Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia

Goheen, M. S. L., M. B. Ducharme, G. P. Kenny, C. E. Johnston, John Frim, Gerald K. Bristow, and Gordon G. Giesbrecht. Efficacy of forced-air and inhalation rewarming by using a humanmodel for severe hypothermia. J. Appl.Physiol. 83(5): 1635-1640, 1997.We recentlydeveloped a nonshivering human model for severe hypothermia by usingmeperidine to inhibit shivering in mildly hypothermic subjects. Thisthermal model was used to evaluate warming techniques. On threeoccasions, eight subjects were immersed for ~25 min in 9°C water.Meperidine (1.5 mg/kg) was injected before the subjects exited thewater. Subjects were then removed, insulated, and rewarmed in anambient temperature of 20°C with either1) spontaneous rewarming (control),2) inhalation rewarming withsaturated air at ~43°C, or 3)forced-air warming. Additional meperidine (to a maximumcumulative dose of 2.5 mg/kg) was given to maintain shiveringinhibition. The core temperature afterdrop was 30-40% less duringforced-air warming (0.9°C) than during control (1.4°C) andinhalation rewarming (1.2°C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-airwarming (2.40°C/h) than during control (0.41°C/h) andinhalation rewarming (0.23°C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.

     

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.

     

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.

     

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.

     

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).

     

Spirometry with a Fleisch pneumotachograph: upstream heat exchanger replaces heating requirement

Miller, Martin R., Ole F. Pedersen, and Torben Sigsgaard.Spirometry with a Fleisch pneumotachograph: upstream heat exchanger replaces heating requirement. J. Appl.Physiol. 82(4): 1053-1057, 1997.The exacttemperature of the head of an unheated Fleisch pneumotachograph (PT)during recording is not known, and variation in its temperature maylead to errors in measuring spirometric indexes. We measured PT headtemperature during blows from five normal subjects, recorded by using aPT with and without an upstream heat exchanger to condition the air tothe ambient temperature that was set in a climate chamber. Group mean(±SD) temperature of a thermocouple (TC) placed inside the PT headwas 11.8 ± 1.9°C with 7°C ambient, 25.4 ± 1.3°C at23°C, and was 37.2 ± 0.3°C at 37°C. The between-subjectrange of temperature for this TC was 7.5° at 7°C, 5.5° at23°C, and 1.1° at 37°C. The mean within-subject within-blowvariation of temperature for this TC was 10.0° and 3.3°C forambient of 7° and 23°C, respectively. At the usual ambient temperature in a laboratory, these differences in temperature lead to a3.6% between-subject bias in recording, and the within-subject differences lead to 2.6% underreading of peak expiratory flow and a0.5% overreading later in the blow, which makesATPS-to-BTPS correction erroneous or difficult to perform. With the use of anupstream heat exchanger, the group mean temperature was 8.7 ± 0.4°, 23.2 ± 0.2°, and 37.1 ± 0.2°C atthe three ambient temperatures, respectively, and the within-subjectwithin-blow variation was reduced to <1°C. A heat exchangerplaced upstream of the PT satisfactorily conditioned expired air to theambient temperature and removed the error.

     

Hypohydration and thermoregulation in cold air

O'Brien, Catherine, Andrew J. Young, and Michael N. Sawka.Hypohydration and thermoregulation in cold air.J. Appl. Physiol. 84(1): 185-189, 1998.This study examined the effects of hypohydration onthermoregulation during cold exposure. In addition, the independentinfluences of hypohydration-associated hypertonicity and hypovolemiawere investigated. Nine male volunteers were monitored for 30 min at25°C, then for 120 min at 7°C, under three counterbalancedconditions: euhydration (Eu), hypertonic hypohydration (HH), andisotonic hypohydration (IH). Hypohydration was achieved 12 h beforecold exposure by inducing sweating (HH) or by ingestion of furosemide(IH). Body weight decrease (4.1 ± 0.2%) caused by hypohydrationwas similar for HH and IH, but differences(P < 0.05) were found between HH andIH in plasma osmolality (292 ± 1 vs. 284 ± 1 mosmol/kgH₂O) andplasma volume reduction (8 ± 2 vs. 18 ± 3%).Heat debt (349 ± 14 among) did not differ(P > 0.05) among trials. Mean skintemperature decreased throughout cold exposure during Eu but plateauedafter 90 min during HH and IH. Forearm-fingertemperature gradient tended (P = 0.06)to be greater during Eu (10.0 ± 0.7°C) than during HH or IH(8.9 ± 0.7°C). This suggests weaker vasoconstrictor tone duringhypohydration than during Eu. Final mean skin temperature was higherfor HH than for Eu or IH (23.5 ± 0.3, 22.6 ± 0.4, and 22.9 ± 0.3°C, respectively), and insulation was lower on HH than onIH (0.13 ± 0.01 vs. 0.15 ± 0.01°C · W¹ · m²,respectively), but not with Eu (0.14 ± 0.01°C · W¹ · m²).This provides some evidence that hypertonicity impairs the vasoconstrictor response to cold. Although mild hypohydration did notaffect body heat balance during 2-h whole body exposure to moderatecold, hypohydration-associated hypertonicity may have subtle effects onvasoconstriction that could become important during a more severe coldexposure.

