Effect of luteal phase elevation in core temperature on forearm blood flow during exercise

Kolka, Margaret A., and Lou A. Stephenson. Effect ofluteal phase elevation in core temperature on forearm blood flow duringexercise. J. Appl. Physiol. 82(4):1079-1083, 1997.Forearm blood flow (FBF) as an index of skinblood flow in the forearm was measured in five healthy women by venousocclusion plethysmography during leg exercise at 80% peak aerobicpower and ambient temperature of 35°C (relative humidity 22%;dew-point temperature 10°C). Resting esophagealtemperature (T_es) was 0.3 ± 0.1°C higher in the midluteal than in the early follicular phase ofthe menstrual cycle (P < 0.05).Resting FBF was not different between menstrual cycle phases. TheT_es threshold for onset of skinvasodilation was higher (37.4 ± 0.2°C) in midluteal than inearly follicular phase (37.0 ± 0.1°C; P < 0.05). The slope of the FBF toT_es relationship was not different between menstrual cycle phases (14.0 ± 4.2 ml · 100 ml¹ · min¹ · °C¹for early follicular and 16.3 ± 3.2 ml · 100 ml¹ · min¹ · °C¹for midluteal phase). Plateau FBF was higher during exercise inmidluteal (14.6 ± 2.2 ml · 100 ml¹ · min¹ · °C¹)compared with early follicular phase (10.9 ± 2.4 ml · 100 ml¹ · min¹ · °C¹;P < 0.05). The attenuation of theincrease in FBF to T_es occurred when T_es was 0.6°C higher andat higher FBF in midluteal than in early follicular experiments(P < 0.05). In summary, the FBF response is different during exercise in the two menstrual cycle phasesstudied. After the attenuation of the increase in FBF and whileT_es was still increasing, thegreater FBF in the midluteal phase may have been due to the effects ofincreased endogenous reproductive endocrines on the cutaneousvasculature.

     

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise

González-Alonso, José, RicardoMora-Rodríguez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function inhyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229-1236, 1997.Weidentified the cardiovascular stress encountered by superimposingdehydration on hyperthermia during exercise in the heat and themechanisms contributing to the dehydration-mediated stroke volume (SV)reduction. Fifteen endurance-trained cyclists [maximalO₂ consumption(O_{2 max}) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinkingfluids. Measurements were made after they continued exercise at 71%O_{2 max} for 30 minwhile 1) euhydrated with anesophageal temperature (T_es) of38.1-38.3°C (control); 2)euhydrated and hyperthermic (39.3°C);3) dehydrated and hyperthermic withskin temperature (T_sk) of34°C; 4) dehydrated withT_es of 38.1°C and T_sk of 21°C; and5) condition4 followed by restored blood volume. Compared withcontrol, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separatelylowered SV 7-8% (11 ± 3 ml/beat;P < 0.05) and increased heart ratesufficiently to prevent significant declines in cardiac output.However, when dehydration was superimposed on hyperthermia, thereductions in SV were significantly (P < 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterialpressure declined 5 ± 2%, and systemic vascular resistanceincreased 10 ± 3% (both P < 0.05). When hyperthermia wasprevented, all of the decline in SV with dehydration was due to reducedblood volume (~200 ml). These results demonstrate that thesuperimposition of dehydration on hyperthermia during exercise in theheat causes an inability to maintain cardiac output and blood pressurethat makes the dehydrated athlete less able to cope with hyperthermia.

     

Thermal and metabolic responses to cold-water immersion at knee, hip, and shoulder levels

