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Aim: In this study, we quantified acute changes in the intracellular and extracellular fluid compartments during upright neutral- and cold-water immersion. We hypothesized that, during short-term cold immersion, fluid shifts would be wholly restricted to the extracellular space., Methods: Seven males were immersed 30 days apart: control (33.3 degrees SD 0.6 degrees C); and cold (18.1 degrees SD 0.3 degrees C). Posture was controlled for 4 h prior to a 60-min seated immersion., Results: Significant reductions in terminal oesophageal (36.9 degrees +/- 0.1 degrees -36.3 degrees +/- 0.1 degrees C) and mean skin temperatures (30.3 degrees +/- 0.3 degrees -23.0 degrees +/- 0.3 degrees C) were observed during the cold, but not the control immersion. Both immersions elicited a reduction in intracellular fluid [20.17 +/- 6.02 mL kg(-1) (control) vs. 22.72 +/- 9.90 mL kg(-1)], while total body water (TBW) remained stable. However, significant plasma volume (PV) divergence was apparent between the trials at 60 min [12.5 +/- 1.0% (control) vs. 6.1 +/- 3.1%; P < 0.05], along with a significant haemodilution in the control state (P < 0.05). Plasma atrial natriuretic peptide concentration increased from 18.0 +/- 1.6 to 58.7 +/- 15.1 ng L(-1) (P < 0.05) during cold immersion, consistent with its role in PV regulation. We observed that, regardless of the direction of the PV change, both upright immersions elicited reductions in intracellular fluid., Conclusion: These observations have two implications. First, one cannot assume that PV changes reflect those of the entire extracellular compartment. Second, since immersion also increases interstitial fluid pressure, fluid leaving the interstitium must have been rapidly replaced by intracellular water.

Using a simultaneous-dilution technique, we investigated body-fluid volume changes during exercise in seven males, during 50 min of cycling (50% maximal work rate) in hot (36.2 degrees C), temperate (22.0 degrees C) and cool conditions (14.4 degrees C). Total body water (TBW), extracellular fluid (ECFV), plasma (PV) and erythrocyte volumes (RCV) were measured, while blood volume (BV), interstitial fluid volume (IFV), extracellular water (ECW) and intracellular water volumes (ICW) were derived. During the initial 10 min of cycling, BV decreased in all environments (P .01), primarily because of a PV reduction (P = 0.01), while IFV, ECFV and ICW were not significantly changed. By 30 min, BV recovered in the temperate and cool conditions, despite mass losses of 563 and 520 mL (respectively), but remained depleted in the hot condition (P = 0.01). The 50-min volume changes revealed that, throughout exercise, body-fluid losses appeared to be drawn primarily from the extracellular space, regardless of air temperature. In the hot condition, the PV change represented 63% of the TBW loss, with the ICW contributing 23%. It was concluded that, during cycling, progressive dehydration mainly affected the extracellular space, with the intravascular and intracellular spaces being defended in less stressful conditions.

The influence of local skin temperature (Tskl) on the control of local and whole-body sweating was evaluated in eight healthy males. A water-perfusion garment (37 degrees C) and a climatic chamber (36.45 +/- 0.78 degrees C; [+/- SD]; relative humidity 60.3 +/- 1.6%) were used to raise and clamp skin and core temperatures. Warm and cool stimuli were applied to four upper-body skin regions (face, arm, forearm, hand) using perfusion patches (249.0 +/- 0.2 cm2). Heating elevated, while cooling suppressed sweat rate (msw) locally, and at other skin surfaces. However, the tendency for Tskl manipulations to induce localized sweat responses was no more powerful than it was at stimulating sweating in non-treated regions (P > 0.05). Accordingly, neither thermal stimulus produced significantly greater local sudomotor influences than were elicited contralaterally (P > 0.05). No statistical support was found for the notion of inter-regional differences in upper-body cutaneous thermal sensitivity for sudomotor control, and, regardless of the stimulation site, whole-body sudomotor responses to localized thermal treatments were equivalent (P > 0.05).

This project sought to evaluate the importance of skin temperature during heat acclimation, using an isothermal-strain model. Two groups of seven matched males, participated (1 h per day, 10 days) in one of two conditions: (i) temperate physical training (TEMP: 22.4 +/- 0.7 degrees C, relative humidity (r.h.) 41.0 +/- 0.9%); or (ii) combined physical training and heat acclimation (HEAT: 38.2 +/- 0.7 degrees C, r.h. 39.7 +/- 1.3%). Isothermal strain was induced in both groups by rapidly elevating rectal temperature by 1 degree C (cycling), then holding it constant by manipulating external work. Subjects completed two three-phase heat stress tests (39.8 +/- 0.1 degrees C, r.h. 38.6 +/- 1.2), consisting of 20 min rest, then 20 min cycling at each of 30% and 45% of peak power, before and after each regimen. While there was a difference of 4.2 degrees C in mean skin temperature between treatments, both regimens elicited a similar peripheral sudomotor increase, indicating a core temperature dependent adaptation. However, based on significant pre- vs. post-acclimation decreases in average auditory canal temperature (0.4 +/- 0.1 degree C), average forehead skin blood flow (26%), average perceived exertion (11%), and a 5% increase in average forehead sweat rate (0.1 +/- 0.04 mg cm-2 min-1), the HEAT regimen elicited a more complete acclimation. While elevation in core temperature is critical to acclimation, it also appears necessary to expose subjects to an external thermal stress. This observation has not been previously demonstrated under conditions of isothermal strain, and verifies the importance of skin temperature elevation in the acclimation process.

