Thyroid hormone effects on contractility and myosin composition of soleus muscle and single fibres from young and old rats.
1. Young (3-6 months) and old (20-24 months) male Wistar rat soleus muscles were examined for myosin isoform composition, fibre type, contractility and sarcoplasmic reticulum (SR) Ca2+ release properties either in control rats or in rats treated with thyroid hormone (3,5,3'-triiodothyronine, T3) for 4 weeks. 2. T3 treatment had a strong impact on myosin heavy chain (MyHC) and light chain (MyLC) isoform composition in both young and old rats. That is, all single fibres co-expressed type I and IIA (type I/IIA fibres) or type I, IIA and IIX MyHCs (type I/IIAX fibres) after treatment. Slow and fast MyLC isoforms, i.e. MyLC1s, MyLC1f, MyLC2s, MyLC2f and MyLC3, co-existed in each of the type I/IIA and I/IIAX fibres in variable proportions. 3. In old rats the maximum velocity of unloaded shortening (V0) was related to MyHC isoform composition: V0 for type I fibres was less than that for type I/IIA fibres which was less than that for type I/IIAX fibres. In young rats, on the other hand, V0 did not differ between pure type I fibres from controls and those co-expressing type I and type II MyHC isoforms from T3-treated rats. 4. Contraction and half-relaxation times of the isometric twitch were significantly longer in old than in young controls. This was paralleled by an age-related decrease in the caffeine threshold of the SR. Four weeks of T3 treatment eliminated the age-related differences in both speed of twitch contraction and caffeine thresholds. V0, on the other hand, was slower in old than in young animals, both control and T3-treated, when cells with a similar MyHC composition were compared. 5. In conclusion, thyroid hormone can substantially reverse at least some of the changes that occur in ageing muscle. Further, the age-related decline in V0 in soleus fibres from control and hyperthyroid rats suggests that: (1) the identification of beta/slow myosin isoforms is incomplete; or (2) the molecular characteristics of MyHC differ between young and old age; or (3) MyHC is not the only determinant of V0.
Li
X
X
Department of Clinical Neurophysiology, Karolinska Hospital, Stockholm, Sweden.
Hughes
S M
SM
Salviati
G
G
Teresi
A
A
Larsson
L
L
D000375:Aging / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D006980:Hyperthyroidism / Q000503:physiopathology*; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D024510:Muscle Development; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000254:growth & development / Q000502:physiology*; D018995:Myosin Heavy Chains / Q000378:metabolism; D018994:Myosin Light Chains / Q000378:metabolism; D009218:Myosins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology*
D018994:Myosin Light Chains; D014284:Triiodothyronine; D018995:Myosin Heavy Chains; D009218:Myosins; D002118:Calcium