation and high-intensity exercise tolerance in humans

The purpose of this investigation was to determine the influence of heat stress on the dynamics of muscle metabolic perturbation during high-intensity exercise. Seven healthy males completed single-legged knee-extensor exercise until the limit of tolerance on two separate occasions. In a randomized order the subjects underwent 40 min of lower-body immersion in warm water at 42°C prior to exercise (HOT) or received no prior thermal manipulation (CON). Following the intervention, muscle metabolism was measured at rest and throughout exercise using (31)P-MRS. The tolerable duration of high-intensity exercise was reduced by 36% after passive heating (CON: 474 ± 146 vs. HOT: 303 ± 76 s; P = 0.005). Intramuscular pH was lower over the first 60 s of exercise (CON: 7.05 ± 0.02 vs. HOT: 7.00 ± 0.03; P = 0.019) in HOT compared to CON. The rate of muscle [PCr] degradation during exercise was greater in the HOT condition (CON: -0.17 ± 0.08 vs. HOT: -0.25 ± 0.10% s(-1); P = 0.006) and pH also tended to change more rapidly in HOT (P = 0.09). Muscle [PCr] (CON: 26 ± 14 vs. HOT: 29 ± 10%), [Pi] (CON: 504 ± 236 vs. HOT: 486 ± 186%) and pH (CON: 6.84 ± 0.13 vs. HOT: 6.80 ± 0.14; P > 0.05) were not statistically different at the limit of tolerance (P > 0.05 for all comparisons). These results suggest that the reduced time-to-exhaustion during high-intensity knee-extensor exercise following lower-body heating might be related, in part, to accelerated rates of change of intramuscular [PCr] and pH towards 'critical' values that limit muscle function.

The effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats

In previous study, heat treatment and AMPK activation by exercise improved glucose tolerance in rat.PURPOSETo determine the effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats.METHODSOtsuka Long‐Evans Tokushima Fatty rat (OLETF: n=16, 305.3±11.4g), an accurate animal model for human type 2 diabetes, and their counter parts (LETO: n=8, 226.7±14.1g) were used. Sixteen OLETF rats were divided into two groups; Control (n=8: CON) and Heat treatment (n=8: HT). HT received a lower‐body heat treatment (41 °C for 20 min) using water bath under anesthesia once a week for twelve weeks. An intraperitoneal glucose tolerance test was performed for each group in week‐11. In week‐12, the soleus muscles were removed 48 h after the last heat treatment. Phospho‐AMPK and total‐AMPK in the muscle was determined by Western blot analysis.RESULTSAt 120 min after glucose injection, blood glucose levels of CON and HT were significantly higher than LETO, whereas blood glucose level of HT was lower than CON. AMPK phosphorylation ratio in the soleus muscle of CON was significantly lower than LETO. However, heat treatment significantly increased AMPK phosphorylation ratio in HT compared with CON, and there was no significant difference between LETO and HT.CONCLUSIONOur results indicate that weekly heat treatment for twelve weeks could increase AMPK activation in skeletal muscle in type 2 diabetic rats.

H eat storage in upper and lower body during high-intensity exercise in athletes with spinal cord injuries

Background: The thermophysiology of athletes with spinal cord injuries (SCI) is not well understood. Spinal cord lesions impact muscle mass, thermoregulatory neural signals and circulatory function. Understanding SCI thermoregulation physiology would benefit exercise function. Therefore, this study was designed to describe heat storage in the upper and lower bodies of SCI and able-bodied (AB) athletes. Procedure: Seven SCI and 8 AB athletes (matched for arm-crank VO2 peak) performed a ramp protocol in an environment similar to an indoor competitive environment (21˚C±1.5˚C, 55±3% relative humidity).Results: SCI athletes experienced similar upper-body heat storage of 0.82±0.59 J.g-1 and lower-body heat storage of 0.47±0.33 J.g-1 compared with that of AB athletes at 0.80±0.61 J.g-1 and 0.27±0.22 J.g-1 for upper and lower body, respectively. There were no significant differences between groups for rectal temperature (Trec) or oesophageal temperature (Tes). However, mean skin temperature (Msk) was significantly higher for SCI throughout the exercise bout (p=0.006). Conclusions: The results of this study suggest that SCI and AB athletes appear to thermoregulate in a similar manner, though SCI tend to store slightly more heat.

The Effect of Heating and Cooling on Time Course of Voluntary and Electrically Induced Muscle Force Variation

The aim of this study was to investigate the effect of heating and cooling on time course of voluntary and electrically induced muscle force variation. Ten volunteers performed 50 maximal voluntary and electrically induced contractions of the knee extensors at an angle of 120 degrees under the control conditions and after passive lower body heating and cooling in the control, heating, and cooling experiments. Peak torque, torque variation, and half-relaxation time were assessed during the exercise. Passive lower body heating increased muscle and core temperatures, while cooling lowered muscle temperature, but did not affect core temperature. We observed significantly lower muscle fatigue during voluntary contraction compared with electrically induced contractions. Body heating (opposite to cooling) increased involuntarily induced muscle force, but caused greater electrically induced muscle fatigue. In the middle of the exercise, the coefficient of correlation for electrically induced muscle torque decreased significantly as compared with the beginning of the exercise, while during maximal voluntary contractions, this relation for torque remained significant until the end of the exercise. It was shown that time course of voluntary contraction was more stable than in electrically induced contractions.

