Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygenuptake (O_{2 max}): 57 ± 6 ml · kg¹ · min¹;35-70ml · kg¹ · min¹]to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age-and height-matched men. The higher maximal workload in highly fit(O_{2 max} > 57 ml · kg¹ · min¹,n = 14) vs. less-fit(O_{2 max} < 56 ml · kg¹ · min¹,n = 15) women caused a higher maximalventilation (E) with increased tidal volume (VT)and breathing frequency (f_b) atcomparable maximal VT/vitalcapacity (VC). More expiratory flow limitation (EFL; 22 ± 4% ofVT) was also observed duringheavy exercise in highly fit vs. less-fit women, causing higherend-expiratory and end-inspiratory lung volumes and greater usage oftheir maximum available ventilatory reserves.HeO₂ (79% He-21%O₂) vs. room air exercise trialswere compared (with screens added to equalize external apparatusresistance). HeO₂ increasedmaximal expiratory flow rates (20-38%) throughout the range ofVC, which significantly reduced EFL during heavy exercise. When EFL wasreduced with HeO₂, VT,f_b, andE (+16 ± 2 l/min) weresignificantly increased during maximal exercise. However, in theabsence of EFL (during room air exercise),HeO₂ had no effect onE. We conclude that smaller lungvolumes and maximal flow rates for women in general, and especiallyhighly fit women, caused increased prevalence of EFL during heavyexercise, a relative hyperinflation, an increased reliance onf_b, and a greater encroachment onthe ventilatory "reserve." Consequently,VT andE are mechanically constrained duringmaximal exercise in many fit women because the demand for highexpiratory flow rates encroaches on the airways' maximum flow-volumeenvelope.

     

Effects of prior exercise on exercise-induced arterial hypoxemia in young women

Twenty-eighthealthy women (ages 27.2 ± 6.4 yr) with widely varying fitnesslevels [maximal O₂consumption (O_{2 max}),31-70 ml · kg¹ · min¹]first completed a progressive incremental treadmill test to O_{2 max} (totalduration, 13.3 ± 1.4 min; 97 ± 37 s at maximal workload), rested for 20 min, and then completed a constant-load treadmill test at maximal workload (total duration, 143 ± 31 s). Atthe termination of the progressive test, 6 subjects had maintained arterial PO₂(Pa_O2) near resting levels, whereas 22 subjects showed a >10 Torr decrease inPa_O2 [78.0 ± 7.2 Torr, arterial O₂ saturation(Sa_O2), 91.6 ± 2.4%], andalveolar-arterial O₂ difference (A-aD_O2,39.2 ± 7.4 Torr). During the subsequent constant-load test, allsubjects, regardless of their degree of exercise-induced arterialhypoxemia (EIAH) during the progressive test, showed a nearly identicaleffect of a narrowed A-aD_O2(4.8 ± 3.8 Torr) and an increase inPa_O2 (+5.9 ± 4.3 Torr) andSa_O2 (+1.6 ± 1.7%) compared with atthe end point of the progressive test. Therefore, EIAH during maximalexercise was lessened, not enhanced, by prior exercise, consistent withthe hypothesis that EIAH is not caused by a mechanismwhich persists after the initial exercise period and is aggravated bysubsequent exercise, as might be expected of exercise-inducedstructural alterations at the alveolar-capillary interface. Rather,these findings in habitually active young women point to a functionallybased mechanism for EIAH that is present only during the exerciseperiod.

