The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise thresholds for vasoconstriction and shivering measured during water immersion. On 2 separate days, seven subjects (six males and one female) were immersed in water (37.5 degrees C) that was subsequently cooled at a constant rate of approximately 6.5 degrees C x h(-1) until the thresholds for vasoconstriction and shivering were clearly established. Water temperature was then increased to 37.5 degrees C. Subjects remained immersed for approximately 20 min, after which they exited the water, were towel-dried and sat in room air (22 degrees C) until both esophageal temperature and mean skin temperature (Tsk) returned to near-baseline values. Subjects then either performed 15 min of cycle ergometry (at 65% maximal oxygen consumption) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. The core temperature thresholds for both vasoconstriction and shivering increased significantly by 0.2 degrees C Post-Exercise (P < 0.05). Because the Tsk at the onset of vasoconstriction and shivering was different during Pre- and Post-Exercise Cooling, we compensated mathematically for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 32.0 degrees C) for vasoconstriction increased significantly from 37.1 (0.3) degrees C to 37.5 ( 0.3) degrees C post-exercise (P < 0.05). Likewise, the shivering threshold increased from 36.2 (0.3) degrees C to 36.5 (0.3) degrees C post-exercise (P < 0.05). In contrast to the post-exercise increase in cold thermal response thresholds, sequential measurements demonstrated a time-dependent similarity in the Pre- and Post-Control thresholds for vasoconstriction and shivering. These data indicate that exercise has a prolonged effect on the post-exercise thresholds for both cold thermoregulatory responses.     

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.

     

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.

     

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.

     

Effect of continuous negative-pressure breathing on skin blood flow during exercise in a hot environment

To assessthe impact of continuous negative-pressure breathing (CNPB) on theregulation of skin blood flow, we measured forearm blood flow (FBF) byvenous-occlusion plethysmography and laser-Doppler flow (LDF) at theanterior chest during exercise in a hot environment (ambienttemperature = 30°C, relative humidity = ~30%). Seven malesubjects exercised in the upright position at an intensity of 60% peakoxygen consumption rate for 40 min with and without CNPB after 20 minof exercise. The esophageal temperature(T_es) in both conditionsincreased to 38.1°C by the end of exercise, without any significantdifferences between the two trials. Mean arterial pressure (MAP)increased by ~15 mmHg by 8 min of exercise, without any significantdifference between the two trials before CNPB. However, CNPB reducedMAP by ~10 mmHg after 24 min of exercise (P < 0.05). The increasein FBF and LDF in the control condition leveled off after 18 min ofexercise above a T_es of37.7°C, whereas in the CNPB trial the increase continued, with arise in T_es despite the decreasein MAP. These results suggest that CNPB enhances vasodilation of skinabove a T_es of ~38°C bystretching intrathoracic baroreceptors such as cardiopulmonarybaroreceptors.

     

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.

     

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.

     

Muscle glycogen accumulation after endurance exercise in trained and untrained individuals

