Biomedical subjects

G E Butterfield

Publications and source records attributed to G E Butterfield.

At least 19 recordsLinked to original sources

PubMed2001

Catecholamine responses to alpha-adrenergic blockade during exercise in women acutely exposed to altitude.

We have previously documented the importance of the sympathetic nervous system in acclimatizing to high altitude in men. The purpose of this investigation was to determine the extent to which alpha-adrenergic blockade affects the sympathoadrenal responses to exercise during acute high-altitude exposure in women. Twelve eumenorrheic women (24.7 +/- 1.3 yr, 70.6 +/- 2.6 kg) were studied at sea level and on day 2 of high-altitude exposure (4,300-m hypobaric chamber) in either their follicular or luteal phase. Subjects performed two graded-exercise tests at sea level (on separate days) on a bicycle ergometer after 3 days of taking either a placebo or an alpha-blocker (3 mg/day prazosin). Subjects also performed two similar exercise tests while at altitude. Effectiveness of blockade was determined by phenylephrine challenge. At sea level, plasma norepinephrine levels during exercise were 48% greater when subjects were alpha-blocked compared with their placebo trial. This difference was only 25% when subjects were studied at altitude. Plasma norepinephrine values were significantly elevated at altitude compared with sea level but to a greater extent for the placebo ( upward arrow 59%) vs. blocked ( upward arrow 35%) trial. A more dramatic effect of both altitude ( upward arrow 104% placebo vs. 95% blocked) and blockade ( upward arrow 50% sea level vs. 44% altitude) was observed for plasma epinephrine levels during exercise. No phase differences were observed across any condition studied. It was concluded that alpha-adrenergic blockade 1) resulted in a compensatory sympathoadrenal response during exercise at sea level and altitude, and 2) this effect was more pronounced for plasma epinephrine.

Adrenergic alpha-Agonists↗

PubMed2000

Sympathoadrenal responses to submaximal exercise in women after acclimatization to 4,300 meters.

The purpose of this investigation was to determine the sympathoadrenal response to exercise in women after acclimatization to high altitude. Sixteen eumenorrheic women (age, 23.6 +/- 1.2 years; weight, 56.2 +/- 4.3 kg) were studied at sea level and after 10 days of high-altitude exposure (4,300 m) in either the follicular (n = 11) or luteal (n = 5) phase. Subjects performed two 45-minute submaximal steady-state exercise tests (50% and 65% peak O2 consumption [VO2 peak]) at sea level on a bicycle ergometer. Exercise tests were also performed on day 10 of altitude exposure (50% VO2 peak at sea level). As compared with rest, plasma epinephrine levels increased 36% in response to exercise at 50% VO2 peak at sea level, with no differences found between cycle phases. This increase was significantly greater (increase 44%) during exercise at 65% VO2 peak. At altitude, the epinephrine response was identical to that found for 65% VO2 peak exercise at sea level (increase 44%), with no differences found between phase assignments. The plasma norepinephrine response differed from that for epinephrine such that the increase with exercise at altitude (increase 61%) was significantly greater compared with 65% Vo2 peak exercise at sea level (increase 49%). Again, no phase differences were observed. It is concluded that the sympathoadrenal response to exercise (1) did not differ between cycle phases across any condition and (2) was similar to that found previously in men, and (3) the relative exercise intensity is the primary factor responsible for the epinephrine response to exercise, whereas altitude had an additive effect on the norepinephrine response to exercise.

Adrenal Glands↗

PubMed2000

Endurance training increases gluconeogenesis during rest and exercise in men.

