scholarly journals Training improves the response in glucose flux to exercise in postmenopausal women

2009 ◽  
Vol 107 (1) ◽  
pp. 90-97 ◽  
Author(s):  
Zinta A. Zarins ◽  
Matthew L. Johnson ◽  
Nastaran Faghihnia ◽  
Michael A. Horning ◽  
Gareth A. Wallis ◽  
...  
Keyword(s):  
Endurance Training ◽  
Postmenopausal Women ◽  
Power Output ◽  
Insulin Response ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Younger Women ◽  
Glucose Flux ◽  
Ergometer Exercise

We examined the effects of endurance training on parameters of glucose flux during rest and exercise in postmenopausal women. Ten sedentary, but healthy women (55 ± 1 yr) completed 12 wk of endurance exercise training on a cycle ergometer [5 days/wk, 1 h/day, 65% peak oxygen consumption (V̇o2peak)]. Flux rates were determined by primed continuous infusion of [6,6-2H]glucose (D2-glucose) during 90 min of rest and 60 min of cycle ergometer exercise during one pretraining exercise trial [65% V̇o2peak (PRE)] and two posttraining exercise trials [the power output that elicited 65% pretraining V̇o2peak (ABT) and 65% posttraining V̇o2peak (RLT)]. Training increased V̇o2peak by 16.3 ± 3.9% ( P < 0.05). Epinephrine and glucagon were lower during ABT and lactate was lower during ABT and RLT ( P < 0.05), but the apparent insulin response was unchanged. Whole body glucose rate of appearance decreased posttraining during exercise at a given power output (4.58 ± 0.39 mg·kg−1·min−1 during ABT compared with 5.21 ± 0.48 mg·kg−1·min−1 PRE, P < 0.05), but not at the same relative workload (5.85 ± 0.36 mg·kg−1·min−1). Training resulted in a 35% increase in glucose MCR during exercise at the same relative intensity (7.16 ± 0.42 ml·kg−1·min−1 during RLT compared with 5.28 ± 0.42 ml·kg−1·min−1 PRE, P < 0.05). Changes in parameters of glucose kinetics during exercise were accomplished without changes in dietary composition, body weight, or body composition. We conclude that despite changes in the hormonal milieu that occur at menopause, endurance training results in a similar magnitude in training-induced alterations of glucose flux as seen previously in younger women.

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

1999 ◽  
Vol 277 (1) ◽  
pp. E81-E92 ◽  
Author(s):  
B. C. Bergman ◽  
G. E. Butterfield ◽  
E. E. Wolfel ◽  
G. D. Lopaschuk ◽  
G. A. Casazza ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Endurance Training ◽  
Power Output ◽  
Whole Body ◽  
Glucose Disposal ◽  
Moderate Intensity ◽  
Active Muscle ◽  
Glucose Kinetics ◽  
Glucose Flux

We evaluated the hypotheses that alterations in glucose disposal rate (Rd) 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 (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 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%V˙o 2 peak. The power output that elicited 66.0 ± 1.1% ofV˙o 2 peak before training elicited 54.0 ± 1.7% after training. Whole body glucose Rd decreased posttraining at ABT (5.45 ± 0.31 mg ⋅ kg−1 ⋅ min−1at 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 Rd 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%V˙o 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%V˙o 2 peak) promotes a glucose shunt from inactive tissues to active muscle.

Isotopic estimation of CO2 production during exercise before and after endurance training

1993 ◽  
Vol 75 (1) ◽  
pp. 70-75 ◽  
Author(s):  
A. R. Coggan ◽  
D. L. Habash ◽  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
C. L. Kien
Keyword(s):  
Endurance Training ◽  
Tricarboxylic Acid Cycle ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Carbohydrate Oxidation ◽  
Whole Body ◽  
Co2 Production ◽  
Acid Oxidation ◽  
Ergometer Exercise ◽  
Before And After

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75–100% VO2peak for 45–90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Twelve weeks of endurance training increases FFA mobilization and reesterification in postmenopausal women

2010 ◽  
Vol 109 (6) ◽  
pp. 1573-1581 ◽  
Author(s):  
M. L. Johnson ◽  
Z. Zarins ◽  
J. A. Fattor ◽  
M. A. Horning ◽  
L. Messonnier ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Training ◽  
Plasma Free Fatty Acid ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Age Related ◽  
Ergometer Exercise ◽  
Body Weights ◽  
Plasma Ffa ◽  
Power Outputs

