Blood-gas measurements adjusted for temperature at three sites during incremental exercise in the horse

Rectal temperature(T_re) is often used to adjustmeasurements of blood gases, but these adjusted measurements may notapproximate temperatures during intense exercise at main sites of gasexchange: muscle and lung. To evaluate differences in blood gasesbetween sites, temperatures (T) were measured with thermocouples in the rectum (re), in mixed venous blood (), ingluteal muscle (mu), and on the skin (sk) in seven Arabian horses asthey underwent an incremental exercise test on a treadmill. Bloodsamples were drawn from the carotid artery and pulmonary artery (mixedvenous) 30 s before each increase in speed and during recovery. Blood gases and pH were measured at 37°C, and all variables were adjusted to T_re,, andT_mu. Adjusted variables duringexercise and recovery were significantly different from each other atthe three sites. Linear and polynomial equations described the timecourse of venous temperature and fromT_re andT_sk during exercise and fromT_sk during recovery.Interpretation of changes in muscle metabolism and gas exchanges basedon blood-gas measurements is improved if they are adjustedappropriately to T_mu or, which may be predicted fromT_sk in addition toT_re during strenuous exercise andfrom T_sk during recovery.

     

Thermoregulatory responses to cold transients: effects of menstrual cycle in resting women

Effects of themenstrual cycle on heat loss and heat production(M) and core and skin temperatureresponses to cold were studied in six unacclimatized female nonsmokers(18-29 yr of age). Each woman, resting supine, was exposed to acold transient (ambient temperature = mean radiant temperature = 20 to5°C at 0.32°C/min, relative humidity = 50 ± 2%, wind speed = 1 m/s) in the follicular (F) phase(days 2-6) and midluteal (L)phase (days 19-23) of her menstrual cycle. Clothed in each of two ensembles with different thermal resistances, women performed multiple experiments in the F andL phases. Thermal resistance was 0.2 and 0.4 m² · K · W¹for ensembles A andB, respectively. Esophagealtemperature (T_es), mean weightedskin temperature(_sk),finger temperature (T_fing), andarea-weighted heat flux were recorded continuously. Rate of heat debt(S) and integrated mean bodytemperature(_b,i)were calculated by partitional calorimetry throughout the cold ramp. Extensive peripheral vasoconstriction in the F phase during early periods of the ramp elevated T_esabove thermoneutral levels. Shivering thermogenesis(M = M  M_basal,W /m²) was highly correlated withdeclines in_sk andT_fing(P <0.0001). There was a reducedslope in M as a function of_b,i inthe L phase with ensembles A(P < 0.02) andB (P < 0.01). Heat flux was higher andS was less in the L phases withensemble A(P < 0.05). An analytic modelrevealed that_sk andT_es contribute as additive inputsand T_fing has a multiplicativeeffect on the total control of Mduring cold transients(R² = 0.9).Endogenous hormonal levels at each menstrual cycle phase, coretemperature and_skinputs, vascular responses, and variations in body heat balance must beconsidered in quantifying thermoregulatory responses in women duringcold stress.

     

Fast and slow components of cerebral blood flow response to step decreases in end-tidal PCO2 in humans

This study examined the dynamics of the middlecerebral artery (MCA) blood flow response to hypocapnia in humans(n = 6) by using transcranial Dopplerultrasound. In a control protocol, end-tidalPCO₂(PET_CO2) was heldnear eucapnia (1.5 Torr above resting) for 40 min. In ahypocapnic protocol, PET_CO2was held near eucapnia for 10 min, then at 15 Torr below eucapnia for20 min, and then near eucapnia for 10 min. During both protocols,subjects hyperventilated throughout andPET_CO2 and end-tidalPO₂ were controlled by using thedynamic end-tidal forcing technique. Beat-by-beat values werecalculated for the intensity-weighted mean velocity (_IWM),signal power (), and theirinstantaneous product(_IWM).A simple model consisting of a delay, gain terms, time constants(_f,on, _f,off) and baseline levels offlow for the on- and off-transients, and a gain term(g_s) and time constant(_s) for a second slower component was fitted to the hypocapnic protocol. The cerebral bloodflow response to hypocapnia was characterized by a significant (P < 0.001) slowprogressive adaptation in_IWM, with g_s = 1.26 %/Torr and_s = 427 s, that persistedthroughout the hypocapnic period. Finally, the responses at the onsetand relief of hypocapnia were asymmetric(P < 0.001), with_f,on (6.8 s) faster than_f,off (14.3 s).