     

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.

     

Intravenous vs. oral rehydration: effects on subsequent exercise-heat stress

Castellani, John W., Carl M. Maresh, Lawrence E. Armstrong,Robert W. Kenefick, Deborah Riebe, Marcos Echegaray, Douglas Casa, andV. Daniel Castracane. Intravenous vs. oral rehydration: effects onsubsequent exercise-heat stress. J. Appl.Physiol. 82(3): 799-806, 1997.This studycompared the influence of intravenous vs. oral rehydration afterexercise-induced dehydration during a subsequent 90-min exercisebout. It was hypothesized that cardiovascular, thermoregulatory, and hormonal variables would be the same between intravenous and oral rehydration because of similar restoration ofplasma volume (PV) and osmolality (Osmo). Eight non-heat-acclimated menreceived three experimental treatments (counterbalanced design) immediately after exercise-induced dehydration (33°C) to 4%body weight loss. Treatments were intravenous 0.45% NaCl (iv; 25 ml/kg), no fluid (NF), and oral saline (Oral; 25 ml/kg).After rehydration and rest (2 h total), subjects walked at 50% maximalO₂ consumption for up to 90 min at36°C. The following observations were made: 1) heart rate was higher(P < 0.05) in Oral vs. ivat minutes 45, 60, and75 of exercise;2) rectal temperature, sweat rate, percent change in PV, and change in plasma Osmo were similar between ivand Oral; 3) change in plasmanorepinephrine decreased less (P < 0.05) in Oral compared with iv at minute45; 4) changes in plasma adrenocorticotropic hormone and cortisol were similar between ivand Oral after exercise was initiated; and5) exercise time was similar betweeniv (77.4 ± 5.4 min) and Oral (84.2 ± 2.3 min). These datasuggest that after exercise-induced dehydration, iv and Oral wereequally effective as rehydration treatments. Thermoregulation, changein adrenocorticotropic hormone, and change in cortisol were notdifferent between iv and Oral after exercise began; this is likely dueto similar percent change in PV and change in Osmo.

     

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.

     

Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans

Ramires, P. R., C. L. M. Forjaz, C. M. C. Strunz, M. E. R. Silva, J. Diament, W. Nicolau, B. Liberman, and C. E. Negrão. Oral glucose ingestion increases endurance capacity in normal anddiabetic (type I) humans. J. Appl.Physiol. 83(2): 608-614, 1997.The effects of anoral glucose administration (1 g/kg) 30 min before exercise onendurance capacity and metabolic responses were studied in 21 type Idiabetic patients [insulin-dependent diabetes mellitus(IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55-60% of maximalO₂ uptake) was performed untilexhaustion. Glucose administration significantly increased endurancecapacity in Con (112 ± 7 vs. 125 ± 6 min,P < 0.05) but only in IDDM patientswhose blood glucose decreased during exercise (70.8 ± 8.2 vs. 82.8 ± 9.4 min, P < 0.05).Hyperglycemia was normalized at 15 min of exercise in Con (7.4 ± 0.2 vs. 4.8 ± 0.2 mM) but not in IDDM patients (12.4 ± 0.7 vs.15.6 ± 0.9 mM). In Con, insulin and C-peptide levels werenormalized during exercise. Glucose administration decreased growthhormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in someIDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.

