‘Compensatory’ muscle hypertrophy in the rat induced by tenotomy of synergistic muscles

Macková, Eva; Hník, P

doi:10.1007/bf02138867

Cited by 21 publications

(9 citation statements)

References 5 publications

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“…With increasing fibre hypertrophy, the acute influence of stretch may be gradually lifted, such that the extra sarcomeres now present in series are lost (Williams & Goldspink, 1973). This subsequent decrease in longitudinal growth may possibly explain the smaller chronicphase enlargement of the overloaded muscle, relative to its larger acute response (Mackova & Hnik, 1973).…”

Section: Discussionmentioning

confidence: 98%

Protein turnover measured in vivo and in vitro in muscles undergoing compensatory growth and subsequent denervation atrophy

Goldspink¹,

Garlick²,

McNurlan³

1983

Biochemical Journal

133

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The rapid growth (1-6 days) of the functionally overloaded soleus muscle, in response to tenotomy of the synergist gastrocnemius, was found to correlate with increases in both the protein synthetic and degradative rates, the change in the former being greater than that of the latter. These conclusions were drawn from two different methods used to measure (in vivo and in vitro) the average rates of protein synthesis and protein breakdown in these soleus muscles. Although the basal rates of synthesis were higher when measured in vivo, and the degradative rates higher in isolated muscle preparations incubated in vitro, both methods gave good agreement concerning the changes in protein turnover induced by tenotomy of the gastrocnemius. The possible involvement of passive stretch in inducing this additional growth is discussed. As an antagonist to the soleus, growth of the extensor digitorum longus muscle was decreased under the same conditions, presumably because of less usage. At 3 days after the cutting of the sciatic nerve, the previously normal or overloaded soleus muscles underwent rapid atrophy. Although in both cases RNA and protein were lost, while protein synthesis decreased and protein breakdown increased, denervation induced larger changes within these parameters of the formerly overloaded muscle. The slowing of growth in the tenotomized gastrocnemius, and its subsequent rapid atrophy after additional denervation, were explained by large increases in protein breakdown, with little or no change in the synthetic rate.

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Section: Discussionmentioning

confidence: 98%

Protein turnover measured in vivo and in vitro in muscles undergoing compensatory growth and subsequent denervation atrophy

Goldspink¹,

Garlick²,

McNurlan³

1983

Biochemical Journal

133

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“…The biochemical mechanism by which use or disuse of muscle and nerve cells regulates cell growth or atrophy is unknown. I n viuo studies of skeletal muscle hypertrophy indicate that passive stretch is an important physiological factor in stimulating cell growth during increased use (Schiaffino and Hanzlikova 1970;Gutmann et al, 1971;Mackova and Hnik, 1973). I t has also been found that passive stretch of organ-cultured adult skeletal muscle causes similar changes to those seen in in viuo hypertrophy: stimulation of amino acid transport, incorporation of amino acids into proteins and inhibition of protein degradation (reviewed in Goldberget al, 1975).…”

Section: Discussionmentioning

confidence: 99%

Stretch‐induced growth of skeletal myotubes correlates with activation of the sodium pump

Vandenburgh

Kaufman

1981

Journal Cellular Physiology

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Skeletal myotubes responded to passive stretch by increased amino acid uptake (as measured with [3H]alpha-aminoisobutyric acid), increased incorporation of amino acids into total cellular protein and myosin heavy chains, and increased accumulation of total cellular protein and myosin heavy chains. These alterations were preceded by an increase in the uptake of ouabain-sensitive rubidium-86 (86Rb+), a potassium tracer used to measure membrane sodium pump activity (Na+K+ATPase). This stretch-induced stimulation of 86Rb+ uptake resulted from a 60-70% increase in the Vmax of the Na pump with little change in the Km. [3H] ouabain binding studies showed no stretch-induced change in the number of membrane Na pumps, indicating that stretch activates the Na pumps that are already present on the cell surface. Since the stretch-induced increases in amino acid transport and amino acid incorporation into proteins were inhibited by ouabain, Na pump activation may be involved in stretch-induced cell growth of skeletal muscle cells by hypertrophy.

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“…Tenotomy, the process of severing the distal tendon of synergist muscles, has been used to study hypertrophy of rat plantaris and soleus muscles. For example, tenotomy of the gastrocnemius muscle results in a rapid weight gain in the plantaris and soleus after surgery (Castle and Reyman, 1984;Goldberg et al, 1975;Mackova and Hnik, 1971;Maltin et al, 1987;Pehme et al, 2004). There is ã 30% increase in muscle wet weight compared to control 7 days postsurgery, but muscle mass is reduced 9-15% at 2-3 weeks postsurgery (Timson, 1990).…”

Section: Resistance Training Using Electrical Stimulationmentioning

confidence: 99%

Muscle Hypertrophy Models: Applications for Research on Aging

Siu¹,

Murlasits²,

Butler³

2005

Can. J. Appl. Physiol.

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Muscle hypertrophy is an adaptive response to overload that requires increasing gene transcription and synthesis of muscle-specific proteins resulting in increased protein accumulation. Progressive resistance training (P(RT)) is thought to be among the best means for achieving hypertrophy in humans. However, hypertrophy and functional adaptations to P(RT) in the muscles of humans are often difficult to evaluate because adaptations can take weeks, months, or even years before they become evident, and there is a large variability in response to P(RT) among humans. In contrast, various animal models have been developed which quickly result in extensive muscle hypertrophy. Several such models allow precise control of the loading parameters and records of muscle activation and performance throughout overload. Scientists using animal models of muscle hypertrophy should be familiar with the advantages and disadvantages of each and thereby choose the model that best addresses their research question. The purposes of this paper are to review animal models currently being used in basic research laboratories, discuss the hypertrophic and functional outcomes as well as applications of these models to aging, and highlight a few mechanisms involved in regulating hypertrophy as a result of applying these animal models to questions in research on aging.

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‘Compensatory’ muscle hypertrophy in the rat induced by tenotomy of synergistic muscles

Cited by 21 publications

References 5 publications

Protein turnover measured in vivo and in vitro in muscles undergoing compensatory growth and subsequent denervation atrophy

Protein turnover measured in vivo and in vitro in muscles undergoing compensatory growth and subsequent denervation atrophy

Stretch‐induced growth of skeletal myotubes correlates with activation of the sodium pump

Muscle Hypertrophy Models: Applications for Research on Aging

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