Host autophagy is exploited by the intracellular parasite Toxoplasma gondii to enhance amino acids levels.

Toxoplasma gondii, a widespread parasite, has the ability to infect nearly any nucleated cell in warm-blooded vertebrates. It is estimated that around 2 billion people globally have been infected by this pathogen. Although most healthy individuals can effectively control parasite replication, certain parasites may evade the immune response, establishing cysts in the brain that are refractory to the immune system and resistance to available drugs. For its chronic persistence in the brain, the parasite relies on host cells' nutrients, particularly amino acids and lipids. Therefore, understanding how latent parasites persist in the brain is crucial for identifying potential drug targets against chronic forms. While shielded within parasitophorous vacuoles (PVs) or cysts, Toxoplasma exploits the host endoplasmic reticulum (ER) metabolism to sustains its persistence in the brain, resulting in host neurological alterations. In this study, we demonstrate that T. gondii disrupts the host ER homeostasis, resulting in accumulation of unfolded protein with the host ER. The host counters this stress by initiating an autophagic pathway known as ER-phagy, which breaks down unfolded proteins into amino acids, promoting their recycling. Remarkably, the persistence of latent forms in cell culture as well as behavioral changes in mice caused by the latent infection could be successfully reversed by restricting the availability of various amino acids during T. gondi infection. Our findings unveil the underlying mechanisms employed by T. gondii to exploit host ER and lysosomal pathways, enhancing nutrient levels during infection. These insights provide new strategies for the treatment of toxoplasmosis. Importance: Intracellular parasites employ several mechanisms to manipulate the cellular environment, enabling them to persist in the host. Toxoplasma gondii , a single-celled parasite, possesses the ability to infect virtually any nucleated cell of warm-blooded vertebrates, including nearly 2 billion people worldwide. Unfortunately, existing treatments and immune responses are not entirely effective in eliminating the chronic persisting forms of the parasite. This study reveals that T. gondii induces the host's autophagic pathway to boost amino acid levels in infected cells. The depletion of amino acids, in turn, influences the persistence of the parasite's chronic forms, resulting in a reduction of neurological alterations caused by chronic infection in mice. Significantly, our investigation establishes the crucial role of host ER-phagy in the parasite's persistence within the host during latent infection.

Towards a continent-wide ecological site condition database using calibrated expert evaluations.

A cost-effective way of undertaking comprehensive, continental-scale, assessments of ecological condition is needed to support large-scale conservation planning, monitoring, reporting, and decision-making. Currently, cross-jurisdictional inconsistency in assessment methods limits the capacity to scale-up monitoring. Here we present a novel way to build a coherent continent-wide site-level ecological condition dataset, using cross-calibration methods to integrate assessments from many observers. We focus on the use of condition assessments from individual expert observers, a currently untapped resource. Our approach has two components: (1) a simple online tool that captures expert assessments at specific locations; (2) a process of calibrating and rescaling disparate expert evaluations that can be applied to the data to provide a consistent dataset for use in conservation assessments. We describe a pilot study, involving 28 experts, who contributed 314 individual site condition assessments across a wide range of ecosystems and regions throughout continental Australia. A correction factor for each expert was used to rescale the contributed site condition assessment scores, based on a set of 77 photographic images, each scored for their condition by multiple experts, using a linear mixed model. Our approach shows strong promise for delivering the volumes of data required to develop continental-scale reference libraries of site condition assessments. Although developed from expert elicitation, the approach could also be used to harmonize the collation of existing condition datasets. The process we demonstrate can also facilitate online citizen scientists to make site condition assessments that can be cross-calibrated using contributed images.

Duration limits for exposure for the whole body and extremities with a military extreme cold protection clothing ensemble at an ambient temperature of -40°C.

