The Visual Politics of Maralinga: Experiences, (Re)presentations, and Vulnerabilities.

Visual cultures are being increasingly discussed in the history of science literature, although relatively very little of that work concerns the nuclear age. In addition, within the discrete yet bourgeoning literature on global nuclear art and culture, Oceania is often overlooked despite its central role in the development of the American, British, and French nuclear weapon capabilities, as well as their associated colonial legacies. This article serves to redress both concerns by examining the visual politics of Maralinga in relation to settler-colonial and Aboriginal experiences, vulnerabilities and (re)presentations. I do so by surveying artworks with a connection to the Australian experience of nuclear colonialism and find that the figure of biological life has been conspicuously left absent from contemporary non-Indigenous Australian depictions of British nuclear testing in Australia.

Identification of a point mutation in the thyrotropin receptor of the hyt/hyt hypothyroid mouse.

The hyt/hyt hypothyroid mouse has an autosomal recessive, fetal-onset, severe hypothyroidism related to TSH hyporesponsiveness and associated with elevated TSH. Our previous work has suggested that the hypothyroidism and TSH hyporesponsiveness may result from a mutation in the hyt/hyt TSH receptor (TSHr) of the thyroid gland. Based on DNA sequencing of the entire coding region of the TSHr gene from the wild-type BALB/cBY +/+ mouse, the +/+ TSHr is 92% and 94% identical at the nucleotide and amino acid residue levels, respectively, compared to the rat TSHr gene. The coding region of the hyt/hyt TSHr, compared to that of the +/+ TSHr, has a single base change, CCG to CTG, at nucleotide position 1666, which leads to the replacement of a highly conserved proline at amino acid position 556 with a leucine in transmembrane domain IV. This mutation was introduced by site-directed mutagenesis into the wild-type human TSHr and transiently expressed in COS-7 cells. Although the size and abundance of the mutant TSHr mRNA suggested that there was no effect on the nature of the mRNA, TSH binding and the response to TSH in transfected cells were abolished. Further studies are necessary to clarify how the Pro to Leu replacement interferes with receptor expression on the cell surface or influences TSH binding. These functional consequences of the mutation appear to account for the observed TSH hyporesponsiveness and hypothyroidism in the hyt/hyt mouse.

A major C-peptide deletion prevents secretion of a mutant human proinsulin from transfected monkey kidney cells.

The biosynthesis and secretion of human proinsulin and a mutant human proinsulin with a major deletion in the C-peptide, (des 38-62)proinsulin, was studied in monkey kidney cells (Cos-7) transfected with cDNAs encoding the respective normal or mutant human preproinsulins. Transfected cells were labelled with [3H]leucine, and insulin-like material was immunoprecipitated and analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. It was found that the prepeptide was removed from both the normal and mutant preproinsulins, and that there was no further processing to insulin. The normal proinsulin was rapidly released from the transfected cells, with little intracellular accumulation, while the mutant proinsulin was retained within the cell, with only small quantities of radio-labelled material in the medium. The intracellular mutant proinsulin was membrane bound and located predominantly within a microsomal fraction. These results suggest that C-peptide plays an important role in the efficient transfer of proinsulin through the early stages of the secretory pathway.

Insulin delivery by somatic cell gene therapy.

