Effect of swimming on prednisolone-induced osteoporosis in elderly rats.

We investigated the possible ameliorating and preventive effect of swimming on prednisolone-induced osteoporosis in elderly rats. A total of 48 female Sabra strain rats were randomly assigned to the following groups and treatments: (1) control (C), (2) swimming (S), (3) prednisolone-treated (CP), and (4) swimming + prednisolone (SP). An additional 8 rats were sacrificed and examined at the onset of the study. Groups C and S were sham injected; groups CP and SP were injected with prednisolone (Ultracorten), 80 mg/kg three times per week for 10 weeks. Groups S and SP swam 1 h daily, 5 days per week for 10 weeks. SP rats swam simultaneously with prednisolone administration. At the end of the swimming period, in vivo bone mineral content (BMC) measurements were performed on rat vertebrae L4-5 by single-photon absorptiometry. Later, the humerus and femur were removed for the following measurements: morphometric, bone density (BD) by Compton scattering technique, bone ion content by atomic absorption, and hydration fraction by proton magnetic resonance (PMR). We found that the humeral BD of S rats was greater by 14% for group S over C and 3% greater for group SP over CP (P less than 0.05). Vertebral BMC was higher by 15% in group S over C and 11% higher for group SP over CP (P less than 0.05). Femoral calcium (mg/g dry bone) ion content was higher by 5% in group S over C and 8% in group SP over CP group (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose and lactate interrelations during moderate-intensity exercise in humans.

To evaluate circulating lactate and glucose kinetics during moderate-intensity exercise, we studied ten healthy endurance-trained men (aged 25 +/- 6 years) during 30 to 50 minutes of supine cycle ergometer exercise at 43% +/- 5% of maximal oxygen consumption (VO2 max) using isotopic tracer techniques. Seven subjects received [U-13C]-lactate and [6-14C]-glucose, and three received [1-14C]-lactate and [U-13C]-glucose. Arterial glucose and lactate concentrations were 94.0 +/- 4.1 and 5.66 +/- 0.87 mg/dL at rest, and 95.7 +/- 3.4 and 8.38 +/- 3.87 mg/dL, respectively, after 25 minutes of exercise. The rate of glucose disappearance (RdG) increased from 2.41 +/- 0.40 at rest to 3.38 +/- 0.77 mg x kg-1 x min-1 during exercise, compared with the much larger rise in the rate of lactate appearance (RaL), which increased from 1.25 +/- 0.20 to 3.47 +/- 0.79 mg x kg-1 x min-1. During exercise RaL was 103% of RdG, compared with only 52% at rest. The rate at which the blood was cleared of lactate increased from 22.7 +/- 2.2 at rest to 44.2 +/- 11.2 ml x kg-1 x min-1 after 25 minutes of exercise. From secondary labeling of lactate with glucose carbons, the rate of glucose conversion to lactate was estimated to be 0.65 +/- 0.16 mg x kg-1 x min-1 during exercise. Twenty percent of the glucose utilization went to lactate formation during exercise, and 20% of the blood lactate appearance came from blood glucose, with the balance presumably coming from muscle glycogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Training does not affect zero-trans lactate transport across mixed rat skeletal muscle sarcolemmal vesicles.

Hindlimb muscle sarcolemmal vesicles were purified from three age-matched groups of female Sprague-Dawley rats: sedentary control (CON; n = 10), sprint trained (ST; n = 8), and endurance trained (ET; n = 9). Membrane isolations from the three groups were not significantly different in protein yield or purification index. Blood lactate concentration was determined in resting CON rats and running ET and ST rats during the final week. Both the ST and ET groups were significantly higher in citrate synthase (vs. CON) in the soleus and mid-vastus lateralis. The time course of 1 mM L-(+)-lactate uptake in vesicles from the three groups showed no significant difference at any of the five time points tested under zero-trans conditions. Saturation kinetics were examined at nine lactate concentrations, and Lineweaver-Burk plots revealed no difference between groups in apparent Michaelis-Menten constant or maximal transport velocity. Vesicles from CON and ET rats were used to investigate cis inhibition of 0.1 mM L-(+)-lactate transport by four unlabeled monocarboxylates: L-(+)-lactate, D-(-)-lactate, pyruvate, and alpha-cyanohydroxycinnamate at 0.1, 1.0, and 10 mM. Under pH gradient-stimulated L-(+)-lactate transport conditions, cis inhibition was affected by neither D-(-)-lactate nor endurance training. We conclude that the lactate transporter has distinct cis-inhibitory specificity, is stereospecific, and is stimulated when confronted with parallel lactate and proton gradients but that spring and endurance training do not alter lactate transport rate or capacity under these conditions.