     

Peripheral O2 diffusion does not affect VO2 on-kinetics in isolated in situ canine muscle

To test thehypothesis that muscle O₂ uptake(O₂) on-kinetics islimited, at least in part, by peripheralO₂ diffusion, we determined theO₂ on-kinetics in1) normoxia (Control);2) hyperoxic gas breathing(Hyperoxia); and 3) hyperoxia andthe administration of a drug (RSR-13, Allos Therapeutics), whichright-shifts the Hb-O₂dissociation curve (Hyperoxia+RSR-13). The study was conducted inisolated canine gastrocnemius muscles(n = 5) during transitions from restto 3 min of electrically stimulated isometric tetanic contractions(200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% peakO₂). In all conditions,before and during contractions, muscle was pump perfused withconstantly elevated blood flow (), at a levelmeasured at steady state during contractions in preliminary trials withspontaneous . Adenosine was infusedintra-arterially to prevent inordinate pressure increases with theelevated . was measuredcontinuously, arterial and popliteal venousO₂ concentrations were determinedat rest and at 5- to 7-s intervals during contractions, andO₂ was calculated as · arteriovenous O₂ content difference.PO₂ at 50%HbO₂saturation (P₅₀) was calculated.Mean capillary PO₂(c_O2)was estimated by numerical integration.P₅₀ was higher in Hyperoxia+RSR-13[40 ± 1 (SE) Torr] than in Control and in Hyperoxia (31 ± 1 Torr). After 15 s of contractions,c_O2was higher in Hyperoxia (97 ± 9 Torr) vs. Control (53 ± 3 Torr) and in Hyperoxia+RSR-13 (197 ± 39 Torr) vs. Hyperoxia. Thetime to reach 63% of the difference between baseline and steady-stateO₂ during contractions was 24.7 ± 2.7 s in Control, 26.3 ± 0.8 s in Hyperoxia, and 24.7 ± 1.1 s in Hyperoxia+RSR-13 (not significant). Enhancement ofperipheral O₂ diffusion (obtainedby increasedc_O2at constant O₂ delivery) duringthe rest-to-contraction (60-70% of peakO₂) transition did notaffect muscle O₂on-kinetics.

     

Cardiac output and mixed venous oxygen content measurements by a tracer bolus method: theory

Clark, Justin S., Yuxiang J. Lin, Michael J. Criddle,Antonio G. Cutillo, Adelbert H. Bigler, Fred L. Farr, and Attilio D. Renzetti, Jr. Cardiac output and mixed venous oxygen content measurements by a tracer bolus method: theory. J. Appl.Physiol. 83(3): 884-896, 1997.We present a bolus method ofinert-gas delivery to the lungs that facilitates application ofmultiple inert gases and the multiple inert-gas-exchange technique(MIGET) model to noninvasive measurements of cardiac output (CO) andcentral mixed venous oxygen contentReduction in recirculation error is made possible by 1)replacement of sinusoidal input functions with impulse inputs and2) replacement of steady-state analyses with transientanalyses. Recirculation error reduction increases the inert-gasselection to include common gases without unusually high (and difficultto find) tissue-to-blood partition coefficients for maximizing thesystemic filtering efficiency. This paper also presents a practicalmethod for determining the recirculation contributions to inert expiredprofiles in animals and determining their specific contributions toerrors in the calculations of CO and from simulationsapplied to published ventilation-perfusion ratio(/) profiles.Recirculation errors from common gases were found to be reducible tothe order of 5% or less for both CO and whereassimulation studies indicate that measurement bias contributions fromrecirculation, / mismatch, andthe / extractionprocess can be limited to 15% for subjects with severe/ mismatch and high inspiredoxygen fraction levels. These studies demonstrate a decreasinginfluence of / mismatch onparameter extraction bias as the number of inert gases are increased.However, the influence of measurement uncertainty on parameterextraction error limits improvement to six gases.

