Letters to the Editor

The following is the abstract of the article discussed in thesubsequent letter:

Venegas, José G., R. Scott Harris, and BrettA. Simon. A comprehensive equation for the pulmonarypressure-volume curve. J. Appl. Physiol. 84(1): 389-395, 1998.Quantification of pulmonary pressure-volume (P-V) curves isoften limited to calculation of specific compliance at a given pressureor the recoil pressure (P) at a given volume (V). These parameters can be substantially different depending on the arbitrary pressure orvolume used in the comparison and may lead to erroneous conclusions. Weevaluated a sigmoidal equation of the form, V = a + b[1 + e^(Pc)/d]¹, for its ability to characterize lung and respiratory system P-V curves obtained under a variety of conditions including normal andhypocapnic pneumoconstricted dog lungs (n = 9), oleicacid-induced acute respiratory distress syndrome (n = 2), andmechanically ventilated patients with acute respiratory distresssyndrome (n = 10). In this equation, a corresponds tothe V of a lower asymptote, b to the V difference between upperand lower asymptotes, c to the P at the true inflection pointof the curve, and d to a width parameter proportional to the Prange within which most of the V change occurs. The equation fittedequally well inflation and deflation limbs of P-V curves with a meangoodness-of-fit coefficient (R²) of 0.997 ± 0.02 (SD). When the data from all analyzed P-V curves were normalized by thebest-fit parameters and plotted as (V  a)/b vs.(P  c)/d, they collapsed into a single and tightrelationship (R² = 0.997). These resultsdemonstrate that this sigmoidal equation can fit with excellentprecision inflation and deflation P-V curves of normal lungs and oflungs with alveolar derecruitment and/or a region of gastrapping while yielding robust and physiologically useful parameters.

     

Cardiovascular adaptations to 10days of cycle exercise

Mier, Constance M., Michael J. Turner, Ali A. Ehsani, andRobert J. Spina. Cardiovascular adaptations to 10 days of cycleexercise. J. Appl. Physiol. 83(6):1900-1906, 1997.We hypothesized that 10 days of training wouldenhance cardiac output (CO) and stroke volume (SV) during peak exerciseand increase the inotropic response to -adrenergic stimulation. Tensubjects [age 26 ± 2 (SE) yr] trained on a cycleergometer for 10 days. At peak exercise, training increasedO₂ uptake, CO, and SV(P < 0.001). Left ventricular (LV)size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training (P < 0.02), whereas LV wall thickness was unchanged. LV contractileperformance was assessed by relating fractional shortening (FS) to theestimated end-systolic wall stress(_ES). Training increased theslope of the FS-_ES relationship (P < 0.05), indicating enhancedsystolic function. The increase in slope correlated with increases inCO (r = 0.71,P < 0.05) and SV(r = 0.70,P < 0.05). The increase in bloodvolume also correlated with increases in CO(r = 0.80, P < 0.01) and SV (r = 0.85, P < 0.004). These datashow that 10 days of training enhance the inotropic response to-adrenergic stimulation, associated with increases in CO and SVduring peak exercise.

     

Fast-twitch skeletal muscles of dystrophic mouse pups are resistant to injury from acute mechanical stress

Loss of the dystrophin-glycoproteincomplex from muscle sarcolemma in Duchenne's muscular dystrophy (DMD)renders the membrane susceptible to mechanical injury, leaky toCa²⁺, and disrupts signaling, but the precise mechanism(s)leading to the onset of DMD remain unclear. To assess the role ofmechanical injury in the onset of DMD, extensor digitorum longus (EDL)muscles from C57 (control), mdx, andmdx-utrophin-deficient [mdx:utrn(/); dystrophic] pups aged 9-12 days were subjected to an acutestretch-injury or no-stretch protocol in vitro. Before the stretches,isometric stress was attenuated for mdx:utrn(/) comparedwith control muscles at all stimulation frequencies (P < 0.05). During the stretches, EDL muscles for each genotypedemonstrated similar mean stiffness values. After the stretches,isometric stress during a tetanus was decreased significantly for bothmdx and mdx:utrn(/) muscles compared withcontrol muscles (P < 0.05). Membrane injury assessedby uptake of procion orange dye was greater for dystrophic comparedwith control EDL (P < 0.05), but, within eachgenotype, the percentage of total cells taking up dye was not different for the no-stretch vs. stretch condition. These data suggest that thesarcolemma of maturing dystrophic EDL muscles are resistant to acutemechanical injury.