The hypothesis that endurance training increases gluconeogenesis (GNG) during rest and exercise was evaluated. We determined glucose turnover with [6,6-(2)H]glucose and lactate incorporation into glucose by use of [3-(13)C]lactate during 1 h of cycle ergometry at two intensities [45 and 65% peak O(2) consumption (VO(2 peak))] before and after training [65% pretraining VO(2 peak)], same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT). Nine males (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer 5 times/wk for 1 h at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) pretraining elicited 54.0 +/- 1.7% posttraining. Rest and exercise arterial glucose concentrations were similar before and after training, regardless of exercise intensity. Arterial lactate concentration during exercise was significantly greater than at rest before and after training. Compared with 65% pretraining, arterial lactate concentration decreased at ABT (4.75 +/- 0.4 mM, 65% pretraining; 2.78 +/- 0.3 mM, ABT) and RLT (3.76 +/- 0.46 mM) (P < 0.05). At rest after training, the percentage of glucose rate of appearance (R(a)) from GNG more than doubled (1.98 +/- 0.5% pretraining; 5.45 +/- 1.3% posttraining), as did the rate of GNG (0.11 +/- 0.03 mg x kg(-1) x min(-1) pretraining, 0.24 +/- 0.06 mg x kg(-1) x min(-1) posttraining). During exercise after training, %glucose R(a) from GNG increased significantly at ABT (2.3 +/- 0.8% at 65% pre- vs. 7.6 +/- 2.1% posttraining) and RLT (6.1 +/- 1.5%), whereas GNG increased almost threefold (P < 0.05) at ABT (0.24 +/- 0.08 mg x kg(-1) x min(-1) 65% pre-, and 0.71 +/- 0.18 mg x kg(-1) x min(-1) posttraining) and RLT (0.75 +/- 0.26 mg x kg(-1) x min(-1)). We conclude that endurance training increases gluconeogenesis twofold at rest and threefold during exercise at given absolute and relative exercise intensities.

Adult↗

PubMed2000

Endurance training, expression, and physiology of LDH, MCT1, and MCT4 in human skeletal muscle.

To evaluate the effects of endurance training on the expression of monocarboxylate transporters (MCT) in human vastus lateralis muscle, we compared the amounts of MCT1 and MCT4 in total muscle preparations (MU) and sarcolemma-enriched (SL) and mitochondria-enriched (MI) fractions before and after training. To determine if changes in muscle lactate release and oxidation were associated with training-induced changes in MCT expression, we correlated band densities in Western blots to lactate kinetics determined in vivo. Nine weeks of leg cycle endurance training [75% peak oxygen consumption (VO(2 peak))] increased muscle citrate synthase activity (+75%, P < 0.05) and percentage of type I myosin heavy chain (+50%, P < 0.05); percentage of MU lactate dehydrogenase-5 (M4) isozyme decreased (-12%, P < 0.05). MCT1 was detected in SL and MI fractions, and MCT4 was localized to the SL. Muscle MCT1 contents were consistent among subjects both before and after training; in contrast, MCT4 contents showed large interindividual variations. MCT1 amounts significantly increased in MU, SL, and MI after training (+90%, +60%, and +78%, respectively), whereas SL but not MU MCT4 content increased after training (+47%, P < 0.05). Mitochondrial MCT1 content was negatively correlated to net leg lactate release at rest (r = -0.85, P < 0.02). Sarcolemmal MCT1 and MCT4 contents correlated positively to net leg lactate release at 5 min of exercise at 65% VO(2 peak) (r = 0.76, P < 0.03 and r = 0. 86, P < 0.01, respectively). Results support the conclusions that 1) endurance training increases expression of MCT1 in muscle because of insertion of MCT1 into both sarcolemmal and mitochondrial membranes, 2) training has variable effects on sarcolemmal MCT4, and 3) both MCT1 and MCT4 participate in the cell-cell lactate shuttle, whereas MCT1 facilitates operation of the intracellular lactate shuttle.

Adult↗

PubMed2000

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.

Adult↗

PubMed2000

Women at altitude: energy requirement at 4,300 m.

To test the hypotheses that prolonged exposure to moderately high altitude increases the energy requirement of adequately fed women and that the sole cause of the increase is an elevation in basal metabolic rate (BMR), we studied 16 healthy women [21.7 +/- 0.5 (SD) yr; 167.4 +/- 1.1 cm; 62.2 +/- 1.0 kg]. Studies were conducted over 12 days at sea level (SL) and at 4,300 m [high altitude (HA)]. To test that menstrual cycle phase has an effect on energetics at HA, we monitored menstrual cycle in all women, and most women (n = 11) were studied in the same phase at SL and HA. Daily energy intake at HA was increased to respond to increases in BMR and to maintain body weight and body composition. Mean BMR for the group rose 6.9% above SL by day 3 at HA and fell to SL values by day 6. Total energy requirement remained elevated 6% at HA [ approximately 670 kJ/day (160 kcal/day) above that at SL], but the small and transient increase in BMR could not explain all of this increase, giving rise to an apparent "energy requirement excess." The transient nature of the rise in BMR may have been due to the fitness level of the subjects. The response to altitude was not affected by menstrual cycle phase. The energy requirement excess is at present unexplained.