     

Respiratory muscle work compromises leg blood flow during maximal exercise

Harms, Craig A., Mark A. Babcock, Steven R. McClaran, DavidF. Pegelow, Glenn A. Nickele, William B. Nelson, and Jerome A. Dempsey.Respiratory muscle work compromises leg blood flow during maximalexercise. J. Appl. Physiol.82(5): 1573-1583, 1997.We hypothesized that duringexercise at maximal O₂ consumption (O_{2 max}),high demand for respiratory muscle blood flow() would elicit locomotor muscle vasoconstrictionand compromise limb . Seven male cyclists(O_{2 max} 64 ± 6 ml · kg¹ · min¹)each completed 14 exercise bouts of 2.5-min duration atO_{2 max} on a cycleergometer during two testing sessions. Inspiratory muscle work waseither 1) reduced via aproportional-assist ventilator, 2)increased via graded resistive loads, or3) was not manipulated (control).Arterial (brachial) and venous (femoral) blood samples, arterial bloodpressure, leg (legs;thermodilution), esophageal pressure, andO₂ consumption(O₂) weremeasured. Within each subject and across all subjects, at constantmaximal work rate, significant correlations existed(r = 0.74-0.90;P < 0.05) between work of breathing(Wb) and legs (inverse), leg vascular resistance (LVR), and leg O₂(O_{2 legs};inverse), and between LVR and norepinephrine spillover. Mean arterialpressure did not change with changes in Wb nor did tidal volume orminute ventilation. For a ±50% change from control in Wb,legs changed 2 l/min or 11% of control, LVRchanged 13% of control, and O₂extraction did not change; thusO_{2 legs}changed 0.4 l/min or 10% of control. TotalO_{2 max} was unchangedwith loading but fell 9.3% with unloading; thusO_{2 legs}as a percentage of totalO_{2 max} was 81% incontrol, increased to 89% with respiratory muscle unloading, anddecreased to 71% with respiratory muscle loading. We conclude that Wbnormally incurred during maximal exercise causes vasoconstriction inlocomotor muscles and compromises locomotor muscle perfusion andO₂.

     

Sonoran Desert Ecosystem transformation by a C4 grass without the grass/fire cycle

Aim Biological invasions facilitate ecosystem transformation by altering the structure and function, diversity, dominance and disturbance regimes. A classic case is the grass–fire cycle in which grass invasion increases the frequency, scale and/or intensity of wildfires and promotes the continued invasion of invasive grasses. Despite wide acceptance of the grass–fire cycle, questions linger about the relative roles that interspecific plant competition and fire play in ecosystem transformations. Location Sonoran Desert Arizona Upland of the Santa Catalina Mountains, Arizona, USA. Methods We measured species cover, density and saguaro (Carnegiea gigantea) size structure along gradients of Pennisetum ciliare invasion at 10 unburned/ungrazed P. ciliare patches. Regression models quantified differences in diversity, cover and density with respect to P. ciliare cover, and residence time and a Fisher’s exact test detected demographic changes in saguaro populations. Because P. ciliare may have initially invaded locations that were both more invasible and less diverse, we ran analyses with and without the plots in which initial infestations were located. Results Richness and diversity decreased with P. ciliare cover as did cover and density of most dominant species. Richness and diversity declined with increasing time since invasion, suggesting an ongoing transformation. The proportion of old‐to‐young Carnegiea gigantea was significantly lower in plots with dominant P. ciliare cover. Main conclusions Rich desert scrub (15–25 species per plot) was transformed into depauperate grassland (2–5 species per plot) within 20 years following P. ciliare invasion without changes to the fire regime. While the onset of a grass–fire cycle may drive ecosystem change in the later stages and larger scales of grass invasions of arid lands, competition by P. ciliare can drive small‐scale transformations earlier in the invasion. Linking competition‐induced transformation rates with spatially explicit models of spread may be necessary for predicting landscape‐level impacts on ecosystem processes in advance of a grass–fire cycle.     