     

A multi-dimensional scaling approach to shape analysis

We propose an alternative to Kendall's shape space for reflectionshapes of configurations in with k labelled vertices, where reflection shape consistsof all the geometric information that is invariant under compositionsof similarity and reflection transformations. The proposed approachembeds the space of such shapes into the space of (k – 1) x (k – 1) real symmetricpositive semidefinite matrices, which is the closure of an opensubset of a Euclidean space, and defines mean shape as the naturalprojection of Euclidean means in on to the embedded copy of the shape space. This approachhas strong connections with multi-dimensional scaling, and themean shape so defined gives good approximations to other commonlyused definitions of mean shape. We also use standard perturbationarguments for eigenvalues and eigenvectors to obtain a centrallimit theorem which then enables the application of standardstatistical techniques to shape analysis in two or more dimensions.     

Protein kinase C modulation of ventilatory response to hypoxia in nucleus tractus solitarii of conscious rats

This study aimedto determine the role of protein kinase C (PKC) in signal transductionmechanisms underlying ventilatory regulation in the nucleus tractussolitarii (NTS). Microinjection of phorbol 12-myristate 13-acetate intothe commissural NTS of nine chronically instrumented, unrestrained ratselicited significant cardiorespiratory enhancements that lasted for atleast 4 h, whereas administration of vehicle(n = 15) or the inactive phorbol ester 4-phorbol 12,13-didecanoate (n = 7)did not elicit minute ventilation (E)changes. Peak hypoxic Eresponses (10% O₂-balanceN₂) were measured in 19 additional animals after NTS microinjection of bisindolylmaleimide(BIM) I, a selective PKC inhibitor (n = 12), BIM V (inactive analog; n = 7),or vehicle (Con; n = 19). In Con,E increased from 139 ± 9 to 285 ± 26 ml/min in room air and hypoxia, respectively, and similarresponses occurred after BIM V. BIM I did not affect room airE but markedly attenuated hypoxia-induced E increases (128 ± 12 to 167 ± 18 ml/min; P < 0.02 vs. Con and BIM V). When BIM I was microinjected into the cerebellum(n = 4), cortex(n = 4), or spinal cord(n = 4),E responses were similar to Con.Western blots of subcellular fractions of dorsocaudal brain stemlysates revealed translocation of PKC, , , , , and  isoenzymes during acute hypoxia, and enhanced overall PKC activity wasconfirmed in the particulate fraction of dorsocaudal brain stem lysatesharvested after acute hypoxia. These studies suggest that, in the adultrat, PKC activation in the NTS mediates essential components of theacute hypoxic ventilatory response.

     

Human ventilatory response to 8h of euoxic hypercapnia

Tansley, John G., Michala E. F. Pedersen, Christine Clar,and Peter A. Robbins. Human ventilatory response to 8 h of euoxic hypercapnia. J. Appl.Physiol. 84(2): 431-434, 1998.Ventilation (E) risesthroughout 40 min of constant elevated end-tidalPCO₂ without reaching steady state(S. Khamnei and P. A. Robbins. Respir. Physiol. 81: 117-134, 1990). The present studyinvestigates 8 h of euoxic hypercapnia to determine whetherE reachessteady state within this time. Two protocols were employed:1) 8-h euoxic hypercapnia (end-tidalPCO₂ = 6.5 Torr above prestudy value,end-tidal PO₂ = 100 Torr) followed by 8-h poikilocapnic euoxia; and2) control, where the inspired gaswas air. Ewas measured over a 5-min period before the experiment and then hourly over a 16-h period. In the hypercapnia protocol,E had notreached a steady state by the first hour(P < 0.001, analysis of variance), but there were no further significant differences inEover hours 2-8 (analysis ofvariance). Efell promptly on return to eucapnic conditions. We conclude that,whereas there is a component of theE responseto hypercapnia that is slow, there is no progressive rise inE throughoutthe 8-h period.

