Seasonal effects on human physiological adaptation factors, thermotolerance and plasma fibronectin.

Plasma fibronectin (PF) influences shock survival and basal levels increase with active conditioning that improves human physiological adaptation factors (PAF) and thermotolerance (TT). To evaluate further PF's relationship with PAF and TT, the effects of passive conditioning with seasonal change (spring vs. summer) in New England on PAF, TT, basal PF level and PF level during hot-humid exercise (HHE; bicycling; 40 +/- 4% VO2max; 35 degrees C; 70% rh; 45 min) were examined in male subjects (28.2 +/- 1.6 years; N = 7; values are means +/- SE). The spring and summer studies were separated by 2 months. In addition, 2 months prior to the spring study, a winter basal PF pre-screening was conducted. Winter (287 +/- 36 micrograms/ml), spring (272 +/- 21 micrograms/ml), and summer (278 +/- 19 micrograms/ml) basal PF levels were similar. The PF response during HHE was unremarkable with seasonal change. PAF were improved, since blood volume (6266 +/- 276 vs. 5895 +/- 251 ml), plasma volume (3896 +/- 198 vs. 3601 +/- 165 ml) and HHE sweat rate (18.7 +/- 5.5 vs. 12.9 +/- 6.4 ml/min) were elevated (p < 0.05) in the summer compared to the spring. However, this was not accompanied by improved TT, since spring and summer rectal temperatures during HHE were similar, while summer heart rate was elevated (p < 0.05) compared to the spring. In contrast to active conditioning, passively-induced improvements in PAF were not associated with elevations in TT or PF level. Unlike PAF, PF elevations might only occur when the conditioning resulted in increased TT, which suggests a potential for PF as a TT marker.

Metabolic and performance responses to uphill and downhill running in distance runners.

Distance running performance is slower on hilly race courses than flat courses even when the start and finish are at the same elevation, resulting in equal amounts of uphill and downhill running. The physiological mechanism limiting performance on these courses is not known. We examined the effects of uphills and downhills with 11 trained male distance runners running three 30 min self-paced competitive races on a treadmill. Race courses consisted of five, 6 min stages. Percent grades were: course A (0, 0, 0, 0, 0), course B (0, +5, 0, -5, 0) and course C (0, -5, 0, +5, 0). Pace, oxygen consumption (VO2), heart rate (HR), blood lactate (LA), and rating of perceived exertion (RPE) did not change significantly (P greater than 0.05) over stages on the control course A. Pace changed inversely with percent grade on courses B and C. The increase in downhill running pace was inadequate to maintain a level VO2 during the race. LA increased on the uphill stages even though running pace decreased. The running paces for courses B and C were slower (P less than 0.05) than course A by 2.8% and 2.4%, respectively. Runners do not maintain constant energy expenditure when racing on hilly courses. Lactate accumulated on uphill stages even though pace decreased. Running pace increased on downhills but not enough to maintain a constant VO2.

Maximal aerobic capacity at several ambient concentrations of carbon monoxide at several altitudes.

In order to assess the combined effects of altitude and acute carbon monoxide exposure, 11 male and 12 female subjects, nonsmokers in good health, were given incremental (two minutes at each workload) maximal aerobic capacity tests at four levels of ambient carbon monoxide (0, 50, 100, and 150 parts per million) at four altitudes (55, 1,524, 2,134, and 3,048 m). Five male and four female subjects completed all 16 experiments. The remaining subjects completed either eight or 12 experiments; at least eight male and eight female subjects were tested at each combination of carbon monoxide and altitude. Test conditions were double-blind. Subjects initially were screened with a medical history questionnaire, a 12-lead electrocardiogram, pulmonary function tests, anthropometric and body fat measurements, blood volume determinations, and a maximal aerobic capacity test. Each subject, after attaining the required altitude and ambient carbon monoxide level, performed the maximal aerobic capacity test (maximum VO2) meeting required conditions to assure that a maximal level was attained. Blood samples were drawn prior to the aerobic capacity test; at workloads of 50 watts, 100 watts, 150 watts, and maximum; at the fifth minute of recovery; and prior to repressurization to sea level. Blood was analyzed for hemoglobin, hematocrit, plasma proteins, lactates, and carboxyhemoglobin. Carbon-monoxide-carboxyhemoglobin uptake rates were derived from the submaximal workloads. Maximum VO2 was similar at 55 m and 1,524 m, and decreased from the 55-m value by 4 percent at 2,134 m and by 8 percent at 3,048 m. Despite increases in carboxyhemoglobin, no additional significant decreases in maximal aerobic capacity were observed. With increasing carbon monoxide, a decrease in maximum VO2 independent of altitude was observed. Carboxyhemoglobin concentrations at maximum VO2 were highest at 55 m and lowest at 3,048 m. Carboxyhemoglobin concentrations were lower in female subjects than in male subjects. Immediately prior to and at maximal workloads, carbon monoxide shifted into extravascular spaces and returned to the vascular space within five minutes after exercise stopped. We demonstrated that altitude hypoxia and carbon monoxide hypoxia act independently on the parameters of the maximal aerobic capacity test. We also demonstrated a decrease in the carbon monoxide concentration to carboxyhemoglobin as altitude increased, which can be attributed to the decrease in driving pressure of carbon monoxide at altitude.