     

Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress

The purpose ofthe present study was to determine the separate and combined effects ofaerobic fitness, short-term heat acclimation, and hypohydration ontolerance during light exercise while wearing nuclear, biological, andchemical protective clothing in the heat (40°C, 30% relativehumidity). Men who were moderately fit [(MF); <50ml · kg¹ · min¹maximal O₂ consumption;n = 7] and highly fit[(HF); >55ml · kg¹ · min¹maximal O₂ consumption;n = 8] were tested while theywere euhydrated or hypohydrated by ~2.5% of body mass throughexercise and fluid restriction the day preceding the trials. Tests wereconducted before and after 2 wk of daily heat acclimation (1-htreadmill exercise at 40°C, 30% relative humidity, while wearingthe nuclear, biological, and chemical protective clothing). Heatacclimation increased sweat rate and decreased skin temperature andrectal temperature (T_re) in HF subjects but had no effecton tolerance time (TT). MF subjects increased sweat rate but did notalter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased T_re and heart rate and decreasedthe respiratory exchange ratio and the TT regardless of acclimationstate. Overall, the rate of rise of skin temperature was less, whileT_re, the rate of rise of T_re, and the TTwere greater in HF than in MF subjects. It was concluded thatexercise-heat tolerance in this uncompensable heat-stress environmentis not influenced by short-term heat acclimation but is significantlyimproved by long-term aerobic fitness.

     

Pulmonary gas exchange during exercise in pigs

Increased ventilation-perfusion(A/)inequality is observed in ~50% of humans during heavy exercise andcontributes to the widening of the alveolar-arterialO₂ difference(A-aD_O2). Despite extensive investigation, the cause remains unknown. As a firststep to more direct examination of this problem, we developed an animalmodel. Eight Yucatan miniswine were studied at rest and duringtreadmill exercise at ~30, 50, and 85% of maximalO₂ consumption (O_{2 max}). Multipleinert-gas, blood-gas, and metabolic data were obtained. TheA-aD_O2increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr duringthe heaviest exercise level, but arterialPO₂(Pa_O2) remained at resting levels during exercise. There was normalA/inequality [log SD of the perfusion distribution(log) = 0.42 ± 0.04] at rest, and moderate increases(log = 0.68 ± 0.04, P < 0.0001) wereobserved with exercise. This result was reproducible on a separate day.TheA/inequality changes are similar to those reported in highly trainedhumans. However, in swine, unlike in humans, there was no inert gasevidence for pulmonary end-capillary diffusion limitation during heavyexercise; there was no systematic difference in the measuredPa_O2 and the Pa_O2 as predicted from the inertgases. These data suggest that the pig animal model iswell suited for studying the mechanism of exercise-inducedA/ inequality.

     

Effects of CO2-HCO<SUP>&minus;</SUP><SUB>3</SUB> on catecholamine efflux from cat carotid body

Iturriaga, Rodrigo, and Julio Alcayaga. Effects ofCO₂-on catecholamine efflux from cat carotid body. J. Appl. Physiol. 84(1): 60-68, 1998.Using achronoamperometric technique with carbon-fiber microelectrodes andneural recordings, we simultaneously measured the effects of thefollowing procedures on catecholamine efflux (CA) andfrequency of chemosensory discharges (f_x) fromsuperfused cat carotid body: 1) theaddition ofCO₂- to Tyrode solution previously buffered withN-2-hydroxyethylpiperazine-N -2-ethanesulfonicacid, maintaining pH at 7.40; 2)hypercapnia (10% CO₂, pH 7.10);3) hypoxia(PO₂ h  40 Torr) with andwithoutCO₂-;and 4) the impact of several bolusesof dopamine (DA; 10-100 µg) on hypoxic and hypercapnic challenges. WithCO₂-,hypoxia increased f_x which preceded CAincreases, whereas hypercapnia raised f_x but didnot consistently increase CA. Repeated stimuli induced similarf_x increases, but attenuated CA. AfterDA, hypoxia produced larger CA, which preceded chemosensoryresponses. WithoutCO₂-, hypoxia produced a similar pattern of CA andf_x responses. Switching to Tyrode solution withCO₂-at pH 7.40 raised f_x but did not increase CA.WithCO₂- and after DA, hypoxic-induced CAs were larger than in its absence. Results suggest that DA release is not essential for chemosensory excitation.