     

Immunocompetence of macrophages in rats exposed to Candida albicans infection and stress

The integration of innate andadaptive immune responses is required for efficient control ofCandida albicans. The present work aimed to assess, at thelocal site of the infection, the immunocompetence of macrophages inrats infected intraperitoneally with C. albicans and exposedsimultaneously to stress during 3 days (CaS group). We studied the1) ability to remove and kill C. albicans,2) tumor necrosis factor- (TNF-) release,3) balance of the inducible enzymes NO synthase (iNOS) andarginase, and 4) expression of interleukin (IL)-1 andIL-1 receptor antagonist (ra) mRNA. Compared with only infected animals(Ca group), the number of colony-forming units was significantly higherin CaS rats (P < 0.01), and the macrophagecandidicidal activity was ~2.5-fold lower (P < 0.01). Release of TNF- was diminished in both unstimulated andheat-killed C. albicans restimulated macrophages of the CaSgroup (Ca vs. CaS, P < 0.03 and P < 0.05, respectively). In Ca- and CaS-group rats, the rates for both thearginase activity and the NO synthesis were significantly enhanced.However, the stress exposure downregulated the activity of both enzymes(CaS vs. Ca, P < 0.05). After in vitro restimulation,the IL-1ra/IL-1 ratio was significantly diminished in CaS-group rats(P < 0.05). Our results indicate that a correlationexists between early impairment of macrophage function and stress exposure.

     

Testosterone and cortisol in relationship to dietary nutrients and resistance exercise

Volek, Jeff S., William J. Kraemer, Jill A. Bush, ThomasIncledon, and Mark Boetes. Testosterone and cortisol inrelationship to dietary nutrients and resistance exercise.J. Appl. Physiol. 82(1): 49-54, 1997.Manipulation of resistance exercise variables (i.e., intensity,volume, and rest periods) affects the endocrine response to exercise;however, the influence of dietary nutrients on basal andexercise-induced concentrations of hormones is less understood. Thepresent study examined the relationship between dietary nutrients andresting and exercise-induced blood concentrations of testosterone (T)and cortisol (C). Twelve men performed a bench press exercise protocol(5 sets to failure using a 10-repetitions maximum load) and a jumpsquat protocol (5 sets of 10 repetitions using 30% of each subject's1-repetition maximum squat) with 2 min of rest between all sets. Ablood sample was obtained at preexercise and 5 min postexercise fordetermination of serum T and C. Subjects also completed detaileddietary food records for a total of 17 days. There was a significant(P  0.05) increase in postexercise Tcompared with preexercise values for both the bench press (7.4%) andjump squat (15.1%) protocols; however, C was not significantly different from preexercise concentrations. Significantcorrelations were observed between preexercise T and percent energyprotein (r = 0.71), percentenergy fat (r = 0.72), saturated fattyacids (g ^· 1,000 kcal^{1 ·} day¹;r = 0.77), monounsaturated fatty acids(g ^· 1,000 kcal^{1 ·} day¹;r = 0.79), the polyunsaturatedfat-to-saturated fat ratio (r = 0.63), and the protein-to-carbohydrate ratio (r = 0.59). There were nosignificant correlations observed between any nutritional variables andpreexercise C or the absolute increase in T and C after exercise. Thesedata confirm that high-intensity resistance exercise results inelevated postexercise T concentrations. A more impressive finding wasthat dietary nutrients may be capable of modulating restingconcentrations of T.