We examined the effects of exercise intensity and training on rates of lipolysis, plasma free fatty acid (FFA) appearance (Ra), disappearance (Rd), reesterification (Rs), and oxidation (RoxP) in postmenopausal (PM) women. Ten sedentary but healthy women (55 ± 0.6 yr) completed 12 wk of supervised endurance exercise training on a cycle ergometer [5 days/wk, 1 h/day, 65% peak oxygen consumption (V̇o2peak)]. Flux rates were determined by continuous infusion of [1-13C]palmitate and [1,1,2,3,3-2H5]glycerol during 90 min of rest and 60 min of cycle ergometer exercise during one pretraining exercise trial [65% V̇o2peak (PRE)] and two posttraining exercise trials [at power outputs that elicited 65% pretraining V̇o2peak (absolute training; ABT) and 65% posttraining V̇o2peak (relative training; RLT)]. Initial body weights (68.2 ± 4.5 kg) were maintained over the course of study. Training increased V̇o2peak by 16.3 ± 3.9% ( P < 0.05) (Zarins ZA, Wallis GA, Faghihnia N, Johnson ML, Fattor JA, Horning MA and Brooks GA. Metabolism 58: 9: 1338–1346, 2009). Glycerol Ra and Rd were elevated in the RLT trial ( P < 0.05), but not the ABT trial after training. Rates of plasma FFA Ra, Rd, and RoxP were elevated during the ABT compared with PRE trial ( P < 0.05). FFA Rs accounted for most (50–70%) of Rd during exercise; training reduced FFA Rs during ABT, but not RLT compared with PRE. We conclude that, despite the large age-related decrease in metabolic scope in PM women, endurance training increases the capacities for FFA mobilization and oxidation during exercises of a given power output. However, after menopause, total lipid oxidation capacity remains low, with reesterification accounting for most of FFA Rd.

Substrate utilization during endurance exercise in men and women after endurance training

2001 ◽  
Vol 280 (6) ◽  
pp. E898-E907 ◽  
Author(s):  
S. L. Carter ◽  
C. Rennie ◽  
M. A. Tarnopolsky
Keyword(s):  
Endurance Training ◽  
Endurance Exercise ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Glucose Flux ◽  
Before And After ◽  
Glycerol Utilization ◽  
Males And Females

We investigated the effect of endurance training on whole body substrate, glucose, and glycerol utilization during 90 min of exercise at 60% peak O2 consumption (V˙o 2 peak) in males and females. Substrate oxidation was determined before and after 7 wk of endurance training on a cycle ergometer, with posttesting performed at the same absolute (ABS, W) and relative (REL, %V˙o 2 peak) intensities. [6,6-2H]glucose and [1,1,2,3,3-2H]glycerol tracers were used to calculate the respective substrate tracee flux. Endurance training resulted in an increase inV˙o 2 peak for both males and females of 17 and 22%, respectively ( P < 0.001). Females demonstrated a lower respiratory exchange ratio (RER) both pretraining and posttraining compared with males during exercise ( P< 0.001). Glucose rate of appearance (Ra) and rate of disappearance (Rd) were not different between males and females. Glucose metabolic clearance rate (MCR) was lower at 75 and 90 min of exercise for females compared with males ( P < 0.05). Glucose Ra and Rd were lower during exercise at both ABS and REL posttraining exercise intensities compared with pretraining ( P < 0.001). Females had a higher exercise glycerol Ra and Rd compared with males both pre- and posttraining ( P < 0.001). Glycerol Ra was not different at either the ABS or REL posttraining exercise intensities compared with pretraining. We concluded that females oxidize proportionately more lipid and less carbohydrate during exercise compared with males both pre- and posttraining, which was cotemporal with a higher glycerol Ra in females. Furthermore, endurance training resulted in a decrease in glucose flux at both ABS and REL exercise intensities after endurance exercise training.

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

1999 ◽  
Vol 87 (5) ◽  
pp. 1684-1696 ◽  
Author(s):  
Bryan C. Bergman ◽  
Eugene E. Wolfel ◽  
Gail E. Butterfield ◽  
Gary D. Lopaschuk ◽  
Gretchen A. Casazza ◽  
...  
Keyword(s):  
Endurance Training ◽  
Power Output ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Lactate Clearance ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Moderate Intensity ◽  
Metabolic Clearance ◽  
Lactate Uptake

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate]a) during continuous exercise by decreasing net lactate release (L˙) and appearance rates (Ra) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O2consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 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%V˙o 2 peak. Compared with the 65%V˙o 2 peakpretraining condition (4.75 ± 0.4 mM), [lactate]a decreased at ABT (41%) and RLT (21%) ( P < 0.05). L˙ 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.

