Effects of a beta-adrenergic agonist on protein turnover in muscle cells in culture

McElligott, Mary Ann; Chaung, L Y; Barreto, Albert

doi:10.1016/0006-2952(89)90077-4

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…␤-Adrenergic receptor agonist administration increases the net uptake of amino acids into the hindlimbs of steers and subsequent muscle protein accretion (37), decreases semitendinosus muscle protein degradation, increases muscle protein content and reduces fat and collagen content in lambs (38), increases the accretion of proteins containing 3-methylhistidine (actin and myosin) through a decrease in the fractional breakdown rate and a reciprocal increase in the fractional synthetic rate in rats (39), increases muscle weight in rats (40), and decreases protein degradation in isolated, perfused rat muscle (41). Conversely, ␣-and ␤-adrenergic receptor blockade after injury in dogs inhibited skeletal muscle protein catabolism without affecting whole body nitrogen loss (42).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

Hamadeh

Devries

Tarnopolsky

2005

The Journal of Clinical Endocrinology & Metabolism

117

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Healthy active men exhibit higher rates of carbohydrate (CHO) and leucine oxidation and lower rates of lipid oxidation compared with their female counterparts both at rest and during moderate intensity endurance exercise. We postulated that this reduced dependence on amino acids as a fuel source in women was due to the female sex hormone estrogen. In a randomized, double-blind, placebo-controlled, cross-over design, we investigated the effect of supplementing 12 recreationally active men with estrogen on whole body substrate oxidation and leucine kinetics at rest and during moderate intensity endurance exercise. Subjects cycled for 90 min at an intensity of 65% maximum O(2) consumption after 8 d of either estrogen supplementation (2 mg 17beta-estradiol/d) or placebo (polycose). After a 2-wk washout period, they repeated the test after 8 d of the alternate treatment. On the test day, after a primed continuous infusion of l-[(13)C]leucine, O(2) consumption, CO(2) production, steady-state breath (13)CO(2), and plasma alpha-[(13)C]ketoisocaproate enrichments were measured at rest and at 60, 75, and 90 min during exercise in the postabsorptive state. Exercise increased energy expenditure more than 5-fold, CHO oxidation more than 6-fold, lipid oxidation more than 4-fold, and leucine oxidation 2.2-fold (all P < 0.0001), whereas it decreased the ratio of lipid to CHO oxidation by 50-70% (P = 0.003) compared with values at rest. Estrogen supplementation decreased respiratory exchange ratio during exercise (P = 0.03). Estrogen supplementation significantly decreased CHO oxidation by 5-16% (P = 0.04) and leucine oxidation by 16% (P = 0.01), whereas it significantly increased lipid oxidation by 22-44% (P = 0.024) at rest and during exercise. We conclude that estrogen influences fuel source selection at rest and during endurance exercise in recreationally active men, characterized by a reduced dependence on amino acids and CHO and an increased reliance on lipids as a fuel source.

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Section: Discussionmentioning

confidence: 99%

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

Hamadeh

Devries

Tarnopolsky

2005

The Journal of Clinical Endocrinology & Metabolism

117

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“…Importantly, this study has identified that ␤ 2 -adrenoceptors are actually present on regenerating skeletal muscle fibers. Although evidence for the existence of ␤ 2 -adrenoceptors on myoblasts and myotubes has been conflicting, it has been postulated that adrenergic stimulation plays an important role in muscle development through increases in adenylate cyclase activity (24,30,38,42). The marked increase in ␤ 2 -adrenoceptor concentration observed in injured muscles from both saline-treated and fenoterol-treated rats at 2 days postinjury indicates that ␤ 2 -adrenoceptors may play an important physiological role in the process of skeletal muscle regeneration.…”

Section: Discussionmentioning

confidence: 99%

β₂-Adrenoceptor agonist fenoterol enhances functional repair of regenerating rat skeletal muscle after injury

