Selected contribution: role of spleen emptying in prolonging apneas in humans.

This study addressed the interaction between short-term adaptation to apneas with face immersion and erythrocyte release from the spleen. Twenty healthy volunteers, including ten splenectomized subjects, participated. After prone rest, they performed five maximal-duration apneas with face immersion in 10 degrees C water, with 2-min intervals. Cardiorespiratory parameters and venous blood samples were collected. In subjects with spleens, hematocrit and hemoglobin concentration increased by 6.4% and 3.3%, respectively, over the serial apneas and returned to baseline 10 min after the series. A delay of the physiological breaking point of apnea, by 30.5% (17 s), was seen only in this group. These parameters did not change in the splenectomized group. Plasma protein concentration, preapneic alveolar PCO2, inspired lung volume, and diving bradycardia remained unchanged throughout the series in both groups. Serial apneas thus triggered the hematological changes that have been previously observed after long apneic diving shifts; they were rapidly reversed and did not occur in splenectomized subjects. This suggests that splenic contraction occurs in humans as a part of the diving response and may prolong repeated apneas.     

Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea

Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. DouglasBradley. Effects of inhaledCO₂ and added dead space on idiopathic central sleep apnea. J. Appl.Physiol. 82(3): 918-926, 1997.We hypothesizedthat reductions in arterial PCO₂ (Pa_CO2) below the apnea threshold play akey role in the pathogenesis of idiopathic central sleep apnea syndrome(ICSAS). If so, we reasoned that raisingPa_CO2 would abolish apneas in thesepatients. Accordingly, patients with ICSAS were studied overnight onfour occasions during which the fraction of end-tidalCO₂ and transcutaneous PCO₂ were measured: during room airbreathing (N1), alternating room airand CO₂ breathing(N2),CO₂ breathing all night(N3), and addition of dead space viaa face mask all night (N4).Central apneas were invariably preceded by reductions infraction of end-tidal CO₂. Bothadministration of a CO₂-enrichedgas mixture and addition of dead space induced 1- to 3-Torr increasesin transcutaneous PCO₂, whichvirtually eliminated apneas and hypopneas; they decreased from43.7 ± 7.3 apneas and hypopneas/h onN1 to 5.8 ± 0.9 apneas andhypopneas/h during N3(P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep duringCO₂ inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients werebreathing through added dead space duringN4 (P < 0.005). Because raisingPa_CO2 through two different meansvirtually eliminated central sleep apneas, we conclude that centralapneas during sleep in ICSA are due to reductions inPa_CO2 below the apnea threshold.

     

Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans.

The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10 degrees C) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion. Oxygen uptake from the lungs decreased during apnea in air (-22% compared with eupneic control) and was further reduced during apnea with face immersion (-25% compared with eupneic control). The plasma lactate concentration increased from control (11%) after apnea in air and even more after apnea with face immersion (20%), suggesting an increased anaerobic metabolism during apneas. The lung oxygen store was depleted more slowly during apnea with face immersion because of the augmented diving response, probably including a decrease in cardiac output. Venous oxygen stores were probably reduced by the cardiovascular responses. The turnover times of these gas stores would have been prolonged, reducing their effect on the oxygen uptake in the lungs. Thus the human diving response has an oxygen-conserving effect.     

Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs

The effects of periodic obstructive apneas onsystemic and myocardial hemodynamics were studied in ninepreinstrumented sedated pigs under four conditions: breathing room air(RA), breathing 100% O₂,breathing RA after critical coronary stenosis (CS) of the left anteriordescending coronary artery, and breathing RA after autonomic blockadewith hexamethonium (Hex). Apneas with RA increased mean arterialpressure (MAP; from baseline 103.0 ± 3.5 to late apnea 123.6 ± 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 ± 22.9% of baseline,P < 0.001) but decreased cardiacoutput (CO; from baseline 2.97 ± 0.15 to late apnea 2.39 ± 0.19 l/min, P < 0.001). Apneas withO₂ increased MAP (from baseline105.1 ± 4.6 to late apnea 110.7 ± 4.8 Torr, P < 0.001). Apneas with CS producedsimilar increases in MAP as apneas with RA but greater decreases in CO(from baseline 3.03 ± 0.19 to late apnea 2.1 ± 0.15 l/min,P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 ± 1.5 to late apnea 7.6 ± 2.0%,P < 0.01) and regionalintramyocardial pH (baseline 7.05 ± 0.03 to late apnea 6.72 ± 0.11, P < 0.001) during apneas withCS but under no other conditions. Apneas with Hex increased to the sameextent as apneas with RA. Myocardial O₂ demand remained unchangedduring apnea relative to baseline. We conclude that obstructiveapnea-induced changes in left ventricular afterload and CO aresecondary to autonomic-mediated responses to hypoxemia. Increased CBFduring apneas is related to regional metabolic effects of hypoxia andnot to autonomic factors. In the presence of limited coronary flowreserve, decreased O₂ supply during apneas can lead to myocardial ischemia, which in turnadversely affects left ventricular function.

