東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Active-muscle and whole-body fat, ca...

Bergman, Bryan Christopher.

FindBook

Google Book

Amazon

博客來

Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men./
作者:	Bergman, Bryan Christopher.
面頁冊數:	207 p.
附註:	Source: Dissertation Abstracts International, Volume: 60-05, Section: B, page: 1939.
Contained By:	Dissertation Abstracts International60-05B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9931185
ISBN:	9780599314023

Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men.
Bergman, Bryan Christopher.

Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men. - 207 p.

Source: Dissertation Abstracts International, Volume: 60-05, Section: B, page: 1939.

Thesis (Ph.D.)--University of California, Berkeley, 1999.

This study was undertaken to evaluate the hypotheses that: (1) endurance training increases intramuscular triglyceride (IMTG) oxidation, (2) alterations in glucose disposal rate (Rd) due to endurance training are the result of changed net glucose uptake in active muscle, (3) blood glucose is shunted to working muscle during exercise requiring high relative power output, (4) active muscle mass is responsible for maintenance of elevated [lactate]a during exercise, and (5) decreased arterial lactate concentration ([lactate] a) after endurance training is due to increased leg and whole body lactate clearance and decreased lactate production. We studied leg net free fatty acid (FFA), glycerol, glucose and lactate exchange, and whole body glucose and lactate turnover during one hour of cycle ergometry at two intensities before (45% and 65% V&dot;O2peak) and after training (65% pre-training V&dot;O 2peak, same absolute workload (ABT), and 65% post-training V&dot;O 2peak, same relative intensity (RLT). Nine male subjects (27.4 +/- 2.0 yr) were tested before and after 9 weeks of cycle ergometer training, 5x/week at 75% V&dot;O2peak. The power output that elicited 66.0 +/- 1.1% of V&dot;O2peak prior to training elicited 54.0 +/- 1.7% after training due to a 14.6 +/- 3.1% increase in V&dot;O 2peak. Training significantly decreased pulmonary RER values at ABT but not RLT. After training leg RQ was not significantly different at either the same absolute or relative workload. Net FFA uptake was increased at RLT but not ABT after training. Net IMTG lipolysis did not change from rest to exercise, or at ABT or RLT compared to 65% pre-training V&dot;O2peak. Muscle biopsies revealed TG storage, not mobilization during exercise. Whole body glucose Rd decreased post-training at ABT, but not RLT. Net glucose uptake was attenuated post-training at ABT, but not RLT. Glycogen degradation also decreased post-training at ABT, but not RLT. Leg net glucose uptake accounted for 61% of blood glucose Rd before training and 81% after training at RLT, and only 38% after ABT. Compared to 65% pre-training V&dot;O2peak [lactate]a concentration decreased at ABT and RLT. Net limb lactate release decreased at ABT, but not RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. Compared to 65% pre-training V&dot;O 2peak, lactate appearance and Rd decreased at ABT but were unchanged at RLT. Lactate clearance was unchanged at ABT, but increased at RLT. Whole body lactate oxidation decreased at ABT and increased at RLT. We conclude: (1) IMTG utilization does not increase after training, (2) muscle glucose uptake decreases for a moderate intensity task after training, (3) hard exercise (65% V&dot;O2peak) promotes a glucose shunt from inactive tissues to active muscle (4) active skeletal muscle is not solely responsible for maintenance of elevated [lactate]a and (5) training increases leg lactate clearance and decreases whole body and leg lactate production at moderate intensity power output, and increases whole body and leg lactate clearance at high relative power outputs. (Abstract shortened by UMI.)

ISBN: 9780599314023Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men.
LDR:04076nmm 2200277 4500 001 1825023
005 20061205094413.5
008 130610s1999 eng d
020 $a 9780599314023
035 $a (UnM)AAI9931185
035 $a AAI9931185
040 $a UnM $c UnM
100 1 $a Bergman, Bryan Christopher. $3 1914048
245 1 0 $a Active-muscle and whole-body fat, carbohydrate, and lactate metabolism after endurance training in men.
300 $a 207 p.
500 $a Source: Dissertation Abstracts International, Volume: 60-05, Section: B, page: 1939.
500 $a Chair: George Austin Brooks.
502 $a Thesis (Ph.D.)--University of California, Berkeley, 1999.
520 $a This study was undertaken to evaluate the hypotheses that: (1) endurance training increases intramuscular triglyceride (IMTG) oxidation, (2) alterations in glucose disposal rate (Rd) due to endurance training are the result of changed net glucose uptake in active muscle, (3) blood glucose is shunted to working muscle during exercise requiring high relative power output, (4) active muscle mass is responsible for maintenance of elevated [lactate]a during exercise, and (5) decreased arterial lactate concentration ([lactate] a) after endurance training is due to increased leg and whole body lactate clearance and decreased lactate production. We studied leg net free fatty acid (FFA), glycerol, glucose and lactate exchange, and whole body glucose and lactate turnover during one hour of cycle ergometry at two intensities before (45% and 65% V&dot;O2peak) and after training (65% pre-training V&dot;O 2peak, same absolute workload (ABT), and 65% post-training V&dot;O 2peak, same relative intensity (RLT). Nine male subjects (27.4 +/- 2.0 yr) were tested before and after 9 weeks of cycle ergometer training, 5x/week at 75% V&dot;O2peak. The power output that elicited 66.0 +/- 1.1% of V&dot;O2peak prior to training elicited 54.0 +/- 1.7% after training due to a 14.6 +/- 3.1% increase in V&dot;O 2peak. Training significantly decreased pulmonary RER values at ABT but not RLT. After training leg RQ was not significantly different at either the same absolute or relative workload. Net FFA uptake was increased at RLT but not ABT after training. Net IMTG lipolysis did not change from rest to exercise, or at ABT or RLT compared to 65% pre-training V&dot;O2peak. Muscle biopsies revealed TG storage, not mobilization during exercise. Whole body glucose Rd decreased post-training at ABT, but not RLT. Net glucose uptake was attenuated post-training at ABT, but not RLT. Glycogen degradation also decreased post-training at ABT, but not RLT. Leg net glucose uptake accounted for 61% of blood glucose Rd before training and 81% after training at RLT, and only 38% after ABT. Compared to 65% pre-training V&dot;O2peak [lactate]a concentration decreased at ABT and RLT. Net limb lactate release decreased at ABT, but not RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. Compared to 65% pre-training V&dot;O 2peak, lactate appearance and Rd decreased at ABT but were unchanged at RLT. Lactate clearance was unchanged at ABT, but increased at RLT. Whole body lactate oxidation decreased at ABT and increased at RLT. We conclude: (1) IMTG utilization does not increase after training, (2) muscle glucose uptake decreases for a moderate intensity task after training, (3) hard exercise (65% V&dot;O2peak) promotes a glucose shunt from inactive tissues to active muscle (4) active skeletal muscle is not solely responsible for maintenance of elevated [lactate]a and (5) training increases leg lactate clearance and decreases whole body and leg lactate production at moderate intensity power output, and increases whole body and leg lactate clearance at high relative power outputs. (Abstract shortened by UMI.)
590 $a School code: 0028.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Health Sciences, Recreation. $3 1018003
690 $a 0433
690 $a 0575
710 2 0 $a University of California, Berkeley. $3 687832
773 0 $t Dissertation Abstracts International $g 60-05B.
790 1 0 $a Brooks, George Austin, $e advisor
790 $a 0028
791 $a Ph.D.
792 $a 1999
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9931185