Lee, Dae T., Michael M. Toner, William D. McArdle, IoannisS. Vrabas, and Kent B. Pandolf. Thermal and metabolic responses tocold-water immersion at knee, hip, and shoulder levels.J. Appl. Physiol. 82(5):1523-1530, 1997.To examine the effect of cold-water immersion atdifferent depths on thermal and metabolic responses, eight men (25 yrold, 16% body fat) attempted 12 tests: immersed to the knee (K), hip(H), and shoulder (Sh) in 15 and 25°C water during both rest (R) orleg cycling [35% peak oxygen uptake; (E)] for up to 135 min. At 15°C, rectal (T_re)and esophageal temperatures(T_es) between R and E were notdifferent in Sh and H groups (P > 0.05), whereas both in K group were higher during E than R(P < 0.05). At 25°C,T_re was higher(P < 0.05) during E than R at alldepths, whereas T_es during E washigher than during R in H and K groups.T_re remained at control levels inK-E at 15°C, K-E at 25°C, and in H-E groups at 25°C,whereas T_es remained unchanged inK-E at 15°C, in K-R at 15°C, and in all 25°C conditions (P > 0.05). During R and E, themagnitude of T_re change wasgreater (P < 0.05) than themagnitude of T_es change in Sh andH groups, whereas it was not different in the K group(P > 0.05). Total heat flow wasprogressive with water depth. During R at 15 and 25°C, heatproduction was not increased in K and H groups from control level(P > 0.05) but it did increase in Shgroup (P < 0.05). The increase inheat production during E compared with R was smaller(P < 0.05) in Sh (121 ± 7 W/m² at 15°C and 97 ± 6 W/m² at 25°C) than in H (156 ± 6 and 126 ± 5 W/m²,respectively) and K groups (155 ± 4 and 165 ± 6 W/m², respectively). These datasuggest that T_re andT_es respond differently duringpartial cold-water immersion. In addition, water levels above knee in15°C and above hip in 25°C cause depression of internal temperatures mainly due to insufficient heat production offsetting heatloss even during light exercise.

     

Effect of estrogen supplementation on exercise thermoregulation in premenopausal women

This studyexamined the effects of 3 days of estrogen supplementation (ES) onthermoregulation during exercise in premenopausal (20-39 yr) adultwomen during the follicular phase of the menstrual cycle. Subjects (11 control, 10 experimental) performed upright cycle ergometer exercise at60% of maximal O₂ consumption ina neutral environment (25°C, 30% relative humidity) for 20 min. Subjects were given placebo (P) or -estradiol (2 mg/tablet, 3 tablets/day for 3 days). All experiments were conductedbetween 6:30 and 9:00 AM after ingestion of the last tablet. Heartrate, forearm blood flow (FBF), mean skin temperature, esophagealtemperature (T_es), and forearmsweat rate were measured. Blood analysis for estrogen and progesteronereflected the follicular phase of the menstrual cycle. MaximalO₂ consumption (37.1 ± 6.2 in P vs. 38.4 ± 6.3 ml · kg¹ · min¹in ES) and body weight-to-surface area ratio (35.58 ± 2.85 in P vs.37.3 ± 2.7 in ES) were similar between groups. Synthesis of 70-kDaheat shock protein was not induced by 3 days of ES. Neither thethreshold for sweating (36.97 ± 0.15 in P vs. 36.90 ± 0.22°C in ES), the threshold for an increase in FBF (37.09 ± 0.22 in P vs. 37.17 ± 0.26°C in ES), the slope ofsweat rate-T_es relationship (0.42 ± 0.16 in P vs. 0.41 ± 0.17 in ES), nor the FBF-T_es relationship (10.04 ± 4.4 in P vs. 9.61 ± 3.46 in ES) was affected(P > 0.05) by 3 days of ES. Weconclude that 3 days of ES by young adult women in the follicular phaseof their menstrual cycle have no effect on heat transfer to the skin,heat dissipation by evaporative cooling, or leukocyte synthesis of70-kDa heat shock protein.

     

Chronic hormone replacement therapy does not alter resting or maximal skin blood flow

