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Biomedical subjects

B Kayser

Publications and source records attributed to B Kayser.

At least 37 records · Page 2Linked to original sources
PubMed1996

Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and in deacclimatization.

Peak blood lactate ([Labl]peak) and blood lactate concentration ([Labl]) vs. workload (W) relationships during acclimatization to altitude and in the deacclimatization were evaluated in 10 Caucasian lowlanders at sea level (SL0); after approximately 1 wk (Alt1wk), 3 wk (Alt3wk), and 5 wk (Alt5wk) at 5,050 m; and weekly during the first 5 wk after return to sea level (SL1wk-SL5wk). Incremental bicycle ergometer exercises (30 W added every 4 min up to exhaustion) were performed. At Alt1wk and at Alt5wk, the experiments were repeated in hypobaric normoxia (Alt1wk-O2 and Alt5wk-O2). [Labl] was determined at rest and during the last approximately 30 s of each W. [Labl]peak was taken as the highest [Labl] during recovery. Acid-base status (pH and concentration of HCO-3 in arterialized capillary blood) was determined at rest. Mean [Labl]peak values were 11.5 (SL0), 8.0 (Alt1wk), 6.4 (Alt3wk), 6.3 (Alt5wk), 8.0 (SL1wk), 9.4 (SL2wk), 10.8 (SL3wk), 11.3 (SL4wk), and 11.6 (SL5wk) mM. At Alt1wk-O2 and Alt5wk-O2, peak W increased, compared with Alt1wk and Alt5wk, whereas no changes were observed for [Labl]peak. [Labl] vs. W was shifted to the left (i.e., higher [Labl] values were found for the same W) at Alt1wk compared with SL0 and partially shifted back to the right (i.e., lower [Labl] values were found for the same W) at Alt3wk and Alt5wk. At Alt1wk-O2 and Alt5wk-O2, [Labl] vs. W values were superimposed on that at SL0. At SL1wk-SL5wk, [Labl] vs. W values were shifted to the right compared with that at SL0. At Alt1wk, a condition of respiratory alkalosis was found, which was only partially compensated for during acclimatization. At SL1wk, the acid-base status was back to normal. We conclude that 1) the reduced [Labl]peak at altitude is still present for 2-3 wk after return from altitude; is not attributable to reduced peak W nor to hypoxia per se, nor to a reduced buffer capacity; alternatively, it could be related to some central determinants of fatigue. 2) The [Labl] vs. W leftward shift at altitude was due to hypoxia per se. 3) The factor(s) responsible for the [Labl] vs. W partial rightward shift during acclimatization could still be effective during the first weeks after return to sea level.

Acclimatization↗
PubMed1996

Muscle ultrastructure and biochemistry of lowland Tibetans.

Muscle ultrastructure and biochemistry in vastus lateralis muscle biopsies and the response to exercise of 8 lowland Tibetans (T) were compared with those of 8 Nepalese lowlanders (N). Blood hemoglobin was lower in T than in N (119 +/- 3 vs. 131 +/- 2 g/l; P < 0.05). Peak O2 consumption per kilogram of body mass was similar [37.9 +/- 2.2 (T) vs. 40.1 +/- 1.36 ml.min-1.kg body mass-1 (N)]. Maximum exercise blood lactate was the same [11.4 (T) +/- 0.5 vs. 11.3 +/- 0.6 mM (N)]. Muscle fiber type distribution was similar [type I, 58.6 +/- 3.4 (N) vs. 57.0 +/- 3.4% (T); type IIa, 24.1 +/- 3.5 vs. 27.1 +/- 1.6%; type IIb, 17.4 +/- 1.4 vs. 15.9 +/- 2.9%]. T had smaller fiber cross-sectional areas [3,413 +/- 677 (T) vs. 3,895 +/- 447 microns 2 (N); P < 0.05] but had similar number of capillaries per muscle fiber [1.35 +/- 0.23 (T) vs. 1.46 +/- 0.08 (N)] and muscle fiber area supplied per capillary [399 +/- 29 (T) vs. 382 +/- 65 mm2 (N)]. Total mitochondrial volume density was much lower in T (3.99 +/- 0.17%) than in N (5.51 +/- 0.19%) (P < 0.025). Mirroring mitochondrial volume density, citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities were lower in T than in N (P < 0.05). The activities of L-lactate dehydrogenase and hexokinase were the same in both groups. T had significantly less muscle fiber lipid droplets than did N, which correlated with the low activity of 3-hydroxyacyl-CoA dehydrogenase (r = 0.57, P = 0.02). In conclusion, lowland-born T have a low mitochondrial volume-to-specific peak O2 consumption ratio, which, based on previous measurements on altitude-born Sherpas (B. Kayser, H. Hoppeler, H. Claassen and P. Cerretelli. J. Appl. Physiol. 70: 1938-1942, 1991), appears to be an inborn feature.