     

Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition

Cardenas, Victor, Jr., Thomas A. Heming, and Akhil Bidani.Kinetics of CO₂ excretion andintravascular pH disequilibria during carbonic anhydrase inhibition.J. Appl. Physiol. 84(2): 683-694, 1998.Inhibition of carbonic anhydrase (CA) activity (activity in redblood cells and activity available on capillary endothelium) results indecrements in CO₂ excretion(CO₂) and plasma-erythrocyteCO₂--H⁺disequilibrium as blood travels around the circulation. To investigate the kinetics of changes in blood PCO₂and pH during progressive CA inhibition, we used our previouslydetailed mathematical model of capillary gas exchange to analyzeexperimental data of CO₂ and blood-gas/pH parameters obtained from anesthetized, paralyzed, andmechanically ventilated dogs after treatment with acetazolamide (Actz,0-100 mg/kg iv). Arterial and mixed venous blood samples werecollected via indwelling femoral and pulmonary arterial catheters, respectively. Cardiac output was measured by thermodilution. End-tidal PCO₂, as a measure of alveolarPCO₂, was obtained from continuousrecords of airway PCO₂ above thecarina. Experimental results were analyzed with the aid of amathematical model of lung and tissue-gas exchange. Progressive CAinhibition was associated with stepwise increments in the equilibratedmixed venous-alveolar PCO₂ gradient(9, 19, and 26 Torr at 5, 20, and 100 mg/kg Actz, respectively). Themaximum decrements in CO₂were 10, 24, and 26% with 5, 20, and 100 mg/kg Actz, respectively,without full recovery ofCO₂ at 1 h postinfusion. Equilibrated arterial PCO₂overestimated alveolar PCO₂, andtissue PCO₂ was underestimated by themeasured equilibrated mixed venous bloodPCO₂. Mathematical model computations predicted hysteresis loops of the instantaneousCO₂--H⁺relationship and in vivo bloodPCO₂-pH relationship due to thefinite reaction times forCO₂--H⁺reactions. The shape of the hysteresis loops was affected by the extentof Actz inhibition of CA in red blood cells and plasma.

     

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.

     

Neural-mechanical coupling of breathing in REM sleep

Smith, C. A., K. S. Henderson, L. Xi, C.-M. Chow, P. R. Eastwood, and J. A. Dempsey. Neural-mechanical coupling of breathing in REM sleep. J. Appl.Physiol. 83(6): 1923-1932, 1997.During rapid-eye-movement (REM) sleep theventilatory response to airway occlusion is reduced. Possiblemechanisms are reduced chemosensitivity, mechanical impairment of thechest wall secondary to the atonia of REM sleep, or phasic REM eventsthat interrupt or fractionate ongoing diaphragm electromyogram (EMG)activity. To differentiate between these possibilities, we studiedthree chronically instrumented dogs before, during, and after15-20 s of airway occlusion during non-REM (NREM) and phasic REMsleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG(Di) was similar or reduced in REM sleep relativeto NREM sleep; 2) for a givenDi in response to airway occlusion and thehyperpnea following occlusion, the mechanical output (flow or pressure)was similar or reduced during REM sleep relative to NREM sleep;3) for comparable durations ofairway occlusion the Di and integratedinspiratory tracheal pressure tended to be smaller and more variable inREM than in NREM sleep, and 4)significant fractionations (caused visible changes in trachealpressure) of the diaphragm EMG during airway occlusion inREM sleep occurred in ~40% of breathing efforts. Thus reducedand/or erratic mechanical output during and after airwayocclusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributable largely to reduced neural activity of the diaphragm, which in turn is likely attributable to REM effects, causing reduced chemosensitivity at the level of theperipheral chemoreceptors or, more likely, at the central integrator.Chest wall distortion secondary to the atonia of REM sleep maycontribute to the reduced mechanical output following airway occlusionwhen ventilatory drive is highest.