Postmenopausal women on estrogen replacementtherapy (ERT) regulate body core temperature at a lower baseline levelat rest in a thermoneutral environment. We conducted a series ofstudies to test whether, in a thermoneutral environment, chronic (2yr) oral ERT significantly alters baseline skin blood flow (SkBF) andcutaneous vascular conductance (CVC) and whether ERT alters maximal CVC(CVC_max) and SkBF inpostmenopausal women. In the first set of studies, forearm blood flow(FBF) was measured by venous-occlusion plethysmography in 24 postmenopausal women: 8 not taking exogenous hormone therapy (No HRTgroup), 8 on ERT, and 8 receiving combination of estrogen andprogesterone therapy, at rest and during prolonged (1 h) local heatingof the forearm at 42°C. Mean arterial pressure (MAP) was measuredby brachial auscultation before each set of FBF measurements tocalculate forearm vascular conductance (FVC = FBF/MAP). SkBF wasmeasured by laser-Doppler flowmetry (LDF), and CVC was calculated asLDF/MAP and standardized as%CVC_max. Baseline FVC,%CVC_max, and maximal FVC were notsignificantly different among the three groups of women. In the secondset of experiments, LDF in ERT and No HRT groups was measured at restin both thermoneutral and warm environments. %CVC_max was again notsignificantly different between ERT and No HRT groups at thermoneutralambient temperatures and increased similarly in the warm environment.Therefore, chronic exogenous ERT does not appear to influence eitherbaseline or maximal SkBF.

     

Esophageal temperature threshold for sweating decreases before ovulation in premenopausal women

The purpose ofthis study was to test the hypothesis that regulated body temperatureis decreased in the preovulatory phase in eumenorrheic women. Six womenwere studied in both the preovulatory phase (Preov-2;days 9-12), which was 1-2days before predicted ovulation when 17-estradiol(E₂) was estimated to peak, andin the follicular phase (F; days2-6). The subjects walked on a treadmill (~225W · m²)in a warm chamber (ambient temperature = 30°C; dew-pointtemperature = 11.5°C) while heavily clothed.E₂, esophageal temperature(T_es), local skin temperatures,and local sweating rate were measured. The estimate of when theE₂ surge would occur was correctfor four of six subjects. In these four subjects,E₂ increased(P  0.05) from 42.0 ± 24.5 pg/mlduring F to 123.2 ± 31.3 pg/ml during Preov-2. RestingT_es was 37.02 ± 0.20°Cduring F and 36.76 ± 0.28°C during Preov-2(P  0.05). TheT_es threshold for sweating wasdecreased (P  0.05) from 36.88 ± 0.27°C during F to 36.64 ± 0.35°C during Preov-2. Both meanskin and mean body temperatures were decreased during rest in Preov-2group. The hypothesis that regulated body temperature is decreasedduring the preovulatory phase is supported.

     

Moderate exercise increases postexercise thresholds for vasoconstriction and shivering

The purpose of this study was to evaluate theeffect of exercise on the subsequent postexercise thresholds forvasoconstriction and shivering. On two separate days, with six subjects(3 women), a whole body water-perfused suit slowly decreased mean skintemperature (~7.0°C/h) until thresholds for vasoconstriction andshivering were clearly established. Subjects were then rewarmed byincreasing water temperature until both esophageal and mean skintemperatures returned to near-baseline values. Subjects eitherperformed 15 min of cycle ergometry (65% maximalO₂ consumption) followed by 30 minof recovery (Exercise) or remained seated with no exercise for 45 min(Control). Subjects were then cooled again. We mathematically compensated for changes in skin temperatures by using the established linear cutaneous contribution of skin to the control ofvasoconstriction and shivering (20%). The calculated core temperaturethreshold (at a designated skin temperature of 30.0°C) forvasoconstriction increased significantly from 36.64 ± 0.20 to 36.89 ± 0.22°C postexercise (P < 0.01). Similarly, the shivering threshold increased from 35.73 ± 0.13 to 36.13 ± 0.12°C postexercise(P < 0.01). In contrast, sequentialmeasurements, without exercise, demonstrate a time-dependent decreasein both the vasoconstriction (0.10°C) and shivering (0.12°C) thresholds. These data indicate that exercise has a prolonged effect byincreasing the postexercise thresholds for both cold thermoregulatoryresponses.

