Respiratory energetics during exercise at high altitude.

The purpose of this study was to assess the effect of high altitude (HA) on work of breathing and external work capacity. On the basis of simultaneous records of esophageal pressure and lung volume, the mechanical power of breathing (Wrs) was measured in four normal subjects during exercise at sea level (SL) and after a 1-mo sojourn at 5,050 m. Maximal exercise ventilation (VEmax) and maximal Wrs were higher at HA than at SL (mean 185 vs. 101 l/min and 129 vs. 40 cal/min, respectively), whereas maximal O2 uptake averaged 2.07 and 3.03 l/min, respectively. In three subjects, the relationship of Wrs to minute ventilation (VE) was the same at SL and HA, whereas, in one individual, Wrs for any given VE was consistently lower at HA. Assuming a mechanical efficiency (E) of 5%, the O2 cost of breathing at HA and SL should amount to 26 and 5.5% of maximal O2 uptake, whereas for E of 20% the corresponding values were 6.5 and 1.4%, respectively. Thus, at HA, Wrs may substantially limit external work unless E is high. Although at SL VEmax did not exceed the critical VE, at which any increase in VE is not useful in terms of body energetics even for E of 5%, at HA VEmax exceeded critical VE even for E of 20%.     

Lactate during exercise at extreme altitude

Maximal exercise at extreme altitude results in profound arterial hypoxemia and, presumably, extreme tissue hypoxia. The best evidence available indicates that the resting arterial PO2 on the summit of Mount Everest is about 28 torr and that it falls even further during exercise. Nevertheless, some 10 climbers have now reached the summit without supplementary oxygen. Paradoxically, blood lactate for a given work rate at high altitude in acclimatized subjects is essentially the same as at sea level. Because work capacity decreases markedly with increasing altitude, maximal blood lactate also falls. Extrapolation of available data up to 6300 m indicates that a climber who reaches the Everest summit will have no increase in blood lactate. The cause of the low blood lactate during exercise at extreme altitude is not fully understood. One possibility is depletion of plasma bicarbonate in acclimatized subjects, which reduces buffering and results in large increases in H+ concentration for a given release of lactate. The consequent local fall in pH may inhibit enzymes, e.g., phosphofructokinase (EC 2.7.1.56), in the glycolytic pathway.     

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.     

Effect of adrenergic blockade on lymphocyte cytokine production at rest and during exercise

To examine the effect of exercise andadrenergic blockade on lymphocyte cytokine production, six men ingestedeither a placebo (control) or an - (prazosin hydrochloride) and-adrenoceptor antagonist (timolol malate) capsule (blockade, or BLK)2 h before performing 19 ± 1 min of supine bicycle exerciseat 78 ± 3% peak pulmonary uptake. Blood was collected before andafter exercise, stimulated with phorbol 12-myristate 13-acetate andionomycin, and surface stained for T (CD3⁺) and naturalkiller [NK (CD3CD56⁺)] lymphocyte surfaceantigens. Cells were permeabilized, stained for the intracellularcytokines interleukin (IL)-2 and interferon (IFN)-, and analyzedusing flow cytometry. BLK had no effect on the resting concentration ofstimulated cytokine-positive T and NK lymphocytes or the amount ofcytokine they were producing. Exercise resulted in an increase (P< 0.05) in the concentration of stimulated T and NK lymphocytesproducing cytokines in the circulation, but these cells produced less(P < 0.05) cytokine post- compared with preexercise.BLK attenuated (P < 0.05) the elevation in theconcentration of lymphocytes producing cytokines during exercise;however, BLK did not affect the amount of IL-2 and IFN- produced.These results suggest that adrenergic stimulation contributes to theexercise-induced increase in the concentration of lymphocytes in thecirculation; however, it does not appear to be responsible for theexercise-induced suppression in cytokine production.

     

Women at altitude: carbohydrate utilization during exercise at 4,300 m.

To evaluate the hypothesis that exposure to high altitude would reduce blood glucose and total carbohydrate utilization relative to sea level (SL), 16 young women were studied over four 12-day periods: at 50% of peak O(2) consumption in different menstrual cycle phases (SL-50), at 65% of peak O(2) consumption at SL (SL-65), and at 4,300 m (HA). After 10 days in each condition, blood glucose rate of disappearance (R(d)) and respiratory exchange ratio were measured at rest and during 45 min of exercise. Glucose R(d) during exercise at HA (4.71 +/- 0.30 mg. kg(-1). min(-1)) was not different from SL exercise at the same absolute intensity (SL-50 = 5.03 mg. kg(-1). min(-1)) but was lower at the same relative intensity (SL-65 = 6.22 mg. kg(-1). min(-1), P < 0.01). There were no differences, however, when glucose R(d) was corrected for energy expended (kcal/min) during exercise. Respiratory exchange ratios followed the same pattern, except carbohydrate oxidation remained lower (-23.2%, P < 0.01) at HA than at SL when corrected for energy expended. In women, unlike in men, carbohydrate utilization decreased at HA. Relative abundance of estrogen and progesterone in women may partially explain the sex differences in fuel utilization at HA, but subtle differences between menstrual cycle phases at SL had no physiologically relevant effects.     

Thermoregulation at rest and during exercise in prepubertal boys

Thermal balance was studied in 11 boys, aged 10-12 years, with various values for maximal oxygen uptake (VO2max), during two standardized sweating tests performed in a climatic chamber in randomized order. One of the tests consisted in a 90-min passive heat exposure [dry bulb temperature (Tdb) 45 degrees C] at rest. The second test was represented by a 60-min ergocycle exercise at 60% of individual VO2max (Tdb 20 degrees C). At rest, rectal temperature increased during heat exposure similar to observations made in adults, but the combined heat transfer coefficient reached higher values, reflecting greater radiative and convective heat gains in the children. Children also exhibited a greater increase in mean skin temperature, and a greater heat dissipation through sweating. Conversely, during the exercise sweating-test, although the increase in rectal temperature did not differ from that of adults for similar levels of exercise, evaporative heat loss was much lower in children, suggesting a greater radiative and convective heat loss due to the relatively greater body surface area. Thermophysiological reactions were not related to VO2max in children, in contrast to adults.     

Arm blood flow at rest and during arm exercise

To test the applicability of a dye-dilution method to quantitate total arm blood flow at rest and during arm exercise, indocyanine green was infused at a constant rate into the brachial artery. Eight subjects performed continuous 30-min arm exercises with an increase in intensity every 10 min (30, 60, and 90 W). The loads corresponded to 29 +/- 1, 48 +/- 2, and 78 +/- 4% (means +/- SE) of the maximal O2 uptake (VO2max 2.13 +/- 0.08 l/min) during arm exercise. VO2max during arm exercise was 61 +/- 1.7% of that during leg exercise. The dye concentration was analyzed in blood samples from three arm veins, two ipsi- and one contralateral, at shoulder level. Corresponding dye concentrations in both ipsilateral veins and a stable concentration difference between ipsi- and contralateral veins were achieved. Total arm blood flow was calculated to be 0.21 +/- 0.04 l/min at rest and 2.43 +/- 0.14 l/min at 90 W. Arm O2 uptake rose from 9 +/- 2 to 323 +/- 21 ml/min. Arm blood flow and O2 uptake each correlated linearly with both work load (r = 0.98) and pulmonary O2 uptake (r greater than or equal to 0.98). Mechanical efficiency for the arm and body was 34-44 and 16-19%, respectively. We conclude that arm blood flow can be determined by continuous infusion of indocyanine green.