Adolescent↗
PubMed1996

Muscle tissue adaptations of high-altitude natives to training in chronic hypoxia or acute normoxia.

Twenty healthy high-altitude natives, residents of La Paz, Bolivia (3,600 m), participated in 6 wk of endurance exercise training on bicycle ergometers, 5 times/wk, 30 min/session, as previously described in normoxia-trained sea-level natives (H. Hoppeler, H. Howald, K. E. Conley, S. L. Lindstedt, H. Claassen, P. Vock, and E. R. Weibel. J. Appl. Physiol. 59: 320-327, 1985). A first group of 10 subjects was trained in chronic hypoxia (HT; barometric pressure = 500 mmHg; inspired O2 fraction = 0.209); a second group of 10 subjects was trained in acute normoxia (NT; barometric pressure = 500 mmHg; inspired O2 fraction = 0.314). The workloads were adjusted to approximately 70% of peak O2 consumption (VO2peak) measured either in hypoxia for the HT group or in normoxia for the NT group. VO2peak determination and biopsies of the vastus lateralis muscle were taken before and after the training program. VO2peak in the HT group was increased (14%) in a way similar to that in NT sea-level natives with the same protocol. Moreover, VO2peak in the NT group was not further increased by additional O2 delivery during the training session. HT or NT induced similar increases in muscle capillary-to-fiber ratio (26%) and capillary density (19%) as well as in the volume density of total mitochondria and citrate synthase activity (45%). It is concluded that high-altitude natives have a reduced capillarity and muscle tissue oxidative capacity; however, their training response is similar to that of sea-level residents, independent of whether training is carried out in hypobaric hypoxia or hypobaric normoxia.

Acclimatization↗
PubMed1996

Lactate and epinephrine during exercise in altitude natives.

We tested the hypothesis that the reported low blood lactate accumulation ([La]) during exercise in altitude-native humans is refractory to hypoxianormoxia transitions by investigating whether acute changes in inspired O2 fraction (FIo2) affect the [La] vs. power output (W) relationship or, alternatively, as reported for lowlanders, whether changes in [La] vs. W on changes in FIo2 are related to changes in blood epinephrine concentration ([Epi]). Altitude natives [n = 8, age 24 +/- 1 (SE) yr, body mass 62 +/- 3 kg, height 167 +/- 2 cm] in La Paz, Bolivia (3,600 m) performed incremental exercise with two legs and one leg in chronic hypoxia and acute normoxia (AN). Submaximal one- and two-leg O2 uptake (Vo2) vs. W relationships were not altered by FIo2. AN increased two-leg peak Vo2 by 10% and peak W by 7%. AN paradoxically decreased one-leg peak Vo2 by 7%, whereas peak W remained the same. The [La] vs. W relationships were similar to those reported in unacclimatized lowlanders. There was a shift to the right on AN, and maximum [La] was reduced by 7 and 8% for one- and two-leg exercises, respectively. [Epi] and [La] were tightly related (mean r = 0.81) independently of FIo2. Thus normoxia attenuated the increment in both [La] and [Epi] as a function of W, whereas the correlation between [La] and [Epi] was unaffected. These data suggest loose linkage of glycolysis to oxidative phosphorylation under influence from [Epi]. In conclusion, high-altitude natives appear to be not fundamentally different from lowlanders with regard to the effect of acute changes in FIo2 on [La] during exercise.