Effects of training on glucose metabolism of gluconeogenesis-inhibited short-term-fasted rats.

To evaluate the effects of endurance training on gluconeogenesis and blood glucose homeostasis, trained as well as untrained short-term-fasted rats were injected with mercaptopicolinic acid (MPA), a gluconeogenic inhibitor, or the injection vehicle. Glucose kinetics were assessed by primed-continuous venous infusion of [U-14C]- and [6-3H]glucose at rest and during submaximal exercise at 13.4 m/min on level grade. Arterial blood was sampled for the determination of blood glucose and lactate concentrations and specific activities. In resting untrained sham-injected rats, blood glucose and lactate were 7.6 +/- 0.2 and 1.3 +/- 0.1 mM, respectively; glucose rate of appearance (Ra) was 71.1 +/- 12.1 mumol.kg-1.min-1. MPA treatment lowered blood glucose, raised lactate, and decreased glucose Ra. Trained animals had significantly higher glucose Ra at rest and during exercise. At rest, trained MPA-treated rats had lower blood glucose, higher blood lactate, and similar glucose Ra and disappearance rates (Rd) than trained sham-injected animals. Exercising sham-injected untrained animals had increased blood glucose and glucose Ra compared with rest. Exercising trained sham-injected rats had increased blood glucose and glucose Ra and Rd but no change in blood lactate compared with untrained sham-injected animals. In the trained animals during exercise, MPA treatment increased blood lactate and decreased blood glucose and glucose Ra and Rd. There was no measurable glucose recycling in trained or untrained MPA-treated animals either at rest or during submaximal exercise. There was no difference in running time to exhaustion between trained and untrained MPA-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Balance of carbohydrate and lipid utilization during exercise: the "crossover" concept.

The "crossover" concept represents a theoretical means by which one can understand the effects of exercise intensity and prior endurance training on the balance of carbohydrate (CHO) and lipid metabolism during sustained exercise. According to the crossover concept, endurance training results in muscular biochemical adaptations that enhance lipid oxidation as well as decrease the sympathetic nervous system responses to given submaximal exercise stresses. These adaptations promote lipid oxidation during mild- to moderate-intensity exercise. In contrast, increases in exercise intensity are conceived to increase contraction-induced muscle glycogenolysis, alter the pattern of fiber type recruitment, and increase sympathetic nervous system activity. Therefore the pattern of substrate utilization in an individual at any point in time depends on the interaction between exercise intensity-induced responses (which increase CHO utilization) and endurance training-induced responses (which promote lipid oxidation). The crossover point is the power output at which energy from CHO-derived fuels predominates over energy from lipids, with further increases in power eliciting a relative increment in CHO utilization and a decrement in lipid oxidation. The contemporary literature contains data indicating that, after endurance training, exercise at low intensities (< or = 45% maximal O2 uptake) is accomplished with lipid as the main substrate. In contrast, the literature also contains reports that are interpreted to indicate that during hard-intensity exercise (approximately 75% maximal O2 uptake) CHO is the predominant substrate. Seen within the context of the crossover concept these apparently divergent results are, in fact, consistent.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory gas-exchange ratios during graded exercise in fed and fasted trained and untrained men.

