Edward T. Mannix

TISSUE WASTING IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE, THE ACQUIRED IMMUNE DEFICIENCY SYNDROME, AND CONGESTIVE HEART FAILURE

Malnutrition is common among individuals suffering from hypoxemic chronic obstructive pulmonary disease (COPD), advanced HIV disease, and in patients with chronic, severe congestive heart failure. Although increased morbidity and mortality has been associated with weight loss in these conditions, the pathophysiology of malnutrition remains somewhat unclear for each. In COPD, the primary postulated mechanism is hypermetabolism resulting in elevated total caloric expenditure arising from increased airway resistance, increased O2 cost of ventilation, increased dietary induced thermogenesis, inefficient substrate use and perhaps, increased levels of proinflammatory cytokines. In AIDS, postulated mechanisms include hypermetabolism arising from increased activation of proinflammatory cytokines, along with futile cycling of fatty acids and de novo lipogenesis early in the course of HIV infection; intestinal malabsorption and anorexia also play a role in many inflicted individuals. In cardiac cachexia, dietary and metabolic factors, and levels and activity of cytokines, thyroid hormone, catecholamines and cortisol have been suggested as being responsible for causing weight loss in a most cases.

Atrial natriuretic peptide and the renin-aldosterone axis during exercise in man.

Under non-exercise conditions, atrial natriuretic peptide (ANP) elevation suppresses plasma renin activity (PRA) and aldosterone (PA). A similar effect of ANP on PRA-PA during exercise has been suggested but not demonstrated. We measured ANP, PRA, PA, plasma potassium (K+), and changes in plasma volume (PV) and blood volume (BV) at rest and during incremental cycle ergometer exercise to exhaustion in ten healthy males. Plasma concentrations (mean +/- SE) of hormones and electrolytes increased (P less than 0.05) during exercise: ANP (68 +/- 14 to 207 +/- 48 pg.ml-1), PA (11.2 +/- 2.2 to 18.8 +/- 3.4 ng.dl-1), PRA (5.1 +/- 1.1 to 8.2 +/- 1.6 ng.ml-1.90 min-1), and K+ (4.2 +/- 0.1 to 5.5 +/- 0.1 mEq). PV and BV declined, reaching maximal deflections from baseline during the 100% stage (12.9 +/- 1.5 and 8.4 +/- 0.8% decreases, respectively). There were positive correlations between ANP and PRA (r = 0.58; P less than 0.01), ANP and PA (r = 0.56; P less than 0.01), and PRA and PA (r = 0.80; P less than 0.001). Increases in K+ did not correlate with increases in PA. The fall in PV correlated with elevations in PRA (r = -0.67; P less than 0.01) and PA (r = -0.58; P less than 0.01), and the fall in BV correlated with elevations in PRA (r = -0.62; P less than 0.01) and PA (r = -0.44; P less than 0.02). ANP production was related to exercise intensity (gauged by heart rate response; r = 0.58; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Airways Hyperresponsiveness in High School Athletes

Adult athletes have a higher prevalence (11%–50%) of exercise‐induced bronchoconstriction (EIB) and airways hyperresponsiveness (AHR) than the population at large (7%–11%): reports describing EIB/AHR in adolescent athletes are scant. Hypotheses: 1) a minimum AHR prevalence of 20% would be revealed in a group of high school athletes; 2) demographic data would predict AHR; 3) AHR‐positive athletes would preferentially choose low ventilation sports. Eucapnic voluntary hyperpnea (EVH) was used to test for AHR in 23% of all athletes (79 of 343) of a midwestern high school. The AHR was defined by at least a 10%, 20%, or 25% decline in FEV1, FEF25–75, or PEFR at 1, 5, 10, or 15‐min post‐EVH, respectively. Results: 30 of 79 (38%) tested positive for AHR; demographic data tended to predict AHR, as correlations between the total number of years exercised with the greatest decline in FEV1 and the total number of days exercised with the greatest decline in FEV1 following the EVH challenge tended to be significant (r = 0.354; p = 0.055 and r = 0.314; p = 0.091, respectively); and 69% of AHR‐positive students played only low ventilation sports. Conclusion: AHR prevalence was 38% in athletes of a midwestern high school; demographic data tended to predict AHR; those with AHR preferentially play low ventilation sports.