     

Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women

Brooks, E. M., A. L. Morgan, J. M. Pierzga, S. L. Wladkowski, J. T. O'Gorman, J. A. Derr, and W. L. Kenney. Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women. J. Appl.Physiol. 83(2): 477-484, 1997.This investigationexamined effects of chronic (2 yr) hormone replacement therapy (HRT),both estrogen replacement therapy (ERT) and estrogen plus progesteronetherapy (E+P), on core temperature and skin blood flow responses ofpostmenopausal women. Twenty-five postmenopausal women [9 not onHRT (NO), 8 on ERT, 8 on E+P] exercised on a cycle ergometer for1 h at an ambient temperature of 36°C. Cutaneous vascularconductance (CVC) was monitored by laser-Doppler flowmetry, and forearmvascular conductance (FVC) was measured by using venous occlusionplethysmography. Iontophoresis of bretylium tosylate was performedbefore exercise to block local vasoconstrictor (VC) activity at oneskin site on the forearm. Rectal temperature (T_re) was ~0.5°C lower forthe ERT group (P < 0.01) comparedwith E+P and NO groups at rest and throughout exercise. FVC: mean body temperature (T_b) and CVC:T_b curves were shifted~0.5°C leftward for the ERT group(P < 0.0001). Baseline CVC wassignificantly higher in the ERT group(P < 0.05), but there was nointeraction between bretylium treatment and groups once exercise wasinitiated. These results suggest that1) chronic ERT likely acts centrally to decrease T_re,2) ERT lowers theT_re at which heat-loss effector mechanisms are initiated, primarily by actions on active cutaneous vasodilation, and 3) addition ofexogenous progestins in HRT effectively blocks these effects.

     

Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand

Peripheral vasoconstriction decreases thermalconductance of hypothermic individuals, making it difficult to transferexternally applied heat to the body core. We hypothesizedthat increasing blood flow to the skin of a hypothermic individualwould enhance the transfer of exogenous heat to the body core, therebyincreasing the rate of rewarming. External auditory meatus temperature(T_EAM) was monitored inhypothermic subjects during recovery from general anesthesia. In 10 subjects, heat (45-46°C, water-perfused blanket) was appliedto a single forearm and hand that had been placed in a subatmosphericpressure environment (30 to 40 mmHg) to distend the bloodvessels. Heat alone was applied to control subjects (n = 6). The application ofsubatmospheric pressure resulted in a 10-fold increase in rewarmingrates as determined by changes inT_EAM [13.6 ± 2.1 (SE)°C/h in the experimental group vs. 1.4 ± 0.1°C/h in thecontrol group; P < 0.001]. Inthe experimental subjects, the rate of change ofT_EAM decreased sharply asT_EAM neared the normothermic range.

     

Hypoxia, temperature, and pH/CO2 effects on respiratory discharge from a turtle brain stem preparation

Johnson, Stephen M., Rebecca A. Johnson, and Gordon S. Mitchell. Hypoxia, temperature, andpH/CO₂ effects on respiratory discharge from a turtle brain stem preparation. J. Appl. Physiol. 84(2): 649-660, 1998.An in vitrobrain stem preparation from adult turtles (Chrysemyspicta) was used to examine the effects of anoxia andincreased temperature and pH/CO₂on respiration-related motor output. At pH ~7.45, hypoglossal (XII)nerve roots produced patterns of rhythmic bursts (peaks) of discharge(0.74 ± 0.07 peaks/min, 10.0 ± 0.6 s duration) that werequantitatively similar to literature reports of respiratory activity inconscious, vagotomized turtles. Respiratory discharge was stable for 6 h at 22°C; at 32°C, peak amplitude and frequency progressivelyand reversibly decreased with time. Two hours of hypoxia had no effecton respiratory discharge. Acutely increasing bath temperature from 22 to 32°C decreased episode and peak duration and increased peakfrequency. Changes in pH/CO₂increased peak frequency from zero at pH 8.00-8.10 to maxima of0.81 ± 0.01 and 1.44 ± 0.02 peaks/min at 22°C (pH 7.32) and32°C (pH 7.46), respectively;pH/CO₂ sensitivity was similar atboth temperatures. We conclude that1) insensitivity to hypoxiaindicates that rhythmic discharge does not reflect gasping behavior,2) increased temperature altersrespiratory discharge, and 3)central pH/CO₂ sensitivity isunaffected by temperature in this preparation (i.e.,Q₁₀ ~1.0).