     

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.     

Abdominal muscle fatigue after maximal ventilation in humans

Kyroussis, Dimitris, Gary H. Mills, Michael I. Polkey,Carl-Hugo Hamnegard, Nicholaos Koulouris, Malcolm Green, and John Moxham. Abdominal muscle fatigue after maximal ventilation inhumans. J. Appl. Physiol. 81(4):1477-1483, 1996.Abdominal muscles are the principal muscles ofactive expiration. To investigate the possibility of abdominal musclelow-frequency fatigue after maximal ventilation in humans, westimulated the nerve roots supplying the abdominal muscles. We used amagnetic stimulator (Magstim 200) powering a 90-mm circular coil andstudied six normal subjects. To assess the optimum level of stimulationand posture, we stimulated at each intervertebral level betweenT₇ andL₁ in the prone, supine, andseated positions. At T₁₀, we usedincreasing power outputs to assess the pressure-power relationship.Care was taken to avoid muscle potentiation. Twitch gastric pressure(Pga) was recorded with a balloon-tipped catheter. Mean (±SD)baseline twitch Pga measured with the subjects in the prone position atT₁₀ was 23.5 ± 5.4 cmH₂O. Within-occasion mean twitchPga coefficient of variation was 4.6 ± 1.1%. Twitch Pga wasmeasured with the subjects in the prone position with stimulation overT₁₀ before and after 2 min ofmaximal isocapnic ventilation (MIV). Twenty minutes after MIV, meantwitch Pga fell by 17 ± 9.1%(P = 0.03) and remained low 90 minafter MIV. We conclude that after maximal ventilation in humans thereis a reduction of twitch Pga and, therefore, of low-frequency fatiguein abdominal muscles.

     

Cerebral vasomotor reactivity at high altitude in humans

The purpose of this study was twofold:1) to determine whether at highaltitude cerebral blood flow (CBF) as assessed during CO₂ inhalation and duringhyperventilation in subjects with acute mountain sickness (AMS) wasdifferent from that in subjects without AMS and2) to compare the CBF as assessedunder similar conditions in Sherpas at high altitude and in subjects atsea level. Resting control values of blood flow velocity in themiddle cerebral artery (V_MCA), pulseoxygen saturation (Sa_O2), andtranscutaneous PCO₂ were measured at4,243 m in 43 subjects without AMS, 17 subjects with AMS, 20 Sherpas,and 13 subjects at sea level. Responses ofCO₂ inhalation andhyperventilation onV_MCA,Sa_O2, and transcutaneous PCO₂ were measured, and the cerebralvasomotor reactivity (VMR = V_MCA/PCO₂)was calculated as the fractional change ofV_MCA per Torrchange of PCO₂, yielding ahypercapnic VMR and a hypocapnic VMR. AMS subjects showeda significantly higher resting controlV_MCA than didno-AMS subjects (74 ± 22 and 56 ± 14 cm/s, respectively;P < 0.001), andSa_O2 was significantly lower (80 ± 8 and 88 ± 3%, respectively; P < 0.001). Resting control V_MCA values inthe sea-level group (60 ± 15 cm/s), in the no-AMS group, and inSherpas (59 ± 13 cm/s) were not different. Hypercapnic VMR valuesin AMS subjects were 4.0 ± 4.4, in no-AMS subjects were 5.5 ± 4.3, in Sherpas were 5.6 ± 4.1, and in sea-level subjects were 5.6 ± 2.5 (not significant). Hypocapnic VMR values were significantly higher in AMS subjects (5.9 ± 1.5) compared with no-AMS subjects (4.8 ± 1.4; P < 0.005) but werenot significantly different between Sherpas (3.8 ± 1.1) and thesea-level group (2.8 ± 0.7). We conclude that AMS subjects havegreater cerebral hemodynamic responses to hyperventilation, higherV_MCAresting control values, and lower Sa_O2 compared with no-AMSsubjects. Sherpas showed a cerebral hemodynamic patternsimilar to that of normal subjects at sea level.     