Adult↗

PubMed1999

Nutrient requirements at high altitude.

Travel to terrestrial altitudes greater than 2500 m, for more than 2 to 3 days, results in acute and long-term physiologic adaptations with the potential to profoundly affect the requirements for some nutrients. This article discusses the evidence for these increased requirements and makes recommendations regarding appropriate intakes at high altitude. Discussion of nutrients includes energy and the food components that supply it (i.e., protein, carbohydrate, and fat), water, vitamins, and minerals. Because the anorexia associated with high altitude exposure may limit the intake of adequate nutrients, a food and water regimen, or "doctrine," is proposed and described.

Altitude↗

PubMed1999

Pre-exercise carbohydrate meals: application of glycemic index.

PURPOSE: The purpose of this study was to compare postprandial glycemic, insulinemic, and physiologic responses to a pre-exercise meal calculated to have a low glycemic index (LGI) with one calculated to have a moderately high glycemic index (HGI); each meal provided three foods totaling 1.5 g carbohydrate/kg body weight. METHODS: After an overnight fast, 10 trained cyclists consumed one of the test meals or water 30 min before cycling 2 h at 70% of maximum oxygen uptake (VO2max), followed by cycling to exhaustion at 100% of VO2max. RESULTS: Plasma insulin levels were significantly lower (P < 0.05) after LGI than after HGI through 20 min of exercise. Significantly higher (P < 0.05) respiratory exchange ratios were observed after HGI than after LGI until 2 h of exercise. At that time plasma glucose levels were significantly higher and ratings of perceived exertion lower (P < 0.05) after LGI compared with after HGI. Time to exhaustion was 59% longer after LGI (206.5+/-43.5 s) than after HGI (129.5+/-22.8 s). CONCLUSIONS: These results suggest a pre-exercise LGI may positively affect maximal performance following sustained exercise. The LGI maintained higher plasma glucose levels at the end of 2 h of strenuous exercise than the HGI, which may have better supported subsequent maximal effort.

Adult↗

PubMed1999

Evaluation of exercise and training on muscle lipid metabolism.

To evaluate the hypothesis that endurance training increases intramuscular triglyceride (IMTG) oxidation, we studied leg net free fatty acid (FFA) and glycerol exchange during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (V(O2) peak)] and after training [65% pretraining V(O2) peak, same absolute workload (ABT), and 65% posttraining V(O2) peak, same relative intensity (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times per week at 75% V(O2) peak. The power output that elicited 66.1 +/- 1.1% of V(O2) peak before training elicited 54.0 +/- 1.7% after training due to a 14.6 +/- 3.1% increase in V(O2) peak. Training significantly (P < 0.05) decreased pulmonary respiratory exchange ratio (RER) values at ABT (0.96 +/- 0.01 at 65% pre- vs. 0.93 +/- 0.01 posttraining) but not RLT (0.95 +/- 0.01). After training, leg respiratory quotient (RQ) was not significantly different at either ABT (0.98 +/- 0.02 pre- vs. 0.98 +/- 0.03 posttraining) or RLT (1.01 +/- 0.02). Net FFA uptake was increased at RLT but not ABT after training. FFA fractional extraction was not significantly different after training or at any exercise intensity. Net glycerol release, and therefore IMTG lipolysis calculated from three times net glycerol release, did not change from rest to exercise or at ABT but decreased at the same RLT after training. Muscle biopsies revealed minor muscle triglyceride changes during exercise. Simultaneous measurements of leg RQ, net FFA uptake, and glycerol release by working legs indicated no change in leg FFA oxidation, FFA uptake, or IMTG lipolysis during leg cycling exercise that elicits 65% pre- and 54% posttraining V(O2) peak. Training increases working muscle FFA uptake at 65% V(O2) peak, but high RER and RQ values at all work intensities indicate that FFA and IMTG are of secondary importance as fuels in moderate and greater-intensity exercise.

Adult↗

PubMed1999

Muscle net glucose uptake and glucose kinetics after endurance training in men.

We evaluated the hypotheses that alterations in glucose disposal rate (R(d)) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative workload (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) before training elicited 54.0 +/- 1.7% after training. Whole body glucose R(d) decreased posttraining at ABT (5.45 +/- 0.31 mg. kg(-1). min(-1) at 65% pretraining to 4.36 +/- 0.44 mg. kg(-1). min(-1)) but not at RLT (5.94 +/- 0.47 mg. kg(-1). min(-1)). Net glucose uptake was attenuated posttraining at ABT (1.87 +/- 0.42 mmol/min at 65% pretraining and 0.54 +/- 0.33 mmol/min) but not at RLT (2.25 +/- 0. 81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose R(d) and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65% VO(2 peak)) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65% VO(2 peak)) promotes a glucose shunt from inactive tissues to active muscle.

