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ellison_chapter - I I) SAY THAT MEN AND WOMEN differ in...

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Unformatted text preview: I I) SAY THAT MEN AND WOMEN differ in many details of llll'il' reproductive physiology is obvious and boring. So let’s start with Ilu‘ opposite statement: men and women are remarkably similar in many details of their reproductive physiology. The central hormonal axis governing gonadal function is the same in lioth sexes. The hypothalamus releases GnRH into the hypophyseal In Il'lill system in quasi—hourly pulses in males just as it does in females. .-\|ieration of the pulsatile GnRH pattern in the direction of either too nmny pulses or too few can result in a disruption of gonadotropin release lw the pituitary gland. Pubertal development normally involves the ap- lu-Llrance of the mature pulsatile pattern of GnRH. Exogenous manipu— Luions of GnRH pulsatilityueither introducing UnRH pulses where IIu-y are absent, or suppressing them (via long-acting GnRH analogs) when they are present—can advance or retard pubertal progression in Individuals with developmental pathologies of hypothalamic origin. When GnRH pulses occur in the mature hourly pattern, the male’s l-miitary responds, as does the female's, by releasing gonadotropins. I'hese gonadotropins are the same ones found in females—follicle stima ulaling hormone (FSH) and luteinizing hormone (LH)—even though males have no follicles to stimulate or to luteinize. In early physiological '-llltli€5, these hormones were given different names in males, referring In their principal functions in the male reproductive system—intersti- Iml cell stimulating hormone instead of follicle stimulating hormone. .md Leydig cell stimulating hormone instead of luteinizing hormone. 252 THE BODY BUILDERS When the composition of these large and complex protein molecules was finally worked out, however, the male and female gonadott‘opins were found to be identical, and the female names were given prece~ dence. Not only are the structures of the gonadotropin molecules the same in males and females, but their targets and actions are analogOus as well. To appreciate this similarity we must first appreciate the anatomical and histological analogies between the ovary and the testis. The gonads de— velop early in embryogenesis around a duct system (the Wolffian ducts} that leads into the developing urinary tract. A secrmd duct system (the Miillerian ducts), outside the developing gonad, also leads to the uri~ nary sinus from the open body cavity near the gonad. The precursor cells to the gametes migrate to the developing gonad from their site ol production near the developing umbilical cord. As they reach the go- nad. which to this point is identical in males and females, the first ex- pression of genes for sex determination comes into play. The proliferat' ing gametogenic cells either locate themselves in the outer layer, or cortex, of the gonad, or migrate deep into the interior, or medulla, oi the gonad to line the system of tubal ducts. This positioning of the go metes determines the direction in which they will travel later in the or- ganism’s life in their quest for gametes of the opposite sex. Those ga metes that are located in the cortex will be shed to the exterior of tin- gonad to be transported by the fallopian tubes (the erstwhile Miillerian ducts) to the uterus. Those gametes that are located in the medulla of the gonad will be shed internally into the semeniferous tubule», thence to the rete testis. epidydimis, and vas deferens (derived from the Wolffian ducts). The location of the gametogenic cells is the first anatomical distim tion between ovary and testis. Subsequently the unused duct system in each sex degenerates to provide another distinction. In each location. however, the gametogenic cells become separated from other tissue. and from the body's blood supply by a surrounding membrane that seal. off tissues on either side. This kind of membrane is called a baseIm-m membrane. Such a membrane defines the follicles in the LIL‘VL'lUI'IlI'I}'_ THE BODY BUILDERS 253 ovary and the seminiferous tubules in the developing testis. Inside the membrane together with the developing gametes are specialized "nurse" cells—granulosa cells in the female, Sertoli cells (also called interstitial cells) in the male. These nurse cells maintain cytoplasmic connections with the gametes as they develop_through which important nutrients and signals for development flow. butside the membrane in each case is a second population of cells that is responsible for the production of steroid hormones necessary for normal gamete maturation. These are theca cells in the female and Leydig cells in the male. lln the female, the theca cells, unlike the granulosa cells, are able to make steroid hormones from scratch, that is to say, from cholesterol. The theca cells respond to LH pulses from the pituitary by producing androgens, primarily testosterone. So it is with the Leydig cells in the male, which make testosterone de novo from cholesterol in response to LH. In the female, the granulosa cells inside the basement membrane support the development of the egg cells and convert testosterone de- rived from the theca cells into estradiol. So it is with the Sertoli cells in the male, which nurse the developing sperm cells and convert testoster' one to estradiol. When follicles are growing and gamete maturation is under way, the granulosa cells in the female also release a protein hor— mone called inhibin, which, upon reaching the pituitary, selectively . suppresses the release of FSH. So it is with the Sertoli cells in the male. As long as spermatogenesis is under way, the Sertoli cells produce in. hibin, which feeds back negatively on FSH release to maintain very low circulating levels. In the female, PSI-I is necessary to initiate follicular maturation at the start of each menstrual cycle. But when steroid pro- _ duction by the dominant follicle reaches a sufficient level, high levels of FSH stimulation are not required for follicular growth and gamete mat— urntion to proceed. So it is in the male. FSH is required to initiate fliunetogenesis, or to restart it if it becomes interrupted. But once estab- ' llnhed, steroid production is sufficient to keep the process going with ' only minimal FSH. If spermatogenesis is interrupted, by starvation for "simple. inhihin production is interrupted as well. When conditions Improve and (MRI! pulses begin again, the pituitary releases FSH in THE BODY BUII I-II yHypothalamus Major components of tln- m -|. reproductive axis. Gan l r. .