     

Heat stroke: opioid-mediated mechanisms

Romanovsky, Andrej A., and Clark M. Blatteis. Heatstroke: opioid-mediated mechanisms. J. Appl.Physiol. 81(6): 2565-2570, 1996.In our previousstudy in guinea pigs, intensive and prolonged intraperitoneal heating(IPH) caused heat stroke characterized by high mortality andaccompanied by two paradoxical phenomena: ear skin vasoconstriction ata high body temperature (T_b)(hyperthermia-induced vasoconstriction) and a post-IPHT_b fall at an ambient temperature (T_a) below thermoneutrality(hyperthermia-induced hypothermia). In this study, we tested thehypothesis that the mechanisms of the two phenomena involve endogenousopioid agonists. Experiments were conducted in 24 unanesthetized,lightly restrained guinea pigs, each chronically implanted with anintraperitoneal thermode and intrahypothalamic thermocouple. Thethermoregulatory effects of a wide-spectrum opioid-receptor antagonist,naltrexone (NTX; 50 or 0 µmol/kg sc), were studied in IPH-inducedheat stroke and under normal conditions. IPH was accomplished byperfusing (50 ml/min; 80 min) water (45°C) through the thermode.T_a was maintained at ~24°C.Skin vasodilation occurred at the onset of IPH but later changed tovasoconstriction despite high T_band continuing IPH. IPH-induced hyperthermia (1.8 ± 0.1°C) was followed by a post-IPH T_b fall (5.1 ± 0.7°C; calculated for the survivors only). The 48-h mortality ratewas 50%. NTX prevented the hyperthermia-induced vasoconstriction andattenuated the hyperthermia-induced hypothermia (1.8 ± 0.4°C). None of the NTX-treated animals died. The effects of NTX onT_b regulation under normalconditions were minor. These results indicate that the phenomena ofboth hyperthermia-induced vasoconstriction and hyperthermia-inducedhypothermia are opioid dependent. The latter is speculated to reflectopioid-mediated inhibition of metabolism; the former is thought toresult from opioid-induced hemodynamic alterations. Because bothphenomena did not occur in the NTX-treated survivors, the skinvasoconstriction at high T_b andthe posthyperthermia T_b fall maybe viewed as markers of the severity of heat stroke. It is suggestedthat opioid antagonists may have therapeutic potential in heat-induceddisorders.

     

Posthemorrhagic antipyresis: what stage of fever genesis is affected?

Romanovsky, Andrej A., and Yelena K. Karman.Posthemorrhagic antipyresis: what stage of fever genesis isaffected? J. Appl. Physiol. 83(2):359-365, 1997.It has been shown that hemorrhage leads to adecreased thermal responsiveness to lipopolysaccharide (LPS). The aimof this study was to clarify what stage of fever genesis[production of endogenous pyrogens such as interleukin-1 (IL-1),increase of the prostaglandin E₂(PGE₂) concentration in braintissue, activation of cold-defense effectors] is deficient inposthemorrhagic antipyresis. In adult rabbits, we evaluated the effectof acute hemorrhage (15 ml/kg) on the rectal temperature (T_re) responses to LPS fromSalmonella typhi (200 ng/kg iv),ethanol-purified preparation of homologous IL-1 (1 ml from 3.5 × 10⁷ cells, 1.5 ml/kg iv), andPGE₂ (1 µg,intracisternal injection). The effect of hemorrhage onT_re was also studied in afebrilerabbits, both at thermoneutrality (23°C) and during ramp cooling(to 7°C). The hemorrhage strongly attenuated the biphasicLPS-induced fever (a T_re rise of0.4 ± 0.1 instead of 1.2 ± 0.2°C at the time of the secondpeak), the monophasic T_re responseto IL-1 (by ~0.5°C for over 1-5 h postinjection), and thePGE₂-induced hyperthermia (0.4 ± 0.1 vs. 0.9 ± 0.1°C, maxima). In afebrileanimals, the hemorrhage neither affectedT_re at thermoneutrality norchanged the T_re response to coldexposure. The data suggest that neither insufficiency of cold-defenseeffectors nor lack of endogenous mediators of fever (IL-1,PGE₂) can be the only or eventhe major cause of posthemorrhagic antipyresis. Wespeculate that fever genesis is altered at a stage occurring after theintrabrain PGE₂ level is increasedbut before thermoeffectors are activated.