     

THERMOREGULATORY EFFECT IN HUMANS OF SUPPRESSED ENDOGENOUS MELATONIN BY PRE-SLEEP BRIGHT-LIGHT EXPOSURE IN A COLD ENVIRONMENT

This study investigated the physiological function of suppressed melatonin through thermoregulation in a cold environment. Interactions between thermoregulation directly affected by exposure to a cold environment and indirectly affected by endogenous melatonin suppression by bright-light exposure were examined. Ten male subjects were exposed to two different illumination intensities (30 and 5000 lux) for 4.5?h, and two different ambient temperatures (15 and 27°C) for 2?h before sleep under dark and thermoneutral conditions. Salivary melatonin level was suppressed by bright light (p?<?0.001), although the ambient temperature condition had no significant effect on melatonin. During sleep, significant effects of pre-sleep exposure to a cold ambient temperature (p?<?0.001) and bright light (p?<?0.01) on rectal temperature (T_re) were observed. Pre-sleep, bright-light exposure led to an attenuated fall in T_re during sleep. Moreover, T_re dropped more precipitously after cold exposure than thermoneutral conditions (cold: ?0.54?±?0.07°C/h; thermoneutral: ?0.16?±?0.03°C/h; p?<?0.001). Pre-sleep, bright-light exposure delayed the nadir time of T_re under thermoneutral conditions (p?<?0.05), while cold exposure masked the circadian rhythm with a precipitous decrease in T_re. A significant correlation between the T_re nadir and melatonin level (r?=??0.774, p?<?0.05) indicated that inter-individual differences with higher melatonin levels lead to a reduction in T_re after cold exposure. These results suggest that suppressed endogenous melatonin inhibits the downregulation of the body temperature set-point during sleep. (Author correspondence: ishibasi@design.kyushu-u.ac.jp)     

Is urodilatin the missing link in exercise-dependent renal sodium retention?

Schmidt, W., A. Bub, M. Meyer, T. Weiss, D. Schneider, N. Maassen, and W. G. Forssmann. Is urodilatin the missing link inexercise-dependent renal sodium retention? J. Appl.Physiol. 84(1): 123-128, 1998.The purpose of thepresent study was to investigate the behavior of plasma atrialnatriuretic peptide [ANP-(99126)] concentration([ANP]) and renal urodilatin [Uro; ANP-(95126)] excretion during and after exercise and theirpossible effects on renal Na⁺retention. Ten male subjects performed a cycle ergometer test for 60 min at 60% of maximum workload. Blood and urine samples were collectedbefore, during, and up to 24 h after exercise. During exercise, plasma[ANP] and renal Uro excretion were oppositely affected:whereas [ANP] increased from 46.5 ± 5.1 to 124.1 ± 10.6 pg/ml, urinary Uro excretion decreased from 120.8 ± 16.0 to49.5 ± 9.8 fmol/min and remained at a lower level until 1 h afterexercise. Glomerular filtration rate showed lowest values duringexercise (from 164.9 ± 15.3 to 75.8 ± 10.1 ml/min), and urineflow and the fractional excretion rate ofNa⁺(FE_Na⁺) andCl()had their nadir during the first hour after exercise. Positiverelationships were observed between Uro excretion andFE_Na⁺(P < 0.05) and, whereas a tendency toward a negative correlation was obtained between[ANP] andFE_Na⁺. It seemspossible that Uro may be, among other factors, involved in theexercise-related regulation of renalNa⁺ retention. The specific rolesUro and ANP play during exercise, however, remain to be investigated.