Manual performance and body temperature responses were assessed in a 1-h trial at an ambient temperature (TAMB) of -40°C for 7 male participants (32 ± 14 (mean ± SD) years) wearing a typical military extreme cold protection clothing ensemble. The purpose was to establish duration limited exposure (DLIM) for these conditions, and it was hypothesized that (i) core temperature (TCORE) would remain normothermic, whereas extremity skin temperature (TSK) would decrease; (ii) decrements of manual performance would be in proportion to decreases of hand TSK; and (iii) DLIM would be determined by the hand or foot TSK responses. Linear regression was employed to assess associations of manual performance scores and body temperatures with DLIM assessed using the Required Clothing Insulation (IREQ) model and extremity temperatures in ISO 11079-2007. Results showed TCORE remained at ~37.3°C, whereas there were significant (0.0001 < p < 0.05) decreases in extremity TSK. Associations between manual performance and hand TSK showed coefficients of determination (R2) ranging from 0.48 < R2 < 0.98; 0.00005 ≤ p ≤ 0.08. The DLIM for the whole-body ensemble ranged from 2.2 h to > 8 h, whereas the DLIM for the extremities was 0.56 ± 0.20 h for TSK decreasing 15°C. In conclusion, the hypotheses of a stable core temperature and decreases of extremity skin temperature giving decrements in manual performance were accepted as was the hypothesis that duration limits for exposure would be determined by extremity skin temperatures of the hand and foot.

Belief in the need for sodium supplementation during ultramarathons remains strong: findings from the Ultrarunners Longitudinal TRAcking (ULTRA) study.

In the past, ultramarathon runners have commonly believed that consuming sodium supplements, as capsules or tablets, will prevent exercise-associated hyponatremia (EAH), dehydration, muscle cramping, and nausea, but accumulating evidence indicates that sodium supplementation during ultramarathons is not necessary and may be potentially dangerous. In this work, beliefs about whether sodium supplements should be made available at ultramarathons were assessed during 2018 among 1152 participants of the Ultrarunners Longitudinal TRAcking (ULTRA) study, of which 85.2% had completed an ultramarathon during 2014-2018. Two-thirds (66.4%) of study participants indicated that sodium supplements should be made available at ultramarathons, supported by beliefs that they prevent EAH (65.5%) and muscle cramping (59.1%). Of those indicating that sodium supplements should not be made available, 85.0% indicated it is because runners can provide their own, 27.9% indicated it is because they are not necessary, and 12.1% indicated they could increase thirst drive and cause overhydration. In general, there was a tendency for those who were older, less active in running ultramarathons in recent years, and with a longer history of ultramarathon running to be less likely to know that sodium supplements do not help prevent EAH, muscle cramping, and nausea. Novelty Ultramarathon runners continue to have misunderstandings about the need for sodium supplementation during ultramarathons. Few ultramarathon runners recognize that supplementing sodium intake beyond that in food and drink is generally not necessary during ultramarathons or that it could result in overhydration. Continued educational efforts are warranted to help ensure safe participation in the sport.

Consecutive non-training days over a weekend for assessing cardiac parasympathetic variation in response to accumulated exercise stress.

Purpose: To examine the association between day-to-day resting cardiac parasympathetic variability over consecutive non-training days (i.e. weekend) and accumulated exercise stress when quantified using indices of cardiovascular strain. Methods: Twelve international calibre female field hockey players training as part of a national team were participants over a four-week mesocycle prior to a 2016 Olympic qualifying tournament. On-field exercise stress was examined using heart rate (HR) dynamics and quantified as; (1) training load and (2) time (min) spent above anaerobic threshold. The square root of the mean squared differences of successive cardiac cycles (R-R intervals) recorded on Saturday and Sunday were individually calculated and log-transformed prior to being averaged (Ln rMSSDweekend). Day-to-day variation in Ln rMSSD over the weekend was expressed using the coefficient of variation (Ln rMSSDCV). Non-linear regression analysis examined the association between accumulated exercise stress and Ln rMSSDCV. Results: A quadratic association between each index of exercise stress and Ln rMSSDCV was identified. After converting the coefficient of determination into a correlation coefficient (90% CL), the respective association between Ln rMSSDCV and training load (AU); r = 0.40 (0.16:0.59) and time above threshold; r = 0.35 (0.06:0.59) were observed. Conclusion: Ln rMSSDCV derived over consecutive non-training days displayed a moderate, yet significant association between accumulated exercise stress when expressed as global or high-intensity indices of cardiovascular strain. Weekend assessments may offer a practical and appropriate juncture between microcycles to assess the magnitude of perturbation in cardiac autonomic homeostasis prior to entering subsequent training periods.