The feasibility of somatic cell gene therapy as a method of insulin delivery has been studied in mice. Murine pituitary AtT20 cells were transfected with a human preproinsulin DNA in a plasmid containing a metallothionein promoter and a gene conferring resistance to the antibiotic G418. The AtT20MtIns-1.4 clone of cells was selected because of its higher insulin-releasing activity compared with other clones. After culturing for 24 h in Dulbecco's medium containing 10 mM glucose, the AtT20MtIns-1.4 cells released human insulin at about 5 ng/10(6) cells per 24 h. Insulin release was not significantly altered by raised concentrations of glucose, potassium or calcium, but insulin release was increased by 20 mM arginine, 5 mM isomethylbutylxanthine and 90 microM zinc. AtT20MtIns-1.4 cells (2 x 10(6)) were implanted intraperitoneally into non-diabetic athymic nude (nu/nu) mice, and the mice were made diabetic by injection of streptozotocin after 7 days. Release of human insulin in vivo was assessed using a specific plasma human C-peptide assay. Human C-peptide concentrations were maintained at about 0.1 pmol/ml throughout the 29 days of the study. The development of streptozotocin-induced hyperglycaemia was delayed in recipients of the cells releasing human insulin, compared with a control group receiving an implant of non-transfected cells. At autopsy the implanted AtT20MtIns-1.4 cells in each recipient had formed a tumour-like aggregation, with an outer region of insulin-containing cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Sorting of PC2 to the regulated secretory pathway in AtT20 cells.

PC2 and PC3 are neuroendocrine specific members of the eukaryotic subtilisin-like proprotein convertase (PC) family. Both are sorted via the regulated secretory pathway into secretory granules. In order to identify sequences in PC2 which are involved in targeting to the regulated secretory pathway we expressed a series of PC2 cDNAs containing mutations in the C terminal or propeptide domains in the mouse corticotrophic AtT20 cell line. Sorting of endogenous PC3 was used as a control. PC2 and PC3 were secreted with similar kinetics and sorted to secretory granules with similar efficiencies. Deletions of up to 50 amino acids from the C-terminus of proPC2 had no effect on secretion or sorting, but larger deletions completely prevented maturation or secretion. Two large deletions within the propeptide also prevented secretion. Smaller deletions between the primary and secondary cleavage sites, or of the primary cleavage site, reduced the amount of protein secreted but did not affect sorting to secretory granules. Replacement of the propeptide of PC2 with that of the endogenous PC3 also had no effect on secretion or sorting. The results indicate that targeting of proPC2 to the regulated secretory pathway is dependent on more than one region within the proPC2 molecule.

Postoperative radiotherapy increases locoregional control of patients with stage IIIA non-small-cell lung cancer treated with induction chemotherapy followed by surgery.

PURPOSE: To determine the effectiveness of postoperative radiotherapy (RT) in patients with Stage IIB and Stage IIIA non-small-cell lung cancer (NSCLC) treated with induction chemotherapy followed by surgery. METHODS AND MATERIALS: We retrospectively reviewed the treatment records of 98 patients (58 men and 40 women; median age 61 years, range 31-91) with Stage IIB and Stage IIIA NSCLC who were treated with induction chemotherapy followed by surgery at our institution between January 1990 and December 2000. Patients were grouped by treatment (chemotherapy/surgery alone vs. chemotherapy/surgery/RT), by disease stage and nodal classification. The rates of local control (LC), disease-specific survival, disease-free survival, and overall survival (OS) were calculated using the Kaplan-Meier method. RESULTS: Of the 98 patients, 40 had Stage IIB and 58 had Stage IIIA. The clinical disease stage and N stage were significantly greater in those patients who underwent RT than in those who did not; however, no statistically significant differences were identified in the additional characteristics between those receiving and not receiving RT within each stage or nodal group. The overall 5-year actuarial LC rate was 81% in the RT group and 54% in the chemotherapy/surgery-alone group (p = 0.07). Postoperative RT significantly improved the 5-year LC rate in patients with Stage IIIA disease (from 35% to 82%, p = 0.01). Postoperative RT did not significantly improve the 5-year OS rate (30% with RT vs. 49% without) for all patients or for patients with Stage IIIA disease. The disease-specific survival and disease-free survival rates did not differ between the treatment groups. Patients who responded to induction chemotherapy had a significantly greater 5-year OS rate (49%) than did those with stable or progressive disease (22%, p = 0.003). CONCLUSION: Postoperative RT in patients with Stage IIIA NSCLC treated with induction chemotherapy followed by surgery significantly improved LC without improving OS. Significantly improved survival was observed in all patients who responded to induction chemotherapy compared with those with stable or progressive disease.