     

Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis

Shah, Ashish R., Thomas G. Keens, and David Gozal.Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis. J. Appl.Physiol. 83(5): 1641-1647, 1997.The effects ofsupplemental O₂ on recovery fromsupramaximal exercise and subsequent performance remain unknown. Ifrecovery from exercise could be enhanced in individuals with chroniclung disease, subsequent supramaximal exercise performance could also be improved. Recovery from supramaximal exercise and subsequent supramaximal exercise performance were assessed after 10 min of breathing 100% O₂ or room air(RA) in 17 cystic fibrosis (CF) patients [25 ± 10 (SD) yrold, 53% men, forced expired volume in 1 s = 62 ± 21%predicted] and 17 normal subjects (25 ± 8 yr old, 59% men,forced expired volume in 1 s = 112 ± 15% predicted). Supramaximalperformance was assessed as the work of sustained bicycling at a loadof 130% of the maximum load achieved during a graded maximal exercise.Peak minute ventilation(E) andheart rate (HR) were lower in CF patients at the end of eachsupramaximal bout than in controls. In CF patients, single-exponentialtime decay constants indicated faster recovery of HR(_HR = 86 ± 8 and 73 ± 6 s in RA and O₂,respectively, P < 0.01). Similarly, fast and slow time constants of two-exponential equations providing thebest fit for ventilatory recovery were improved in CF patients duringO₂ breathing ( = 132.1 ± 10.5 vs. 82.5 ± 10.4 s; = 880.3 ± 300.1 vs. 368.6 ± 107.1 s,P < 0.01). However, no such improvements occurred in controls. Supramaximal performance after O₂ improved in CF patients (109 ± 6% of the 1st bout after O₂ vs. 94 ± 6% in RA, P < 0.01).O₂ supplementation had no effect on subsequent performance in controls (97 ± 3% inO₂ vs. 93 ± 3% in RA). Weconclude that supplemental O₂after a short bout of supramaximal exercise accelerates recovery andpreserves subsequent supramaximal performance in patients with CF.

     

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.

     

Quantitative analysis of transpleural flux in the isolated lung

Li, M. H., J. Hildebrandt, and M. P. Hlastala.Quantitative analysis of transpleural flux in the isolated lung.J. Appl. Physiol. 82(2): 545-551, 1997.In this study, the loss of inert gas through the pleura of anisolated ventilated and perfused rabbit lung was assessed theoreticallyand experimentally. A mathematical model was used to represent an idealhomogeneous lung placed within a box with gas flow(box) surrounding the lung. Thealveoli are assumed to be ventilated with room air(A) andperfused at constant flow () containinginert gases (x) with various perfusate-air partition coefficients(_p,x).The ratio of transpleural flux of gas(pl_x)to its total delivery to the lung via pulmonary artery( ),representing fractional losses across the pleura, can be shown todepend on four dimensionless ratios:1)_p,x,2) the ratio of alveolar ventilation to perfusion(A/), 3) the ratioof the pleural diffusing capacity(Dpl_x) to the conductance ofthe alveolar ventilation (Dpl_x /A_g,where _g is the capacitancecoefficient of gas), and 4) theratio of extrapleural (box) ventilation to alveolar ventilation(box/A).Experiments were performed in isolated perfused and ventilated rabbitlungs. The perfusate was a buffer solution containing six dissolvedinert gases covering the entire 10⁵-fold range of_p,x usedin the multiple inert gas elimination technique. Steady-state inert gasconcentrations were measured in the pulmonary arterial perfusate,pulmonary venous effluent, exhaled gas, and box effluent gas. Theexperimental data could be described satisfactorily by thesingle-compartment model. It is concluded that a simple theoreticalmodel is a useful tool for predicting transpleural flux from isolatedlung preparations, with known ventilation and perfusion, for inertgases within a wide range of .

     

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.