Monitoring the Prescribed and Experienced Heart Rate-Derived Training Loads in Elite Field Hockey Players.

Perrotta, AS, Taunton, JE, Koehle, MS, White, MD, and Warburton, DER. Monitoring the prescribed and experienced heart rate-derived training loads in elite field hockey players. J Strength Cond Res 33(5): 1394-1399, 2019-This study examined the congruence between the prescribed and experienced heart rate-derived training loads over a 5-week periodized mesocycle. Twenty-four elite female field hockey players training as part of a national team were monitored before an (FIH) Hockey World League tournament. Three on-field training sessions per week were prospectively designed focusing on technical, tactical, and physiologically oriented hockey drills. A training load value, modeling the periodized weekly loading scheme, was prescribed for each training session and was calculated using normative training load responses from performing on-field hockey drills. Magnitude-based inferences focusing on the effect size (ES) and a Pearson correlation coefficient (r) were used to examine the degree of difference and the strength of correlation between the prescribed and experienced training loads. A significant correlation was observed between the experienced and prescribed training loads over the 5-week mesocycle (r = 0.92, 90% confidence limit [CL] [0.84-0.96]). The percentage difference and the ES between the achieved and prescribed training loads were as follows: week 1 demonstrated a 2.0% difference (ES = 0.10, 90% CL [-0.22-0.41]), week 2 a -5.4% difference (ES = -0.41, 90% CL [-0.75 to -0.07]), week 3 a -1.5% difference (ES = -0.09, 90% CL [-0.37 to 0.20]), week 4 a 7.1% difference (ES = 0.46, 90% CL [0.14-0.78]), and week 5 a 3.5% difference (ES = 0.18, 90% CL [-0.17 to 0.53]). This investigation demonstrates the efficacy for coaches to prospectively design on-field training sessions using normative training load data to enhance the congruence between the prescribed and experienced training loads over a periodized mesocycle.

Panting as a human heat loss thermoeffector.

The human autonomic nervous system participates in the control of thermoregulatory responses that are employed to regulate core temperature following deviations of skin temperature and/or core temperature from their respective resting values. This permits a regulation of the core temperature (TC) at 37.0 ± 1°C with superimposed circadian variations in both sexes and menstrual cycle-associated variations in premenopausal women. When rendered hyperthermic, passively by heat exposure while at rest or actively during exercise, humans engage heat loss or thermolytic responses, including eccrine sweating and cutaneous vasodilatation. A third, less studied, human thermolytic response is thermal panting, and this response is the focus of this review. Human thermal panting was first described over a century ago. It has since been shown to be a reproducible response showing some similar patterns of breathing in species that employ panting as their sole thermolytic heat loss response. The contribution of human panting as a thermolytic response, however, remains controversial. This review highlights both past and recent evidence supporting that hyperthermic humans have a panting pattern of breathing that plays an important role in human thermoregulation.

Efficacy of Hot Yoga as a Heat Stress Technique for Enhancing Plasma Volume and Cardiovascular Performance in Elite Female Field Hockey Players.