We evaluated the hypotheses that endurance training increases relative lipid oxidation over a wide range of relative exercise intensities in fed and fasted states and that carbohydrate nutrition causes carbohydrate-derived fuels to predominate as energy sources during exercise. Pulmonary respiratory gas-exchange ratios [(RER) = CO2 production/O2 consumption (VO2)] were determined during four relative, graded exercise intensities in both fed and fasted states. Seven untrained (UT) men and seven category 2 and 3 US Cycling Federation cyclists (T) exercised in the morning in random order, with target power outputs of 20 and 40% peak VO2 (VO2 peak) for 2 h, 60% VO2 peak for 1.5 h, and 80% VO2 peak for a minimum of 30 min after either a 12-h overnight fast or 3 h after a standardized breakfast. Actual metabolic responses were 22 +/- 0.33, 40 +/- 0.31, 59 +/- 0.32, and 75 +/- 0.39% VO2 peak. T subjects showed significantly (P < 0.05) decreased RER compared with UT subjects at absolute workloads when fed and fasted. Fasting significantly decreased RER values compared with the fed state at 22, 40, and 59% VO2 peak in T and at 40 and 59% VO2 peak in UT subjects. Training decreased (P < 0.05) mean RER values compared with UT subjects at 22% VO2 peak when they fasted, and at 40% VO2 peak when fed or fasted, but not at higher relative exercise intensities in either nutritional state. Our results support the hypothesis that endurance training enhances lipid oxidation in men after a 12-h overnight fast at low relative exercise intensities (22 and 40% VO2 peak). However, a training effect on RER was not apparent at high relative exercise intensities (59 and 75% VO2 peak). Because most athletes train and compete at exercise intensities >40% maximal VO2, they will not oxidize a greater proportion of lipids compared with untrained subjects, regardless of nutritional state.

Effects of a 36-hour fast on human endurance and substrate utilization.

To determine if prolonged fasting affects substrate utilization and endurance time, seven trained men exercised to exhaustion on a cycle ergometer at 50% maximum oxygen consumption (VO2max) in an overnight-fasted [postabsorptive (PA)] state and after a 36-h fast (F). Fasting produced significant elevations in the resting concentrations of blood free fatty acids (FFA; 1.16 +/- 0.05 vs. 0.56 +/- 0.06 mM, F vs. PA, respectively, a 107% increase), beta-hydroxybutyrate (beta-OH, 2.06 +/- 0.66 vs. 0.15 +/- 0.06 mM, a 1,270% increase), and glycerol (0.12 +/- 0.03 vs. 0.04 +/- 0.01 mM, a 200% increase), with a significant decline in glucose (79.79 +/- 2.12 vs. 98.88 +/- 3.11 mg/dl, a 19% decrease). Exercise in the F trial increased FFA, decreased glucose, and significantly elevated beta-OH and glycerol over the PA trial. There was no difference in blood glucose concentration between trials at exhaustion. However, F produced a significant decrement in exercise endurance time compared with the PA trial (88.9 +/- 18.3 vs. 144.4 +/- 22.6 min, F vs. PA, a 38% decrease). Based on the respiratory exchange ratio, fasting led to a greater utilization of lipids during rest and exercise. It was concluded that 1) a 36-h fast significantly altered substrate utilization at rest and throughout exercise to exhaustion, 2) glucose levels do not appear to be the single determinant of time to exhaustion in submaximal exercise, and 3) despite the apparent sparing of carbohydrate utilization with the 36-h fast, endurance performance was significantly decreased.

Acute anemia results in an increased glucose dependence during sustained exercise.

We evaluated whether acute anemia results in altered blood glucose utilization during sustained exercise at 26.8 m/min on 0% grade, which elicited approximately 60-70% maximal O2 consumption. Acute anemia was induced in female Sprague-Dawley rats by isovolumic plasma exchange transfusion. Hemoglobin and hematocrit were reduced 33% by exchange transfusion to 8.6 +/- 0.4 g/dl and 26.5 +/- 1%, respectively. Glucose kinetics were determined by primed continuous infusion of [6-3H]glucose. Rates of O2 consumption were similar during rest (pooled means 25.1 +/- 1.8 ml.kg-1.min-1) and exercise (pooled means 46.8 +/- 3.0 ml.kg-1.min-1). Resting blood glucose and lactate concentrations were not different in anemic animals (pooled means 5.1 +/- 0.2 and 0.9 +/- 0.02 mM, respectively). Exercise resulted in significantly decreased blood glucose (4.0 +/- 0.2 vs. 4.6 +/- 0.1 mM) and elevated lactate (6.1 +/- 0.4 vs. 2.3 +/- 0.5 mM) concentrations in anemic animals. Glucose turnover rates (Rt) were not different between anemic and control animals at rest and averaged 58.8 +/- 3.6 mumol.kg-1.min-1. Exercise resulted in a 30% greater increase in Rt in anemic (141.7 +/- 3.2 mumol.kg-1.min-1) than in control animals (111.2 +/- 5.2 mumol.kg-1.min-1). Metabolic clearance rates (MCR = Rt/[glucose]) were not different at rest (11.6 +/- 7.4) but were significantly greater in anemic (55.2 +/- 5.7 ml.kg-1.min-1) than in control animals (24.3 +/- 1.4 ml.kg-1.min-1) during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Induced lactacidemia does not affect postexercise O2 consumption.

