Relationship between cortisone and muscle work in determining muscle size

Abstract

SUMMARY1. Large doses of cortisone caus3d marked atrophy of the plantaris muscle and other pale muscles of hind limbs of hypophysectomized rats, but hormone treatment had little effect on the size of the red soleus muscle.2. Denervation increased the sensitivity of the soleus and plantaris to the catabolic effects of cortisone.3. Increased work induced by tenotomy of the synergistic gastrocnemius made the plantaris muscle less sensitive to cortisone-induced atrophy.4. Since the catabolic effects of cortisone are more pronounced in the less active muscles, it is suggested that in mobilizing body protein for gluconeogenesis the hormone spares those muscles physiologically most active. 5. The rapidity with which muscles lose weight in response to cortisone indicates that the hormone must decrease protein half-lives as well as decrease protein synthesis.

A histochemical and morphological study of skeletal muscle from obese hyperglycaemic ob/ob mice

“…Perhaps of relevance in this context, circulating glucocorticoids are reported to be elevated in both diabetic rats [29] and obese mice [11,12] before 3 weeks of age, and have been shown to cause decreased synthesis of DNA and the preferential loss of white muscle [15,29]. Further evidence for the involvement of corticosteroids has been provided by work using adrenalectomized mice.…”

“…It could be argued also that the marked hypoactivity of obese mice may trigger a reduction in size of their presumably less frequently used fast twitch skeletal muscle fibres. However, the soleus muscle is a continually active postural muscle, and constant contractile activity has been shown to be a fundamental determinant of muscle mass which can take precedence over endocrine signals for muscle protein depletion [15,36]. Decreased long bone growth in obese mice is unlikely to be the cause of the decreased muscle size since the soleus and gastrocnemius muscles share the same tendon but only the latter is smaller.…”

“…Plasma corticosteroid levels are also elevated in ob/ob mice [11,12] and may cause accelerated protein degradation and diversion of amino-acids into excessive gluconeogenesis [13]. If these metabolic abnormalities in obese mice are responsible for their decreased skeletal muscle mass, one would predict that fast and slow phasic muscles would respond differently, since either st~eptozotocin-induced diabetes [14] or corticosteroid injections in rats [15] cause large glycolytic fibres and fast phasic muscles, to lose most weight.We investigated the number, type, and size of fibres il~ the biceps brachii muscles of lean and obese mice to determine whether the smaller muscles in the latter show differential changes in fibre size and type. The biceps brachii muscle was chosen since it contains a good mixture of red and white fibres.…”

Communications

“…The change in gain may result partly from activation of dynamic y motoneurones. (Goldberg & Goodman, 1969) that the contra.tile activity of a particular muscle may influence the extent to which it responds to these steroids.…”

Participação do estresse oxidativo na disfunção muscular esquelética em ratos diabéticos.

“…Além da insulina, o diabetes tipo 1 apresenta outras alterações hormonais, como elevação plasmática de glicocorticóides (Roy et al, 1990) e redução do fator de crescimento semelhante à insulina-1 (IGF-1 -insulin-like growth factor-1) (Masaoka et al, 2003), o primeiro contribuindo para maior catabolismo (Goldberg, Goodman, 1969) e o segundo para menor síntese proteica muscular (Glass, 2005;Sandri, 2008). Conforme revisado por Brownlee (2001), a hiperglicemia típica do quadro diabético causa ativação da via dos polióis e da proteína quinase C (PKC) -β e -δ, aumento do fluxo de metabólitos pela via das hexosaminas e formação de produtos avançados de glicação (AGE -advanced glycation end products).…”