Perrotta, AS, White, MD, Koehle, MS, Taunton, JE, and Warburton, DER. Efficacy of hot yoga as a heat stress technique for enhancing plasma volume and cardiovascular performance in elite female field hockey players. J Strength Cond Res 32(10): 2878-2887, 2018-This investigation examined the efficacy of hot yoga as an alternative heat stress technique for enhancing plasma volume percentage (PV%) and cardiovascular performance. Ten international caliber female field hockey players completed six 60-minute hot yoga sessions using permissive dehydration over 6 days, followed by a 6-day national team camp. Changes in PV% were examined throughout the intervention and postintervention period. A graded maximal exercise test was performed in a thermoneutral environment (23.2 ± 1.0° C) 24 hours before and 24 hours after intervention. Six days of hot yoga initiated a moderate state of hypovolemia (PV% = -3.5%, 90% confidence limit [CL] [-6.9 to -0.13]), trivial improvements in maximal aerobic power (V[Combining Dot Above]O2max) (effect size [ES] = 0.06, 90% CL [-0.16 to 0.28]), and run time to exhaustion (ES = 0.11, 90% CL [-0.07 to 0.29]). Small meaningful improvements were observed in running speed (km·h) at ventilatory threshold (VT1) (ES = 0.34, 90% CL [-0.08 to 0.76]), VT2 (ES = 0.53, 90% CL [-0.05 to 1.1]), along with adaptations in the respiratory exchange ratio during high-intensity exercise (ES = -0.25, 90% CL [-0.62 to 0.12]). A large plasma volume expansion transpired 72 hours after intervention (PV% = 5.0%, 90% CL [1.3-8.7]) that contracted to a small expansion after 6 days (PV% = 1.6%, 90% CL [-1.0 to 4.2]). This investigation provides practitioners an alternative heat stress technique conducive for team sport, involving minimal exercise stress that can preserve maximal cardiovascular performance over periodized rest weeks within the yearly training plan. Furthermore, improvements in submaximal performance and a delayed hypervolemic response may provide a performance-enhancing effect when entering a 6-day competition period.

A condition metric for Eucalyptus woodland derived from expert evaluations.

The evaluation of ecosystem quality is important for land-management and land-use planning. Evaluation is unavoidably subjective, and robust metrics must be based on consensus and the structured use of observations. We devised a transparent and repeatable process for building and testing ecosystem metrics based on expert data. We gathered quantitative evaluation data on the quality of hypothetical grassy woodland sites from experts. We used these data to train a model (an ensemble of 30 bagged regression trees) capable of predicting the perceived quality of similar hypothetical woodlands based on a set of 13 site variables as inputs (e.g., cover of shrubs, richness of native forbs). These variables can be measured at any site and the model implemented in a spreadsheet as a metric of woodland quality. We also investigated the number of experts required to produce an opinion data set sufficient for the construction of a metric. The model produced evaluations similar to those provided by experts, as shown by assessing the model's quality scores of expert-evaluated test sites not used to train the model. We applied the metric to 13 woodland conservation reserves and asked managers of these sites to independently evaluate their quality. To assess metric performance, we compared the model's evaluation of site quality with the managers' evaluations through multidimensional scaling. The metric performed relatively well, plotting close to the center of the space defined by the evaluators. Given the method provides data-driven consensus and repeatability, which no single human evaluator can provide, we suggest it is a valuable tool for evaluating ecosystem quality in real-world contexts. We believe our approach is applicable to any ecosystem.

Effect of a patent foramen ovale in humans on thermal responses to passive cooling and heating.

Humans with a patent foramen ovale (PFO) have a higher esophageal temperature (Tesoph) than humans without a PFO (PFO-). Thus the presence of a PFO might also be associated with differences in thermal responsiveness to passive cooling and heating such as shivering and hyperpnea, respectively. The purpose of this study was to determine whether thermal responses to passive cooling and heating are different between PFO- subjects and subjects with a PFO (PFO+). We hypothesized that compared with PFO- subjects PFO+ subjects would cool down more rapidly and heat up slower and that PFO+ subjects who experienced thermal hyperpnea would have a blunted increase in ventilation. Twenty-seven men (13 PFO+) completed two trials separated by >48 h: 1) 60 min of cold water immersion (19.5 ± 0.9°C) and 2) 30 min of hot water immersion (40.5 ± 0.2°C). PFO+ subjects had a higher Tesoph before and during cold water and hot water immersion (P < 0.05). However, the rate of temperature change was similar between groups for each condition. Within a subset of 18 subjects (8 PFO+) who experienced thermal hyperpnea, PFO+ subjects experienced thermal hyperpnea at a higher absolute Tesoph but with a blunted magnitude compared with PFO- subjects. These data suggest that PFO+ subjects have a higher Tesoph at rest and have blunted thermal hyperpnea during passive heating.NEW & NOTEWORTHY Patent foramen ovale (PFO) is found in ~25-40% of the population. The presence of a PFO appears to be associated with a greater core body temperature and blunted ventilatory responses during passive heating. The reason for this blunted ventilatory response to passive heating is unknown but may suggest differences in thermal sensitivity in PFO+ subjects compared with PFO- subjects.

