Enzymatic adaptation to physical training under beta-blockade in the rat. Evidence of a beta 2-adrenergic mechanism in skeletal muscle.

Ji, Li Li; Lennon, Doris L.F.; Kochan, R. G.; Nagle, F. J.; Lardy, Henry A.

doi:10.1172/jci112639

Cited by 56 publications

(28 citation statements)

References 38 publications

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“…The data are in agreement with reports that ß-blocking drugs did not change the bw either in rats or human cardiac patients [3]. However, the results were in contrast to that observed in a previ ous experiment [4], where we found that the bw gain of growing male rats chronically injected with propranolol (30 mg/kg bw, 5 days/wk, i.p.) and subjected to an exer cise training program was significantly lower as com pared to the trained rats not receiving the drug.…”

Section: Results Discussionsupporting

confidence: 92%

See 1 more Smart Citation

The effects of beta-adrenergic blockade on body composition in free-fed and diet-restricted rats.

Ji¹,

Doan²,

Lennon³

et al. 1987

Journal of the American College of Nutrition

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The effects of the non-selective beta-adrenergic blocking agent propranolol (known for its anti-lipolytic activity) on body composition were investigated in growing male rats on normal unrestricted diet (N = 7) and on diet restriction (N = 7, 95% of controls). Three animals in each group were injected i.p. with 30 mg propranolol per kg body weight (bw) dissolved in saline, 5 days/week. This dose attenuates exercising heart rate by 25% and exercise training-induced enzyme activity. The remaining animals received saline. Fat, glycogen, moisture and non-ether extractable residue were determined in the homogenized residue of the whole animal. After 9 weeks on the experimental regimen, bw gain was significantly lower in the diet restricted rats, whereas propranolol had no effect on the bw gain. The percentage of fat, moisture and non-ether extractable residue were unchanged by either propranolol or diet restriction. However, glycogen content was significantly lower in the beta-blocked rats either with or without diet restriction. These data indicated that neither beta-adrenergic blockade nor minimal diet restriction influences the percentage body fat, whereas body glycogen content is decreased under both conditions.

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Section: Results Discussionsupporting

confidence: 92%

“…The drug was dissolved in 1 ml saline. This dose has been shown previously to decrease the exercise heart rate by 25% as compared to non-drug controls and to attenuate exercise traininginduced enzymic activity [4]. Overall physical activity did not appear to be reduced by ß-blockade.…”

Section: A T E R I a L A N D M E T H O D Smentioning

confidence: 67%

The effects of beta-adrenergic blockade on body composition in free-fed and diet-restricted rats.

Ji¹,

Doan²,

Lennon³

et al. 1987

Journal of the American College of Nutrition

Self Cite

View full text Add to dashboard Cite

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“…At rest, treatments with selective β-adrenergic agonist/antagonist have shown to induce or inhibit PGC-1α expression in rodents, respectively (Miura et al, 2007). Moreover in rodents, treatment with β-adrenergic antagonists have shown to attenuate the increase in PGC-1α mRNA following acute exercise (Miura et al, 2007) and mitochondrial biogenesis following endurance training (Ji et al, 1986). These studies support the findings by Puigserver et al (1998) and implicate adrenergic mechanisms in the regulation of PGC-1α and mitochondrial biogenesis.…”

Section: β-Adrenergic Stimulationsupporting

confidence: 67%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

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PGC-1α is regarded as a key regulator of mitochondrial biogenesis due to its central role in regulating the activity of key transcription factors associated with encoding mitochondrial components. Additionally, PGC-1α has shown to mediate adaptations that increase fat metabolism and angiogenesis, contributing to the overall oxidative phenotype of the muscle. While it is well established that exercise is a potent stimulator of PGC-1α, recent evidence indicates that heat and cold exposures may also influence mitochondrial biogenesis through the up-regulation of PGC-1α. This highlights the potential use of these modalities in conjunction with exercise to enhance training adaptations. As such, the purpose of this review is to describe the possible mechanisms and pathways by which exercise, as well as hot and cold exposures may influence mitochondrial biogenesis. It is clear that changes in intracellular calcium, oxidative stress and phosphorylation potential are major up-regulators of PGC-1α during exercise. Moreover, there is evidence implicating calcium signalling, in addition to β-adrenergic activation in cold-induced mitochondrial biogenesis, while PGC-1α during heat exposure is likely triggered by changes in phosphorylation potential and nitric oxide signalling. However, these mechanisms appear to change considerably when cold/heat is administered following exercise, and seem to be dependent on the experimental models used (i.e. in vitro vs. in vivo, rodent vs. human). Understanding the effects heat/cold exposure and its interaction with exercise may lead to the optimisation and development of temperature-related interventions to enhance training adaptations, or aid in the treatment of mitochondrial related diseases.