Adult↗

PubMed1999

Active muscle and whole body lactate kinetics after endurance training in men.

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate](a)) during continuous exercise by decreasing net lactate release () and appearance rates (R(a)) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O(2) consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT)]. Nine men (27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75% VO(2 peak). Compared with the 65% VO(2 peak) pretraining condition (4.75 +/- 0.4 mM), [lactate](a) decreased at ABT (41%) and RLT (21%) (P < 0.05). decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate](a); and 2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.

Adult↗

PubMed1998

Beta-adrenergic blockade does not prevent polycythemia or decrease in plasma volume in men at 4300 m altitude.

When humans ascend to high altitude (ALT) their plasma volume (PV) and total blood volume (BV) decrease during the first few days. With continued residence over several weeks, the hypoxia-induced stimulation of erythropoietin increases red cell production which tends to restore BV. Because hypoxia also activates the beta-adrenergic system, which stimulates red blood cell production, we investigated the effect of adrenergic beta-receptor inhibition with propranolol on fluid volumes and the polycythemic response in 11 healthy unacclimatized men (21-33 years old exposed to an ALT of 4300 m (barometric pressure 460 Torr) for 3 weeks on Pikes Peak, Colorado. PV was determined by the Evans blue dye method (PVEB), BV by the carbon monoxide method (BVCO), red cell volume (RCV) was calculated from hematocrit (Hct) and BVCO, and serum erythropoietin concentration ([EPO]) and reticulocyte count, were also determined. All determinations were made at sea level and after 9-11 (ALT-10) and 19-20 (ALT-20) days at ALT. At sea level and ALT, six men received propranolol (pro, 240 mg x day[-1]), and five received a placebo (pla). Effective beta-blockade did not modify the mean (SE) maximal values of [EPO] [pla: 24.9 (3.5) vs pro: 24.5 (1.5) mU x ml(-1)] or reticulocyte count [pla: 2.7 (0.7) vs pro: 2.2 (0.5)%]; nor changes in PVEB [pla: -15.8 (3.8) vs pro: -19.9 (2.8)%], RCVCO [pla: +7.0 (6.7) vs pro: + 10.1 (6.1)%], or BVCO [pla: -7.3 (2.3) vs pro: -7.1 (3.9)%]. In the absence of weight loss, a redistribution of body water with no net loss is implied. Hence, activation of the beta-adrenergic system did not appear to affect the hypovolemic or polycythemic responses that occurred during 3 weeks at 4300 m ALT in these subjects.

Adrenergic beta-Antagonists↗

PubMed1998

Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude.

We evaluated the hypotheses that on acute exposure to hypobaric hypoxia, sympathetic stimulation leads to augmented muscle lactate production and circulating [lactate] through a beta-adrenergic mechanism and that beta-adrenergic adaptation to chronic hypoxia is responsible for the blunted exercise lactate response after acclimatization to altitude. Five control and 6 beta-blocked men were studied during rest and exercise at sea level (SL), on acute exposure to 4,300 m (A1), and after a 3-wk sojourn at altitude (A2). Exercise was by leg cycling at 49% of SL peak O2 consumption (VO2 peak) (65% of altitude VO2 peak or 87 +/- 2.6 W); beta-blockade was by propranolol (80 mg 3x daily), femoral arterial and venous blood was sampled; leg blood flow (Q) was measured by thermodilution, leg lactate net release [ = (2) (1-leg Q) venous-arterial concentrationL] was calculated, and vastus lateralis needle biopsies were obtained. Muscle [lactate] increased with exercise and acute altitude exposure but regressed to SL values with acclimatization; beta-blockade had no effect on muscle [lactate]. Arterial [lactate] rose during exercise at SL (0.9 +/- 0.1 to 1.5 +/- 0.3 mM); exercise at A1 produced the greatest arterial [lactate] (4.4 +/- 0.8 mM), and exercise at A2 an intermediate response (2.1 +/- 0.6 mM). beta-Blockade reduced circulating [lactate] approximately 45% during exercise under all altitude conditions. increased transiently at exercise onset but then declined over time under all conditions. Blood and muscle "lactate paradoxes" occurred independent of beta-adrenergic influences, and the hypotheses relating the blood lactate response at altitude to beta-adrenergic mechanisms are rejected. During exercise at altitude, arterial [lactate] is determined by factors in addition to hypoxemia, circulating epinephrine, and net lactate release from active muscle beds.