Insulin-releasing pituitary cells as a model for somatic cell gene therapy in diabetes mellitus.

Insulin delivery by somatic cell gene therapy was evaluated using murine pituitary AtT20MtIns-1.4 cells. These cells have been stably transfected to release human insulin by the introduction of a recombinant plasmid bearing a human preproinsulin cDNA under the control of a zinc-sensitive metallothionein promoter. 6 x 10(7) AtT20MtIns-1.4 cells were implanted subcutaneously into streptozotocin-diabetic mice immunosuppressed with cyclosporin A. Release of human insulin was assessed using a specific plasma human C-peptide assay. On days 1 and 2 after implantation human C-peptide concentrations were about 0.02 pmol/ml. Consumption of zinc sulphate solution (500 mg/l) as drinking fluid for days 3-5 increased plasma human C-peptide concentrations to 0.11 +/- 0.01 pmol/ml (mean +/- S.E.M.), n = 11, P < 0.01, and concentrations declined when zinc was discontinued. The extent of hyperglycaemia was slightly lower (P < 0.05) than in a group implanted with non-transfected AtT20 cells. The study was terminated after 9 days, and tumour-like aggregations of implanted cells were identified at autopsy. These comprised a large necrotic core with insulin-containing cells at the periphery. The study provides support for the view that somatic cell gene therapy offers a potential approach to insulin delivery in diabetes mellitus.

Preferred room temperature of young vs aged males: the influence of thermal sensation, thermal comfort, and affect.

BACKGROUND: While research has demonstrated that aged persons may show impaired thermoregulatory control, we do not know whether dysthermia in the aged results from altered behavioral or autonomic responses. Consequently, we investigated age-related differences concerning the ability to regulate room temperature. METHODS: Two groups of matched healthy males (22.9 yr and 66.9 yr) were subjects of this study. After equilibration at 24 degrees C (rh 50%), chamber temperature controllers were set into cooling mode. Using a dual position switch, subjects adjusted this temperature when air temperature moved outside their preferred range. Switch operation resulted in maximal cooling or heating, without a steady state. Subjective ratings of thermal sensation, discomfort, and affect were provided at each activation. RESULTS: Both groups controlled temperature equivalently: 24.9 degrees C (+/- 1.3, young) and 24.5 degrees C (+/- 1.5, elderly; p > .05). At cold-induced change points, the skin temperatures of the calf, thigh, chest, and hand were significantly lower in the elderly subjects. During the heat-induced changes, chest, hand, upper arm, and mean skin temperatures were also lower (p < .05). At cold-induced change points, the elderly group felt colder (p < .05), were less uncomfortable (p < .05), and felt better than the young subjects (p < .05). During heat-induced changes, thermal sensation was equivalent, the elderly were more comfortable (p < .05), and felt better (p < .05). CONCLUSIONS: Assuming thermal discomforture drives behavior, it is possible that elderly people may require a more intense thermal stimulus to elicit the appropriate behavioral responses in the home. It is also possible that such stimuli will result in a greater heat flow, elevating the risk of dysthermia in the aged.

Static respiratory muscle work during immersion with positive and negative respiratory loading.

Upright immersion imposes a pressure imbalance across the thorax. This study examined the effects of air-delivery pressure on inspiratory muscle work during upright immersion. Eight subjects performed respiratory pressure-volume relaxation maneuvers while seated in air (control) and during immersion. Hydrostatic, respiratory elastic (lung and chest wall), and resultant static respiratory muscle work components were computed. During immersion, the effects of four air-delivery pressures were evaluated: mouth pressure (uncompensated); the pressure at the lung centroid (PL,c); and at PL,c +/-0.98 kPa. When breathing at pressures less than the PL,c, subjects generally defended an expiratory reserve volume (ERV) greater than the immersed relaxation volume, minus residual volume, resulting in additional inspiratory muscle work. The resultant static inspiratory muscle work, computed over a 1-liter tidal volume above the ERV, increased from 0.23 J. l(-1), when subjects were breathing at PL,c, to 0.83 J. l(-1) at PL,c -0.98 kPa (P < 0.05), and to 1.79 J. l(-1) at mouth pressure (P < 0.05). Under the control state, and during the above experimental conditions, static expiratory work was minimal. When breathing at PL,c +0.98 kPa, subjects adopted an ERV less than the immersed relaxation volume, minus residual volume, resulting in 0.36 J. l(-1) of expiratory muscle work. Thus static inspiratory muscle work varied with respiratory loading, whereas PL,c air supply minimized this work during upright immersion, restoring lung-tissue, chest-wall, and static muscle work to levels obtained in the control state.