     

Differential effects of phorbol ester (PMA) on blocker-sensitive ENaCs of frog skin and A6 epithelia

Activation ofprotein kinase C with phorbol 12-myristate 13-acetate (PMA) causedcomplex transient perturbations of amiloride-sensitive short-circuitNa⁺ currents(I_Na) in A6epithelia and frog skins that were tissue and concentration dependent.A noninvasive channel blocker pulse method of noise analysis (18) wasused to investigate how PMA caused time-dependent changes of apicalmembrane epithelial Na⁺ channel(ENaC) single-channel currents, channel open probabilities (P_o), andchannel densities(N_T). In A6epithelia, 5 and 50 nM PMA caused within 7 min concentration-dependentsustained decreases ofP_o (~55% belowcontrol, 50 nM) and rapid compensatory transient increases ofN_T within 7 min(~220% above control, 50 nM), resulting in either small transientincreases of I_Naat 5 nM PMA or small biphasic decreases ofI_Na at 50 nM PMA.In contrast to A6 epithelia, 50 and 500 nM PMA in frog skin causedafter a delay of at least 10 min transient increases ofN_T to~60-70% above control at 30-60 min. Unlike A6 epithelia,P_o was increased~15% above control within 7 min and remained within±10-15% of control for the duration of the 2-h experiments.Despite differences in the time courses of secondary inhibition oftransport in A6 epithelia and frog skin, the delayed downregulation oftransport was due to time-dependent decreases ofN_T from theirpreelevated levels in both tissues. WhereasP_o is decreasedwithin minutes in A6 epithelia as measured by noise analysis or bypatch clamp (8), the discrepancy in regulation ofN_T in A6epithelia as measured by noise analysis and patch clamp is most likelyexplained by the inability of on-cell patches formed before treatmentof tissues with PMA to respond to regulation of their channeldensities.

     

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

We used anexercise paradigm with repeated bouts of heavy forearm exercise to testthe hypothesis that alterations in local acid-base environment thatremain after the first exercise result in greater blood flow andO₂ delivery at the onset of the second bout of exercise.Two bouts of handgrip exercise at 75% peak workload were performed for5 min, separated by 5 min of recovery. We continuously measured bloodflow using Doppler ultrasound and sampled venous blood forO₂ content, PCO₂, pH, and lactateand potassium concentrations, and we calculated muscle O₂uptake (O₂). Forearm blood flow waselevated before the second exercise compared with the first andremained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was notdifferent at 5 min. Arteriovenous O₂ content difference waslower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 mlO₂/dl) and higher by 30 s of exercise(11.2 ± 0.7 vs. 10.8 ± 0.7 ml O₂/dl,P < 0.05). Muscle O₂was unchanged before the start of exercise but was elevated during thefirst 30 s of the transition to the second exercise bout(26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood PCO₂, pH, andlactate concentration were consistent with reduced reliance onanaerobic glycolysis at the onset of the second exercise bout. Thesedata show that limitations of muscle blood flow can restrict theadaptation of oxidative metabolism at the onset of heavy muscular exertion.

     

Influence of hydrostatic pressure gradients on regulation of plasma volume after exercise