To study the effects of circulatory occlusion on the time course and magnitude of postexercise O2 consumption (VO2) and blood lactate responses, nine male subjects were studied twice for 50 min on a cycle ergometer. On one occasion, leg blood flow was occluded with surgical thigh cuffs placed below the buttocks and inflated to 200 mmHg. The protocol consisted of a 10-min rest, 12 min of exercise at 40% peak O2 consumption (VO2 peak), and a 28-min resting recovery while respiratory gas exchange was determined breath by breath. Occlusion (OCC) spanned min 6-8 during the 12-min work bout and elicited mean blood lactate of 5.2 +/- 0.8 mM, which was 380% greater than control (CON). During 18 min of recovery, blood lactate after OCC remained significantly above CON values. VO2 was significantly lower during exercise with OCC compared with CON but was significantly higher during the 4 min of exercise after cuff release. VO2 was higher after OCC during the first 4 min of recovery but was not significantly different thereafter. Neither total recovery VO2 (gross recovery VO2 with no base-line subtraction) nor excess postexercise VO2 (net recovery VO2 above an asymptotic base line) was significantly different for OCC and CON conditions (13.71 +/- 0.45 vs. 13.44 +/- 0.61 liters and 4.93 +/- 0.26 vs. 4.17 +/- 0.35 liters, respectively). Manipulation of exercise blood lactate levels had no significant effect on the slow ("lactacid") component of the recovery VO2.

Physiological and biochemical correlates of increased work in trained iron-deficient rats.

We investigated physiological and biochemical factors associated with the improved work capacity of trained iron-deficient rats. Female 21-day-old rats were assigned to one of four groups, two dietary groups (50 and 6 ppm dietary iron) subdivided into two levels of activity (sedentary and treadmill trained). Iron deficiency decreased hemoglobin (61%), maximal O2 uptake. (VO2max) (40%), skeletal muscle mitochondrial oxidase activities (59-90%), and running endurance (94%). In contrast, activities of tricarboxylic acid (TCA) cycle enzymes in skeletal muscle were largely unaffected. Four weeks of mild training in iron-deficient rats resulted in improved blood lactate homeostasis during exercise and increased VO2max (15%), TCA cycle enzymes of skeletal muscle (27-58%) and heart (29%), and liver NADH oxidase (34%) but did not affect any of these parameters in the iron-sufficient animals. In iron-deficient rats training affected neither the blood hemoglobin level nor any measured iron-dependent enzyme pathway of skeletal muscle but substantially increased endurance (230%). We conclude that the training-induced increase in endurance in iron-deficient rats may be related to cardiovascular improvements, elevations in liver oxidative capacity, and increases in the activities of oxidative enzymes that do not contain iron in skeletal and cardiac muscle.

Interactive effects of anemia and muscle oxidative capacity on exercise endurance.