     

Cerebellar modulation of cough motor pattern in cats

Xu, Fadi, Donald T. Frazier, Zhong Zhang, David M. Baekey,and Roger Shannon. Cerebellar modulation of cough motor pattern incats. J. Appl. Physiol. 83(2):391-397, 1997.The cerebellum modulates respiratory muscleactivity in part via its influence on the central respiratory patterngenerator. Because coughing requires well-coordinated respiratorymuscle activity, studies were conducted to determine whether thecerebellum influences the centrally generated cough motor pattern.Integrated phrenic and lumbar efferent neurograms(PN and LN, respectively)were monitored in decerebrated, paralyzed, and ventilated cats.Mechanical probing of the intrathoracic trachea was used to evokefictive coughs; i.e., large increases inPN and LN amplitudes.Cerebellectomy resulted in a decrease in the number of coughsper trial (cough frequency) and LN peakamplitudes without any consistent change inPN peak amplitudes. Cerebellar nuclei [therostral interposed nucleus (INr) and the rostral fastigial nucleus(FNr)] known to be involved in respiratory control were ablatedto determine their potential role in the cough response. Control(eupneic) respiratory frequency was not affected by cerebellectomy orINr/FNr lesions. Cough frequency was depressed by lesion of the INr butnot by ablation of the FNr. No significant changes inPN and LN amplitudes wereobserved after lesion of either the INr or FNr. These results suggestthat the cerebellum, specifically the INr, is involved in modulation ofthe frequency of centrally generated coughing.

     

RTN TRH causes prolonged respiratory stimulation

Cream, Carlos L., Aihua Li, and Eugene E. Nattie. RTNTRH causes prolonged respiratory stimulation. J. Appl.Physiol. 83(3): 792-799, 1997.We injectedthyrotropin-releasing hormone (TRH; 10 nl; 0.25, 0.5, 1.0, or 10 mM),its inactive free acid form (TRHOH; 1 mM), or a metabolite with lowTRH-receptor binding affinity, histidine-proline diketopiperazine (cHP;1 mM), into the retrotrapezoid nucleus of anesthetized rats. Injectionlocation was verified by anatomic analysis. Lower doses (0.25-0.5mM) significantly increased both the product of integrated phrenicamplitude and frequency(Phr · f) and f for 20-30min compared with artificial cerebrospinal fluid control injections. Higher doses (1.0-10 mM) produced greater and long-lastingstimulation of Phr · f,Phr, and f and of blood pressure. Thisstimulation reached values 150% of baseline and durations of 270 minafter a single injection. TRHOH (1 mM ) or cHP (1 mM) had no effect onPhr but increased f, as did 1 mM TRH. We concludethat TRH has a very powerful stimulatory effect in the retrotrapezoidnucleus region on Phr · f, withthe Phr response seemingly specific for TRHreceptors. Similar responses of f to TRHOH and cHP suggest it may benonspecific.

     

Thermal drive contributes to hyperventilation during exercise in sheep

The etiology of exercise hypocapnia is unknown.The contributions of exercise intensity (ExInt), lactic acid,environmental temperature, rectal temperature(T_re), and physicalconditioning to the variance in arterialCO₂ tension(Pa_CO2) in the exercising sheep werequantified. We hypothesized that thermal drive contributes tohyperventilation. Four unshorn sheep were exercised at ~30, 50, and70% of maximal O₂ consumption for30 min, or until exhaustion, both before and after 5 wk of physicalconditioning. In addition, two of the sheep were shorn and exercised ateach intensity in a cold (<15°C) environment.T_re andO₂ consumption were measured continuously. Lactic acid and Pa_CO2 weremeasured at 5- to 10-min intervals. Data wereanalyzed by multiple regression onPa_CO2. During exercise,T_re rose andPa_CO2 fell, except at the lowest ExIntin the cold environment. T_reexplained 77% of the variance in Pa_CO2,and ExInt explained 5%. All other variables were insignificant. Weconclude that, in sheep, thermal drive contributes to hyperventilation during exercise.