Adult↗
PubMed1996

Comparison of static and dynamic intrinsic positive end-expiratory pressure using the Campbell diagram.

Intrinsic positive end-expiratory pressure (PEEPi) due to dynamic hyperinflation has been measured as a plateau airway opening pressure during airway occlusion (PEEPi,stat). PEEPi has also been dynamically determined as a fall in esophageal pressure (Pes) before the inspiratory flow starts (PEEPi,dyn). The aims of the current study were to systematically compare PEEPi,stat and PEEPi,dyn and to explain the underlying mechanisms of their difference. The study was performed in healthy subjects with dynamic hyperinflation induced by expiration through a Starling resistor. The Campbell diagram was constructed for each subject by determining the static pressure-volume curves of the lung (Pst,[l]) and chest wall (Pst,[w]). For a given end-expiratory volume, PEEPi,stat was measured on the Campbell diagram as the pressure difference between Pst(w) and -Pst(l). PEEPi,dyn was measured as mentioned above. The effects of respiratory muscle recruitment on PEEPi,dyn were estimated by the Pes values when Pes started to fall relative to Pst(w). We found that: (1) there was a great variability of the PEEPi,dyn/PEEPi,stat ratio among and within subjects; (2) expiratory muscle recruitment was evident on most occasions; (3) persistent inspiratory muscle activity during expiration was present in some subjects; (4) the Pes values at the start of inspiratory flow were frequently on the left of -Pst(l), which contributed to the difference between PEEPi,stat and PEEPi,dyn and implied a greater dynamic than static elastance presumably due to viscoelastic properties; (5) chest wall distortions characterized by inflation of the abdomen with deflation of the rib cage during the initial inspiratory efforts were observed in three subjects. In conclusion, interpretation of PEEPi,dyn needs to be cautious because both expiratory and tonic inspiratory muscle activities that lead to significant over- or underestimation of PEEPi by PEEPi,dyn, respectively, are associated with acute dynamic hyperinflation. In addition, the effects of viscoelastic properties and chest wall distortions on PEEPi,dyn need to be further investigated.

Adult↗
PubMed1995

Hypertrophic response of human skeletal muscle to strength training in hypoxia and normoxia.

The purpose of this study was to test the hypothesis that work-induced skeletal muscle hypertrophy may be reduced by training in chronic hypobaric hypoxia compared to normoxia. Five healthy males [mean age 34.4 (SEM 2.2) years] performed strength training of the elbow flexors for 1 month, at altitude (A) (5050 m) and with the same absolute loads at sea level (SL), 8 months later. The EF cross-sectional area (CSA), determined at mid-arm by nuclear magnetic resonance imaging, increased by 11.3 (SEM 3.7)% (P < 0.05) at A and 17.7 (SEM 4.5)% (P < 0.05) at SL. Isometric maximal voluntary contraction (MVC) increased by 9.5 (SEM 2.6)% (P < 0.05) at A and 13.6 (SEM 2.4)% (P < 0.05) at SL. The CSA and MVC changes in A were significantly smaller than at SL (P < 0.05). Muscle specific tension did not change in either condition. No changes in muscle plus bone or MVC of the untrained, controlateral arm were observed. Thus, although there was no indication of muscle wasting at A, the hypertrophic response of skeletal muscle when trained in chronic hypoxia seemed to be significantly lower than that produced in normoxia. This effect could have arisen either from a direct depression of protein synthesis and/or hormonal changes provoked by hypoxia.