Oxygen delivery and cardiac output during exercise following oral phosphate-glucose

Phosphate has been proposed as an ergogenic aid since it may enhance O2 delivery and cardiac work efficiency by increasing plasma phosphate (P Pi), red blood cell phosphate (RBC Pi), 2,3-diphosphoglycerate (DPG), RBC adenosine triphosphate (ATP), and P50. In 10 normal, fasting males we measured cardiac output (Q) by CO2 rebreathing, heart rate (HR), O2 deficit (O2DEF), and O2 consumption (VO2) during cycle ergometer exercise (60% of peak VO2). Stroke volume (SV) and arteriovenous O2 difference (A-VO2) were calculated. Following a baseline blood sample (BASE) for P Pi, RBC Pi, DPG, RBC ATP, and P50 (3 h before exercise), a single oral dose of dicalcium phosphate (129 mmol) and glucose (500 ml/10% sol, PHOS), or placebo (PLA), was administered in a random, crossover, double-blind fashion. Blood sampling was repeated immediately before and after exercise (PRE-EX and POST-EX). PHOS induced increases in P Pi (3.87 to 4.35 mg.dl-1, P less than 0.05), RBC Pi (3.86 to 4.63 mg.dl-1, P = 0.08), DPG (11.8 to 13.1 mumol.g-1 Hb, P less than 0.05), RBC ATP (4.2 to 4.4 mumol.g-1 Hb, P less than 0.05), and P50 (26.8 to 27.9 mm Hg, P less than 0.05) from BASE to PRE-EX. All variables remained elevated through the exercise period, as evidenced by higher levels than BASE at POST-EX (P less than 0.05). However, P50 was not different across conditions at PRE-EX (PHOS P50 = 27.9, PLA P50 = 28.3 mm Hg) or POST-EX (PHOS P50 = 28.0, PLA P50 = 28.1 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic, renal, and hormonal responses to lower body positive pressure in human subjects

Studies in healthy human subjects subjected to lower body positive pressure (LBPP) have failed to elucidate many of the physiologic effects of this maneuver. In 7 healthy, well-hydrated men we studied the following responses to LBPP (35 mm Hg, 1 hour, supine position): systemic and renal hemodynamics; urine volume (UV), urine osmolality (Uosm), and urine sodium level (UNaV); free water (CH20) and osmolar (Cosm) clearances; plasma renin activity (PRA); levels of aldosterone (PA), cortisol (CORT), norepinephrine (NE), atrial natriuretic peptide (ANP), and vasopressin (AVP); osmolality (Posm); and serum sodium level. Subjects were restudied on a control day with zero trouser pressure. The recorded changes (p < 0.05) when comparing the LBPP day with the control day were as follows: fractional Na+ reabsorption increased (98.7% +/- 0.2% to 99.3% +/- 0.1%) and UNaV decreased (0.19 +/- 0.03 mEq/min to 0.10 +/- 0.01 mEq/min), with concomitant increases in PRA (1.7 +/- 0.2 ng/ml/90 min to 4.5 +/- 1.8 ng/ml/90 min), PA (7.7 +/- 0.7 ng/dl to 9.3 +/- 1.5 ng/dl), and CORT (13.0 +/- 2.6 mg/dl to 19.2 +/- 3 mg/dl); the increase in blood pressure with LBPP (96 +/- 3 mm Hg to 112 +/- 4 mm Hg) was greater than that during control conditions. Renal plasma flow tended to display an interactive pattern across days, with a slight decline during LBPP (5%) and a slight elevation under control conditions (9%). On the LBPP day only, filtered Na+ declined (15 +/- I mEq/min to 12 +/- 1 mEq/min) as a function of reduced glomerular filtration rate (112 +/- 5 ml/min to 91 +/- 7 ml/min), blood volume decreased (by 2.7% +/- 0.7%), CO decreased (5.5 +/- 0.3 L/min to 4.7 +/- 0.3 L/min), and stroke volume declined (101 +/- 6 ml to 84 +/- 3 ml). On both days, NE increased (control, 221 +/- 23 pg/ml to 340 +/- 33 pg/ml; LBPP, 236 +/- 17 pg/ml to 369 +/- 31 pg/ml) and ANP increased (control, 47 +/- 7 pg/ml to 97 +/- 21 pg/ml; LBPP, 49 +/- 10 pg/ml to 104 +/- 30 pg/ml). We concluded that LBPP reduces renal sodium excretion. The mechanism for this reduction is not known, although it did occur in association with an increase in plasma renin activity, which in turn results from mechanical reduction of renal perfusion, stress-related CORT stimulation, a reflex-based elevation in peripheral vascular resistance leading to a reflex increase in plasma renin activity, or a combination of these.

The Role of Physical Activity, Exercise, and Nutrition in the Treatment of Obesity

The increasing prevalence of obesity and overweight has caused many experts to declare that a “health care epidemic of being overweight and obese” is gripping our nation and becoming a significant health care problem. According to a published report cited by The National Institutes for Health (NIH) (1), as of the late 1990s, more than half of the adults in the United States are overweight (body mass index [BMI] ≥25 kg/m2, including those who are obese) and nearly one-quarter of US adults are obese (BMI ≥30 kg/m2) (2). Unfortunately, the prevalence of overweight and obesity has steadily increased in nearly all ethnic and racial groups over the latter portion of the 20th century, as a 3.2% increase in the prevalence of the overweight category occurred during the years 1960 through 1994, along with a 66.4% increase in the prevalence of obesity during the same time period (2). Tragically, each year approx 280,000 adult deaths in the United States are attributed to obesity (3), with a total annual cost of

Exercise-induced asthma in figure skaters.

99.2 billion in the year 1995 (4).