     

Protein kinase C{varepsilon} contributes to regulation of the sarcolemmal Na+-K+ pump

A reduction in angiotensinII (ANG II) in vivo by treatment of rabbits with theangiotensin-converting enzyme inhibitor, captopril, increasesNa⁺-K⁺ pump current (I_p)of cardiac myocytes. This increase is abolished by exposure of myocytesto ANG II in vitro. Because ANG II induces translocation of the-isoform of protein kinase C (PKC), we examined whether thisisozyme regulates the pump. We treated rabbits with captopril, isolatedmyocytes, and measured I_p of myocytes voltageclamped with wide-tipped patch pipettes. I_p ofmyocytes from captopril-treated rabbits was larger thanI_p of myocytes from controls. ANG II superfusionof myocytes from captopril-treated rabbits decreasedI_p to levels similar to controls. Inclusion ofPKC-specific blocking peptide in pipette solutions used to perfusethe intracellular compartment abolished the effect of ANG II. Inclusionof RACK, a PKC-specific activating peptide, in pipettesolutions had an effect on I_p that was similarto that of ANG II. There was no additive effect of ANG II andRACK. We conclude that PKC regulates the sarcolemmalNa⁺-K⁺ pump.

     

Effects of dopamine and domperidone on ventilatory sensitivity to hypoxia after 8h of isocapnic hypoxia

Acclimatization to altitude involves an increase in the acutehypoxic ventilatory response (AHVR). Because low-dose dopamine decreases AHVR and domperidone increases AHVR, the increase in AHVR ataltitude may be generated by a decrease in peripheral dopaminergicactivity. The AHVR of nine subjects was determined with and without aprior period of 8 h of isocapnic hypoxia under each of threepharmacological conditions: 1)control, with no drug administered;2) dopamine (3 µg · min¹ · kg¹);and 3) domperidone (Motilin, 40 mg).AHVR increased after hypoxia (P  0.001). Dopaminedecreased (P  0.01), and domperidone increased (P  0.005) AHVR. The effect of both drugs on AHVR appearedlarger after hypoxia, an observation supported by a significantinteraction between prior hypoxia and drug in the analysis of variance(P  0.05). Although the increasedeffect of domperidone after hypoxia of 0.40 l · min¹ · %saturation¹[95% confidence interval (CI) 0.11 to 0.92 l · min¹ · %¹]did not reach significance, the lower limit for this confidence interval suggests that little of the increase in AHVR after sustained hypoxia was brought about by a decrease in peripheral dopaminergic inhibition.

     

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

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

     

Letters to the Editor

The following is the abstract of the article discussed in thesubsequent letter:

Batterham, Alan M., Keith Tolfrey, and Keith P. George. Nevill's explanation of Kleiber's 0.75 mass exponent: anartifact of collinearity problems in least squares models? J. Appl. Physiol. 82(2): 693-697, 1997.Intraspecificallometric modeling (Y = a · mass^b,where Y is the physiological dependent variable and ais the proportionality coefficient) of peak oxygen uptake(O_2peak) has frequentlyrevealed a mass exponent (b) greater than that predicted fromdimensionality theory, approximating Kleiber's 3/4 exponent for basalmetabolic rate. Nevill (J. Appl. Physiol. 77: 2870-2873,1994) proposed an explanation and a method that restores the inflatedexponent to the anticipated 2/3. In human subjects, the method involvesthe addition of "stature" as a continuous predictor variable in amultiple log-linear regression model: ln Y = ln a + c · ln stature + b · ln mass + ln , where c is the general body size exponent and  isthe error term. It is likely that serious collinearity confounds mayadversely affect the reliability and validity of the model. The aim ofthis study was to critically examine Nevill's method in modelingO_2peak in prepubertal,teenage, and adult men. A mean exponent of 0.81 (95% confidenceinterval, 0.65-0.97) was found when scaling by mass alone.Nevill's method reduced the mean mass exponent to 0.67 (95%confidence interval, 0.44-0.9). However, variance inflation factors and tolerance for the log-transformed stature and mass variables exceeded published criteria for severe collinearity. Principal components analysis also diagnosed severe collinearity in twoprincipal components, with condition indexes >30 and variance decomposition proportions exceeding 50% for two regressioncoefficients. The derived exponents may thus be numerically inaccurateand unstable. In conclusion, the restoration of the mean mass exponentto the anticipated 2/3 may be a fortuitous statistical artifact.

