Mixed-model ANOVA was used to assess main effects of time, treatment, and their interactions for total and free testosterone, oxygen-carrying capacity, energy and macronutrient intake, energy balance, substrate oxidation, nitrogen balance, glycogen, and mRNA expressions. Mixed-model ANOVA with fat mass and fat-free mass as covariates was used to assess energy expenditure main effects of time (balance vs deficit), treatment (TEST vs PLA), and their interactions. Total body mass, fat-free mass, and fat mass were primary outcomes of the parent study (7) and are reported in this article as a change from balance to deficit. After completing the balance phase, participants were admitted to an inpatient unit at the PBRC for the 28-d controlled diet- and exercise-induced energy deficit (55% below total energy needs) phase of the study. This study included a 14-d energy balance phase, followed by a 28-d inpatient phase of controlled diet- and exercise-induced energy deficit (Fig. 1). We also hypothesized that testosterone administration would increase the transcription of energy metabolism and fat oxidation–related genes compared with placebo after 28 d of 55% energy deficit.
T-cell mediated immune response was analysed with ANCOVA models including body mass at the sampling date and resistance to free radicals as covariates. Finally, since the rate of peroxidation of lipids of the red blood cell membrane determines the capacity to resist the free radical aggression (e.g. Brzezinska-Slebodzinska 2001; Nagasaka et al. 2004), this assay would also reflects the degree of oxidation suffered in the recent past. The androgen-receptor antagonist activity of flutamide in this species is supported by the results from a recent study (Tomaszycki et al. 2006). Testosterone also regulates the expression of the trait, probably by upregulating the synthesis of lipoproteins that carry the pigment (Cynx & Nottebohm 1992; McGraw et al. 2006). Following von Schantz et al. (1999), several other studies have postulated that testosterone has pro-oxidant properties (e.g. Royle et al. 2001; Gil et al. 2004; Rutkowska et al. 2005), even though a closer scrutiny of available data reveals a more complex pattern. In addition, some testosterone-dependent ornaments are produced by pigments with antioxidant properties (e.g. Stoehr & Hill 2001; Jayasooriya et al. 2002; Alvarez et al. 2005).
As shown in Figure 1D, Serca2a protein expression was significantly decreased in the OQT group and this decrease was prevented by testosterone replacement. To identify carbonyl groups that are introduced into the amino acid side chains after oxidative modification of proteins, 2D-oxyblot analysis was performed (29). In conclusion, our findings demonstrate that testosterone deficiency leads to reduced myocardial contractility and impaired cardiac interfibrillar mitochondrial function. Orchidectomy increased total left ventricular mitochondrial protein in the SSM, but not in IFM. Considering the intimate connection between oxidative metabolism and myocardial contractility, we determined the effects of testosterone deficiency on the two spatially distinct subpopulations of cardiac mitochondria, subsarcolemmal (SSM) and interfibrillar (IFM). Associations between 24-h energy expenditure and fat-free mass during energy balance (A) and…