Induction of thermogenesis in brown and beige adipose tissues: molecular markers, mild cold exposure and novel therapies.

PURPOSE OF REVIEW: The purpose of this short review paper is to summarize recent developments in the understanding of the activation, growth and function of brown adipose tissue (BAT). RECENT FINDINGS: Transcriptional markers for increased BAT activity and differentiation of white adipocytes to 'beige' or 'brite' adipocytes include amongst others peroxisome proliferator-activated receptor γ, cytosine-enhancer-binding protein, positive regulatory domain 16 and bone morphogenetic proteins. These markers induce uncoupling protein 1 expression in brown and 'beige' or 'brite' adipocytes which allows energy from macronutrients to be expended as heat. Acute and repeated mild cold exposures of 17-19 °C in adult humans increase BAT volume and activity and this is a novel method for increasing their energy expenditure. Emerging evidence suggests that irisin and melatonin hormones may be involved in BAT activation. Additionally, brown adipocyte stem cell therapy transplantation is a means to stimulate this increased thermogenesis from brown and 'beige' or 'brite' adipocytes. SUMMARY: Markers for increased BAT activation and for white adipocyte differentiation into beige/brite adipocytes have been identified, and these lead to an uncoupling protein 1-mediated increase in metabolic rate. Mild cold exposure and brown adipocyte stem cell transplantation are two potential strategies for inducing activation and growth of BAT for the treatment of human obesity.

Effect of change in ambient temperature on core temperature during the daytime.

In this study, the hypothesis is tested that continuous increases in ambient temperature (Ta) during daytime would give elevated core and skin temperatures, and consequently better thermal sensation and comfort. Rectal temperature (Tre), skin temperatures and regional dry heat losses at 7 sites were continuously measured for 10 Japanese male subjects in three thermal conditions: cond. 1, stepwise increases in Ta from 26 °C at 9 h00 to 30 °C at 18 h00; cond. 2, steady Ta at 28 °C from 9 h00 to 18 h00 and cond. 3, stepwise decreases in Ta from 30 °C at 9 h00 to 26 °C at 18 h00. Oxygen consumption was measured and thermal sensation and comfort votes were monitored at 15 min intervals. Body weight loss was measured at 1 h intervals. While Tre increased continuously in the morning period in any condition, it increased to a significantly greater (p<0.05) 36.9±0.3 °C at 18 h00 in cond. 1 relative to 36.7±0.28 °C in Cond. 2 and 36.5±0.37 °C in cond. 3. Better thermal comfort was observed in the afternoon and the evening in Cond.1 as compared with the other 2 conditions. Thus, a progressive and appropriate increase in Ta may induce optimal cycle in core temperature during daytime, particularly for a resting person.

Central chemoreflex ventilatory responses in humans following passive heat acclimation.

Since there is temperature dependence of pulmonary ventilation (V˙(E)) in response to the normal modulators (i.e. [Formula: see text] , [Formula: see text] ), it was asked in this study if passive heat acclimation (HA) modifies the human central chemoreflex ventilatory response to CO(2). Nine males performed normothermic- and hyperthermic modified Read re-breathing tests before and after HA. Heat acclimation consisted of 2hday(-1) exposures to 50°C and 20% RH for 10 consecutive days and each exposure elevated rectal temperature to between 38.5 and 39.0°C. Ventilatory recruitment thresholds (VRTs) and central chemosensitivity were assessed before and after HA during normothermia with an oesophageal temperature (T(es)) of ∼37°C and in hyperthermia when T(es) was 38.5-39.0°C. Results showed VRT and central chemosensitivities were unaltered by HA (p≥0.375) and hyperthermia increased pre- (p=0.010) but not post-acclimation (p=0.332) central chemosensitivity. Additionally, during hyperthermia V˙(E) became progressively greater (p=0.027) relative to corresponding normothermic values in the re-breathing tests. In conclusion, the ventilatory response to hyperoxic CO(2) was unaltered by heat Acclimation State.

