Cardiac growth and respiratory enzyme levels in male rats subjected to a running program

Lb, Oscai; Mole, P. A.; Brei, B; Holloszy, J. O.

doi:10.1152/ajplegacy.1971.220.5.1238

Cited by 73 publications

(15 citation statements)

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“…We were not able to measure myocardial glycogen content in the present study. In experimental animals physical training does not alter heart glycogen (50) or water content ( 18). If the same is true in man, changes in myocardial glycogen content in the athlete's heart were not 2270 Nuutila et al responsible for the decreased glucose uptake.…”

Section: Discussionmentioning

confidence: 97%

“…Thus, the observed increase in insulin sensitivity was due to chronic aerobic training rather than a consequence of acute exercise. Regarding the qualitative changes in muscle tissue leading to enhanced insulin sensitivity, factors such as enhanced capillary density (46), increased glycogen synthase activity (47,48), increased mitochondrial volume and activity of oxidative enzymes ( 18) have been suggested to be involved. In the current study, we did not take muscle biopsies to examine possible differences in the muscle fiber composition or capillary density.…”

Section: Discussionmentioning

confidence: 99%

“…In skeletal muscle, physical training increases the total activity of mitochondrial enzymes involved in betaoxidation and respiratory chain. This is accounted for by the increase in the mitochondrial size and number ( 18). However, no changes occur in the heart mitochondrial size or enzyme activity ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

“…This is accounted for by the increase in the mitochondrial size and number ( 18). However, no changes occur in the heart mitochondrial size or enzyme activity ( 18 ). Since the enzymatic responses to physical training are different in the skeletal muscle and the heart, one would anticipate differences also in the metabolic adjustment of the skeletal muscle and myocardium.…”

Section: Introductionmentioning

confidence: 99%

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Different alterations in the insulin-stimulated glucose uptake in the athlete's heart and skeletal muscle.

Nuutila¹,

Knuuti²,

Heinonen³

et al. 1994

J. Clin. Invest.

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Physical training increases skeletal muscle insulin sensitivity. Since training also causes functional and structural changes in the myocardium, we compared glucose uptake rates in the heart and skeletal muscles of trained and untrained individuals. Seven male endurance athletes (VO2max 72±2 ml/kg/min) and seven sedentary subjects matched for characteristics other than VO2max (43±2 ml/kg/min) were studied. Whole body glucose uptake was determined with a 2-h euglycemic hyperinsulinemic clamp, and regional glucose uptake in femoral and arm muscles, and myocardium using "F-fluoro-2-deoxy-D-glucose and positron emission tomography. Glucose uptake in the athletes was increased by 68% in whole body (P < 0.0001), by 99% in the femoral muscles (P < 0.01), and by 62% in arm muscles (P = 0.06), but it was decreased by 33% in the heart muscle (P < 0.05) as compared with the sedentary subjects. The total glucose uptake rate in the heart was similar in the athletes and control subjects. Left ventricular mass in the athletes was 79% greater (P < 0.001) and the meridional wall stress smaller (P < 0.001 ) as estimated by echocardiography. VO2max correlated directly with left ventricular mass (r = 0.87, P < 0.001) and inversely with left ventricular wall stress (r = -0.86, P < 0.001). Myocardial glucose uptake correlated directly with the rate-pressure product (r = 0.75, P < 0.02) and inversely with left ventricular mass (r = -0.60, P < 0.05) or with the whole body glucose disposal (r = -0.68, P < 0.01). Thus, in athletes, (a) insulin-stimulated glucose uptake is enhanced in the whole body and skeletal muscles, (b) whereas myocardial glucose uptake per muscle mass is reduced possibly due to decreased wall stress and energy requirements or the use of alternative fuels, or both. (J. Clin. Invest. 1994Invest. . 2267Invest. -2274

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Different alterations in the insulin-stimulated glucose uptake in the athlete's heart and skeletal muscle.

Nuutila¹,

Knuuti²,

Heinonen³

et al. 1994

J. Clin. Invest.

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show abstract

“…The adaptation to exercise training is dependent on factors such as training load, duration and frequency. Swimming is recognized for its efficiency in inducing myocardial hypertrophy and a significant increase in left ventricular end-diastolic volume in rats (10,11). In the present study, we developed a robust and reproducible exercise training protocol for the development of cardiac hypertrophy in mice.…”

Section: Introductionmentioning

confidence: 97%

Duration-controlled swimming exercise training induces cardiac hypertrophy in mice

Evangelista

Brum

Krieger

2003

Braz J Med Biol Res

123

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Exercise training associated with robust conditioning can be useful for the study of molecular mechanisms underlying exercise-induced cardiac hypertrophy. A swimming apparatus is described to control training regimens in terms of duration, load, and frequency of exercise. Mice were submitted to 60-vs 90-min session/day, once vs twice a day, with 2 or 4% of the weight of the mouse or no workload attached to the tail, for 4 vs 6 weeks of exercise training. Blood pressure was unchanged in all groups while resting heart rate decreased in the trained groups (8-18%). Skeletal muscle citrate synthase activity, measured spectrophotometrically, increased (45-58%) only as a result of duration and frequency-controlled exercise training, indicating that endurance conditioning was obtained. In groups which received duration and endurance conditioning, cardiac weight (14-25%) and myocyte dimension (13-20%) increased. The best conditioning protocol to promote physiological hypertrophy, our primary goal in the present study, was 90 min, twice a day, 5 days a week for 4 weeks with no overload attached to the body. Thus, duration-and frequency-controlled exercise training in mice induces a significant conditioning response qualitatively similar to that observed in humans. Correspondence

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Regulation of Mitochondrial Biogenesis and GLUT4 Expression by Exercise

Holloszy

2011

Comprehensive Physiology

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Endurance exercise training can induce large increases mitochondria and the GLUT4 isoform of the glucose transporter in skeletal muscle. For a long time after the discovery in the 1960s that exercise results in an increase in muscle mitochondria, there was no progress in elucidation of the mechanisms involved. The reason for this lack of progress was that nothing was known regarding how expression of the genes-encoding mitochondrial proteins is coordinately regulated. This situation changed rapidly after discovery of transcription factors that control transcription of genes-encoding mitochondrial proteins and, most importantly, the discovery of peroxisome proliferator-gamma coactivator-1α (PGC-1α). This transcription coactivator binds to and activates transcription factors that regulate transcription of genes-encoding mitochondrial proteins. Thus, PGC-1α activates and coordinates mitochondrial biogenesis. It is now known that exercise rapidly activates and induces increased expression of PGC-1α. The exercise-generated signals that lead to PGC-1α activation and increased expression are the increases in cytosolic Ca(2+) and decreases in ATP and creatine phosphate (∼P). Ca(2+) mediates its effect by activating CAMKII, while the decrease in ∼P mediates its effect via activation of AMPK. Expression of the GLUT4 isoform of the glucose transporter is regulated in parallel with mitochondrial biogenesis via the same signaling pathways. This review describes what is known regarding the regulation of mitochondrial biogenesis and GLUT4 expression by exercise. A major component of this review deals with the physiological and metabolic consequences of the exercise-induced increase in mitochondria and GLUT4.

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Cardiac growth and respiratory enzyme levels in male rats subjected to a running program

Cited by 73 publications

References 0 publications

Different alterations in the insulin-stimulated glucose uptake in the athlete's heart and skeletal muscle.

Different alterations in the insulin-stimulated glucose uptake in the athlete's heart and skeletal muscle.

Duration-controlled swimming exercise training induces cardiac hypertrophy in mice

Regulation of Mitochondrial Biogenesis and GLUT4 Expression by Exercise

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