We used endurance training and acute anemia to assess the interactions among maximal oxygen consumption (VO2max), muscle oxidative capacity, and exercise endurance in rats. Animals were evaluated under four conditions: untrained and endurance-trained with each group subdivided into anemic (animals with reduced hemoglobin concentrations) and control (animals with unchanged hemoglobin concentrations). Anemia was induced by isovolemic plasma exchange transfusion. Hemoglobin concentration and hematocrit were decreased by 38 and 41%, respectively. Whole body VO2max was decreased by 18% by anemia regardless of training condition. Anemia significantly reduced endurance by 78% in untrained rats but only 39% in trained animals. Endurance training resulted in a 10% increase in VO2max, a 75% increase in the distance run to exhaustion, and 35, 45, and 58% increases in skeletal muscle pyruvate-malate, alpha-ketoglutarate, and palmitylcarnitine oxidase activities, respectively. We conclude that endurance is related to the interactive effects of whole body VO2max and muscle oxidative capacities for the following reasons: 1) anemic untrained and trained animals had similar VO2max but trained rats had higher muscle oxidative capacities and greater endurance; 2) regardless of training status, the effect of acute anemia was to decrease VO2max and endurance; and 3) trained anemic rats had lower VO2max but had greater muscle oxidative capacity and greater endurance than untrained controls.

Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2.

The necessity for defining hypoxia as O2-limited energy flux rather than low partial pressure is explored from a systems perspective. Oxidative phosphorylation, the Krebs cycle, glycolysis, substrate supply, and cell energetics interact as subsystems; the set point is a match between ATP demand and aerobic ATP production. To this end the transport subsystem must match the transcapillary and mitochondrial O2 fluxes. High transcapillary O2 flux requires intracellular PO2 in the range 1-10 Torr. In this range the O2 drive on electron transport must be compensated by adaptive changes in the phosphorylation and redox drives. Thus the metabolic subsystem supports diffusive O2 transport by maintaining O2 flux at intracellular partial pressures required for O2 release from blood. Since responses to stress are distributed according to the state of the entire system, several simultaneous metabolic measurements, including intracellular PO2 (or a known direction of change in intracellular PO2) and the O2 dependence of a measurable function are required to judge the adequacy of O2 supply. ATP demand and aerobic capacity must also be evaluated, because the hypoxic threshold depends on the ratio of ATP demand to aerobic capacity. The application and limitation of commonly used criteria of hypoxia are discussed, and a more precise terminology is proposed.

Blood glutathione oxidation during human exercise.

To examine the effects of increased O2 utilization on the glutathione antioxidant system in blood, eight moderately trained male volunteers were exercised to peak O2 consumption (VO2peak) and for 90 min at 65% of VO2peak on a cycle ergometer. Blood samples were taken during exercise, and for up to 4 days of recovery from submaximal exercise. During exercise to VO2peak, blood reduced glutathione (GSH) and total glutathione [GSH + oxidized glutathione (GSSG)] did not change significantly. Lactate (L), pyruvate (P), and L/P increased significantly from rest values (P less than 0.01). During prolonged submaximal exercise, GSH decreased 60% from control, and GSSG increased 100%. Total glutathione, glucose, pyruvate, and lactate concentrations and L/P did not change significantly during sustained exercise. During recovery, GSH and GSH/GSSG increased from exercise levels and significantly overshot preexercise levels, reaching maximum values after 3 days. Oxidation of GSH during submaximal exercise and its reduction in recovery suggest increased formation of active O2-. species in blood during physical exercise in moderately trained males.

Disposal of blood [1-13C]lactate in humans during rest and exercise.

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.

Antioxidant status and indexes of oxidative stress during consecutive days of exercise.

We tested whether consecutive days of prolonged submaximal exercise would result in oxidant stress sufficient to alter blood antioxidant profiles, progressively change and exhaust blood and plasma antioxidants, and damage RNA. Eleven moderately trained males (24.3 +/- 1.1 yr) exercised 90 min at 65% peak O2 uptake on a cycle ergometer for 3 consecutive days. During day 1 exercise, blood reduced glutathione (GSH) declined 55 +/- 10% and oxidized glutathione (GSSG) increased 28 +/- 7% within 15 min. Total blood glutathione did not significantly change during exercise. GSH levels returned to baseline after 15 min of recovery. On day 3, preexercise GSH and GSSG levels were not significantly different from day 1 preexercise values; essentially similar results were obtained during exercise and recovery. During day 1 exercise, plasma total ascorbate (ascorbate + dehydroascorbate) increased from 53.8 +/- 9.3 to 59.0 +/- 11.3 microM, and percent reduced ascorbate increased from 77.6 +/- 9.3 to 87.3 +/- 9.7%. During day 3 exercise, plasma ascorbate changes were similar to those on day 1. Plasma vitamin E did not change due to exercise on either day 1 or 3. RNA adducts, urinary 8-hydroxyguanosine, did not change significantly due to exercise. Observed increases in GSH oxidation indicate the presence of oxidant stress during prolonged submaximal exercise. Similar redox changes on consecutive days of exercise, with recovery to preexercise values within 15 min, indicate no evidence of persistent or cumulative exercise effects on blood glutathione redox status.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle mitochondrial ultrastructure in exercise-trained iron-deficient rats.