Adult↗
PubMed1995

Kinetics of oxygen consumption during maximal exercise at different muscle temperatures.

The aim of this study was to test at maximal exercise the hypothesis of the temperature-dependence of the kinetics of O2 consumption (VO2), which predicts a greater O2 deficit as muscle temperature is decreased. Six male subjects underwent 3 min exercise bouts at the minimum power eliciting maximum O2 consumption (VO2max), at normal temperature (A) and after cooling the thigh muscles by water immersion (C). Breath-by-breath VO2 was measured together with muscle blood flow (Qm), blood lactate accumulation ("early lactate", eLa), heart rate and muscle temperature (Tm). The O2 deficit was calculated by standard procedure. Net VO2max was 2.92 +/- 0.85 (SD) and 3.19 +/- 0.71 l center dot min-1 in C and A respectively (P < 0.05). Correspondingly, maximum power was 20 W lower in C than in A. At exercise start, Tm was 35.0 +/- 1.2 and 27.5 +/- 1.8 degrees C in A and C respectively. O2 deficit was 2.25 +/- 0.53 and 3.05 +/- 1.12 l in A and C respectively. The corresponding eLa was 7.7 +/- 2.5 and 13.8 +/- 2.5 mM, (P < 0.05) while Qm was 376 +/- 92 and 290 +/- 50 ml center dot kg-1 center dot min-1 (P < 0.05) in A and C, respectively. The eLa increase in C is associated with an impaired muscle blood flow and decreased muscle O2 unloading, and does not completely explain the greater O2 deficit in C. The unexplained fraction of the latter is perhaps accounted for by a greater net alactic O2 deficit, in agreement with a temperature-dependent decrease of the velocity constants of oxidative reactions, as suggested by the tested hypothesis.

Adult↗
PubMed1995

Maximal exercise performance in chronic hypoxia and acute normoxia in high-altitude natives.

Maximal O2 uptake (VO2max) was determined on a bicycle ergometer in chronic hypoxia (CH) and during acute exposure to normoxia (AN) in 50 healthy young men who were born and had lived at 3,600 m altitude (La Paz, Bolivia). VO2max was significantly improved (approximately 8%) by AN. However, the difference in VO2max measured in CH and AN (delta VO2max) was lower than that reported in sea-level natives (SN) who exercised in chronic normoxia and acute hypoxia. It is shown that high-altitude natives (HN) and SN have a similar VO2max in normoxia, but highlanders can attain a greater VO2max when O2 availability is reduced by altitude exposure. In addition, in HN, the higher the subject's VO2max in hypoxia, the smaller his delta VO2max. These results contrast with the data obtained in 14 lowlanders acclimatized to high altitude who showed that their delta VO2max was positively related to their VO2max in hypoxia, as previously reported in SN who exercised in acute hypoxia (A. J. Young, A. Cymerman, and R. L. Burse. Eur. J. Appl. Physiol. Occup. Physiol. 54: 12-15, 1985). Furthermore, arterial O2 saturation of HN behaved differently from acclimatized lowland natives, inasmuch as it fell less during exercise both in CH and AN. HN with high aerobic capacity display a lower exercise ventilation and a reduced arterial saturation, which could explain their inability to improve VO2max with normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1995

Training in hypoxia vs. training in normoxia in high-altitude natives.