     

Nerve-responsive troponin I slow promoter does not respond to unloading

We examined theregulation of the troponin I slow (TnIs) promoter during skeletalmuscle unloading-induced protein isoform transition, by using atransgenic mouse line harboring the 4,200 to +12 base pairsregion of the human TnIs promoter. Eighteen female transgenic mice(~30 g body mass) were randomly divided into two groups:weight-bearing (WB) controls (n = 9)and hindlimb unloaded (HU; n = 9). TheHU mice were tail suspended for 7 days. Body mass was unchanged in theWB group but was reduced (6%; P < 0.05) after the HU treatment.Absolute soleus muscle mass (25%) and soleus mass relative tobody mass (16%) were both lower(P < 0.05) in the HU group comparedwith the WB mice. Northern blot analyses indicate that 7 days of HUresult in a 64% decrease (P < 0.05)in the abundance of endogenous TnIs mRNA (µg/mg muscle) in the mousesoleus. Furthermore, there is a trend for the abundance of the fasttroponin I mRNA to be increased (+34%). Analysis of transgenicchloramphenicol acetyltransferase activity in the soleus musclerevealed no difference (P > 0.05)between WB and HU groups. We conclude that additional elements arenecessary for the TnIs gene to respond to an unloading-induced,slow-to-fast isoform transition stimulus.

     

Susceptibility to periodic breathing with assisted ventilation during sleep in normal subjects

Assisted ventilation with pressure support (PSV)or proportional assist (PAV) ventilation has the potential to produceperiodic breathing (PB) during sleep. We hypothesized that PB willdevelop when PSV level exceeds the product of spontaneous tidal volume (VT) and elastance(VT_sp · E)but that the actual level at which PB will develop[PSV(PB)] will be influenced by thePCO₂ (difference between eupneicPCO₂ andCO₂ apneic threshold) and by RR[response of respiratory rate (RR) to PSV]. We also wishedto determine the PAV level at which PB develops to assess inherentventilatory stability in normal subjects. Twelve normal subjectsunderwent polysomnography while connected to a PSV/PAV ventilatorprototype. Level of assist with either mode was increased in smallsteps (2-5 min each) until PB developed or the subject awakened.End-tidal PCO₂,VT, RR, and airway pressure (Paw) were continuously monitored, and the pressure generated byrespiratory muscle (Pmus) was calculated. The pressure amplification factor (PAF) at the highest PAV level was calculated from[(Paw + Pmus)/Pmus], where Paw is peak Paw  continuous positive airway pressure. PB with central apneas developedin 11 of 12 subjects on PSV. PCO₂ranged from 1.5 to 5.8 Torr. Changes in RR with PSV were small andbidirectional (+1.1 to 3.5min¹). With use ofstepwise regression, PSV(PB) was significantly correlated withVT_sp(P = 0.001), E(P = 0.00009),PCO₂ (P = 0.007), and RR(P = 0.006). The final regressionmodel was as follows: PSV(PB) = 11.1 VT_sp + 0.3E  0.4 PCO₂  0.34 RR  3.4 (r = 0.98). PBdeveloped in five subjects on PAV at amplification factors of1.5-3.4. It failed to occur in seven subjects, despite PAF of upto 7.6. We conclude that 1) aPCO₂ apneic threshold exists duringsleep at 1.5-5.8 Torr below eupneicPCO₂,2) the development of PB during PSVis entirely predictable during sleep, and3) the inherent susceptibility to PBvaries considerably among normal subjects.

     