A screening programme for hypertension in general practice.

It is recommended that hypertensive patients with a diastolic blood pressure of 100 mmHg be treated. However, it has been proposed that only 50% of hypertensives are diagnosed, and of these, 50% are not treated. We therefore set out to identify hypertensive patients in our practice, who were then actively treated, some in a clinical trial of ketanserin. Of the 3,384 patients (1,667 males and 2,707 females) who were invited to our surgery for a blood pressure measurement, 2,606 patients (77%) attended. The overall prevalence of hypertension in the patients, aged 35-65 years was 2.9%. This prevalence increased with age: from 1.0% in the 35-44 year age group to 3.5% at 45-54 years, and 4.4% at 55-64 years. The mean systolic but not diastolic blood pressure increased with age. There were more male hypertensives than females, except over 55 years of age. Of the 84 hypertensives identified after one visit, the majority remained hypertensive after an additional visit, and 31 agreed to participate in a clinical trial. After a four-week placebo run-in, 22 patients had a diastolic blood pressure above 95 mmHg and were randomly allocated to receive ketanserin 40 mg twice daily or metoprolol 100 mg twice daily. Treatment continued double-blind for three months. There were no significant differences in blood pressure reduction between the treatment groups. The heart rate was reduced more by metoprolol. There were no withdrawals for side effects and no major differences in subjective complaints between the two treatment groups.

Eccrine sweat glands. Adaptations to physical training and heat acclimation.

Heat dissipation, under conditions of thermal stress, is mediated primarily by evaporation of sweat. Physical training has been shown to enhance sweat production by eliciting changes in the sensitivity of eccrine glands, total sweat output and distribution of gland activity. These adaptations afford partial acclimation. Heat acclimation produces similar changes, and also results in reduced sweat thresholds. To account for these different responses it has been hypothesised that physical training induces peripheral adaptations, while acclimation produces both peripheral and central modifications. It is suggested that repeated cutaneous heat detection may be essential to the development of central sudomotor changes.

Exercise-induced skeletal muscle growth. Hypertrophy or hyperplasia?

Postnatal skeletal muscle growth in humans is generally ascribed to enlargement of existing muscle fibres rather than to cellular proliferation. Some evidence of muscle fibre division or splitting was provided in the nineteenth century. This evidence has more recently been supported by fibres obtained from regenerating muscle, and from muscle which has undergone stress-induced growth. Numerous investigators have reported indirect evidence for exercise-induced hypertrophy and hyperplasia. These findings are largely founded on secondary observations of fibre size or number differences expressed relative to muscle cross-sectional area. Since these observations in humans are open to methodological criticism, researchers have developed 3 animal models to represent exercise-induced human muscle growth. These include compensatory hypertrophy, stretch-induced hypertrophy, and weight lifting in trained animals. The results and criticisms of the experiments which have used these models are discussed in this review. In studies of muscle cross-sectional area, errors are created by fibres terminating intrafascicularly. Longitudinal growth of such fibres result in an overestimation of fibre number, and with the use of penniform muscles where fibres do not run parallel to the longitudinal axis of the muscle, the error is compounded. It was concluded that hyperplasia is not yet substantiated, and that new fibres, if present, may be the result of the development of satellite cells. Further experiments are required before a definitive answer can be provided. It is suggested that rigidly controlled exercise studies using contralateral control, fusiform muscles with analysis of individually teased muscle fibres be performed.

