Energy cost of sport rock climbing in elite performers.
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OBJECTIVES: To assess oxygen uptake (VO2), blood lactate concentration ([La(b)]), and heart rate (HR) response during indoor and outdoor sport climbing. METHODS: Seven climbers aged 25 (SE 1) years, with a personal best ascent without preview or fall (on sight) ranging from 6b to 7a were assessed using an indoor vertical treadmill with artificial rock hand/foot holds and a discontinuous protocol with climbing velocity incremented until voluntary fatigue. On a separate occasion the subjects performed a 23.4 m outdoor rock climb graded 5c and taking 7 min 36 s (SE 33 s) to complete. Cardiorespiratory parameters were measured using a telemetry system and [La(b)] collected at rest and after climbing. RESULTS: Indoor climbing elicited a peak oxygen uptake (VO2climb-peak) and peak HR (HRpeak) of 43.8 (SE 2.2) ml/kg/min and 190 (SE 4) bpm, respectively and increased blood lactate concentration [La(b)] from 1.4 (0.1) to 10.2 (0.6) mmol/l (p < 0.05). During outdoor climbing VO2 and HR increased to about 75% and 83% of VO2climb-peak and HRpeak, respectively. [La(b)] increased from 1.3 (0.1) at rest to 4.5 mmol/l (p < 0.05) at 2 min 32 s (8 s) after completion of the climb. CONCLUSIONS: The results suggest that for elite climbers outdoor sport rock climbs of five to 10 minutes' duration and moderate difficulty require a significant portion of the VO2climb-peak. The higher HR and VO2 for outdoor climbing and the increased [La(b)] could be the result of repeated isometric contractions, particularly from the arm and forearm muscles. (+info)
Barometric pressures on Mt. Everest: new data and physiological significance.
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Barometric pressures (PB) near the summit of Mt. Everest (altitude 8, 848 m) are of great physiological interest because the partial pressure of oxygen is very near the limit for human survival. Until recently, the only direct measurement on the summit was 253 Torr, which was obtained in October 1981, but, despite being only one data point, this value has been used by several investigators. Recently, two new studies were carried out. In May 1997, another direct measurement on the summit was within approximately 1 Torr of 253 Torr, and meteorologic data recorded at the same time from weather balloons also agreed closely. In the summer of 1998, over 2,000 measurements were transmitted from a barometer placed on the South Col (altitude 7,986 m). The mean PB values during May, June, July, and August were 284, 285, 286, and 287 Torr, respectively, and there was close agreement with the PB-altitude (h) relationship determined from the 1981 data. The PB values are well predicted from the equation PB = exp (6.63268 - 0.1112 h - 0.00149 h2), where h is in kilometers. The conclusion is that on days when the mountain is usually climbed, during May and October, the summit pressure is 251-253 Torr. (+info)
Exaggerated endothelin release in high-altitude pulmonary edema.
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BACKGROUND: Exaggerated pulmonary hypertension is thought to play an important part in the pathogenesis of high-altitude pulmonary edema (HAPE). Endothelin-1 is a potent pulmonary vasoconstrictor peptide that also augments microvascular permeability. METHODS AND RESULTS: We measured endothelin-1 plasma levels and pulmonary artery pressure in 16 mountaineers prone to HAPE and in 16 mountaineers resistant to this condition at low (580 m) and high (4559 m) altitudes. At high altitude, in mountaineers prone to HAPE, mean (+/-SE) endothelin-1 plasma levels were approximately 33% higher than in HAPE-resistant mountaineers (22.2+/-1.1 versus 16.8+/-1.1 pg/mL, P<0.01). There was a direct relationship between the changes from low to high altitude in endothelin-1 plasma levels and systolic pulmonary artery pressure (r=0.82, P<0.01) and between endothelin-1 plasma levels and pulmonary artery pressure measured at high altitude (r=0.35, P=0.05). CONCLUSIONS: These findings suggest that in HAPE-susceptible mountaineers, an augmented release of the potent pulmonary vasoconstrictor peptide endothelin-1 and/or its reduced pulmonary clearance could represent one of the mechanisms contributing to exaggerated pulmonary hypertension at high altitude. (+info)
Energy metabolism increases and regional body fat decreases while regional muscle mass is spared in humans climbing Mt. Everest.