Central and peripheral adaptations of the gas transport system to one-leg training

1981 ◽  
Vol 59 (11) ◽  
pp. 1146-1154 ◽  
Author(s):  
S. G. Thomas ◽  
D. A. Cunningham ◽  
M. J. Plyley ◽  
D. R. Boughner ◽  
R. A. Cook
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Maximal Oxygen Uptake ◽  
Enzyme Activities ◽  
Cardiovascular Responses ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Enzyme Analysis ◽  
Ergometer Exercise

The role of central and peripheral adaptations in the response to endurance training was examined. Changes in cardiac structure and function, oxygen extraction, and muscle enzyme activities following one-leg training were studied.Eleven subjects (eight females, three males) trained on a cycle ergometer 4 weeks with one leg (leg 1), then 4 weeks with the second leg (leg 2). Cardiovascular responses to exercise with both legs and each leg separately were evaluated at entry (T1), after 4 weeks of training (T2), and after a second 4 weeks of training (T3). Peak oxygen uptake ([Formula: see text] peak) during exercise with leg 1 (T1 to T2 increased 19.8% (P < 0.05) and during exercise with leg 2 (T2 to T3 increased 16.9% (P < 0.05). Maximal oxygen uptake with both legs increased 7.9% from T1 to T2 and 9.4% from T2 to T3 (P < 0.05). During exercise at 60% of [Formula: see text] peak, cardiac output [Formula: see text] was increased significantly only when the trained leg was exercised. [Formula: see text] increased 12.2% for leg 1 between T1 and T2 and 13.0% for leg 2 between T2 and T3 (P < 0.05). M-mode echocardiographic assessment of left ventricular internal diameter at diastole and peak velocity of circumferential fibre shortening at rest or during supine cycle ergometer exercise at T1 and T3 revealed no training induced changes in cardiac dimensions or function. Enzyme analysis of muscle biopsy samples from the vastus lateralis (At T1, T2, T3) revealed no consistent pattern of change in aerobic (malate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase) or anaerobic (phosphofructokinase, lactate dehydroginase, and creatine kinase) enzyme activities. Increases in cardiac output and maximal oxygen uptake which result from short duration endurance training can be achieved, therefore, without measurable central cardiac adaptation. The absence of echocardio-graphically determined changes in cardiac dimensions and contractility and the absence of an increase in cardiac output during exercise with the nontrained leg following training of the contralateral limb support this conclusion.

Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating

2005 ◽  
Vol 99 (1) ◽  
pp. 237-243 ◽  
Author(s):  
Takashi Ichinose ◽  
Kazunobu Okazaki ◽  
Shizue Masuki ◽  
Hiroyuki Mitono ◽  
Mian Chen ◽  
...  
Keyword(s):  
Endurance Training ◽  
Exercise Intensity ◽  
Plasma Osmolality ◽  
Young Male ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Cutaneous Vasodilation ◽  
Thermoregulatory Responses ◽  
Before And After ◽  
The Individual

It is well known that hyperosmolality suppresses thermoregulatory responses and that plasma osmolality (Posmol) increases with exercise intensity. We examined whether the decreased esophageal temperature thresholds for cutaneous vasodilation (THFVC) and sweating (THSR) after 10-day endurance training (ET) are caused by either attenuated increase in Posmol at a given exercise intensity or blunted sensitivity of hyperosmotic suppression. Nine young male volunteers exercised on a cycle ergometer at 60% peak oxygen consumption rate (V̇o2 peak) for 1 h/day for 10 days at 30°C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% V̇o2 peak in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by ∼10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, V̇o2 peak and blood volume (BV) both increased by ∼4% ( P < 0.05), followed by a decrease in THFVC ( P < 0.05) but not by that in THSR. Although there was no significant decrease in Posmol at the thresholds after ET, the sensitivity of increase in THFVC at a given increase in Posmol [ΔTHFVC/ΔPosmol,°C·(mosmol/kgH2O)−1], determined by hypertonic infusion, was reduced to 0.021 ± 0.005 from 0.039 ± 0.004 before ET ( P < 0.05). The individual reductions in ΔTHFVC/ΔPosmol after ET were highly correlated with their increases in BV around THFVC ( r = −0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of THFVC after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV.