Hickner, R. C., J. S. Fisher, P. A. Hansen, S. B. Racette,C. M. Mier, M. J. Turner, and J. O. Holloszy. Muscle glycogen accumulation after endurance exercise in trained and untrained individuals. J. Appl. Physiol. 83(3):897-903, 1997.Muscle glycogen accumulation was determined in sixtrained cyclists (Trn) and six untrained subjects (UT) at 6 and either48 or 72 h after 2 h of cycling exercise at ~75% peakO₂ uptake(O_{2 peak}), which terminated with five 1-min sprints. Subjects ate 10 gcarbohydrate · kg¹ · day¹for 48-72 h postexercise. Muscle glycogen accumulation averaged 71 ± 9 (SE) mmol/kg (Trn) and 31 ± 9 mmol/kg (UT) during the first 6 h postexercise (P < 0.01) and 79 ± 22 mmol/kg (Trn) and 60 ± 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogenconcentration was 164 ± 21 mmol/kg (Trn) and 99 ± 16 mmol/kg(UT) 48-72 h postexercise (P < 0.05). Muscle GLUT-4 content immediately postexercise was threefoldhigher in Trn than in UT (P < 0.05)and correlated with glycogen accumulation rates (r = 0.66, P < 0.05). Glycogen synthase in theactive I form was 2.5 ± 0.5, 3.3 ± 0.5, and 1.0 ± 0.3 µmol · g¹ · min¹in Trn at 0, 6, and 48 or 72 h postexercise, respectively;corresponding values were 1.2 ± 0.3, 2.7 ± 0.5, and 1.6 ± 0.3 µmol · g¹ · min¹in UT (P < 0.05 at 0 h). Plasmainsulin and plasma C-peptide area under the curve were lower in Trnthan in UT over the first 6 h postexercise(P < 0.05). Plasma creatine kinaseconcentrations were 125 ± 25 IU/l (Trn) and 91 ± 9 IU/l (UT)preexercise and 112 ± 14 IU/l (Trn) and 144 ± 22 IU/l(UT; P < 0.05 vs.preexercise) at 48-72 h postexercise (normal: 30-200 IU/l).We conclude that endurance exercise training results in an increasedability to accumulate muscle glycogen after exercise.

     

Prostaglandin production contributes to exercise-induced vasodilation in heart failure

Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor,and John R. Wilson. Prostaglandin production contributes toexercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933-1940, 1997.Endothelial release of prostaglandins may contribute toexercise-induced skeletal muscle arteriolar vasodilation in patientswith heart failure. To test this hypothesis, we examined the effect ofindomethacin on leg circulation and metabolism in eight chronic heartfailure patients, aged 55 ± 4 yr. Central hemodynamics and legblood flow, determined by thermodilution, and leg metabolic parameterswere measured during maximum treadmill exercise before and 2 h afteroral administration of indomethacin (75 mg). Leg release of6-ketoprostaglandin F₁ was alsomeasured. During control exercise, leg blood flow increased from 0.34 ± 0.03 to 1.99 ± 0.19 l/min(P < 0.001), legO₂ consumption from 13.6 ± 1.8 to 164.5 ± 16.2 ml/min (P < 0.001), and leg prostanoid release from 54.1 ± 8.5 to267.4 ± 35.8 pg/min (P < 0.001).Indomethacin suppressed release of prostaglandinF₁(P < 0.001) throughout exercise anddecreased leg blood flow during exercise(P < 0.05). This was associated witha corresponding decrease in leg O₂ consumption (P < 0.05) and a higher level offemoral venous lactate at peak exercise(P < 0.01). These data suggest thatrelease of vasodilatory prostaglandins contributes to skeletal musclearteriolar vasodilation in patients with heart failure.

     

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.

     

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.

     

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.

     

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.

     

Ventilatory response to exercise in subjects breathing CO2 or HeO2

Babb, T. G. Ventilatory response to exercise insubjects breathing CO₂ orHeO₂.J. Appl. Physiol. 82(3): 746-754, 1997.To investigate the effects of mechanical ventilatory limitationon the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycleergometry to exhaustion once while breathing room air; once whilebreathing 3% CO₂-21%O₂-balanceN₂; and once while breathing HeO₂ (79% He and 21%O₂). Minute ventilation(E) and respiratory mechanics weremeasured continuously during each 1-min increment in work rate (10 or20 W). Data were analyzed at rest, at ventilatory threshold (VTh),and at maximal exercise. When the subjects were breathing 3%CO₂, there was an increase(P < 0.001) inE at rest and at VTh but not duringmaximal exercise. When the subjects were breathingHeO₂,E was increased(P < 0.05) only during maximalexercise (24 ± 11%). The ventilatory response to exercise belowVTh was greater only when the subjects were breathing 3% CO₂(P < 0.05). Above VTh, theventilatory response when the subjects were breathingHeO₂ was greater than whenbreathing 3% CO₂(P < 0.01). Flow limitation, aspercent of tidal volume, during maximal exercise was greater(P < 0.01) when the subjects werebreathing CO₂ (22 ± 12%) thanwhen breathing room air (12 ± 9%) or when breathingHeO₂ (10 ± 7%)(n = 7). End-expiratory lung volumeduring maximal exercise was lower when the subjects were breathingHeO₂ than when breathing room airor when breathing CO₂(P < 0.01). These data indicate thatolder subjects have little reserve for accommodating an increase inventilatory demand and suggest that mechanical ventilatory constraintsinfluence both the magnitude of Eduring maximal exercise and the regulation ofE and respiratory mechanics duringheavy-to-maximal exercise.

