There is a growing body of evidence suggesting that the effects of testosterone are energetically expensive, and may play an energy-allocating role in the life history trade off between reproduction and survival (Charnov 1993; Folstad and Karter 1992; Muehlenbein 2008; Muehlenbein and Bribiescas 2005). High testosterone levels are hypothesized to lead to increased investment in reproduction, including behavioral strategies and secondary sexual characteristics (Muehlenbein and Bribiescas 2005). Testosterone plays an important role in increasing and maintaining male muscle mass, which can enhance competitive ability and mate attraction (Bhasin and others 1996; Bribiescas 2001). This comes at a cost: not only is muscle energetically expensive (Lassek and Gaulin 2009), but high levels of testosterone also increase the catabolism of fat tissues, depleting reserves that could be essential during periods of food shortage (Bhasin and others 2005).
Studies of male human and non-human primates suggest that short-term fasts can have significant down-regulatory effects on the hypothalamic-pituitary-gonadal (HPG) axis, prior to any change in body weight or composition (Aloi and others 1997; Bergendahl and Veldhuis 1995; Cameron and others 1991). In human males, fasting appears to significantly reduce the number, and amplitude of gonadotropin releasing hormone (GnRH) pulses, thus decreasing luteinizing hormone (LH) pulsatility (Aloi and others 1997; Rojdmark 1987). It is difficult to directly measure GnRH in humans, as it exists solely within the brain, but administration of intravenous GnRH during caloric restriction restores LH pulses, suggesting that fasting down regulates GnRH production (Aloi and others 1997). Problems with direct testing for GnRH make it difficult to ascertain whether it is the frequency of GnRH pulses, or their amplitude that is affected by short term fasting (Aloi and others 1997). Administration of intravenous GnRH has also been shown to restore testosterone levels in fasting subjects (Rojdmark 1987).
Once a fast is broken, LH pulsatility rebounds in male subjects; both in human and non-human primates (Friedl and others 2000; Parfitt and others 1991; Schreihofer and others 1993a; Schreihofer and others 1993b). LH secretion begins within twenty-to-forty minutes of re-feeding, and is monotonically related to the size of the re-feeding meal (Parfitt and others 1991). Resumption of LH secretion is unrelated to the actual act of eating; macaques re-fed via gastric cannulae showed an LH rebound statistically identical to macaques that were re-fed naturally (Schreihofer and others 1993a). When normal weight primates were overfed just prior to the onset of fasting, there was no effect on LH secretion, suggesting that acute caloric deficit plays an important role in hormonal down regulation (Cameron 1996; Schreihofer and others 1993b).
Previous studies find that multi-day fasts cause a reduction in LH and testosterone. This project tests the responsiveness of the male HPG and HPA to a brief caloric deficit. We hypothesize that the male reproductive axis is sensitive to even minor energetic disruptions, with reductions in LH and testosterone the morning following a missed evening meal. We also hypothesize that testosterone will return to normal levels rapidly after re-feeding. Cortisol is hypothesized to rise due to HPA activation from the psychological and physiological stress of fasting. Understanding the effects of short term caloric reduction on the endocrine system will provide insight into the role of testosterone in the trade-off between survival and reproduction in human males.
Studies of male human and non-human primates suggest that short-term fasts can have significant down-regulatory effects on the hypothalamic-pituitary-gonadal (HPG) axis, prior to any change in body weight or composition (Aloi and others 1997; Bergendahl and Veldhuis 1995; Cameron and others 1991). In human males, fasting appears to significantly reduce the number, and amplitude of gonadotropin releasing hormone (GnRH) pulses, thus decreasing luteinizing hormone (LH) pulsatility (Aloi and others 1997; Rojdmark 1987). It is difficult to directly measure GnRH in humans, as it exists solely within the brain, but administration of intravenous GnRH during caloric restriction restores LH pulses, suggesting that fasting down regulates GnRH production (Aloi and others 1997). Problems with direct testing for GnRH make it difficult to ascertain whether it is the frequency of GnRH pulses, or their amplitude that is affected by short term fasting (Aloi and others 1997). Administration of intravenous GnRH has also been shown to restore testosterone levels in fasting subjects (Rojdmark 1987).
Once a fast is broken, LH pulsatility rebounds in male subjects; both in human and non-human primates (Friedl and others 2000; Parfitt and others 1991; Schreihofer and others 1993a; Schreihofer and others 1993b). LH secretion begins within twenty-to-forty minutes of re-feeding, and is monotonically related to the size of the re-feeding meal (Parfitt and others 1991). Resumption of LH secretion is unrelated to the actual act of eating; macaques re-fed via gastric cannulae showed an LH rebound statistically identical to macaques that were re-fed naturally (Schreihofer and others 1993a). When normal weight primates were overfed just prior to the onset of fasting, there was no effect on LH secretion, suggesting that acute caloric deficit plays an important role in hormonal down regulation (Cameron 1996; Schreihofer and others 1993b).
Previous studies find that multi-day fasts cause a reduction in LH and testosterone. This project tests the responsiveness of the male HPG and HPA to a brief caloric deficit. We hypothesize that the male reproductive axis is sensitive to even minor energetic disruptions, with reductions in LH and testosterone the morning following a missed evening meal. We also hypothesize that testosterone will return to normal levels rapidly after re-feeding. Cortisol is hypothesized to rise due to HPA activation from the psychological and physiological stress of fasting. Understanding the effects of short term caloric reduction on the endocrine system will provide insight into the role of testosterone in the trade-off between survival and reproduction in human males.