Acclimatization↗

PubMed1998

Catecholamine response during 12 days of high-altitude exposure (4, 300 m) in women.

We have previously demonstrated that acclimatization to high altitude elicits increased sympathetic nerve activity in men. The purpose of this investigation was to determine 1) whether women respond in a similar manner as found previously in men and 2) the extent to which menstrual cycle phase influences this response. Sixteen eumenorrheic women (age, 23.6 +/- 1.2 yr; weight, 56.2 +/- 4. 3 kg) were studied at sea level and during 12 days of high-altitude exposure (4,300 m) in either their follicular (F; n = 11) or luteal (L; n = 5) phase. Twenty-four-hour urine samples were collected at sea level and during each day at altitude. Catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Compared with sea-level values, urinary norepinephrine excretion increased significantly during altitude exposure, peaking on days 4-6. Thereafter, levels remained constant throughout the duration of altitude exposure. The magnitude of this increase was similar between the F (138%) and L (93%) phase. Urinary epinephrine levels were elevated on day 2 of altitude exposure compared with sea-level values for both F and L subjects (93%). Thereafter, urinary epinephrine excretion returned to sea-level values, and no differences were found between F and L subjects. Plasma catecholamine content was consistent with urinary values and supports the concept of an elevation in sympathetic activity over time at altitude. Mean and diastolic blood pressure as well as heart rate adjustments to high altitude correlated significantly with urinary norepinephrine excretion rates. It was concluded that 1) urinary and plasma catecholamine responses to 12 days of high-altitude exposure in women are similar to those previously documented to occur for men; 2) whereas no differences in catecholamine levels were observed between F- and L-phase assignments, for a given urinary norepinephrine excretion rate, blood pressure and heart rates were lower for F vs. L subjects; and 3) several cardiovascular adaptations associated with high-altitude exposure correlated with 24-h urinary norepinephrine excretion rates and thus sympathetic nerve activity.

Adrenal Glands↗

PubMed1998

O2 extraction maintains O2 uptake during submaximal exercise with beta-adrenergic blockade at 4,300 m.

Whole body O2 uptake (VO2) during maximal and submaximal exercise has been shown to be preserved in the setting of beta-adrenergic blockade at high altitude, despite marked reductions in heart rate during exercise. An increase in stroke volume at high altitude has been suggested as the mechanism that preserves systemic O2 delivery (blood flow x arterial O2 content) and thereby maintains VO2 at sea-level values. To test this hypothesis, we studied the effects of nonselective beta-adrenergic blockade on submaximal exercise performance in 11 normal men (26 +/- 1 yr) at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol (240 mg/day), and five subjects received placebo. At sea level, during submaximal exercise, cardiac output and O2 delivery were significantly lower in propranolol- than in placebo-treated subjects. Increases in stroke volume and O2 extraction were responsible for the maintenance of VO2. At 4,300 m, beta-adrenergic blockade had no significant effect on VO2, ventilation, alveolar PO2, and arterial blood gases during submaximal exercise. Despite increases in stroke volume, cardiac output and thereby O2 delivery were still reduced in propranolol-treated subjects compared with subjects treated with placebo. Further reductions in already low levels of mixed venous O2 saturation were responsible for the maintenance of VO2 on arrival and after 21 days at 4,300 m in propranolol-treated subjects. Despite similar workloads and VO2, propranolol-treated subjects exercised at greater perceived intensity than subjects given placebo at 4,300 m. The values for mixed venous O2 saturation during submaximal exercise in propranolol-treated subjects at 4,300 m approached those reported at simulated altitudes >8,000 m. Thus beta-adrenergic blockade at 4,300 m results in significant reduction in O2 delivery during submaximal exercise due to incomplete compensation by stroke volume for the reduction in exercise heart rate. Total body VO2 is maintained at a constant level by an interaction between mixed venous O2 saturation, the arterial O2-carrying capacity, and hemodynamics during exercise with acute and chronic hypoxia.