Effect of different levels of hyperoxia on breathing in healthy subjects

Becker, Heinrich F., Olli Polo, Stephen G. McNamara, MichaelBerthon-Jones, and Colin E. Sullivan. Effect of different levelsof hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683-1690, 1996.Wehave recently shown that breathing 50%O₂ markedly stimulates ventilationin healthy subjects if end-tidal PCO₂(PET_CO2) ismaintained. The aim of this study was to investigate apossible dose-dependent stimulation of ventilation byO₂ and to examine possiblemechanisms of hyperoxic hyperventilation. In eight normalsubjects ventilation was measured while they were breathing 30 and 75%O₂ for 30 min, withPET_CO2 being held constant.Acute hypercapnic ventilatory responses were also tested in thesesubjects. The 75% O₂ experimentwas repeated without controllingPET_CO2 in 14 subjects, andin 6 subjects arterial blood gases were taken at baseline and at theend of the hyperoxia period. Minute ventilation(I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75%O₂ without any control onPET_CO2 led toa 16% increase inI, butPET_CO2 decreased by3.6 Torr (9%). There was a linear correlation(r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withI more than doubling after 30 min of75% O₂. If isocapnia is notmaintained, hyperventilation is attenuated by a decrease in arterialPCO₂. There is a correlation betweenhyperoxic and hypercapnic ventilatory responses. On the basis of datafrom the literature, we concluded that the Haldane effect seems to bethe major cause of hyperventilation duringboth isocapnic and poikilocapnichyperoxia.

     

Effects of the combination of skin cooling and hyperpnea of frigid air in asthmatic and normal subjects

McDonald, James S., Joann Nelson, K. A. Lenner, Melissa L. McLane, and E. R. McFadden, Jr. Effects of the combination of skincooling and hyperpnea of frigid air in asthmatic and normal subjects.J. Appl. Physiol. 82(2): 453-459, 1997.To investigate whether reducing integumental temperatures influences pulmonary mechanics and interacts with inhaling cold air, 10 normal and 10 asthmatic subjects participated in a three-part trial in which coolingthe skin of the head and thorax and isocapnic hyperventilation offrigid air were undertaken as isolated challenges and then administeredin combination. Integumental cooling for 30 min caused airwayobstruction to develop in both populations [change in 1-s forcedexpiratory volume (FEV₁)asthmatic subjects = 10%; normal subjects = 6%)].Hyperventilation, however, only affected the asthmatic subjects(FEV₁ asthmatic subjects = 18%; normal subjects = 3%). In contrast to expectations, the combinedchallenge did not produce a summation effect(FEV₁ asthmatic subjects = 21%; normal subjects = 7%). These data demonstrate that the skin of the trunk and head is cold sensitive and when stimulated causes similardegrees of bronchial narrowing in both normal subjects and patientswith airway disease independent of any ventilatory effect. They alsoindicate that cooling of the skin does not add to the obstructiveconsequences of hyperpnea.