Desert grassland dynamics estimated from carbon isotopes in grass phytoliths and soil organic matter

Abstract. We document the potential for using carbon isotopes in both soil organic matter (SOM) and grass phytoliths in soil to increase the temporal and taxonomic resolutions of long term vegetation dynamics. Carbon isotope values from both SOM and phytoliths are expected to describe both the age of material through ¹⁴C dating, and the photosynthetic pathway of the source plant material through ratios of ¹²C/¹³C. Taxonomic resolution is increased because the phytoliths examined are specific to grasses, whereas the SOM reflects the contribution of all the vegetation. Temporal resolution is increased because phytoliths are less mobile in the soil profile than SOM, and can therefore provide older dates from the same soil depth. Our results, from a desert grassland site in southwestern North America, largely confirm these expectations, and show that C₄ species have dominated the grass composition for the last 8000 yr, C₃ non‐grass vegetation increased about 100–350 yrBP, and no significant C₃ grass or non‐grass vegetation existed between 350–2000 yr BP.     

Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise

We have recently demonstrated that changes inthe work of breathing during maximal exercise affect leg blood flow andleg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573-1583,1997). Our present study examined the effects of changesin the work of breathing on cardiac output (CO) during maximalexercise. Eight male cyclists [maximalO₂ consumption(O_{2 max}):62 ± 5 ml · kg¹ · min¹]performed repeated 2.5-min bouts of cycle exercise atO_{2 max}. Inspiratorymuscle work was either 1) at controllevels [inspiratory esophageal pressure (Pes): 27.8 ± 0.6 cmH₂O],2) reduced via a proportional-assistventilator (Pes: 16.3 ± 0.5 cmH₂O), or 3) increased via resistive loads(Pes: 35.6 ± 0.8 cmH₂O).O₂ contents measured in arterialand mixed venous blood were used to calculate CO via the direct Fickmethod. Stroke volume, CO, and pulmonaryO₂ consumption(O₂) were not different(P > 0.05) between control andloaded trials atO_{2 max} but were lower(8, 9, and 7%, respectively) than control withinspiratory muscle unloading atO_{2 max}. Thearterial-mixed venous O₂difference was unchanged with unloading or loading. We combined thesefindings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effectson the cardiovascular system: 1) upto 14-16% of the CO is directed to the respiratory muscles; and2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.

     

Role of expiratory flow limitation in determining lung volumes and ventilation during exercise.

We determined the role of expiratory flow limitation (EFL) on the ventilatory response to heavy exercise in six trained male cyclists [maximal O2 uptake = 65 +/- 8 (range 55-74) ml. kg-1. min-1] with normal lung function. Each subject completed four progressive cycle ergometer tests to exhaustion in random order: two trials while breathing N2O2 (26% O2-balance N2), one with and one without added dead space, and two trials while breathing HeO2 (26% O2-balance He), one with and one without added dead space. EFL was defined by the proximity of the tidal to the maximal flow-volume loop. With N2O2 during heavy and maximal exercise, 1) EFL was present in all six subjects during heavy [19 +/- 2% of tidal volume (VT) intersected the maximal flow-volume loop] and maximal exercise (43 +/- 8% of VT), 2) the slopes of the ventilation (DeltaVE) and peak esophageal pressure responses to added dead space (e.g., DeltaVE/DeltaPETCO2, where PETCO2 is end-tidal PCO2) were reduced relative to submaximal exercise, 3) end-expiratory lung volume (EELV) increased and end-inspiratory lung volume reached a plateau at 88-91% of total lung capacity, and 4) VT reached a plateau and then fell as work rate increased. With HeO2 (compared with N2O2) breathing during heavy and maximal exercise, 1) HeO2 increased maximal flow rates (from 20 to 38%) throughout the range of vital capacity, which reduced EFL in all subjects during tidal breathing, 2) the gains of the ventilatory and inspiratory esophageal pressure responses to added dead space increased over those during room air breathing and were similar at all exercise intensities, 3) EELV was lower and end-inspiratory lung volume remained near 90% of total lung capacity, and 4) VT was increased relative to room air breathing. We conclude that EFL or even impending EFL during heavy and maximal exercise and with added dead space in fit subjects causes EELV to increase, reduces the VT, and constrains the increase in respiratory motor output and ventilation.