Inter-compartmental body-fluid distribution is contingent upon posture, exercise state and environmental temperature. This investigation aimed at quantifying the distribution of intra- and extravascular fluid volumes during postural manipulations. Fluid shifts were measured in eight males utilizing a simultaneous, radionuclide dilution technique, in which radioiodinated serum fibrinogen, radiochromated erythrocytes, radiobromine and tritiated water were used to measure plasma, red cell, extracellular and total body water volumes. Subjects were exposed to three postural changes [seated (control), supine and standing] for 30 min at an air temperature of 22.0 degrees C, with each posture separated by 30 min seated rest. Total body water content remained stable throughout postural changes (P = 0.842). Relative to seated volumes, BV increased by 89 mL when supine, and decreased by 406 mL while standing (P = 0.003), with such shifts being primarily a result of plasma movement (P = 0.011). Red cell volume changes were not significant. Vascular fluid lost during standing was filtered into the interstitial compartment (P = 0.014), with the extracellular and intracellular volumes remaining unaffected. (P = 0.271 and P = 0.800, respectively). These observations confirmed the influence of posture on inter-compartmental body-fluid distribution. The intravascular fluid loss when standing was caused by the filtration of plasma into the interstitium, while, during supine rest, intravascular volume increased, reflecting fluid flux from the interstitium to the circulation.

Elastic properties of the lung are typically assessed using the static pressure-volume relaxation manoeuvre. Although dynamic methods have produced equivalent results in normal healthy subjects, their use under obstructive pulmonary disease states and during certain conditions has been questioned. Static (Cst(1)) and dynamic (Cdyn(1)) pulmonary compliance were measured in eight subjects in air (control) and during immersion. Cdyn(1) decreased from 2.94 to 1.61 l kPa-1 following immersion, during which subjects breathed air supplied at mouth pressure (P < 0.05), while Cst(1) remained approximately equivalent (3.16 and 4.07 l kPa-1 respectively, P > 0.05). When immersed subjects were supplied with breathing gas at lung centroid pressure (PLC), Cdyn(1) returned to control status (2.89 l kPa-1; P > 0.05), while Cst(1) remained stable at 3.60 l kPa-1 (P > 0.05). The difference between Cst(1) and Cdynm(1) may imply that flow-resistive properties are included within the latter measurement. It is recommended that Cdyn(1), under these conditions, be interpreted as an index of peripheral airway patency, rather than as an assessment of lung elasticity.

Tracheal gas density breathing heliox at 31.3 atmospheres absolute (O2 at 0.42 ATA) is 6.287 g l-1, or approximately 5.5 times greater than air at 1 ATA. This constitutes a significant respiratory load, previously shown to induce respiratory adaptation. During a saturation dive to 31.3 ATA, five divers were exposed to this load for 16 days. This project aimed at investigating possible hysteresis in pulmonary function during dive compression, adaptation and decompression phases. Pulmonary function tests were performed at the surface in air, and at four pressure stops during compression and decompression, with divers breathing the helium-oxygen gas mixture. Significant hysteresis patterns were observed for pooled maximal voluntary ventilation, forced expired volume at 1 s, peak expiratory flow, and maximum expiratory flows (P < 0.05), with post-adaptation flows consistently exceeding those observed during compression. Two mechanisms may explain these observations. Differences may be attributable to positive effort-dependence in the forced expiratory flow; or it is possible the subjects adapted to the respiratory load by modifying neural input to airway smooth muscle, thereby modifying airway resistance.

This paper focuses upon flow-resistive pulmonary work during upright immersion, and during changes in the air delivery pressure. Nine male non-smokers (aged 26.2 +/- 3.5 years), with normal lung function history, performed spontaneous respiration while seated in air (control) and during total immersion. During the immersed state subjects were supplied with air at four hydrostatic pressures: mouth pressure (PM; simulating a mouth-held demand regulator), lung centroid pressure (PLC; + 1.33 kPa relative to the sternal notch), and 0.98 kPa (10 cmH2O) above and below the lung centroid pressure. Inspiratory, expiratory and total flow-resistive pulmonary work were computed from the integration of transpulmonary pressure (difference between oesophageal and mouth pressure) with respect to lung volume change. When breathing air delivered at mouth pressure, immersion significantly elevated all total flow-resistive pulmonary work components (P less than 0.05). Each increment in breathing pressure resulted in a progressive reduction in expiratory and total flow-resistive pulmonary work, so that when air was provided at lung centroid pressure and lung centroid pressure +0.98 kPa both components were similar to control values (P greater than 0.05). Inspiratory was always less than expiratory pulmonary work. During immersion inspiratory pulmonary work was significantly reduced when air supply pressure was increased above mouth pressure (P less than 0.05). Subsequent pressure increments failed to produce further changes in inspiratory pulmonary work. The difference in response between the inspiratory and expiratory components of total flow resistive pulmonary work was attributed primarily to the volume-dependence of the expiratory component.