To investigate effects of endurance training and iron deficiency, as well as the combination of these two conditions, on mitochondrial ultrastructure, weanling rats at 3 wk of age were assigned to iron-deficient (Fe-) and iron-sufficient (Fe+) groups. Subsequently, groups were subdivided into exercise-trained (T) and sedentary (S) groups. Electron microscopy showed subsarcolemmal and intrafibrillar mitochondria in the Fe-T animals to be enlarged with sparse cristae and vacuole-like areas compared with the other groups. An increase in the number of lipid droplets in both Fe- groups was observed. Stereological measurements revealed a 99% increase in the volume occupied by muscle mitochondria in the Fe-T animals (11.9 +/- 0.8%) over the Fe+T (5.9 +/- 0.4%) and Fe+S (6.0 +/- 0.3%) groups and a 55% increase over the Fe-S groups (7.7 +/- 0.3%). The ratio of mitochondrial surface area to tissue volume was significantly decreased only in the Fe-T group. These results indicate that the combined stresses of iron deficiency and training produce mitochondrial ultrastructural changes far greater than those of iron deficiency or training alone. Because this is also the case with the disproportion among mitochondrial enzymes, it is possible that the ultrastructural changes are indicative of morphological responses that maintain ATP turnover during exercise in iron deficiency when oxygen transport and electron transport chain activities are reduced.

Increased dependence on blood glucose in smokers during rest and sustained exercise.

To evaluate the hypothesis that smoking increases the dependence on blood glucose as a fuel, seven male smokers [28.7 +/- 1.7 (SE) yr. 77.7 +/- 4.3 kg] and seven nonsmokers (NS; 29.1 +/- 0.9 yr, 78.7 +/- 5.3 kg) were studied in the postabsorptive condition. NS received a primed continuous infusion of [6,6-2H]glucose and [1-13C]glucose during 90 min of rest and 60 min of exercise at 49.7 +/- 0.8% of peak O2 consumption on one occasion; chronic smokers continued their overnight abstinence from smoking (CS) for one trial but, on another occasion, acutely smoked (AS) two cigarettes immediately before resting measurements and another cigarette before exercise. Plasma glucose levels were similar among all groups at all times during the trials; however, the glucose rates of appearance (Ra) at rest in CS (1.96 +/- 0.14 mg.kg-1 x min-1) and AS (2.02 +/- 0.14) were higher than in NS (1.41 +/- 0.15, P < 0.05). With exercise, the glucose Ra values rose in all groups above resting values but were significantly greater in CS (4.76 +/- 0.50) and AS (4.71 +/- 0.53) than in NS (3.31 +/- 0.16). Glucose oxidation during exercise was elevated in smokers (2.31 +/- 0.37 mg.kg-1 x min-1 in CS and 2.18 +/- 0.34 in AS) compared with NS (1.09 +/- 0.18, P < 0.05). Nicotine levels correlated with the glucose Ra in AS (r = 0.93, P < 0.01). In conclusion, the results indicate that long-term smoking, independent of acute smoking, increases the dependence on blood glucose as a fuel during rest and sustained submaximal exercise.

Effects of iron deficiency and training on mitochondrial enzymes in skeletal muscle.

