Moreover, testosterone can also increase locomotor activity as a consequence of changes in behaviour (Wikelski et al. 1999; Lynn et al. 2000) and a high muscle activity might enhance oxidative stress (e.g. Finaud et al. 2006 and references therein). Finally, if testosterone generates oxidative stress, we expect red blood cell resistance to free radicals to be the highest in F-males and the lowest in T-males. In this study, we tested the hypothesis that testosterone generates measurable costs in terms of oxidative stress in a bird species, the zebra finch, whose males harbour a testosterone-dependent ornament. Von Schantz et al. (1999) were the first to suggest a role for oxidative stress in the trade-off between the benefits of sexual signalling and the costs derived from sustaining high testosterone levels. The age of animal subjects and strain-specific attributes may affect results, reflecting the dynamic nature of testosterone levels, as well as cardiac and mitochondrial functions. One interesting aspect of our data is that catalase expression was increased in SSM but reduced in IFM.
In older men with low testosterone (hypogonadism), exogenous testosterone decreases resting respiratory exchange ratio (RER) as a result of increased fat oxidation (13). Testosterone administration may elicit whole-body and skeletal muscle energy metabolic adaptations in older men during energy balance conditions (13,14). Increased muscle mass with testosterone administration seems to result from molecular adaptations within skeletal muscle (9–11).
We have previously shown, however, that testosterone has additional actions on hepatic and aortic lipid accumulation in Tfm mice even with aromatase inhibition and ER blockade 16, 17. The present study indicates that testosterone may signal, at least in part, beyond its classical nuclear AR to modulate targets of lipid and glucose metabolism and that these actions are further differentially dependent on the target tissue. Indeed, Tfm mice from the present study have elevated total cholesterol and LDL compared to wild-type mice .
Mitochondrial calcium signaling plays a key role in the regulation of cellular energy metabolism, cardiac excitation–contraction coupling and the generation of ATP for contraction. It is well known that testosterone plays a significant role in cardiac contraction coupling and that the lack of this hormone decreases myocardial contractility due to a decrease in Serca2a activity (32–35). In addition, while the yield of SSM in the heart was increased after testosterone deprivation, the structure and function of these mitochondria was not substantially altered.

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