The impact of posture on the immediate recoveryof intravascular fluid and protein after intense exercise wasdetermined in 14 volunteers. Forces which govern fluid and proteinmovement in muscle interstitial fluid pressure(P_ISF), interstitial colloid osmotic pressure (COP_i), andplasma colloid osmotic pressure(COP_p) were measured before andafter exercise in the supine or upright position. During exercise,plasma volume (PV) decreased by 5.7 ± 0.7 and 7.0 ± 0.5 ml/kgbody weight in the supine and upright posture, respectively. Duringrecovery, PV returned to its baseline value within 30 min regardless ofposture. PV fell below this level by 60 and 120 min in the supine andupright posture, respectively (P < 0.05). Maintenance of PV in the upright position was associated with adecrease in systolic blood pressure, an increase inCOP_p (from 25 ± 1 to 27 ± 1 mmHg; P < 0.05), and an increasein P_ISF (from 5 ± 1 to 6 ± 2 mmHg), whereas COP_i wasunchanged. Increased P_ISFindicates that the hydrostatic pressure gradient favors fluid movementinto the vascular space. However, retention of the recaptured fluid inthe plasma is promoted only in the upright posture because of increasedCOP_p.

     

HSP70 expression in the CNS in response to exercise and heat stress in rats

We havepreviously documented the regional distribution of 70-kDa heat shockprotein (HSP70) in brains of rats made hyperthermic by brief exposureto high-powered microwaves (HPM; 2.06 GHz). We now compare HSP70expression induced by HPM exposure to that induced by exertionaland/or environmental heat stress. Rats were chronicallyimplanted with a temperature probe guide in the hypothalamic region ofthe brain (T_br). After recovery,the following treatment groups were examined: HPM; sham exposed;treadmill exercise at room temperature (24°C; Ex-1); treadmillexercise in a warm environment (34°C; Ex-2); and sedentary groups(Sed-1 and Sed-2), in which ambient temperature was adjusted so thatthe T_br mimicked the T_br in the corresponding exercisegroups. Significant HSP70 expression occurred only in the hyperthermic(Ex-2, Sed-2, and HPM) groups. The pattern of HSP70 expression wassimilar among Ex-2 and Sed-2 rats but differed from that in HPM rats.We conclude that 1) the pattern ofHSP70 expression differs between HPM and nonmicrowave heating, and2) exercise alone was not sufficientto induce central HSP70 expression.

     

Thermogenesis in newborn rats after prenatal or postnatal hypoxia

Oxygenconsumption (O₂)was measured in normoxia as ambient temperature(T_a) was lowered from 40 to15°C, at the rate of 0.5°C/min (thermoneutrality ~33°C).In 2-day-old rats born in hypoxia after hypoxic gestation, theT_a-O₂relationship was as in controls; their interscapular brown adiposetissue (IBAT) was hypoplastic (less proteins and DNA), with lowerconcentration of the mitochondrial uncoupling proteinthermogenin. In 8-day-old rats exposed to hypoxiapostnatally (day 2 today 8), at anyT_a below thermoneutralityO₂ was higher than incontrols; also, in this group IBAT was hypoplastic with decreasedthermogenin. Additional measurements under variousexperimental conditions indicated that the increased thermogeniccapacity was not explained by the smaller body mass and increased bloodoxygen content or by the eventuality of intermittent cold stimuliduring the chronic hypoxia. On the other hand, chronic hypercapnia (3%CO₂ in normoxia, fromday 2 to day8) also resulted in increased normoxic thermogenesis. We conclude that chronic hypoxia in the perinatal period1) reduces IBAT mass andthermogenin concentration and2) can increase the newborn's thermogenic capacity because of stress-related mechanisms not specific to hypoxia.

     