We measured mitochondrial enzyme activities in skeletal muscle under conditions of iron deficiency and endurance training to assess the effects of these interventions on the contents and proportions of non-iron-containing and iron-dependent enzymes and proteins. Male Sprague-Dawley rats, 21 days of age, received a diet containing either 6 (iron deficient) or 50 mg iron/kg diet (iron sufficient). At 35 days of age animals were subdivided into sedentary and endurance training groups (running at 0.7 mph, 0% grade, 45 min/day, 6 days/wk). By 70 days of age, iron deficiency had decreased gastrocnemius muscle cytochrome c by 62% in sedentary animals. In contrast, the activities of tricarboxylic acid cycle enzymes were increased, remained unchanged or were slightly decreased, indicating that iron deficiency markedly altered mitochondrial composition. Endurance training increased cytochrome c (35%), tricarboxylic acid cycle enzymes (approximately 15%), and manganese superoxide dismutase (33%) in iron-deficient rats, whereas the same exercise regimen had no effect on the skeletal muscle of iron-sufficient animals. The interactive effect of dietary iron deficiency and mild exercise on mitochondrial enzymes suggests that adaptation to a training stimulus is, to some extent, geared to the relationship between the energy demand of exercise and the capacity for O2 transport and utilization.

Vitamin E deficiency and vitamin C supplements: exercise and mitochondrial oxidation.

The effects of dietary antioxidant vitamins E and C on exercise endurance capacity and mitochondrial oxidation were investigated in rats. The endurance capacity of both vitamin E-deficient and vitamin C-supplemented, E-deficient rats was significantly (P less than 0.05) lower (38.1 and 33.6%, respectively) than control animals. Compared with the normal and vitamin E-deficient rats, there was a significant (P less than 0.05) increase in the concentration of vitamin C in blood and liver of the vitamin E-deficient, C-supplemented animals. Hence dietary vitamin C supplementation does not prevent the inhibition of exercise endurance capacity or increased hemolysis seen in vitamin E deficiency. The mitochondrial activities for the oxidation of palmitoyl carnitine and alpha-ketoglutarate were significantly (P less than 0.05) decreased by a single bout of exercise in brown adipose tissue but not in muscle, heart, or liver from vitamin C-supplemented, E-deficient groups of rats when compared with the activities in the tissue from the same group of rats killed at rest. Similar results were also seen in brown adipose tissue from vitamin E-deficient rats. The results suggest a tissue-specific role for vitamins E and C in substrate oxidation and show that the poor endurance capacity of vitamin E-deficient rats cannot be attributed to any changes in the mitochondrial activity in skeletal or cardiac muscles. It is also concluded that vitamin C supplementation, at least at the dose employed in the present study, cannot counteract the detrimental effects associated with vitamin E deficiency.

Increased energy intake minimizes weight loss in men at high altitude.

The hypothesis that high-altitude weight loss can be prevented by increasing energy intake to meet energy requirement was tested in seven men, 23.7 +/- 4.3 (SD) yr, taken to 4,300 m for 21 days. Energy intake required to maintain body weight at sea level was found to be 3,118 +/- 300 kcal/day, as confirmed by nitrogen balance. Basal metabolic rate (BMR), determined by indirect calorimetry, increased 27% on day 2 at altitude and then decreased and reached a plateau at 17% above the sea level BMR by day 10. Energy expended during strenuous activities was 37% lower at altitude than at sea level. Fecal excretion of energy, nitrogen, total fiber, and total volatile fatty acids was not significantly affected by altitude. Energy intake at altitude was adjusted after 1 wk, on the basis of the increased BMR, to 3,452 +/- 452 kcal/day. Mean nitrogen balance at altitude was negative (-0.25 +/- 0.71 g/day) before energy intake was adjusted but rose significantly thereafter (0.20 +/- 0.71 and 0.44 +/- 0.66 g/day during weeks 2 and 3). Mean body weight decreased 2.1 +/- 1.0 kg over the 3 wk of the study, but the rate of weight loss was significantly diminished after the increase in energy intake (201 +/- 75 vs. 72 +/- 48 g/day). Individual regression lines drawn through 7-day segments of body weight showed that in four of seven subjects the slopes of body weight were not significantly different from zero after the 2nd wk. Thus weight loss ceased in four of seven men in whom increased BMR at altitude was compensated with increased energy intake.(ABSTRACT TRUNCATED AT 250 WORDS)