     

Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata

Lopatko, Olga V., Sandra Orgeig, Christopher B. Daniels, andDavid Palmer. Alterations in the surface propertiesof lung surfactant in the torpid marsupial Sminthopsiscrassicaudata. J. Appl.Physiol. 84(1): 146-156, 1998.Torpor changes thecomposition of pulmonary surfactant (PS) in the dunnartSminthopsis crassicaudata [C.Langman, S. Orgeig, and C. B. Daniels. Am. J. Physiol. 271 (Regulatory IntegrativeComp. Physiol. 40): R437-R445, 1996]. Herewe investigated the surface activity of PS in vitro. Five micrograms ofphospholipid per centimeter squared surface area of whole lavage (frommice or from warm-active, 4-, or 8-h torpid dunnarts) were applieddropwise onto the subphase of a Wilhelmy-Langmuir balance at 20°Cand stabilized for 20 min. After 4 h of torpor, the adsorption rateincreased, and equilibrium surface tension (ST_eq), minimal surface tension(ST_min), and the %areacompression required to achieveST_min decreased, compared with thewarm-active group. After 8 h of torpor,ST_min decreased [from 5.2 ± 0.3 to 4.1 ± 0.3 (SE) mN/m]; %area compressionrequired to achieve ST_min decreased (from 43.4 ± 1.0 to 27.4 ± 0.8); the rate ofadsorption decreased; and ST_eqincreased (from 26.3 ± 0.5 to 38.6 ± 1.3 mN/m). ST-areaisotherms of warm-active dunnarts and mice at 20°C had a shoulderon compression and a plateau on expansion. These disappeared on theisotherms of torpid dunnarts. Samples of whole lavage (from warm-activeand 8-h torpor groups) containing 100 µg phospholipid/ml were studiedby using a captive-bubble surfactometer at 37°C. After 8 h oftorpor, ST_min increased (from 6.4 ± 0.3 to 9.1 ± 0.3 mN/m) and %area compressiondecreased in the 2nd (from 88.6 ± 1.7 to 82.1 ± 2.0) and 3rd(from 89.1 ± 0.8 to 84.9 ± 1.8) compression-expansion cycles, compared with warm-active dunnarts. ST-area isotherms ofwarm-active dunnarts at 37°C did not have a shoulder oncompression. This shoulder appeared on the isotherms of torpiddunnarts. In conclusion, there is a strong correlation between in vitrochanges in surface activity and in vivo changes in lipid composition of PS during torpor, although static lung compliance remained unchanged (see Langman et al. cited above). Surfactant from torpid animals ismore active at 20°C and less active at 37°C than that ofwarm-active animals, which may represent a respiratory adaptation tolow body temperatures of torpid dunnarts.

     

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.

     

Left ventricular dysfunction following rewarming from experimental hypothermia

This study was aimed at elucidating whetherventricular hypothermia-induced dysfunction persisting after rewarmingthe unsupported in situ dog heart could be characterized as a systolic,diastolic, or combined disturbance. Core temperature of 8 mongrel dogswas gradually lowered to 25°C and returned to 37°C over aperiod of 328 min. Systolic function was described by maximum rate ofincrease in left ventricular (LV) pressure(dP/dt_max),relative segment shortening (SS%), stroke volume (SV), and theload-independent contractility index, preload recruitable stroke work(PRSW). Diastolic function was described by the isovolumic relaxationconstant () and the LV wall stiffness constant(K_p). Comparedwith prehypothermic control, a significant decrease in LV functionalvariables was measured at 25°C:dP/dt_max 2,180 ± 158 vs. 760 ± 78 mmHg/s, SS% 20.1 ± 1.2 vs.13.3 ± 1.0%, SV 11.7 ± 0.7 vs. 8.5 ± 0.7 ml, PRSW 90.5 ± 7.7 vs. 29.1 ± 5.9 J/m · 10²,K_p 0.78 ± 0.10 vs. 0.28 ± 0.03 mm¹, and  78.5 ± 3.7 vs. 25.8 ± 1.6 ms. After rewarming, the significant depression ofLV systolic variables observed at 25°C persisted: dP/dt_max 1,241 ± 108 mmHg/s, SS% 10.2 ± 0.8 J, SV 7.3 ± 0.4 ml, and PRSW52.1 ± 3.6 m · 10², whereasthe diastolic values ofK_p and  returned to control. Thus hypothermia induced a significant depressionof both systolic and diastolic LV variables. After rewarming, diastolicLV function was restored, in contrast to the persistently depressed LVsystolic function. These observations indicate that cooling inducesmore long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction than on sarcoplasmicreticulum Ca²⁺trapping dysfunction or interstitial fluid content, makingposthypothermic LV dysfunction a systolic perturbation.