A non-linear effect of ambient temperature on apparent glucose tolerance.

Increased ambient temperature affects apparent oral glucose tolerance to an extent which may have clinical implications for the diagnosis of impaired glucose tolerance and gestational diabetes. As a first step in order to better define the nature of this effect, we have examined, in a climate chamber, the effects of ambient temperature at four levels (20, 25, 30, and 35 degrees C) on glucose and insulin responses to a standard 75 g oral glucose tolerance test in seven non-diabetic male subjects. Plasma glucose responses to ambient temperature were compared with the responses of core (auditory canal) and skin temperatures. The 2-h plasma glucose was affected in a nonlinear manner by ambient temperature (5.4 +/- 0.2, 5.3 +/- 0.4, 6.5 +/- 0.3, 6.4 +/- 0.4 mmol/l at 20, 25, 30, and 35 degrees C, P = 0.015) with the effect localised between 25 and 30 degrees C (P = 0.012). Core temperature responded in a similar manner (36.6 +/- 0.1, 36.6 +/- 0.1, 36.9 +/- 0.1, 37.0 +/- 0.1, (P = 0.0005) with the effect localised 25 and 30 degrees C (P = 0.011). However skin temperature increased significantly with each 5 degrees C increase in ambient temperature (30.2 +/- 0.5, 33.0 +/- 0.5, 34.2 +/- 0.2, 35.2 +/- 0.2, P < or = 0.0001). We conclude that the acute effect of ambient temperature on apparent glucose tolerance is most likely due to redistribution of blood flow between cutaneous and visceral beds driven by changes in core temperature. The absence of temperature effects between the two lowest, and between the two highest temperatures, provides workable guidelines for the standardisation of conditions during oral glucose tolerance tests in circumstances where temperature may have clinically significant effects.

Whole-body hyperhydration in endurance-trained males determined using radionuclide dilution.

Despite evidence of hypervolemia following endurance training, there is little information regarding corresponding extravascular fluid volumes. Quantification of such volumes relies upon radionuclide dilution methods, previously hampered by the loss of plasma albumin. It was our purpose to measure human body-fluid distribution in eight endurance-trained males, using a simultaneous radionuclide dilution technique, incorporating radioiodinated serum fibronogen (RISF). Fluid distribution was measured on three occasions, using 2 microCi of RISF, 8 microCi of 51 Cr-labeled erythrocytes, and 20 microCi of Na82Br and 450 microCi of 3H2O; to measure PV, erythrocyte (RCV), extracellular (ECFV), and total-body water (TBW) volumes, respectively. Respective volume means, standard deviations, and coefficients of variation were: 46.6 (+/- 4.9; 8.44%), 33.3 (+/- 2.9; 3.89%), 258.1 (+/- 12.1; 4.93%), and 654.2 (+/- 13.4; 3.24%) ml.kg-1. The incorporation of RISF provided a reliable modification to previous methods, and revealed a body-fluid expansion in endurance-trained males. It was concluded that such subjects were hyperhydrated, possessing proportionately expanded fluid volumes throughout both intravascular and extravascular spaces. This was attributed to training history and accompanying reductions in adiposity.

Short-term tests for transplacentally active carcinogens. A comparison of sister-chromatid exchange and the micronucleus test in mouse foetal liver erythroblasts.