Human body temperature and new approaches to constructing temperature-sensitive bacterial vaccines.

Many of the live human and animal vaccines that are currently in use are attenuated by virtue of their temperature-sensitive (TS) replication. These vaccines are able to function because they can take advantage of sites in mammalian bodies that are cooler than the core temperature, where TS vaccines fail to replicate. In this article, we discuss the distribution of temperature in the human body, and relate how the temperature differential can be exploited for designing and using TS vaccines. We also examine how one of the coolest organs of the body, the skin, contains antigen-processing cells that can be targeted to provoke the desired immune response from a TS vaccine. We describe traditional approaches to making TS vaccines, and highlight new information and technologies that are being used to create a new generation of engineered TS vaccines. We pay particular attention to the recently described technology of substituting essential genes from Arctic bacteria for their homologues in mammalian pathogens as a way of creating TS vaccines.

The effects of lower body positive and negative pressure on the hypoxic ventilatory decline.

PURPOSE: Lower body negative pressure (LBNP) augments the acute hypoxic ventilatory response (AHVR) in humans, presumably through altered central integration of baro- and chemoreceptor afferents. This study investigated the effects of LBNP and lower body positive pressure (LBPP) on hypoxic ventilatory decline (HVD) in humans. METHODS: Nine individuals (4 females and 5 males) were tested in a supine position with the lower body supported inside a hypo/hyperbaric chamber. During each test the participant was exposed in a random order to LBNP at -37.5mmHg, LBPP at +37.5mmHg and to ambient pressure (LBAP) at 0mmHg. Blood pressure, expired gases and haemoglobin O(2) saturation were continuously recorded. Hypoxia was administered in a single step to a PET O2 of 50mmHg for 20min. For all tests PET CO2 was maintained at the pre-hypoxic resting level. RESULTS: The peak ventilation was significantly greater during LBNP (36.0+/-10.8Lmin(-1)) than during ambient pressure (29.4+/-8.1Lmin(-1); p=0.032). However, peak ventilation was not significantly different between LBPP and ambient pressure. The HVD was not significantly different across the three conditions (p=0.144). Both mean arterial pressure and pulse pressure were not affected by 37.5mmHg of either LBPP (p=0.941) or LBNP (p=0.275). Baroreflex slope was decreased by both hypoxia and LBNP. CONCLUSION: These data suggest that LBNP increases AHVR through an effect on the baroreflex, while LBPP has no effect on AHVR. Since LBNP increases AHVR without affecting HVD, these findings support that the mechanism accounting for the HVD includes afferent output originating from the peripheral rather than the central chemosensitive tissues.

No effect of skin temperature on human ventilation response to hypercapnia during light exercise with a normothermic core temperature.

Hyperthermia potentiates the influence of CO(2) on pulmonary ventilation (.V(E)). It remains to be resolved how skin and core temperatures contribute to the elevated exercise ventilation response to CO(2). This study was conducted to assess the influences of mean skin temperature (_T(SK)) and end-tidal PCO(2) (P(ET)CO(2)) on .V(E) during submaximal exercise with a normothermic esophageal temperature (T(ES)). Five males and three females who were 1.76 +/- 0.11 m tall (mean +/- SD), 75.8 +/- 15.6 kg in weight and 22.0 +/- 2.2 years of age performed three 1 h exercise trials in a climatic chamber with the relative humidity (RH) held at 31.5 +/- 9.5% and the ambient temperature (T (AMB)) maintained at one of 25, 30, or 35 degrees C. In each trial, the volunteer breathed eucapnic air for 5 min during a rest period and subsequently cycle ergometer exercised at 50 W until T (ES) stabilized at approximately 37.1 +/- 0.4 degrees C. Once T (ES) stabilized in each trial, the volunteer breathed hypercapnic air twice for approximately 5 min with P(ET)CO(2) elevated by approximately +4 or +7.5 mmHg. The significantly (P < 0.05) different increases of P(ET)CO(2) of +4.20 +/- 0.49 and +7.40 +/- 0.51 mmHg gave proportionately larger increases in .V(E) of 10.9 +/- 3.6 and 15.2 +/- 3.6 L min(-1) (P = 0.001). This hypercapnia-induced hyperventilation was uninfluenced by varying the _T(SK) to three significantly different levels (P < 0.001) of 33.2 +/- 1.2 degrees C, to 34.5 +/- 0.8 degrees C to 36.4 +/- 0.5 degrees C. In conclusion, the results support that skin temperature between approximately 33 and approximately 36 degrees C has neither effect on pulmonary ventilation nor on hypercapnia-induced hyperventilation during a light exercise with a normothermic core temperature.