     

Effect of heat stress on glucose kinetics during exercise

Hargreaves, Mark, Damien Angus, Kirsten Howlett, Nelly MarmyConus, and Mark Febbraio. Effect of heat stress on glucose kinetics during exercise. J. Appl.Physiol. 81(4): 1594-1597, 1996.To identify themechanism underlying the exaggerated hyperglycemia during exercise inthe heat, six trained men were studied during 40 min of cyclingexercise at a workload requiring 65% peak pulmonary oxygen uptake(O_{2 peak}) on twooccasions at least 1 wk apart. On one occasion, the ambient temperaturewas 20°C [control (Con)], whereas on the other, it was40°C [high temperature (HT)]. Rates ofglucose appearance and disappearance were measured by using a primedcontinuous infusion of[6,6-²H]glucose. Nodifferences in oxygen uptake during exercise were observed betweentrials. After 40 min of exercise, heart rate, rectal temperature,respiratory exchange ratio, and plasma lactate were all higher in HTcompared with Con (P < 0.05). Plasmaglucose levels were similar at rest (Con, 4.54 ± 0.19 mmol/l; HT,4.81 ± 0.19 mmol/l) but increased to a greater extent duringexercise in HT (6.96 ± 0.16) compared with Con (5.45 ± 0.18;P < 0.05). This was the result of ahigher glucose rate of appearance in HT during the last 30 min ofexercise. In contrast, the glucose rate of disappearance and metabolicclearance rate were not different at any time point during exercise.Plasma catecholamines were higher after 10 and 40 min of exercise in HTcompared with Con (P < 0.05),whereas plasma glucagon, cortisol, and growth hormone were higher in HTafter 40 min. These results indicate that the hyperglycemia observedduring exercise in the heat is caused by an increase in liver glucoseoutput without any change in whole body glucoseutilization.

     

Effect of epinephrine on muscle glycogenolysis during exercise in trained men

Febbraio, M. A., D. L. Lambert, R. L. Starkie, J. Proietto,and M. Hargreaves. Effect of epinephrine on muscle glycogenolysis during exercise in trained men. J. Appl.Physiol. 84(2): 465-470, 1998.To test thehypothesis that an elevation in circulating epinephrine increasesintramuscular glycogen utilization, six endurance-trained men performedtwo 40-min cycling trials at 71 ± 2% of peak oxygen uptake in20-22°C conditions. On the first occasion, subjects wereinfused with saline throughout exercise (Con). One week later, afterdetermination of plasma epinephrine levels in Con, subjects performedthe second trial (Epi) with an epinephrine infusion, which resulted ina twofold higher (P < 0.01) plasmaepinephrine concentration in Epi compared with Con. Although oxygenuptake was not different when the two trials were compared, respiratoryexchange ratio was higher throughout exercise in Epi compared with Con(0.93 ± 0.01 vs. 0.89 ± 0.01; P < 0.05). Muscle glycogenconcentration was not different when the trials were comparedpreexercise, but the postexercise value was lower(P < 0.01) in Epi compared with Con.Thus net muscle glycogen utilization was greater during exercise withepinephrine infusion (224 ± 37 vs. 303 ± 30 mmol/kg for Con andEpi, respectively; P < 0.01). Inaddition, both muscle and plasma lactate and plasma glucoseconcentrations were higher (P < 0.05) in Epi compared with Con. These data indicate that intramuscularglycogen utilization, glycolysis, and carbohydrate oxidation areaugmented by elevated epinephrine during submaximal exercise in trainedmen.

     

Effects of nandrolone decanoate on respiratory and peripheral muscles in male and female rats

Bisschop, Anja, Ghislaine Gayan-Ramirez, HélèneRollier, P. N. Richard Dekhuijzen, René Dom, Vera de Bock, andMarc Decramer. Effects of nandrolone decanoate on respiratory and peripheral muscles in male and female rats. J. Appl.Physiol. 82(4): 1112-1118, 1997.Thirty maleand 18 female adult rats received weekly an intramuscular injection ofeither saline (control; C), 1.5 mg/kg (low-dose; LD) nandrolonedecanoate or 7.5 mg/kg (high-dose; HD) nandrolone decanoate during 5 wk. Compared with respective C, growth rate was stunted in male HD ratsfrom 2 wk of treatment on, whereas it was enhanced in female LD and HDrats after 1 wk. Mass of all muscles studied varied proportionally tobody weight, except for the gastrocnemius (males: 0.49 ± 0.04 vs. C: 0.52 ± 0.03%, not significant; females: 0.17 ± 0.01 vs. C: 0.15 ± 0.01%, P < 0.05). In vitro contractile andfatigue properties of the diaphragm remained unchanged, except for adecrease in twitch kinetics (time to peak tension: C, 21 ± 2; LD,19 ± 1; HD, 19 ± 2 ms, P < 0.05; half-relaxation time: C, 26 ± 5, LD, 25 ± 5, HD, 23 ± 3 ms, P < 0.01).Histochemistry of the diaphragm and the gastrocnemius revealed asignificant increase in type IIx/b dimensions. In the gastrocnemius,type I fiber dimensions also increased. A pair-fed study, includinganother 24 female rats, showed that the changes in oral food intakeonly partly accounted for the observed anabolic effects.

