ellis
Jeszcze o CPT I
In human studies, skeletal muscle CPT I is unaffected by LCD. This was demonstrated at the level of maximal enzyme activity following a 6 d LCD (~3% CHO) [12], and mRNA levels following a 5 d LCD (19% CHO) [31]. However, in skeletal muscle of rats fed a high-fat diet, CPT I enzyme activity capacity was increased up to 1.3 to 2-fold at 10 weeks, depending on the fatty acid composition of the diet [33]. In another rat study, increased gene expression of CPT I mRNA appears to be restricted to type I slow oxidative muscle fibers, since a significant increase was only documented in the soleus muscle, and not the extensor digitorum longus following 8 weeks of a high-fat LCD (0% CHO) [34]. Taken together, these studies suggest that the short term 5–6 d LCD perturbation may not be prolonged enough to evoke a significant change in activity or gene expression of this enzyme which regulates transport of fatty acids into the mitochondria for oxidation. This is further supported by the fact that in well trained human subjects, maximal CPT activity was modestly increased following a prolonged (4 week) very low LCD (<20 g CHO), although it is not clear from this data whether this measurements included CPT I and CPT II activity together [35].
Być może tak jak mówiłem potrzebna jest dłuższa adaptacja...
In human studies, skeletal muscle CPT I is unaffected by LCD. This was demonstrated at the level of maximal enzyme activity following a 6 d LCD (~3% CHO) [12], and mRNA levels following a 5 d LCD (19% CHO) [31]. However, in skeletal muscle of rats fed a high-fat diet, CPT I enzyme activity capacity was increased up to 1.3 to 2-fold at 10 weeks, depending on the fatty acid composition of the diet [33]. In another rat study, increased gene expression of CPT I mRNA appears to be restricted to type I slow oxidative muscle fibers, since a significant increase was only documented in the soleus muscle, and not the extensor digitorum longus following 8 weeks of a high-fat LCD (0% CHO) [34]. Taken together, these studies suggest that the short term 5–6 d LCD perturbation may not be prolonged enough to evoke a significant change in activity or gene expression of this enzyme which regulates transport of fatty acids into the mitochondria for oxidation. This is further supported by the fact that in well trained human subjects, maximal CPT activity was modestly increased following a prolonged (4 week) very low LCD (<20 g CHO), although it is not clear from this data whether this measurements included CPT I and CPT II activity together [35].
Być może tak jak mówiłem potrzebna jest dłuższa adaptacja...
Seewy
slawekop
Biniu
toft