Airway thermal volume in humans and its relation to body size

Serikov, Vladimir B., E. Heidi Jerome, Neal W. Fleming,Peter G. Moore, Frederick A. Stawitcke, and Norman C. Staub.Airway thermal volume in humans and its relation to body size.J. Appl. Physiol. 83(2): 668-676, 1997.The objective of this study was to investigate the influence ofvolume ventilation(E) andcardiac output () on the temperature of the expiredgas at the distal end of the endotracheal tube in anesthetized humans.In 63 mechanically ventilated adults, we used a step decrease in thehumidity of inspired gas to cool the lungs. After change from humid todry gas ventilation, the temperature of the expired gas decreased. Weevaluated the relationship between the inverse monoexponential timeconstant of the temperature fall (1/) and eitherE or . WhenE wasincreased from 5.67 ± 1.28 to 7.14 ± 1.60 (SD) l/min(P = 0.02), 1/ did not changesignificantly [from 1.25 ± 0.38 to 1.21 ± 0.51 min¹,P = 0.81]. In the 11 patients in whom changed during the study period(from 5.07 ± 1.81 to 7.38 ± 2.45 l/min,P = 0.02), 1/ increasedcorrespondingly from 0.89 ± 0.22 to 1.52 ± 0.44 min¹(P = 0.003). We calculated the airwaythermal volume (ATV) as the ratio of the measured values to 1/ and related it to the body height (BH):ATV (liters) = 0.086 BH (cm)  9.55 (r = 0.90).

     

Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response toexercise in diabetic subjects with autonomic neuropathy.J. Appl. Physiol. 81(5):1978-1986, 1996.We have used diabetic autonomic neuropathy as amodel of chronic pulmonary denervation to study the ventilatoryresponse to incremental exercise in 20 diabetic subjects, 10 with(Dan+) and 10 without (Dan) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan subjectsachieved lower O₂ consumption andCO₂ production(CO₂) thancontrol subjects at peak of exercise, they attained similar values ofeither minute ventilation(E) oradjusted ventilation (E/maximalvoluntary ventilation). The increment of respiratory rate withincreasing adjusted ventilation was much higher in Dan+ than inDan and control subjects (P < 0.05). The slope of the linearE/CO₂relationship was 0.032 ± 0.002, 0.027 ± 0.001 (P < 0.05), and 0.025 ± 0.001 (P < 0.001) ml/min inDan+, Dan, and control subjects, respectively. Bothneuromuscular and ventilatory outputs in relation to increasingCO₂ were progressivelyhigher in Dan+ than in Dan and control subjects. At peak ofexercise, end-tidal PCO₂ was muchlower in Dan+ (35.9 ± 1.6 Torr) than in Dan (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects.We conclude that pulmonary autonomic denervation affects ventilatoryresponse to stressful exercise by excessively increasing respiratoryrate and alveolar ventilation. Reduced neural inhibitory modulationfrom sympathetic pulmonary afferents and/or increasedchemosensitivity may be responsible for the higher inspiratoryoutput.

     

Responses of Soybean Leaf Angle, Photosynthesis and Stomatal Conductance to Leaf and Soil Water Potential

The hypothesis that soil water potential (_s) is better correlatedto heliotropic leaf orientation, photosaturated photosyntheticCO₂ assimilation and stomatal conductance during periods oflimited water availability than is bulk leaf water potential(₁) was examined in greenhouse-grown soybean (Glycine max) plants,submitted to a progressive drought. Paired plants were exposedto either 1000 or 100 µmol m^–2 s^–1 photonflux densities (PFD) for 45–60 mins. The higher irradianceinduced short-term decreases in ₁, due to increased transpiration,while _l in the plant exposed to low PFD did not decrease. Thesechanges in ₁ occurred independently of changes in soil waterstatus. Concurrent to the light treatments, a single attachedleaf from each of the two plants was isolated from the restof the plant by shading, and the pulvinus of its terminal leafletwas exposed to a perpendicular PFD of 500 µmol m–²S^–1. Leaf movement of this leaflet was recorded in responseto this light, until a stable leaflet angle was achieved. Valuesof _s and _l (before and after light treatment), and photosaturatedrates of photosynthesis and stomatal conductance, were thenmeasured on these leaves. Leaflet angle and gas exchange werebetter correlated with _s (r² = 0.50, 0.50 and 0.57 for angle,photosynthesis and conductance, respectively) than with _l especiallywhen _l was the result of short-term, high-light induced changesin leaf water status (r² = 0.36, 0.32 and 0.49, for the sameparameters). Leaflet angle was also correlated with stomatalconductance (r² = 0.61) and photosynthetic rate (r² = 0.60),suggesting a close association between leaf orientation, leafmetabolism and soil water availability. Glycine max (L.) Merr. cv. Essex, soybean, heliotropism, water potential, photosynthesis, stomatal conductance, solar tracking     

