Influence of a high ambient temperature and administration of clenbuterol on body composition in rats.

Katsumata, Masaya; Yano, Hideo; Ishida, Naohiko; Miyazaki, Akira

doi:10.3177/jnsv.36.569

Cited by 30 publications

(21 citation statements)

References 33 publications

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“…Since oxygen consumption in heat-acclimated organisms is lower, metabolic adjustments designed to enhance energy reserves take place in order to guarantee long-term performance to fight the lowered oxygen supply [3]. In this sense, there is an enhancement of the metabolic machinery to elevate the energy potential of heat-acclimated organism which is accompanied by a decrease of the rate of the whole body metabolism [4,5]. Metabolic changes which are most evident during heat acclimation are: energy sparing, which is manifested as a rebound of liver glycogen (Glk) in rats [6][7][8] and hamsters [9] (as a result of increased activity of enzymes involved in a direct Glk synthesis), and decreased glucose (Glu) production [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Heat acclimation-induced changes in heart glycogen/glucose metabolism in rats

et al. 2011

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Based on the observation that heat acclimation is a slowly developing response, evoked by continuous exposure to moderate heat, we investigated the time-dependent acclimatory changes of heart glycogen metabolism. Cardiac levels of key carbohydrate-related enzymes and substrates were studied in the function of the duration of short-term (STHA; 6, 12, 24 and 48 h) and long-term heat acclimation (LTHA; 7, 14, 21 and 30 days) to high environmental temperature (35 ± 1°C). The changes in heart glycogen metabolism during STHA could be separated in two phases: up to 12 h exposure, where significant decrease of the heart glycogen (Glk), glucose-6-phosphate (G6P), hexokinase (HK) activity as well as increase of heart glucose was observed; and from 24 to 48 h exposure, manifested with elevation of Glk, Glu, glycogen phosphorylase a (GPa), phosphofructokinase (PFK) and HK activities. The metabolic changes in the period of LTHA could also be seen as separate phases: in a period of 7-14 days of heat exposure there was an increase of heart Glk, Glu, G6P, HK, as well as a decrease of GPa and PFK, while in the period of 21-28 days there was more intensive rebound of Glk and G6P, increase of GPa activity and non-significant changes of Glu, HK and PFK. The results obtained have showed that acclimation to moderate hyperthermic environment has caused significant changes in examined parameters which differ depending on duration to the exposure: intensive stress-induced glycogenolytic and glycolytic processes in the period of STHA and intensive energy sparing, manifested by Glk deposition in the period of LTHA.

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Section: Introductionmentioning

confidence: 99%

Heat acclimation-induced changes in heart glycogen/glucose metabolism in rats

et al. 2011

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“…It also has potent anabolic properties (2,9,14,35); thus its usage as a drug for doping is banned by many athletic committees (33). However, there are still unclear effects on lipid metabolism, thermogenesis, and hyperglycemia (25,43). The higher distribution of ␤ 2 -receptors in slow-twitch muscle (i.e., the increased intracellular cAMP via the receptor) is one of the plausible explanations of the specific effect of clenbuterol on the slowtype muscles, including the transition of myosin types from slow to fast and the metabolic shift from oxidative to anaerobic glycolysis (22,39).…”

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confidence: 99%

Decreased monocarboxylate transporter 1 in rat soleus and EDL muscles exposed to clenbuterol

Kitaura

Tsunekawa

Hatta

2001

Journal of Applied Physiology

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We hypothesized that a shift in muscle fiber type induced by clenbuterol would change monocarboxylate transporter 1 (MCT1) content and activity of lactate dehydrogenase (LDH) and isoform pattern and shift myosin heavy chain (MHC) pattern in soleus (Sol) and extensor digitorum longus (EDL) of male rats. In the clenbuterol-administered rats (2.0 mg x kg(-1) x day(-1) subcutaneously for 4 wk), the ratio of muscle weight to body weight increased in the Sol (P < 0.05) and the EDL (P < 0.01). Clenbuterol induced the appearance of fast MHC(2D) and decreased slow MHC(1) in Sol (13%) but had no effect on EDL. The MHC pattern of Sol changed from slow to fast type. Clenbuterol increased LDH-specific activity (P < 0.01) and the ratio of the muscle-type isozyme of LDH to the heart type (P < 0.05) in Sol. The LDH total activity of the EDL muscle was also increased (P < 0.05). Furthermore, MCT1 content significantly (P < 0.05) decreased in both Sol and EDL (27 and 52%, respectively). This study suggests that clenbuterol might mediate the shift of MHC from slow to fast type and the changes in the regulation of lactate metabolism. Novel to this study is the observation that clenbuterol decreases MCT1 content in the hindlimb muscles and that the decrease in MCT1 is not muscle-type specific. It may suggest that the genetic expressions of individual factors involving slow-type MHC, heart-type isozyme of LDH, and MCT1 are associated with one another but are regulated independently.

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“…2, C:C 1 ). Namely, our previous results showed that the processes of direct glycogen synthesis, same like the indirect process of glycogenoneogenesis, are favored during long-term acclimation, which finally results in rebound of the hepatic glycogen and causes decrease of the blood glucose level (Katsumata et al, 1990;Zhao et al, 1995;Mitev et al, 2005). On the other side, the decreased blood glucose in heat-acclimated rats could be a result of the increased peripheral glucose needs and disposal according to Torlinska et al (1984).…”

Section: Factorial (Two-way) Anovamentioning

confidence: 92%

“…Exposition to high environmental temperature induces considerable structural and functional changes in different tissues. In this sense, heat-acclimated rats showed enlarging of liver (Sod-Moriah et al, 1983;Katsumata et al, 1990), heart and kidney (Zhao et al, 1995), as well as decrease in glucose level (Mitev et al, 2005;Dinevska-Chovkarovska, 1998;Miova et al, 2008) and increase in insulin concentration (Kuroshima et al, 1982). On the other side, changes in AST and ALT activity was found (Hubbard et al, 1979;Heijnen and van Veen, 2001) as a result of heat-induced disorders in the organism (short term exposure of rats to hyperthermic environment).…”

Section: Introductionmentioning

confidence: 91%