To determine the interactions between endurance training and hypoxia on maximal exercise performance, we performed a study on sedentary high-altitude natives who were trained in normoxia at the same relative (n = 10) or at the same absolute (n = 10) intensity of work as hypoxia-trained subjects (n = 10). The training-induced improvement of maximal oxygen uptake (VO2max) in hypoxia-trained subjects was similar to that obtained in normoxia-trained sea-level natives submitted to the same training protocol (H. Hoppeler, H. Howald, K. Conley, S. L. Lindstedt, H. Claassen, P. Vock, and E. W. Weibel. J. Appl. Physiol. 59: 320-327, 1985). Training at the same absolute work intensity in the presence of increased oxygen delivery failed to provide a further increase in VO2max. VO2max was not improved to a greater extent by simultaneously increasing absolute work intensity and O2 delivery during the training sessions. In addition, training in normoxia is accompanied by an increased blood lactate accumulation during maximal exercise, leading to greater drops in arterial pH, bicarbonate concentration, and base excess. We conclude that, in high-altitude natives, 1) training at altitude does not provide any advantage over training at sea level for maximal aerobic capacity, whether assessed in chronic hypoxia or in acute normoxia; 2) VO2max improvement with training cannot be further enhanced by increasing O2 availability alone or in combination with an increased work intensity during the exercising sessions; and 3) training in normoxia in these subjects results in a reduced buffer capacity.

Adult↗
PubMed1995

Maximal rate of blood lactate accumulation during exercise at altitude in humans.

The lower peak lactate accumulation in blood ([La(b)]p) at altitude may be associated with a reduced maximal glycolytic flux. Based on certain assumptions, the latter can be indirectly evaluated in vivo, during short supramaximal exercises, by measuring the maximal rate of lactate accumulation in blood (delta [La(b)]max). delta [La(b)]max was determined on six white subjects at sea level (SL1), after approximately 1 wk (Alt1) and 4 wk (Alt2) of a 35-day sojourn at 5,050 m, and 1 wk after return to sea level (SL2). The subjects performed exercises of increasing duration (5, 15, 25, 35, 45 s or until exhaustion) on a bicycle ergometer at loads = 200% of the individual Wmax. The latter was previously determined in each condition as the greatest work rate that could be sustained for 2-4 min during an incremental exercise. Net [La(b)] accumulation (delta [La(b)]) was measured after each exercise bout. delta [La(b)] resulted to be linearly related to exercise duration. The slopes of the individual delta [La(b)] vs. exercise duration lines were taken as delta [La(b)]max. Exhaustion times were approximately 30-45 s in all conditions. [La(b)]p (in mM) during recovery after the exhaustive load was higher at SL1 (10.22 +/- 1.09; means +/- SD) than at Alt1 (5.08 +/- 0.82), Alt2 (8.13 +/- 2.67), and SL2 (8.18 +/- 1.43). delta [La(b)]max was lower at Alt1 (0.09 +/- 0.02) and at Alt2 (0.17 +/- 0.05) than at SL1 (0.25 +/- 0.05) and SL2 (0.23 +/- 0.06). Both [La(b)]p and delta [La(b)]max increased during acclimatization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1995

Human intramuscular temperature and heat flow transients at rest.

A general model for heat exchange, comprising the major models in the literature, was developed. Temperature changes as a function of space and time were determined in six resting humans (age 32.7 +/- 4.5 yr) during temperature transients by magnetic resonance imaging (MRI), so that the exact solution of the model was obtained. These results allowed application of the model, e.g., the analysis of transient muscle heat flow changes, which could not be assessed by previous steady-state analyses. A microthermocouple was inserted in muscle vastus lateralis 2-3 cm below the skin surface. The measured temperature was used for calibrating the pixel intensity of a temporal series of transaxial magnetic resonance images obtained with a spin echo sequence around the microthermocouple position. After muscle temperature was increased by immersion in a controlled water bath, MRI acquisition was performed while muscle temperature was decreasing. Temperature maps relative to space and time inside a homogeneous region of interest were reconstructed by neural networks, showing specific temperature patterns. Subsequently calculated heat flows (with negative sign) appeared to increase linearly as temperature decreased, until a maximum was attained at a critical temperature, below which dramatic consistent heat flow changes were found. In conclusion, MRI is indeed a powerful technique, useful to study the determinants of muscle temperature and heat flow changes in space and time.

Adult↗
PubMed1994

Autonomic nervous control of heart rate at altitude (5050 m).