Adrenergic beta-Agonists↗

PubMed1998

Women at altitude: changes in carbohydrate metabolism at 4,300-m elevation and across the menstrual cycle.

We hypothesized that, in women, the blood glucose response to a meal (BGR) would be lower after exposure to 4,300 m compared with sea level (SL) and that BGR would be reduced in the presence of estrogen plus progesterone (E+P) relative to estrogen alone (E). Sixteen women were studied in both the E and E+P conditions at SL and in either the E or E+P condition at 4,300 m. On day 9 in each condition, blood was sampled before, and every 30 min for 2 h after, the subjects ate a high-carbohydrate meal. At 4,300 m, BGR peaked at a lower value (5.73 +/- 0.94 mM) than at SL (6.44 +/- 1.45 mM) and returned to baseline more slowly (P < 0.05). Plasma insulin values were the same but C peptide was slightly higher at 4,300 m (P < 0. 05). At SL, BGR returned to baseline more slowly in E+P condition (5. 13 +/- 0.89 and 5.21 +/- 0.91 mM at 60 and 90 min, respectively) relative to E condition (4.51 +/- 0.52 and 4.69 +/- 0.88 mM, respectively) (P < 0.05). Insulin and C peptide were not different between E and E+P conditions. The data indicate that BGR is lower in women at high altitude compared with the SL, possibly due to greater suppression of hepatic glucose production or stimulation of peripheral glucose uptake by insulin. BGR was lower in E condition relative to E+P condition at SL and possibly at 4,300 m, but the relative concentrations of ovarian hormones do not appear to alter the magnitude of the change in BGR when women are exposed to high altitude.

Adult↗

PubMed1998

Effects of human growth hormone, insulin-like growth factor I, and diet and exercise on body composition of obese postmenopausal women.

To determine the effects of GH and insulin-like growth factor I (IGF-I) administration, diet, and exercise on weight loss, body composition, basal metabolic rate (BMR), muscle strength, and psychological status, 33 moderately obese postmenopausal women (67.1 +/- 5.2 yr) participated in a 12-week randomized, double blind study. Participants were placed on a diet that provided 500 Cal/day less than that needed for weight maintenance, and they walked 3 days and strength trained 2 days each week. Subjects also self-injected GH (0.025 mg/kg BW.day), IGF-I (0.015 mg/kg BW.day), a combination of these doses of GH and IGF-I, or placebo (P). Twenty-eight women completed the study, as five subjects dropped out due to intolerable side-effects (e.g. edema). Weight loss occurred in all groups, with the largest decrease occurring in the GH plus IGF-I group (5.6 +/- 1.4 kg). Fat mass significantly decreased in all groups, with the largest losses observed in GH and GH plus IGF-I groups (6.3 +/- 1.8 and 8.4 +/- 2.8 kg, respectively). Despite weight loss, BMR was maintained in all groups. Muscle strength increased with training for all groups, and depression and anxiety scores decreased in groups receiving IGF-I. These data show that obese postmenopausal women can lose weight and fat without compromising fat free mass, BMR, or gains in muscle strength, and that GH and IGF-I given together may enhance fat loss over either given alone.

Aged↗

PubMed1997

Effects of diet and exercise on energy expenditure in postmenopausal women.

The purpose of this study was to determine the effect of a 24-wk diet + exercise (DE) or diet-only program on basal metabolic rate (BMR), bone mineral density (BMD), energy expended during daily activities, muscle strength, and maximal oxygen consumption (VO2max) in 40 postmenopausal women. Daily energy need was determined by measuring BMR and assessing physical activity with 8-d self-reported activity records. The DE group consumed 2092 kJ/d less than the daily energy need and walked and performed strength-training exercises during which they expended an additional 837 kJ/d. The two diet-only groups consumed either 2092 kJ/d (D-2092) or 2929 kJ/d (D-2929) less than the daily energy need. BMD, BMR, muscle strength, VO2max, and energy expended during lying, sitting, standing, and walking were measured at baseline and after 12 and 24 wk of treatment. A significant decrease in BMR and energy expended during sitting and walking occurred in all groups, with no significant differences observed among groups. Although the declines in BMR were significant, they were small and may not have been physiologically relevant. No changes in BMD or VO2max occurred, whereas strength increased significantly in the DE group. The results showed that postmenopausal women significantly improved their body composition over a period of 6 mo without experiencing a large decline in BMR, BMD, or select components of energy expenditure.

Aged↗