     

Physiological and Genomic Consequences of Intermittent Hypoxia: Selected Contribution: Chemoreflex responses to CO2 before and after an 8-h exposure to hypoxia in humans

The ventilatorysensitivity to CO₂, in hyperoxia, is increased after an 8-hexposure to hypoxia. The purpose of the present study was to determinewhether this increase arises through an increase in peripheral orcentral chemosensitivity. Ten healthy volunteers each underwent 8-hexposures to 1) isocapnic hypoxia, with end-tidalPO₂ (PET_O2) = 55 Torr and end-tidal PCO₂(PET_CO2) = eucapnia; 2)poikilocapnic hypoxia, with PET_O2 = 55 Torr and PET_CO2 = uncontrolled;and 3) air-breathing control. The ventilatory response toCO₂ was measured before and after each exposure with theuse of a multifrequency binary sequence with two levels of PET_CO2: 1.5 and 10 Torr above the normalresting value. PET_O2 was held at 250 Torr.The peripheral (Gp) and the central (Gc) sensitivities were calculatedby fitting the ventilatory data to a two-compartment model. There wereincreases in combined Gp + Gc (26%, P < 0.05),Gp (33%, P < 0.01), and Gc (23%, P = not significant) after exposure to hypoxia. There were no significant differences between isocapnic and poikilocapnic hypoxia. We conclude that sustained hypoxia induces a significant increase inchemosensitivity to CO₂ within the peripheral chemoreflex.

     

Oximetry of retinal vessels by dual-wavelength imaging: calibration and influence of pigmentation

A method for noninvasive measurement of HbO₂ saturation(SO₂) inretinal blood vessels by digital imaging was developed and tested.Images of vessels were recorded atO₂-sensitive andO₂-insensitive wavelengths (600 and 569 nm, respectively) by using a modified fundus camera with animage splitter coupled to an 18-bit digital camera. Retinal arterialSO₂ wasvaried experimentally by having subjects breathe mixtures ofO₂ andN₂ while systemic arterial SO₂ wasmonitored with a pulse oximeter. Optical densities (ODs) of vascularsegments were determined using a computer algorithm to track the pathof reflected light intensity along vessels. During graded hypoxia theOD ratio (ODR = OD₆₀₀/OD₅₆₉)bore an inverse linear relationship to systemicSO₂.Compensation for the influence of choroidal pigmentation significantlyreduced variation in the arterialSO₂measurements among subjects. An O₂sensitivity of 0.00504 ± 0.00029 (SE) ODRunits/%SO₂was determined. Retinal venousSO₂ atnormoxia was 55 ± 3.38% (SE). Breathing 100%O₂ increased venousSO₂ by19.2 ± 2.9%. This technique, when combined with bloodflow studies in human subjects, will enable the study of retinalO₂ utilization under experimentaland various disease conditions.     

Phosphocreatine hydrolysis during submaximal exercise: the effect of FIO2

There isevidence that the concentration of the high-energy phosphatemetabolites may be altered during steady-state submaximal exerciseby the breathing of different fractions of inspiredO₂ (FI_O2). Whereasit has been suggested that these changes may be the result ofdifferences in time taken to achieve steady-state O₂ uptake(O₂) at differentFI_O2 values, we postulated that they are due to a direct effect ofO₂ tension. We used³¹P-magnetic resonancespectroscopy during constant-load, steady-state submaximal exercise todetermine 1) whether changes inhigh-energy phosphates do occur at the sameO₂ with variedFI_O2 and2) that these changes are not due todifferences in O₂onset kinetics. Six male subjects performed steady-state submaximal plantar flexion exercise [7.2 ± 0.6 (SE) W] for 10 minwhile lying supine in a 1.5-T clinical scanner. Magnetic resonancespectroscopy data were collected continuously for 2 min beforeexercise, 10 min during exercise, and 6 min during recovery. Subjectsperformed three different exercise bouts at constant load with theFI_O2 switched after 5 min ofthe 10-min exercise bout. The three exercise treatments were1)FI_O2 of 0.1 switched to0.21, 2)FI_O2 of 0.1 switched to1.00, and 3)FI_O2 of 1.00 switched to0.1. For all three treatments, theFI_O2 switch significantly (P  0.05) altered phosphocreatine:1) 55.5 ± 4.8 to 67.8 ± 4.9% (%rest); 2) 59.0 ± 4.3 to72.3 ± 5.1%; and 3) 72.6 ± 3.1 to 64.2 ± 3.4%, respectively. There were no significantdifferences in intracellular pH for the three treatments. The resultsdemonstrate that the differences in phosphocreatine concentration withvaried FI_O2 are not theresult of different O₂onset kinetics, as this was eliminated by the experimental design.These data also demonstrate that changes in intracellular oxygenation,at the same work intensity, result in significant changes in cell homeostasis and thereby suggest a role for metabolic control by O₂ even during submaximalexercise.