The effectiveness of 6 chemicals (benzo[a]pyrene, (BaP), cyclophosphamide (CP), diethylnitrosamine (DEN), methyl methanesulphonate (MMS), mitomycin C (MC) and procarbazine (PC) ) as inducers of micronuclei in foetal liver and maternal bone marrow erythroblasts has been determined, and related to that of gamma-radiation. CP, DEN, MMS and PC were all more effective in the foetal liver. The induction of micronuclei and SCEs by each chemical in foetal erythroblasts after in vivo exposure was measured. When expressed as induction of sister-chromatid exchanges (SCEs) per erythroblast/induction of micronuclei per erythroblast (/microM/kg), the ratios obtained were MC 580, BaP 470, DEN 430, CP 258, MMS 140 and PC 13. The lowest doses detected as potentially genotoxic by each test in foetal liver erythroblasts are (with the exception of PC which is a relatively ineffective inducer of SCEs) similar. When isolated foetal livers were exposed in vitro, SCE dose responses to BaP, MC, MMS and PC could be directly related to those from in vivo exposure, indicating the role of the foetal liver in metabolic activation, but CP was considerably more cytotoxic. The transplacental micronucleus test, and in vivo/in vitro method for SCEs in foetal liver erythroblasts, provide sensitive, complementary assays for genotoxic effects of chemicals during prenatal life. Since foetal liver possesses greater metabolic potential than adult bone marrow, the transplacental tests respond to genotoxic agents not detected by bone-marrow systems.

Computer integrated measurement of respiratory compliance.

Respiratory compliance is obtained from the ratio of lung volume change to change in differential pressure across the chest wall, and is classically derived from the slope of the static, transrespiratory pressure-volume relationship. The need to remove subjectivity from the derivation of respiratory compliance, has prompted the development of a computer-based system which facilitates compliance measurement with minimal experimenter error. This paper outlines the basic algorithms necessary to analyse static, quasi-static and dynamic pressure-volume data, and describes how these data may be entered into a graphics package (Sigmaplot) to derive best-fit polynomial curves.

Physiological assessment of the RNZAF constant wear immersion suit: laboratory and field trials.

Laboratory and field immersion trials were undertaken to determine the thermal protection afforded by a constant wear immersion suit (CWIS) in operation with the Royal New Zealand Air Force (RNZAF). Six males wore each of two ensembles during head-out laboratory immersions in 5.0 +/- 0.1 degree C (mean +/- SD) water for a maximum of 3 h. Ensembles 1 and 2 consisted of the CWIS in addition to minimal and maximal likely undergarment insulations, respectively. Open sea field trials (water temperature = 13.8 +/- 0.7 degree C; Beaufort wind state = 0-4; Sea state = 0-2) were conducted for a maximum of 2 h, with subjects wearing ensemble two and remaining strike aircrew apparel (ensemble three). Analysis of rectal temperature (Tre) changes permitted calculation of time to hypothermia (t35) and the survival estimate of 34 degrees C (t34). Mean (+/- SEM) t35 was 78 +/- 11 (n = 6), 187 +/- 20 (n = 5, p < 0.05) and 98 +/- 5 min (n = 3) for ensembles one, two and three, respectively. Mean t34 was 96 +/- 15, 259 +/- 31 (p < 0.05), and 119 +/- 5 min, respectively. Immersed insulations of ensembles one and two were 0.035 +/- 0.002 and 0.150 +/- 0.015 degree C.m2.W-1, respectively. Thus, the difference between minimal and maximal operational insulation was a 4.3-fold increase in insulation, which facilitated a 2.7-fold increase in mean t34. The thermal protection afforded by the CWIS during field trials was not sufficient to ensure survival for the 12-h expected rescue time.(ABSTRACT TRUNCATED AT 250 WORDS)

Forehead skin temperature and thermal sensation during exercise in cool and thermoneutral environments.