     

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.

     

Hydration effects on physiological strain of horses during exercise-heat stress

This study examined the effects ofhyperhydration, exercise-induced dehydration, and oral fluidreplacement on physiological strain of horses during exercise-heatstress. On three occasions, six horses completed a 90-min exerciseprotocol (50% maximal O₂ uptake,34.5°C, 48% relative humidity) divided into two 45-min periods(exercise I andexercise II) with a 15-min recoverybetween exercise bouts. In random order, horses receivedno fluid (NF), 10 liters of water (W), or a carbohydrate-electrolytesolution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (), stroke volume (SV), corebody temperature, sweating rate (SR), or sweating sensitivity duringexercise I. In contrast, afterexercise II, exercise-induceddehydration in NF (decrease in body mass: NF, 5.6 ± 0.8%; W, 1.1 ± 0.4%; CE, 1.0 ± 0.2%) resulted in greater heat storage,with core body temperature ~1.0°C higher compared with W and CE.In exercise II, the greater thermalstrain in NF was associated with significant(P < 0.05) decreases in (10 ± 2%), SV (9 ± 3%), SR, and sweatingsensitivity. We concluded that 1)preexercise hyperhydration provided no thermoregulatory advantage;2) maintenance of euhydration byoral fluid replacement (~85% of sweat fluid loss) during exercise inthe heat was reflected in higher , SV, and SR withdecreased heat storage; and 3) W oran isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

     

Transcapillary escape rate of albumin in humans during exercise-induced hypervolemia

Haskell, Andrew, Ethan R. Nadel, Nina S. Stachenfeld, KeiNagashima, and Gary W. Mack. Transcapillary escape rate of albuminin humans during exercise-induced hypervolemia. J. Appl. Physiol. 83(2): 407-413, 1997.To test thehypotheses that plasma volume (PV) expansion 24 h after intenseexercise is associated with reduced transcapillary escape rate ofalbumin (TER_alb) and that localchanges in transcapillary forces in the previously active tissues favorretention of protein in the vascular space, we measured PV,TER_alb, plasma colloid osmoticpressure (COP_p), interstitialfluid hydrostatic pressure (Pi), and colloid osmotic pressure in legmuscle and skin and capillary filtration coefficient (CFC) in the armand leg in seven men and women before and 24 h after intense uprightcycle ergometer exercise. Exercise expanded PV by 6.4% at 24 h (43.9 ± 0.8 to 46.8 ± 1.2 ml/kg, P < 0.05) and decreased total protein concentration (6.5 ± 0.1 to6.3 ± 0.1 g/dl, P < 0.05) andCOP_p (26.1 ± 0.8 to 24.3 ± 0.9 mmHg, P < 0.05), although plasmaalbumin concentration was unchanged. TER_alb tended to decline (8.4 ± 0.5 to 6.5 ± 0.7%/h, P = 0.11) and was correlated with the increase in PV(r = 0.69,P < 0.05). CFC increased in the leg(3.2 ± 0.2 to 4.3 ± 0.5 µl · 100 g¹ · min¹ · mmHg¹,P < 0.05), and Pi showed a trend toincrease in the leg muscle (2.8 ± 0.7 to 3.8 ± 0.3 mmHg, P = 0.08). These datademonstrate that TER_alb isassociated with PV regulation and that local transcapillary forcesin the leg muscle may favor retention of albumin in the vascular spaceafter exercise.

     

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.

     

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).