Abstract
Organisms in natural environments often undergo life history stage transitions that optimize behaviors (i.e., migration, reproduction, and foraging) with environmental conditions. These changes in behavior are facilitated by changes in physiology such as metabolism and energy production. Previous work on seasonally breeding songbirds observed that elevated levels of sex steroids during reproduction are accompanied by increases in basal metabolic rate (BMR), the minimum energy required to live for an adult organism. This increase in BMR is also associated with increasing daylengths in long-day seasonally breeding animals. Whether, and to what extent, the seasonal increase in BMR is a direct result of testosterone or in response to increases in duration and amount of activity occurring during longer days is not fully known. Experimental studies indicate that testosterone is capable of modulating mitochondrial function through activation of androgen and estrogen receptors within the mitochondria. However, whether testosterone directly influences BMR, and if it is related to changes in mitochondrial abundance remains unclear. Mitochondrial abundance can be quantified by assessing mitochondrial DNA copy number (mtDNAcn) which has been positively correlated with oxidative capacity and ATP production. Here, we assessed BMR of individual male house sparrows (Passer domesticus) during three experimental treatment periods: non-breeding short day photoperiods prior to hormonal manipulation (SD), followed by testosterone implants while still on non-breeding short days (SD + T), and then photostimulated on long days (LD) after implant removal, mimicking natural breeding conditions. We also collected blood samples to quantify testosterone and mtDNAcn of red blood cells (RBC mtDNAcn). Our results indicate testosterone did not directly alter BMR and that BMR was only elevated under longer daylengths associated with longer active periods. The total minutes of the day the birds were active increased under LD, thus indicating activity, and not increases in sex hormones, is likely responsible for the increases in BMR. We also observed no effect of treatment period on RBC mtDNAcn. Combined, the results from this study indicate that testosterone is not affecting BMR through changes in mitochondrial density (mtDNAcn) in red blood cells. However, changes in photoperiod affected BMR by either increasing daily activity or by stimulating the growth of reproductive tissues in seasonally breeding birds.