Effect of hydration state of circulatory and thermal regulations

1980 ◽  
Vol 49 (4) ◽  
pp. 715-721 ◽  
Author(s):  
E. R. Nadel ◽  
S. M. Fortney ◽  
C. B. Wenger
Keyword(s):  
Blood Flow ◽  
Body Weight Loss ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Ergometer Exercise ◽  
Hydration State ◽  
A Minor ◽  
Cutaneous Blood ◽  
Influence Of Hydration ◽  
Volume Decrease

To determine the influence of hydration state upon circulatory controls, we studied four relatively fit subjects during duplicate 30-min cycle ergometer exercise bouts (55% VO2max) in euhydrated, hypohydrated, and hyperhydrated conditions. Ambient temperature was 35 degrees C. Hypohydration was achieved by 4 days of diuretic administration and resulted in a whole-body weight loss of 2.2 kg and a plasma volume decrease of approximately 700 ml. Hyperhydration was achieved by ADH administration plus ingestion of 2 liters water but caused only a minor increase volume. Hypohydration resulted in a significantly reduced cardiac output during exercise; this the result of a reduction in stroke volume of 17 ml.beat-1 without adequate elevation in heart rate. the internal temperature (Tes) threshold for cutaneous vasodilation was elevated by 0.42 degree C in hypohydrated conditions; but once vasodilation occurred, the slope of the arm blood flow:Tes relation was unchanged from control. Maximal arm blood flow was reduced by nearly 50% in hypohydration. These restrictions in cutaneous blood flow served to maintain an already compromised venous return, but due to the limitation of core-to-skin heat transfer, forced Tes to nearly 39 degrees C, significantly higher than in euhydrated conditions.

Endurance training increases fatty acid turnover, but not fat oxidation, in young men

1999 ◽  
Vol 86 (6) ◽  
pp. 2097-2105 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Anton Usaj ◽  
George A. Brooks
Keyword(s):  
Fatty Acid ◽  
Endurance Training ◽  
Exercise Intensity ◽  
Young Men ◽  
Plasma Free Fatty Acid ◽  
Fat Oxidation ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Plasma Ffa ◽  
Total Fat

We examined the effects of exercise intensity and a 10-wk cycle ergometer training program [5 days/wk, 1 h, 75% peak oxygen consumption (V˙o 2 peak)] on plasma free fatty acid (FFA) flux, total fat oxidation, and whole body lipolysis in healthy male subjects ( n= 10; age = 25.6 ± 1.0 yr). Two pretraining trials (45 and 65% ofV˙o 2 peak) and two posttraining trials (same absolute workload, 65% of oldV˙o 2 peak; and same relative workload, 65% of newV˙o 2 peak) were performed by using an infusion of [1-13C]palmitate and [1,1,2,3,3-2H]glycerol. An additional nine subjects (age 25.4 ± 0.8 yr) were treated similarly but were infused with [1,1,2,3,3-2H]glycerol and not [1-13C]palmitate. Subjects were studied postabsorptive for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, plasma FFA kinetics were inversely related to exercise intensity with rates of appearance (Ra) and disappearance (Rd) being significantly higher at 45 than at 65%V˙o 2 peak(Ra: 8.14 ± 1.28 vs. 6.64 ± 0.46, Rd: 8.03 ± 1.28 vs. 6.42 ± 0.41 mol ⋅ kg−1 ⋅ min−1) ( P ≤ 0.05). After training, when measured at the same absolute and relative intensities, FFA Ra increased to 8.84 ± 1.1, 8.44 ± 1.1 and Rd to 8.82 ± 1.1, 8.35 ± 1.1 mol ⋅ kg−1 ⋅ min−1, respectively ( P ≤ 0.05). Total fat oxidation determined from respiratory exchange ratio was elevated during exercise compared with rest, but did not differ among the four conditions. Glycerol Ra was elevated during exercise compared with rest but did not demonstrate significant intensity or training effects during exercise. Thus, in young men, plasma FFA flux is increased during exercise after endurance training, but total fat oxidation and whole-body lipolysis are unaffected when measured at the same absolute or relative exercise intensities.

O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate

1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Blood Lactate ◽  
Time Constant ◽  
Exercise Intensity ◽  
Power Output ◽  
Cycle Ergometer ◽  
O2 Uptake ◽  
Ergometer Exercise ◽  
Lactate Levels ◽  
Power Outputs ◽  
O2 Deficit

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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