Beitzel

Gregorevic²,

Ryall³

et al. 2004

Journal of Applied Physiology

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Beta(2)-adrenoceptor agonists such as fenoterol are anabolic in skeletal muscle, and because they promote hypertrophy and improve force-producing capacity, they have potential application for enhancing muscle repair after injury. No previous studies have measured the beta(2)-adrenoceptor population in regenerating skeletal muscle or determined whether fenoterol can improve functional recovery in regenerating muscle after myotoxic injury. In the present study, the extensor digitorum longus (EDL) muscle of the right hindlimb of deeply anesthetized rats was injected with bupivacaine hydrochloride, which caused complete degeneration of all muscle fibers. The EDL muscle of the left hindlimb served as the uninjured control. Rats received either fenoterol (1.4 mg x kg(-1) x day(-1)) or an equal volume of saline for 2, 7, 14, or 21 days. Radioligand binding assays identified a approximately 3.5-fold increase in beta(2)-adrenoceptor density in regenerating muscle at 2 days postinjury. Isometric contractile properties of rat EDL muscles were measured in vitro. At 14 and 21 days postinjury, maximum force production (P(o)) of injured muscles from fenoterol-treated rats was 19 and 18% greater than from saline-treated rats, respectively, indicating more rapid restoration of function after injury. The increase in P(o) in fenoterol-treated rats was due to increases in muscle mass, fiber cross-sectional area, and protein content. These findings suggest a physiological role for beta(2)-adrenoceptor-mediated mechanisms in muscle regeneration and show clearly that fenoterol hastens recovery after injury, indicating its potential therapeutic application.

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“…The &agonist cimaterol may increase protein synthesis and concomitantly retard protein degradation (Young et al, 1990). However, several similar P-adrenergic agonists did not alter protein metabolism directly in rat myotube (Klasing and Jamell, 1985;Roeder et al, 1987) or L-8 myotube cultures (McElligott et al, 1989). The intent of the present study was to define the direct effects of isoproterenol (ISO) on muscle protein metabolism by using primary myotube cultures.…”

Section: Introductionmentioning

confidence: 88%

“…Decreased rate of muscle protein degradation in response to p-agonist treatment has been reported previously in animals (Eadara et al., 1989;Morgan et al, 1989) and in cultured muscle cells (Rogers and Fagan, 1988; Young et aL, 1988). However, other research has demonstrated that p-agonists may not affect protein degradation directly (Forsberg and Merrill, 1986;McElligott et al, 1989) but increase protein synthesis (Emery et al, 1984;Claeys et al, 1989). The &agonist cimaterol may increase protein synthesis and concomitantly retard protein degradation (Young et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Effects of the beta-adrenergic agonist isoproterenol on protein accretion, synthesis, and degradation in primary chicken muscle cell cultures1

Orcutt

1991

Journal of Animal Science

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Seven-day-old primary myotube cultures derived from embryonic chicken limb muscles were used to determine the effects of the beta-adrenergic agonist isoproterenol (ISO) on muscle protein metabolism in vitro. Isoproterenol increased (P less than .05) total protein accumulation after 2 h of acute exposure and after chronic exposure for 24 and 48 h. Isoproterenol did not consistently retard rate of protein degradation of the total protein (TP), myofibrillar protein (MFP) pools, and myosin heavy-chain subunit (MHC); degradation of these protein pools tended to be slowed by inclusion of ISO in the culture medium. After acute treatment of 1 X 10(-4) M ISO for 2 h, TP, but not MFP and MHC, synthesis rate was increased, and after chronic exposure to 1 X 10(-4), 1 X 10(-5), and 1 X 10(-6) M ISO, TP, MFP, and MHC synthesis rates and net accumulation of TP, cytoplasmic protein, and MHC fractions were enhanced (P less than .05). The beta-adrenergic antagonist propranolol (1 X 10(-5) M) blocked chronic stimulatory effects of ISO. Furthermore, after 48 h of exposure to ISO, effects on protein synthesis were less pronounced than those observed after 24 h of exposure. Isoproterenol imparted a more pronounced effect on protein synthesis than on protein degradation, indicating that increased muscle protein accretion observed in animals after ISO treatment is likely a function of enhanced protein synthesis.

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Effects of a beta-adrenergic agonist on protein turnover in muscle cells in culture

Cited by 9 publications

References 18 publications

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

β₂-Adrenoceptor agonist fenoterol enhances functional repair of regenerating rat skeletal muscle after injury

Effects of the beta-adrenergic agonist isoproterenol on protein accretion, synthesis, and degradation in primary chicken muscle cell cultures1

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Effects of a beta-adrenergic agonist on protein turnover in muscle cells in culture

Cited by 9 publications

References 18 publications

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

Estrogen Supplementation Reduces Whole Body Leucine and Carbohydrate Oxidation and Increases Lipid Oxidation in Men during Endurance Exercise

β2-Adrenoceptor agonist fenoterol enhances functional repair of regenerating rat skeletal muscle after injury

Effects of the beta-adrenergic agonist isoproterenol on protein accretion, synthesis, and degradation in primary chicken muscle cell cultures1

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β₂-Adrenoceptor agonist fenoterol enhances functional repair of regenerating rat skeletal muscle after injury