Beck, Ken C.

Background Physical activity has been proposed as a risk factor for altitude illness however it is unclear whether the total amount or intensity of activity determines illness. Purpose To examine activity patterns relative to the incidence of acute mountain sickness (AMS) in United States Antarctic Program workers rapidly transported to the South Pole (SP, 9303 ft). Methods 53 medically screened subjects (age=37±10yr, BMI=24±3 kg/m 2 ) were transported by a 3 hour flight from McMurdo Station (sea level, SL) to the SP. Physical activity was monitored at SL and for 3 days after ascent using BodyMedia® activity monitors. Symptoms of AMS were assessed using Lake Louise Questionnaires. Results 53% of subjects displayed AMS between SP days 1–3 (23% day 1, 43% day 2, 15% day 3). Energy expenditure at SP was 3414±944, 3458±781, & 3543±869 Calories/day for days 1–3, respectively. Steps/day at SP was 12593±4926, 13124±4392, & 12966±4482 for days 1–3, respectively. Overall, more activity at higher intensity (>3 METS) on SP day 1 was associated with higher AMS incidence the next morning (p<0.05). Also, calorie expenditure with activity at >3 METS and time of activity at >6 METS in the first 24 hours after ascent independently increased the odds of AMS on SP day 2 (p<0.05). Conclusions With rapid transport to altitude, moderate to intense activity within the first 24 hours of ascent contributes to the incidence of AMS. NSF ANT 0540710

Maximal expiratory flows (MEF) are dependent on gas density, lung volume, subject effort and airway characteristics. Variable changes in MEF occur after ascent to altitude which may represent an interaction between gas density changes, catecholamine stimulation and mild interstitial edema. Hypoxia induced catecholamine up‐regulation has also been associated with acute mountain sickness (AMS). This study examined the association between MEF variability and AMS symptoms in United States Antarctic Program personnel (n=198, age 37±1 yrs, 3% asthma) rapidly transported to the South Pole (SP, 9302 ft). Spirometric parameters, epinephrine (Epi), norepinepherine (NE) and SaO2 levels were recorded at sea level (SL, McMurdo Station) and after the 2 nd night at SP. AMS was assessed using Lake Louise questionnaires (score ≥ 3). FVC, FEV 1 , FEF 25 , FEF 75 and FEF 25–75 increased by 0, 3, 17, 10 and 14% from SL to SP, respectively. On day 2, AMS incidence was 31% and Epi and NE increased by 44 and 71%. Changes in MEF ranged from −64 to +93% in FEF 25–75 and −63 to +70% in FEF 75 . Subjects with the greatest increase in MEF had higher incidence of AMS (24 vs 41%) and higher NE levels, while the subjects with the greatest decrease in MEF had lower SaO2 values (88 vs 90%). Subjects with increased MEF had increased AMS and bronchodilation while subjects with decreased MEF displayed values consistent with mild interstitial edema.

Microspheres (MS) are often used to measure the distribution of pulmonary blood flow in the assumption that the number of MS trapped in a region is proportional to blood flow. However, regional distribution of trapped MS has not been directly compared with regional blood flow in the lung. Regional trapping of MS was compared with regional flow of erythrocytes (RBC's) in isolated, perfused left lungs of dogs. Radioactivity from labeled MS and RBC's was measured by external detection using a gamma camera. We defined six regions of interest in the image of the left lateral surface of the lung: a dorsocaudal, a caudal, two ventral, an apical, and a central region. In each lung, regional trapping of MS was measured from the image of radioactivity obtained after slow injection of a suspension of MS into the arterial perfusion tubing. A radioactive bolus of labeled RBC's was injected during rapid imaging of the lung to obtain radioactivity vs. time curves from each region. The peaks of the regional radioactivity vs. time curves were used to estimate regional flows, though compensation had to be made for overlap of the washout and washin phases of the bolus of labeled RBC's. The results indicated that there were no differences in the regional distribution of MS compared with the regional distribution of RBC flow in isolated, perfused dog lungs.

Abstract To demonstrate physiologic changes associated with asthma symptoms that many patients with asthma develop during exercise, we used sustained constant-load and interval exercise protocols with subjects breathing dry room temperature air. In constant-load exercise, subjects pedaled a stationary bicycle at 50% of their maximal power capacity for 36 min. In interval protocols, subjects pedaled at 60% of maximal capacity for 6 min and then 40% of maximal for 6 min; the 12-min cycle was repeated three times for a total exercise time of 36 min. Maximal expiratory flow versus volume maneuvers (MEFV) were obtained before, at 6-min intervals during, and at 5-min intervals after exercise. Changes in peak expiratory flow (PEF), forced expiratory volume in 1 s (FEV1), and forced expiratory flow at 50% of pre-exercise vital capacity (FEF50) were compared with pre-exercise values. Within 15 min after a maximal 1-min incremental exercise protocol, mean flows decreased compared with pre-exercise (PEF, mean -22%, range -46 to 5%; FEV1, mean -21%, range -42 to -3%; FEF50, mean -41%, range -80 to 3%; all p &lt; 0.05). There were no significant changes in MEFV flows until 18 min of constant-load exercise, when FEV1 and FEF50 fell (FEV1, mean -6%, range -15 to 2%; FEF50, mean -14%, range -32 to 6%; both p &lt; 0.05), although changes in PEF were minimal and were not significantly different compared with pre-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Background— The gene encoding ACE exhibits an insertion/deletion polymorphism resulting in 3 genotypes (DD, ID, and II), which affects serum and tissue ACE activity as well as other vasoactive substances. Pulmonary function is frequently abnormal in patients with congestive heart failure (CHF), the mechanism of which has not been completely characterized. ACE inhibition has been shown to improve diffusion across the alveolar-capillary membrane and to improve exercise capacity and gas exchange in CHF. The aim of the current study was to determine if ACE genotype is associated with altered pulmonary function and exercise intolerance in patients with treated CHF. Methods and Results— Fifty-seven patients (stratified according to ACE genotype as17 DD, 28 ID, 12 II) with ischemic and dilated cardiomyopathy, left ventricular ejection fraction (LVEF) <35%, and <10 pack-years of smoking history were studied. All patients were receiving standard therapy for left ventricular systolic dysfunction. Pulmonary function, LVEF, serum ACE, plasma angiotensin II, atrial natriuretic peptide, and brain natriuretic peptide were measured at baseline. Peak V̇ o 2 and gas exchange measurements were assessed with graded exercise. Resting LVEF was similar among the genotype groups (25% to 28%), and no differences were observed in diastolic function or pulmonary artery pressures ( P >0.05). Mean peak V̇ o 2 and forced vital capacity (% Pred) were significantly reduced ( P <0.05), whereas mean serum ACE activity and plasma angiotensin II concentration were highest in DD homozygotes. Subjects homozygous for the D-allele also demonstrated higher mean ventilatory equivalents for carbon dioxide (V̇ e /V̇ co 2 ) during exercise ( P <0.05). Conclusions— ACE DD genotype is associated with decreased exercise tolerance in CHF, possibly mediated by altered pulmonary function. Pharmacological strategies effecting more complete inhibition of serum and tissue ACE and/or potentiation of bradykinin may improve exercise capacity in patients with CHF and ACE DD genotype.