Heat acclimation does not reduce the impact of hyperthermia on central fatigue

We tested the hypothesis that improved physiological symptoms of passively induced heat acclimation (HA) might impair the impact of hyperthermia on central fatigue and consequently cause greater peripheral fatigue. Subjects in the experimental group (7 males and 6 females) completed seven sessions of HA involving passive heating of the lower body by immersion up to the waist in a water bath at approximately 44 degrees C (air T 23 degrees C, rh 40%) for 45 min, repeated every other day for 2 weeks. During the first and the last HA sessions, participants performed a 2-min MVC of the knee extensors. A TT100 Hz was superimposed on the contraction at about 3, 14, 29, 44, 59, 74, 89, 104, and 119 s. At about 30, 60, 90, and 120 s, the knee extensors were relaxed for 2-3 s and a control TT100 Hz was delivered. The participants in the control group (6 males and 6 females) followed the same exercise protocol on days 1 and 14 in a thermoneutral condition. Peak torque and the muscle voluntary activation and half-relaxation time were assessed during the exercise. The attainment of HA was confirmed by significant decreases in the resting and final rectal temperatures (approximately 0.3 degrees C), heart rate, and physiological stress index, and increased sweating capacity. Lower-body heating resulted in greater central and peripheral fatigue when compared with the thermoneutral condition during the 2-min MVC. Following HA, central and peripheral fatigues were unchanged. We conclude that passively induced HA for 2 weeks improved the physiological symptoms, but did not change central or peripheral fatigue during exercise in hyperthermia.

Heat Treatment Improves Glucose Tolerance and Prevents Skeletal Muscle Insulin Resistance in Rats Fed a High-Fat Diet

OBJECTIVE—Heat treatment and overexpression of heat shock protein 72 (HSP72) have been shown to protect against high-fat diet–induced insulin resistance, but little is known about the underlying mechanism or the target tissue of HSP action. The purpose of this study is to determine whether in vivo heat treatment can prevent skeletal muscle insulin resistance.RESEARCH DESIGN AND METHODS—Male Wistar rats were fed a high-fat diet (60% calories from fat) for 12 weeks and received a lower-body heat treatment (41°C for 20 min) once per week.RESULTS—Our results show that heat treatment shifts the metabolic characteristics of rats on a high-fat diet toward those on a standard diet. Heat treatment improved glucose tolerance, restored insulin-stimulated glucose transport, and increased insulin signaling in soleus and extensor digitorum longus (EDL) muscles from rats fed a high-fat diet. Heat treatment resulted in decreased activation of Jun NH2-terminal kinase (JNK) and inhibitor of κB kinase (IKK-β), stress kinases implicated in insulin resistance, and upregulation of HSP72 and HSP25, proteins previously shown to inhibit JNK and IKK-β activation, respectively. Mitochondrial citrate synthase and cytochrome oxidase activity decreased slightly with the high-fat diet, but heat treatment restored these activities. Data from L6 cells suggest that one bout of heat treatment increases mitochondrial oxygen consumption and fatty acid oxidation.CONCLUSIONS—Our results indicate that heat treatment protects skeletal muscle from high-fat diet–induced insulin resistance and provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for obesity-induced insulin resistance.

A new, reliable lower-body nociception device for unrestrained animals yields data comparable to a new portable version of the face-rub test

A novel lower body heating device is described for use in lower body analgesiometry with freely-moving, small animals. It consists of a resistor in contact with a hindlimb. The defensive biting response to heat shows reliable dose-response effects with morphine which compare well with our similar upper body device (Rosenfeld et al. 1978). Issues dealing with upper versus lower body nociception effects may be tested with the new device set described.

The effect of elevated temperature on the vasculature of mouse jejunum.

The effect of elevated temperature on mouse jejunal vasculature was investigated. Both local and lower-body heating were employed, using a hot water bath; heating time was kept constant at 1 hour, bath temperatures ranging from 40.0 degrees C to 43.0 degrees C. Animals were sacrificed after heating, the erythrocytes were stained with benzidine and H2O2 and the blood vessels revealed by mounting in a clearing resin. The earliest damage seen was the disappearance of capillaries, followed by loss of progressively larger vessels. Loss is interpreted as destruction, not merely as interruption of blood flow. A gradient of sensitivity occurs from the inner layer of the jejunum to the outer, the threshold heating temperature required to produce vascular damage being lowest at the inside. Neither temperature gradient, nor early release of gastric juice from the stomach, appears responsible for this differential response. The mean length of intact venous tree was employed as a parameter for assessing the damage.