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“…Overexpression of cAMP-activated CREB coactivators is also sufficient to induce mitochondrial proliferation in cultured myotubes (242). In rats, the ␤-adrenergic antagonist propranolol blunted activation of mitochondrial enzyme activity after endurance treadmill training (115), but a histological examination of fiber types was not shown in that study. In additional studies, propranolol substantially reduced normal increases in mitochondrial enzyme activity of rat muscles (91), although the effects varied among fiber types (227).…”

Section: Camp In Functional Adaptation Of Skeletal Musclementioning

confidence: 70%

“…Adaptive functions of sustained GPCR signaling have been identified using chronic treatment with agonists and antagonists in humans and model organisms (9,18,43,57,63,86,91,101,115,121,154,155,197) as well as by targeted genetic approaches in mice (42,163,164). These and other studies have revealed striking myofiber hypertrophy and fiber-type transitions to faster fiber types with prolonged activation of ␤-AR signaling in particular.…”

Section: Camp In Functional Adaptation Of Skeletal Musclementioning

confidence: 99%

cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

Berdeaux

Stewart

2012

American Journal of Physiology-Endocrinology and Metabolism

154

115

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Berdeaux R, Stewart R. cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration. Am J Physiol Endocrinol Metab 303: E1-E17, 2012. First published February 21, 2012 doi:10.1152/ajpendo.00555.2011.-Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instructions from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger adenosine 3=,5=-monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. Strikingly, sustained activation of cAMP signaling leads to pronounced hypertrophic responses in skeletal myofibers through largely elusive molecular mechanisms. These pathways can promote hypertrophy and combat atrophy in animal models of disorders including muscular dystrophy, agerelated atrophy, denervation injury, disuse atrophy, cancer cachexia, and sepsis. cAMP also participates in muscle development and regeneration mediated by muscle precursor cells; thus, downstream signaling pathways may potentially be harnessed to promote muscle regeneration in patients with acute damage or muscular dystrophy. In this review, we summarize studies implicating cAMP signaling in skeletal muscle adaptation. We also highlight ligands that induce cAMP signaling and downstream effectors that are promising pharmacological targets. cyclic AMP; skeletal muscle; cell signaling; muscle regeneration; atrophy; protein kinase A ORIGINALLY DISCOVERED by Sutherland and Rall in liver homogenates in 1958 (218), adenosine 3=,5=-monophosphate (cyclic AMP, or cAMP) has since been intensively studied and is one of the best-characterized signaling molecules. In skeletal muscle, acute cAMP signaling has been implicated in regulation of glycogenolysis (213), contractility (32,83,84,88,138,234), sarcoplasmic calcium dynamics (58,147,184,204), and recovery from sustained contractile activity (44, 162). The net result of acute cAMP action on the order of minutes in skeletal muscle can generally be described as increased contractile force and rapid recovery of ion balance, especially during prolonged contractions. These acute changes are most pertinent to muscle contraction and energy utilization during exercise, when epinephrine is rapidly released into the circulation (92) and cAMP accumulates in muscle (72).Many studies have shown, however, that cAMP-inducing agents or genetic modification of proteins involved in cAMP signaling can also have adaptive effects on skeletal muscle by increasing myofiber size and promoting fiber-type transitions to glycolytic fibers (9,18,42,43,57,63,86,91,101,121,128,154,155,163,190,193,194,215). The prohypertrophic actions of ␤-adrenergic receptor (␤-AR) agonists and corticotropin-releasing factor recept...

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Enzymatic adaptation to physical training under beta-blockade in the rat. Evidence of a beta 2-adrenergic mechanism in skeletal muscle.

Cited by 56 publications

References 38 publications

The effects of beta-adrenergic blockade on body composition in free-fed and diet-restricted rats.

The effects of beta-adrenergic blockade on body composition in free-fed and diet-restricted rats.

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

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