     

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.

     

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.

     

Caffeine ingestion and metabolic responses of tetraplegic humans during electrical cycling

Normally, caffeineingestion results in a wide spectrum of neural and hormonal responses,making it difficult to evaluate which are critical regulatory factors.We examined the responses to caffeine (6 mg/kg) ingestion in a group ofspinal cord-injured subjects [7 tetraplegic(C_5-7) and 2 paraplegic(T₄) subjects] at rest andduring functional electrical stimulation of their paralyzed limbs tothe point of fatigue. Plasma insulin did not change, caffeine had noeffect on plasma epinephrine, and there was a slight increase(P < 0.05) in norepinephrine after15 min of exercise. Nevertheless, serum free fatty acids were increased (P < 0.05) after caffeine ingestionafter 60 min of rest and throughout the first 15 min of exercise, butthe respiratory exchange ratio was not affected. The exercise time wasincreased (P < 0.05) by 6% or 1.26 ± 0.57 min. These data suggest that caffeine had direct effects onboth the adipose tissue and the active muscle. It is proposed that theergogenic action of caffeine is occurring, at least in part, by adirect action of the drug on muscle.

     

Effects of Repetitive Drying, Acid Immersion, and Red Light Treatments on Phytochrome- and Gibberellin A3-mediated Germination of Skotodormant Lettuce Seeds

Ten-30 d imbibed skotodormant lettuce seeds (Lactuca sativaL. cv. Grand Rapids) showed no germination with water alone.However, following a single treatment of red light (R), gibberellinA₃ (GA₃) or 1 h acid immersion (pH 0–1) plus water rinse,7% germinated. These imbibed skotodormant seeds germinated 85%or higher if acid immersion was carried out before R or GA₃.Similar values were obtained with imbibed skotodormant seedsunder acid immersion plus drying treatment applied at day 10or 20 plus R or GA3 treatment applied 10 d later. One or twodrying treatments alone reduced the degree of skotodormancyand made seeds more responsive to R but not GA₃. Seeds withone R plus drying treatment at day 10 or 20 germinated about50% with or without an additional R, and 80% or more with GA₃on day 20 or 30. The 20 or 30 d skotodormant seeds having R(with or without drying) or acid plus R and drying treatmenton day 10 or 20 and additional dark incubation in water for10d showed 85 to 100% germination with only acid immersion.The skotodormancy was eliminated by the acid immersion but itwas initiated again if R or GA₃ treatment was not given immediately.It is concluded that the drying treatment, after eliminationof skotodormancy by acid or acid + R pretreatment, preventsthese seeds re-entering skotodormancy and maintains a high germinationpotential under dark storage for up to 20 d. Key words: Dark reversion of phytochrome, gibberellin A₃, acidification, skotodormancy, induction and breakage of seed dormancy     

Alveolar PCO2 and PO2 of high-altitude natives living at sea level

León-Velarde, Fabiola, Manuel Vargas, Carlos Monge-C.,Robert W. Torrance, and Peter A. Robbins. AlveolarPCO₂ andPO₂ of high-altitude natives livingat sea level. J. Appl.Physiol. 81(4): 1605-1609, 1996.Thisstudy was designed to determine whether subjects born at high altitude(HA; 2,000 m or above) who subsequently move to near sea level (SL)develop end-tidal PCO₂(PET_CO2) andPO₂(PET_O2) valuesthat equal those of SL natives living near SL. A total of 108 male HAnatives living near SL were identified by survey of a district in Lima,Peru, and a further 108 male SL natives from the same district wereidentified as control subjects. Of these subjects, satisfactory datafor inclusion in the study were obtained from 93 HA and 82 SL subjects.Mean PET_CO2 and PET_O2 values were 37.7 ± 2.5 (SD) and 104.7 ± 3.2 Torr, respectively, in HA subjects and37.7 ± 2.2 and 104.8 ± 3.0 Torr, respectively, in SL subjects.The average difference between SL natives and HA natives forPET_CO2 was 0.07 Torr(0.64 to 0.78; 95% confidence interval) and forPET_O2 was 0.05 Torr(0.89 to 0.99, 95% confidence interval). The average age andweight of the SL and HA subjects did not differ, but the HA subjectswere shorter and tended to have larger vital capacities, consistentwith their origin at HA. We conclude that thePET_CO2 andPET_O2 near SL of SL nativesand HA natives do not differ.