BACKGROUND: The influence of forehead and mean skin temperature on thermal sensation during exercise in hot, cool, and thermoneutral environments is unclear. HYPOTHESIS: We hypothesized that forehead temperature, in contrast to other skin sites, would contribute significantly to thermal sensation during exercise in hot, cool, and thermoneutral environments. METHOD: Volunteer males (N = 14) performed 30 min of constant load exercise on a cycle ergometer during which thermal sensation, skin and rectal temperatures, and heart rate were collected. Each subject participated in a control (24 degrees C), hot (40 degrees C), and cool (8 degrees C) condition. RESULTS: Significantly higher mean skin temperatures occurred during exercise in the hot condition (M = 37.22 +/- 0.20 degrees C) compared to exercise in the neutral (M = 33.34 +/- 0.51 degrees C) and cool conditions (M = 27.92 +/- 0.22 degrees C). Forehead skin temperature in the neutral and cool conditions was significantly greater than forearm, hand, thigh, and calf skin temperatures (p < 0.05). In the hot condition, forehead temperature was significantly greater than back, chest, upper arm, and hand skin temperatures (p < 0.05). In contrast to the neutral and hot conditions, forehead skin temperature was significantly associated with thermal sensation during exercise in the cool condition (r consistently > 0.67). CONCLUSIONS: We conclude that forehead skin temperature, in contrast to other skin sites, contributed significantly to thermal sensation during exercise in the cool.

Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.

AIM: This experiment was designed to test the hypothesis that the plasma volume is not selectively defended during exercise- and heat-induced dehydration following humid-heat acclimation. METHODS: Eight physically active males were heat acclimated (39.8 °C, relative humidity 59.2%) using 17 days of controlled hyperthermia (core temperature: 38.5 °C). Inter-compartmental fluid losses and movements were tracked (radioisotopes and Evans blue dye) during progressive dehydration (cycling) in these same conditions and also during a resting recovery without fluid replacement (28 °C), before (day 1), during (day 8) and after heat acclimation (day 22). RESULTS: On days 8 and 22, there were significant increases in total body water, interstitial fluid and plasma volume (P < 0.05), but the intracellular compartments did not change (P > 0.05). The baseline plasma volume remained expanded throughout: 43.4 [±2.6 (day 1)], 49.1 [±2.4 (day 8); P < 0.05] and 48.9 mL kg(-1) [±3.0 (day 22); P < 0.05]. During progressive dehydration, plasma reductions of 9.0% (±0.9: day 1), 12.4% (±1.6: day 8) and 13.6% (±1.2: day 22) were observed, with day 8 and 22 losses significantly exceeding day 1 (P < 0.05). During recovery, plasma volume restoration commenced, with the intracellular fluid contribution becoming more pronounced as acclimation progressed. CONCLUSION: It is concluded that the plasma volume was not defended more vigorously following humid-heat acclimation. Indeed, a greater fluid loss may well underlie the mechanisms for enhancing plasma volume recovery when heat acclimation is induced using the controlled-hyperthermia technique.

Does intramuscular thermal feedback modulate eccrine sweating in exercising humans?

AIM: Few investigators have considered the possibility that skeletal muscles might contain thermosensitive elements capable of modifying thermoeffector responses. In this experiment, the temporal relationships between dynamic changes in deep-body and intramuscular temperatures and eccrine sweat secretion were explored during rhythmical and reproducible variations in heat production. METHODS: Eight subjects performed semi-recumbent cycling (25 °C) at a constant load to first establish whole-body thermal and sudomotor steady states (35 min), followed by a 24-min block of sinusoidal workload variations (three, 8-min periods) and then returning to steady-state cycling (20 min). Individual oesophageal, mean skin and intramuscular (vastus lateralis) temperatures were independently cross-correlated with simultaneously measured forehead sweat rates to evaluate the possible thermal modulation of sudomotor activity. RESULTS: Both intramuscular and oesophageal temperatures showed strong correlations with sinusoidal variations in sweating with respective maximal cross-correlation coefficients of 0.807 (±0.044) and 0.845 (±0.035), but these were not different (P = 0.40). However, the phase delay between intramuscular temperature changes and sweat secretion was significantly shorter than the delay between oesophageal temperature and sweating [25.6 s (±12.6) vs. 46.9 s (±11.3); P = 0.03]. CONCLUSION: The temporal coupling of eccrine sweating to intramuscular temperature, combined with a shorter phase delay, was consistent with the presence of thermosensitive elements within skeletal muscles that appear to participate in the modulation of thermal sweating.