     

Role of inhibition of nitric oxide production in monocrotaline-induced pulmonary hypertension

Mathew, Rajamma, Elizabeth S. Gloster, T. Sundararajan, Carl I. Thompson, Guillermo A. Zeballos, andMichael H. Gewitz. Role of inhibition of nitric oxide productionin monocrotaline-induced pulmonary hypertension. J. Appl. Physiol. 82(5): 1493-1498, 1997.Monocrotaline (MCT)-induced pulmonary hypertension (PH) isassociated with impaired endothelium-dependent nitric oxide(NO)-mediated relaxation. To examine the role of NO in PH,Sprague-Dawley rats were given a single subcutaneous injection ofnormal saline [control (C)], 80 mg/kg MCT, or the same doseof MCT and a continuous subcutaneous infusion of 2 mg · kg¹ · day¹of molsidomine, a NO prodrug (MCT+MD). Two weeks later, plasma NO₃ levels, pulmonary arterialpressure (Ppa), ratio of right-to-left ventricular weights (RV/LV) toassess right ventricular hypertrophy, and pulmonary histology wereevaluated. The plasma NO₃ level inthe MCT group was reduced to 9.2 ± 1.5 µM(n = 12) vs. C level of 17.7 ± 1.8 µM (n = 8; P < 0.02). In the MCT+MD group,plasma NO₃ level was 12.3 ± 2.0 µM (n = 8). Ppa and RV/LV in theMCT group were increased compared with C [Ppa, 34 ± 3.4 mmHg(n = 6) vs. 19 ± 0.8 mmHg(n = 8) and 0.41 ± 0.01 (n = 9) vs. 0.25 ± 0.008 (n = 8), respectively;P < 0.001]. In the MCT+MDgroup, Ppa and RV/LV were not different when compared with C [19 ± 0.5 mmHg (n = 5) and 0.27 ± 0.01 (n = 9), respectively;P < 0.001 vs. MCT]. Medial wall thickness of lung vessels in the MCT group was increased comparedwith C [31 ± 1.5% (n = 9)vs. 13 ± 0.66% (n = 9);P < 0.001], and MDpartially prevented MCT-induced pulmonary vascular remodeling [22 ± 1.2% (n = 11);P < 0.001 vs. MCT and C].These results indicate that a defect in the availability of bioactive NO may play an important role in the pathogenesis of MCT-induced PH.

     

Windchill and the risk of tissue freezing

Danielsson, Ulf. Windchill and the risk of tissuefreezing. J. Appl. Physiol. 81(6): 2666-2673, 1996.Low air temperatures and high wind speeds are associated with anincreased risk of freezing of the exposed skin. P. A. Siple and C. F. Passel (Proc. Am. Phil. Soc. 89: 177-199, 1945) derivedtheir windchill index from cooling experiments on a water-filledcylinder to quantify the risk of frostbite. Their results arereexamined here. It is found that their windchill index does notcorrectly describe the convective heat transfer coefficient(h_c) for such a cylinder; theeffect of the airspeed (v) isunderestimated. New risk curves have been developed, based on theconvection equations valid for cylinders in a cross flow,h_c  v^0.62, and tissuefreezing data from the literature. An analysis of the data reveals alinear relationship between the frequency of finger frostbite and thesurface temperature. This relation closely follows a normaldistribution of finger-freezing temperatures, with an SD of 1°C. Asthe skin surface temperature falls from 4.8 to 7.8°C,the risk of frostbite increases from 5 to 95%. These data indicatethat the risk of finger frostbite is minor above an air temperature of10°C, irrespective of v,but below 25°C there is a pronounced risk, even at lowv.