     

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.

     

Protein kinase C reduces the KCa current of rat tail artery smooth muscle cells

The hypothesis that protein kinase C (PKC) isable to regulate the whole cell Ca-activated K(K_Ca) current independently of PKC effects on local Ca release events was tested using the patch-clamp technique and freshly isolated rat tail artery smooth muscle cells dialyzed with a strongly buffered low-Ca solution. The active diacylglycerol analog1,2-dioctanoyl-sn-glycerol (DOG) at 10 µM attenuated the current-voltage(I-V)relationship of the K_Ca current significantly and reduced the K_Cacurrent at +70 mV by 70 ± 4% (n = 14). In contrast, 10 µM DOG after pretreatment of the cells with 1 µM calphostin C or 1 µM PKC inhibitor peptide, selective PKCinhibitors, and 10 µM1,3-dioctanoyl-sn-glycerol, aninactive diacylglycerol analog, did not significantly alter theK_Ca current. Furthermore, thecatalytic subunit of PKC (PKC_C)at 0.1 U/ml attenuated theI-Vrelationship of the K_Ca currentsignificantly, reduced the K_Cacurrent at +70 mV by 44 ± 3% (n = 17), and inhibited the activity of singleK_Ca channels at 0 mV by 79 ± 9% (n = 6). In contrast, 0.1 U/mlheat-inactivated PKC_C did notsignificantly alter the K_Cacurrent or the activity of singleK_Ca channels. Thus these resultssuggest that PKC is able to considerably attenuate theK_Ca current of freshly isolatedrat tail artery smooth muscle cells independently of effects of PKC onlocal Ca release events, most likely by a direct effect on theK_Ca channel.     

Recovery of diaphragmatic function in awake sheep after two approaches to thoracic surgery

Imanaka, Hideaki, William R. Kimball, John C. Wain, MasajiNishimura, Kenichi Okubo, Dean Hess, and Robert M. Kacmarek. Recovery of diaphragmatic function in awake sheep after two approaches to thoracic surgery. J. Appl.Physiol. 83(5): 1733-1740, 1997.Video-assistedthoracoscopic surgery (VATS) is replacing thoracotomy, but no study hasaddressed the extent or duration of VATS-induced diaphragmaticalteration. We hypothesized that VATS would impair diaphragmaticfunction less and return diaphragmatic function faster thanthoracotomy. In eight sheep, sonomicrometers were randomly implanted onthe right costal diaphragm via VATS or thoracotomy. Diaphragmaticresting length, shortening fraction, and respiratory function weremeasured weekly during quiet breathing (QB) andCO₂ rebreathing for 4 wk. ForVATS, shortening fraction was smallest onpostoperative days 1 (POD 1) (6.4 ± 3.4 and12.9 ± 8.7% during QB and 10%CO₂ rebreathing, respectively) and7 (6.3 ± 3.4 and 16.9 ± 4.0%during QB and 10% CO₂rebreathing, respectively) and recovered by 3 wk (13.2 ± 1.8 and28.9 ± 8.0% during QB and 10%CO₂ rebreathing, respectively).For thoracotomy, shortening fraction at 10%CO₂ rebreathing was smaller onPODs 1, 7, 14 (15.9 ± 7.1, 13.6 ± 5.4, and 19.0 ± 6.9%) than onPOD 28 (29.9 ± 8.2%), but notduring QB on POD 1 or7 (7.5 ± 3.8 and 3.4 ± 2.6%)compared with POD 28 (10.7 ± 8.7%). Shortening fraction did not differ between surgeries. There wasno group difference in minute ventilation, respiratory rate,transdiaphragmatic pressure, or esophageal and gastric pressures. Inconclusion, although shortening fraction recovered faster for VATS,this translated into insignificant functional differences.