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The objectives of the study were to determine regional changes in body composition, energy expenditure by means of doubly labeled water, and net energy balance during exposure to high and extreme altitudes (5,300-8,848 m). This study focuses on a subset of subjects who consumed the doubly labeled water (three base camp personnel and seven climbers). Regional body composition was determined by measuring skinfold thicknesses and circumferences at 10 different sites on the body. Energy expenditure was measured by doubly labeled water excretion. Discrepancies between actual energy expenditure and data obtained from diet records and body weight changes suggested a chronic underreporting of dietary energy intake, especially by those subjects who reached the highest altitudes. This underreporting may be due in part to diminished cognition or to a preferential focus on survival, rather than on filling out diet records accurately. Mean adjusted dietary intakes were 10.50 +/- 0. 65 MJ/d (2510 +/- 155 kcal/d) for those who remained at base camp, and 20.63 +/- 6.56 MJ/d (4931 +/- 1568 kcal/d) for those who climbed above base camp. Energy expenditure averaged 2.5-3.0 times sea level resting energy expenditure. Differential changes in regional body composition suggested a preferential loss of fat mass and a relative sparing of muscle mass, despite insufficient energy intake to maintain body weight. (+info)
Downregulation in muscle Na(+)-K(+)-ATPase following a 21-day expedition to 6,194 m.
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To investigate the hypothesis that acclimatization to altitude would result in a downregulation in muscle Na(+)-K(+)-ATPase pump concentration, tissue samples were obtained from the vastus lateralis muscle of six volunteers (5 males and 1 female), ranging in age from 24 to 35 yr, both before and within 3 days after a 21-day expedition to the summit of Mount Denali, Alaska (6,194 m). Na(+)-K(+)-ATPase, measured by the [(3)H]ouabain-binding technique, decreased by 13.8% [348 +/- 12 vs. 300 +/- 7.6 (SE) pmol/g wet wt; P < 0.05]. No changes were found in the maximal activities (mol. kg protein(-1). h(-1)) of the mitochondrial enzymes, succinic dehydrogenase (3.63 +/- 0.20 vs. 3.25 +/- 0.23), citrate synthase (4. 76 +/- 0.44 vs. 4.94 +/- 0.44), and malate dehydrogenase (12.6 +/- 1. 8 vs. 12.7 +/- 1.2). Similarly, the expedition had no effect on any of the histochemical properties examined, namely fiber-type distribution (types I, IIA, IIB, IC, IIC, IIAB), area, capillarization, and succinic dehydrogenase activity. Peak aerobic power (52.3 +/- 2.1 vs. 50.6 +/- 1.9 ml. kg(-1). min(-1)) and body mass (76.9 +/- 3.7 vs. 75.5 +/- 2.9 kg) were also unaffected. We concluded that acclimatization to altitude results in a downregulation in muscle Na(+)-K(+)-ATPase pump concentration, which occurs without changes in oxidative potential and other fiber-type histochemical properties. (+info)
Effects of prolonged hypobaric hypoxia on human skeletal muscle function and electromyographic events.
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This study tested the hypothesis that a prolonged decrease in arterial oxygen pressure in resting or contracting skeletal muscles alters their ability to develop force through an impairment of energy-dependent metabolic processes and also through an alteration of electrophysiological events. The experiment was conducted during a 32-day simulated ascent of Mt. Everest (8848 m altitude) (Everest III Comex '97), which also allowed testing of the effects of re-oxygenation on muscle function. Maximal voluntary contractions (MVCs) of the flexor digitorum, and static handgrips sustained at 60% of MVC, were performed by eight subjects before the ascent (control), then during the stays at simulated altitudes of 5000 m, 6000 m and 7000 m, and finally 1 day after the return to 0 m. The evoked muscle compound action potential (M-wave) was recorded at rest and during the manoeuvres at 60% of MVC. The changes in median frequency of electromyographic (EMG) power spectra were also studied during the contraction at 60% of MVC. In four individuals, transient re-oxygenation during the ascent allowed us to test the reversibility of hypoxia-induced MVC and M-wave changes. At rest, a significant decrease in M-wave amplitude was noted at 5000 m. This effect was associated with a prolonged M-wave conduction time at 6000 m and an increased M-wave duration at 7000 m, and persisted after the return to 0 m. Re-oxygenation did not modify the changes in M-wave characteristics. A significant decrease in MVC was measured only during the ascent (-10 to -24%) in the non-dominant forearm of subjects who underwent re-oxygenation; this intervention slightly improved muscle strength at 6000 m and 7000 m. During the ascent and after the return to 0 m, there was a significant reduction of the median frequency decrease throughout contraction at 60% of MVC compared with the EMG changes measured before the ascent. It is concluded that prolonged exposure to hypoxia slows the propagation of myopotentials and alters sensorimotor control during sustained effort. Re-oxygenation did not affect the hypoxia-induced EMG changes and had a modest influence on muscle strength. (+info)
Stress Doppler echocardiography for identification of susceptibility to high altitude pulmonary edema.