H2O2 increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin

Wells, U. M., S. Duneclift, and J. G. Widdicombe.H₂O₂increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin. J. Appl.Physiol. 82(2): 621-631, 1997.Exogenous hydrogenperoxide(H₂O₂)causes airway epithelial damage in vitro. We have studied the effectsof luminalH₂O₂in the sheep trachea in vivo on tracheal permeability tolow-molecular-weight hydrophilic (technetium-99m-labeleddiethylenetriamine pentaacetic acid;^99mTc-DTPA) and lipophilic([¹⁴C]antipyrine;[¹⁴C]AP) tracers andon the tracheal vascular response to luminal capsaicin, whichstimulates afferent nerve endings. A tracheal artery was perfused, andtracheal venous blood was collected. H₂O₂exposure (10 mM) reduced tracheal potential difference(42.0 ± 6.4 mV) to zero. It increased arterial andvenous flows (56.7 ± 6.1 and 57.3 ± 10.0%,respectively; n = 5, P < 0.01, paired t-test) but not tracheal lymph flow(unstimulated flow 5.0 ± 1.2 µl ^· min^{1 ·} cm¹,n = 4). DuringH₂O₂exposure, permeability to ^99mTc-DTPA increased from2.6 to 89.7 × 10⁷ cm/s(n = 5, P < 0.05), whereas permeability to[¹⁴C]AP (3,312.6 × 10⁷ cm/s,n = 4) was not altered significantly(2,565 × 10⁷cm/s). Luminal capsaicin (10 µM) increased tracheal blood flow (10.1 ± 4.1%, n = 5)and decreased venous ^99mTc-DTPAconcentration (19.7 ± 4.0, P < 0.01), and these effects weresignificantly greater after epithelial damage (28.1 ± 6.0 and45.7 ± 4.3%, respectively,P < 0.05, unpairedt-test). Thus H₂O₂increases the penetration of a hydrophilic tracer into tracheal bloodand lymph but has less effect on a lipophilic tracer. It also enhancesthe effects of luminal capsaicin on blood flow and tracer uptake.

     

Cardiovascular responses to treadmill and cycle ergometer exercise in children and adults

Turley, Kenneth R., and Jack H. Wilmore. Cardiovascularresponses to treadmill and cycle ergometer exercise in children andadults. J. Appl. Physiol. 83(3):948-957, 1997.This study was conducted to determine whethersubmaximal cardiovascular responses at a given rate of work aredifferent in children and adults, and, if different, what mechanismsare involved and whether the differences are exercise-modalitydependent. A total of 24 children, 7 to 9 yr old, and 24 adults, 18 to26 yr old (12 males and 12 females in each group), participated in bothsubmaximal and maximal exercise tests on both the treadmill and cycleergometer. With the use of regression analysis, it was determined thatcardiac output () was significantly lower(P  0.05) at a givenO₂ consumption level(O₂, l/min) in boys vs. menand in girls vs. women on both the treadmill and cycle ergometer. Thelower in the children was compensated for by asignificantly higher (P  0.05)arterial-mixed venous O₂difference to achieve the same or similarO₂. Furthermore, heart rateand total peripheral resistance were higher and stroke volume was lowerin the children vs. in the adult groups on both exercise modalities.Stroke volume at a given rate of work was closely related to leftventricular mass, with correlation coefficients ranging fromr = 0.89-0.92 andr = 0.88-0.93 in the males and females, respectively. It was concluded that submaximal cardiovascular responses are different in children and adults and that these differences are related to smaller hearts and a smaller absolute amountof muscle doing a given rate of work in the children. The differenceswere not exercise-modality dependent.

     

What hypothesis tests are not: a reply to Johnson

We are sorry that Johnson's pleasure at reading our recent paper(Colegrave and Ruxton, 2003) was so short-lived. Johnson (2005)is correct that the definition of the P value that we use inthe paper is incorrect, and we are grateful