To investigate possible changes in autonomic regulation of heart rate as a result of acclimatization to high altitude, indexes of autonomic nervous activity were obtained non invasively by spectrum analysis of heart rate variability on five healthy male subjects [age, 31 (SEM 2) years] during a postural change from supine to seated, both at sea level and after 1 month of exposure to an altitude of 5050 m. Heart rate fluctuations at the respiratory frequency (high frequency, HF) are mediated by the parasympathetic system whereas fluctuations at about 0.1 Hz (low frequency, LF) are due to both sympathetic and parasympathetic nervous systems. Maximal heart rate, as measured during an incremental exercise test, decreased from 184 (SEM 5) beats.min-1 at sea level to 152 (SEM 2) beats.min-1 at 5050 m. At sea level, the change in posture from supine to seated induced an increase in LF amplitude accompanied by an increase or a decrease in HF amplitude, whereas after 1 month at altitude the HF amplitude decreased in all subjects, with little or no change in LF amplitude. These results indicate a changed strategy of heart rate regulation after acclimatization to high altitude. At sea level, the postural change induced an increase in sympathetic activity in all subjects with different individual vagal responses, whereas at altitude the postural change induced a net decrease in vagal tone in all subjects, with little or no change in sympathetic activity. These results corroborate the reported reduced sensitivity of the heart to adrenergic drive in chronic hypoxia, which may, at least in part, explain the decreased maximal heart rate in altitude-acclimatized human subjects.

Acclimatization↗
PubMed1994

The metabolic and ventilatory response to exercise in Tibetans born at low altitude.

The exercise response of 20 Tibetans (T) born and living in Kathmandu, Nepal (1300 m) was compared to that of 21 age- and sex-matched local lowlanders. The subjects carried out an incremental exercise protocol on a bicycle ergometer (30 watt steps every 4 min) until exhaustion. The kinetics of readjustment of VO2 measured as half time (t-on) upon a 90 watt constant load exercise was also determined. Breath-by-breath gas exchange, heart rate (HR) and blood lactate concentration ([La]) were measured at rest, at the end of each load and during recovery. The slope of the straight line relating VO2 to work load was 10.8 ml.watt-1 in both groups which corresponds to a mechanical efficiency of 0.26 (assuming a RQ of 0.89 and an energy equivalent of 20.9 kJ.L-1 O2). At submaximal loads T were characterized by higher VE (P < 0.05), VE.VO2(-1) (P < 0.01) and VCO2 levels (P < 0.001) than N. The found higher VE in T, resulting from a lower tidal volume coupled to a higher respiratory frequency, led to higher PETO2 (P < 0.001) and SaO2 (P < 0.001) at all work levels. Absolute VO2max in the two investigated groups were 1977 +/- 72 (T) and 2095 +/- 80 (N) ml.min-1 (NS). Specific (i.e. per kg body weight) VO2max were identical (37.0 +/- 1.1 [T] vs. 36.7 +/- 1.1 ml.kg-1.min-1 [N]). [La]max were 11.4 +/- 0.4 (T) vs. 12.3 +/- 0.4 (N) mM (NS). [La] accumulation in blood as a function of workload and its rate of disappearance during recovery were similar. t-on at 90 watt was 30.7 +/- 2.4 sec in T and 28.9 +/- 2.3 sec in N (NS). The corresponding average contracted O2 deficit were 971 ml for T and 994 ml for N (NS). In conclusion, Tibetans born at low altitude do not seem to differ from lowlanders with regard to their metabolic response whereas their ventilatory response to exercise is greater.

Adolescent↗
PubMed1994

Fatigue and exhaustion in chronic hypobaric hypoxia: influence of exercising muscle mass.