Adaptation of exercise ventilation during an actively-induced hyperthermia following passive heat acclimation.

Hyperthermia-induced hyperventilation has been proposed to be a human thermolytic thermoregulatory response and to contribute to the disproportionate increase in exercise ventilation (VE) relative to metabolic needs during high-intensity exercise. In this study it was hypothesized that VE would adapt similar to human eccrine sweating (E(SW)) following a passive heat acclimation (HA). All participants performed an incremental exercise test on a cycle ergometer from rest to exhaustion before and after a 10-day passive exposure for 2 h/day to either 50 degrees C and 20% relative humidity (RH) (n = 8, Acclimation group) or 24 degrees C and 32% RH (n = 4, Control group). Attainment of HA was confirmed by a significant decrease (P = 0.025) of the esophageal temperature (T(es)) threshold for the onset of E(SW) and a significantly elevated E(SW) (P < or = 0.040) during the post-HA exercise tests. HA also gave a significant decrease in resting T(es) (P = 0.006) and a significant increase in plasma volume (P = 0.005). Ventilatory adaptations during exercise tests following HA included significantly decreased T(es) thresholds (P < or = 0.005) for the onset of increases in the ventilatory equivalents for O(2) (VE/VO(2)) and CO(2) (VE/VCO(2)) and a significantly increased VE (P < or = 0.017) at all levels of T(es). Elevated VE was a function of a significantly greater tidal volume (P = 0.003) at lower T(es) and of breathing frequency (P < or = 0.005) at higher T(es). Following HA, the ventilatory threshold was uninfluenced and the relationships between VO(2) and either VE/VO(2) or VE/VCO(2) did not explain the resulting hyperventilation. In conclusion, the results support that exercise VE following passive HA responds similarly to E(SW), and the mechanism accounting for this adaptation is independent of changes of the ventilatory threshold or relationships between VO(2) with each of VE/VO(2) and VE/VCO(2).

Performance of a compact end-tidal forcing system.

The purpose of the present study was to develop and validate a new compact, portable end-tidal forcing (ETF) system capable of reliably controlling end-tidal gases. The system consists of compressed gas sources (air, N(2) and CO(2)) that are connected via three solenoid valves to a humidification chamber and an inspiratory reservoir bag from which the participant breathes. This computer-controlled system compares actual end-tidal gas partial pressures with target pressures and mixes the gases on a breath-by-breath basis. This leaves no unused exhaust gas and keeps gas requirements to a minimum. Eight participants underwent two different 30-min protocols that included each possible combination of end-tidal O(2) partial pressure (PET O2) and end-tidal CO(2) partial pressure (PET O2) control at two different levels (PET O2 at 55 and 75 mmHg; and PET CO2 at 4 and 7 mmHg above resting). The ETF system maintained the mean PET CO2 at 0.13 mmHg from the target values, with a pooled S.D. across conditions of +/-0.91 mmHg and a 95% confidence interval (CI) of +/-0.63 mmHg. The mean PET CO2 was held at 0.49 mmHg from its target values, with a pooled S.D. across conditions of +/-1.31 mmHg and a 95% CI of +/-0.91 mmHg. To demonstrate suitability of this system for measuring chemosensitivity to hypoxia, hypoxic ventilatory response (HVR) tests were conducted in a subset of five participants. During a 20-min HVR test both PET CO2 and PET O2 were not significantly different from their target values. These data demonstrate the performance of a portable, compact, economical system that controls PET CO2 within 1 mmHg and PET O2 within 2 mmHg of their respective target values.