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OBJECTIVE: This prospective single-blinded study was performed to quantitate noninvasive pulmonary artery systolic pressure (PASP) responses to prolonged acute hypoxia and normoxic exercise. BACKGROUND: Hypoxia-induced excessive rise in pulmonary artery pressure is a key factor in high-altitude pulmonary edema (HAPE). We hypothesized that subjects susceptible to HAPE (HAPE-S) have increased pulmonary artery pressure response not only to hypoxia but also to exercise. METHODS: PASP was estimated at 45, 90 and 240 min of hypoxia (FiO2 = 12%) and during supine bicycle exercise in normoxia using Doppler-echocardiography in nine HAPE-S and in 11 control subjects. RESULTS: In the control group, mean PASP increased from 26+/-2 to 37+/-4 mm Hg (deltaPASP 10.3+/-2 mm Hg) after 90 min of hypoxia and from 27+/-4 to 36+/-3 mm Hg (deltaPASP 8+/-2 mm Hg) during exercise. In contrast, all HAPE-S subjects revealed significantly greater increases (p = 0.002 vs. controls) in mean PASP both during hypoxia (from 28+/-4 to 57+/-10 mm Hg, deltaPASP 28.7+/-6 mm Hg) and during exercise (from 28+/-4 to 55+/-11 mm Hg, deltaPASP 27+/-8 mm Hg) than did control subjects. Stress echocardiography allowed discrimination between groups without overlap using a cut off PASP value of 45 mm Hg at work rates less than 150 W. CONCLUSIONS: These data indicate that HAPE-S subjects may have abnormal pulmonary vascular responses not only to hypoxia but also to supine bicycle exercise under normoxic conditions. Thus, Doppler echocardiography during supine bicycle exercise or after 90 min of hypoxia may be useful noninvasive screening methods to identify subjects susceptible to HAPE. (+info)
The effect of amlodipine on respiratory and pulmonary vascular responses to hypoxia in mountaineers.
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Calcium antagonists are known to reduce the incidence of high-altitude pulmonary oedema, but the mechanism is unclear. The aim of this study was to examine the effects of the calcium antagonist, amlodipine, on cardiac and respiratory responses in normoxia and hypoxia. Fourteen normal subjects aged 31+/-4 yrs who had climbed to altitudes of 5,000-7,500 m without problems were randomly assigned to a double-blind crossover trial of amlodipine versus placebo, using sea-level inspiratory hypoxia to simulate altitude. Doppler echocardiographic estimates of resting pulmonary haemodynamics and cycle ergometer test results of cardiorespiratory responses to exercise were recorded in normoxia and hypoxia. It was found that, although hypoxic pulmonary vasoconstriction (HPV) was not significantly reduced by amlodipine, the effect of the drug on HPV was inversely related to the serum level of amlodipine. Amlodipine did not alter left ventricular function measured echocardiographically. During exercise, amlodipine increased breathlessness, measured using standard scales, in both normoxia and hypoxia but had no effect on ventilatory variables. It was concluded that amlodipine has the potential to block hypoxic pulmonary vasoconstriction as evidenced by a drug concentration-related decrease in resting tricuspid regurgitation jet velocity without any change in resting myocardial contractility. However, with amlodipine, the subjects felt more breathless during exercise. The reasons for this increase in breathlessness are not clear. (+info)