Exhaustive dynamic exercise with large muscle groups in chronic hypobaric hypoxia may be limited by central (nervous) rather than peripheral (metabolic) fatigue. Six males [32 +/- 4 (SD) yr] at sea level (SL) and after 1-mo acclimatization at 5,050 m (HA) performed exhaustive dynamic forearm exercise at a constant absolute load, requiring regional maximum aerobic power at SL, and exhaustive cycle exercise at prevailing maximal O2 uptake (HA approximately equal to 80% SL). Exhaustion time (t(ex)), blood O2 saturation (SaO2), and heart rate (HR) were measured during each exercise bout. Before and after both arm and leg exercise, lactate concentration ([La]), PO2, PCO2, and pH were measured in arterialized blood samples. Integrated electromyogram activity (IEMG) and mean (MPF) and centroid (CPF) power frequencies of the EMG power spectrum during exercise were calculated for forearm flexors and vastus lateralis muscle. t(ex) for forearm exercise at the same absolute load was the same at SL and HA. Similar increases of IEMG (+214% at SL vs. +172% at HA) and decreases of CPF (-13% at SL vs. -16% at HA) and MPF (-22% at SL vs. -21% at HA) were observed. By contrast, at HA, for similar t(ex), leg exercise had to be performed at the same relative (i.e., prevailing maximal O2 uptake) but lower absolute load (approximately equal to 80% of SL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Energy balance at high altitude of 6,542 m.

Weight loss due to malnutrition and possibly intestinal malabsorption is a well-known phenomenon in high-altitude climbers. Up to approximately 5,000 m, energy balance may be attained and intestinal energy digestibility remains normal. To see whether 1) energy balance may also be attained at 6,542 m and, if not, 2) whether decreased energy digestibility would play a significant role in the energy deficit, energy intake (EI), energy expenditure, body composition, and energy digestibility of 10 subjects (4 women, 6 men; 27-44 yr) were assessed during a 21-day sojourn on the summit of Mt. Sajama, Bolivia (6,542 m). EI was measured during two 3-day intervals: EI1 (days 7-9) and EI2 (days 17-19). Total fecal energy loss during EI1 was calculated from fecal energy measured by bomb calorimetry. Average daily metabolic rate (ADMR) at altitude was measured in six subjects (2 women, 4 men) using doubly labeled water over a 10-day interval (days 9-19). Basal metabolic rate was measured before and after the expedition by respiratory gas analysis. Body composition was estimated from skinfolds and body mass before and during the altitude sojourn. Subjects were in negative energy balance throughout the observation period (EI1-ADMR = -2.9 +/- 1.8 MJ/day and EI2-ADMR = -2.3 +/- 1.8 MJ/day based on a gross energy digestibility of 95%). The activity level, expressed as ADMR to basal metabolic rate, was 1.56-2.39. The loss of fat mass (3.7 +/- 1.5 kg) represented 74 +/- 15% of the loss of body mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1994

Nutrition and energetics of exercise at altitude. Theory and possible practical implications.

Altitude exposure may lead to considerable weight loss. Most reports, showing weight losses of 3% in 8 days at 4300m and up to 15% after 3 months at 5300 to 8000m, appear to indicate that this weight loss is a function of both absolute altitude and the duration of exposure. Based on the available scientific evidence to date, it is concluded that altitude weight loss is because of an initial loss of water and subsequent loss of fat and muscle mass due to malnutrition. Up to 5500m, malabsorption of macronutrients does not occur. Up to altitudes around 5000m, weight loss from a reduction of fat and muscle appears to be avoidable by maintaining adequate dietary intake. Primary anorexia, lack of comfort and palatable food, detraining, and possibly direct effects of hypoxia on protein metabolism seem inevitably to lead to weight loss during longer exposures at higher altitudes. To minimise losses, it is advisable to acclimatise properly, reduce the length of stay at extreme altitude as much as possible and maintain a high and varied nutrient intake. With sojourns at intermediate altitude for training purposes, adequate energy intake should be maintained taking into account the decrease in aerobic training intensity and the increase in basal metabolic rate that ensue from the hypoxic environment.

Altitude↗