Modification of active cutaneous vasodilation by oral contraceptive hormones

Charkoudian, Nisha, and John M. Johnson. Modificationof active cutaneous vasodilation by oral contraceptive hormones. J. Appl. Physiol. 83(6):2012-2018, 1997.It is not clear whether the alteredthermoregulatory reflex control of the cutaneous circulation seen amongphases of the menstrual cycle also occurs with the synthetic estrogenand progesterone in oral contraceptive pills and whether any suchmodifications include altered control of the cutaneous activevasodilator system. To address these questions, we conducted controlledwhole body heating experiments in seven women at the end of the thirdweek of hormone pills (HH) and at the end of the week of placebo/nopills (LH). A water-perfused suit was used to control body temperature.Laser Doppler flowmetry was used to monitor cutaneous blood flow at acontrol site and at a site at which noradrenergic vasoconstrictorcontrol had been eliminated by iontophoresis of bretylium (BT),isolating the active cutaneous vasodilator system. The oral temperature(T_or) thresholds for cutaneousvasodilation were higher in HH at both control [37.09 ± 0.12 vs. 36.83 ± 0.07°C (LH), P < 0.01] and BT-treated [37.19 ± 0.05 vs. 36.88 ± 0.12°C (LH), P < 0.01]sites. The T_or threshold forsweating was similarly shifted (HH: 37.15 ± 0.11°C vs. LH: 36.94 ± 0.11°C, P < 0.01). Arightward shift in the relationship of heart rate toT_or was seen in HH. Thesensitivities (slopes of the responses vs.T_or) did not differstatistically between phases. The similar threshold shifts at controland BT-treated sites suggest that the hormones shift the function ofthe active vasodilator system to higher internal temperatures. Thesimilarity of the shifts among thermoregulatory effectors suggests acentrally mediated action of these hormones.

     

Sodium alterations in isolated rat heart during cardioplegic arrest

Schepkin, V. D., I. O. Choy, and T. F. Budinger. Sodiumalterations in isolated rat heart during cardioplegic arrest. J. Appl. Physiol. 81(6):2696-2702, 1996.Triple-quantum-filtered (TQF) Na nuclearmagnetic resonance (NMR) without chemical shift reagent is used toinvestigate Na derangement in isolated crystalloid perfused rat heartsduring St. Thomas cardioplegic (CP) arrest. Theextracellular Na contribution to the NMR TQF signal of a rat heart isfound to be 73 ± 5%, as determined by wash-out experiments atdifferent moments of ischemia and reperfusion. With the use of thiscontribution factor, the estimated intracellular Na([Na⁺]_i)TQF signal is 222 ± 13% of preischemic level after 40 min of CParrest and 30 min of reperfusion, and the heart rate pressure productrecovery is 71 ± 8%. These parameters aresignificantly better than for stop-flow ischemia: 340 ± 20% and 6 ± 3%, respectively. At 37°C, the initial delay of 15 min in[Na⁺]_igrowth occurs during CP arrest along with reduced growth later (~4.0%/min) in comparison with stop-flow ischemia (~6.7%/min). The hypothermia (21°C, 40 min) for the stop-flow ischemia and CPdramatically decreases the[Na⁺]_igain with the highest heart recovery for CP (~100%). These studiesconfirm the enhanced sensitivity of TQF NMR to[Na⁺]_iand demonstrate the potential of NMR without chemical shift reagent tomonitor[Na⁺]_iderangements.

     

Regional deposition of inhaled particles in human lungs: comparison between men and women

We measured detailed regional depositionpatterns of inhaled particles in healthy adult male(n = 11; 25 ± 4 yr of age) and female (n = 11; 25 ± 3 yr of age)subjects by means of a serial bolus aerosol delivery technique formonodisperse fine [particle diameter(D_p) = 1 µm] and coarse aerosols(D_p = 3 and 5 µm). The bolus aerosol (40 ml half-width) was delivered to a specificvolumetric depth (Vp) of the lung ranging from 100 to 500 ml with a50-ml increment, and local deposition fraction (LDF) was assessed for each of the 10 local volumetric regions. In all subjects, the deposition distribution pattern was very uneven with respect to Vp,showing characteristic unimodal curves with respect to particle sizeand flow rate. However, the unevenness was more pronounced in women.LDF tended to be greater in all regions of the lung in women than inmen for D_p = 1 µm. For D_p = 3 and 5 µm, LDF showed a marked enhancement in the shallow region of Vp  200 ml in women compared with men(P < 0.05). LDF in women wascomparable to or smaller than those of men in deep lung regions of Vp > 200 ml. Total lung deposition was comparable between men and womenfor fine particles but was consistently greater in women than men forcoarse particles regardless of flow rates used: the difference rangedfrom 9 to 31% and was greater with higher flow rates(P < 0.05). The results indicatethat 1) particledeposition characteristics differ between healthy men and women undercontrolled breathing conditions and2) deposition in women is greaterthan that in men.