- leased ll'l pulses {TCPITI thl' l|\|"' thalamus, stimulating Illr I'l .- duction and release of F5} I n. l Lll from the anterior pIIIII|.u-_ Together FSH and LH .\'Ill1n| late production ofsperm :m-l production of the hormnm . testosterone and illhihin. I. tosterone modulates l'inH -r|. | lamic and pituitary activin while inhibin suppresses Ili- production of F5} |. Testosterone inhihin quantity as well as LH until spermatogenesis is reestablished. All” that, only a low circulating amount of FSH is necessary to suslmu aromatization of testosterone to estradiol by the granulosa Ct‘llh “I Sertoli cells in either sex? This recitation of the similarities of male and female reprodm I n- physiology helps to set the important differences in relief. Among tho-.- differences two are paramount. Males produce gametes in protligiou quantities, not one at a time, and do so continuously, not at monthly m tervals. All along the length of the semeniferous tubules (which an rulul extend for dOZens of meters if uncoiled) mitotically active spermzuu gonia divide to produce sperm cells. The developing sperm cells In. dergo an extended process of maturation under the nurturnm-t- .m-I guidance of the Sertoli cells, migrating in the process from their hllt‘ t-I TIIH BODY BUILDERS 255 mlgin next to the basement membrane toward the open lumen at the Gunter of the tubule. The entire eourse of maturation takes around sew titty—four days, but it proceeds in asynchronous waves along the length Ill. the seminiferous tubule, and new crops of sperm cells are mitotically produced in any given location before the previous crop has completed ltll course. The result is a continuous flow of mature sperm cells into the lumen of the semeniferous tubules, from which they are collected into the epidydimis to await ejaculation or eventual death and resorption. Superficially, the maturation of a sperm cell looks like the opposite till the maturation of an egg cell. Where the egg cell increases in size and lactiumulates cytoplasm, the sperm cell shrinks in size and sheds cytoa plusm. It assumes a highly specialized morphology dedicated to the task 'tll'fettilization. In the end, it consists ofa head containing the paternal R! of chromosomes topped by a special cap of enzymes known as the acrosome. The enzymes of the acrosome will be used to digest the veils of cellular and secreted material that surround the egg, including the Cumulus oophorus and the zona pellucida. Behind the head is the mid, piece of the sperm cell in which are packed all the cell’s mitochondria, the engine that. will provide energy to the propeller. The propeller is represented by the tail of the sperm cell, a long, mobile filament compa- table in form and function to the flagellae that many unicellular organ— lllns use to propel themselves through their aqueous world. Stripped to the bare essentials, the sperm cell depends on its imme— tllule environment to provide it with nearly everything it will need to .eumplete its mission of fertilization. The seminal fluid, which is pro— duced by the prostate gland and seminal vesicles, is rich in simple car— hill‘IYtlt‘ateS that the mitochondria of the midpiece can use for fuel, as Well as carbonates to neutralize the acidic environment of the vagina. Once through the cervix into the uterine cavity, the sperm cell will rely on nutrients provided by the secretory glands of the endometrium for fuel. Although the sperm cell has a propeller of sorts, it has no rudder. It depends on its immediate environment to provide it with direction as well as fuel. In the middle of the menstrual cycle, under the influence l'll ll l, lhe mucus Illill normally lills the cervix becomes thin, and the THE BODY EU | LDEIl‘x 256 individual mucin strands become stretched to lie parallel to the axis through the cervix, rather than presenting a tangled mass as they Hill: during most of the rest of the menstrual cycle. The sperm-cells use It w parallel traclts provided by the mucin strands to orient their swrmming. The thermal oscillations produced in the mucin strands by the woman s body heat also resonate with the beating of the sperm cell’s tail to aid Ilh progress. Further up the woman’s reproductive tract the steady current of fluid passing down the fallopian tube toward the uterus—a currentl produced by the beating of the microscopic cilia lining the tube at: carrying the egg cell toward its site of potential implantation—T—wtir '- like wind on a weather vane to keep the sperm cells swrmming up stream. A LIMITING DIFFERENCE It‘s a hazardous journey, and only a small fraction of the sperm cells Illul enter the vagina at ejaculation ever arrive in the vicinity of the oot'yh to have a chance at fertilization. This fact alone might seem suffieiml to account for the high rate of production of male sperm cells. But it n- ally is only part of the story. It may help to remember that continuuu. production ofa large number of gametes is the primitive pattern mlm ited by all vertebrates from their invertebrate ancestors. It is a. patlrm that female mammals have abandoned for specific reasons tled -lll|I mately to their necessarily heavy physiological investment in relatm-li few offspring. The fact that males still follow the ancnent pattern ul '3: mete production suggests that male reproductive success is not sulxlu I to the same energetic constraints. Because male mammals do noI ’11". tate or suckle their own offspring, male reproductive output is not Inn ited by the rate at which nutrients can flow across the placenln on through the nipple. ‘ TWhat primarily limits male reproductive output 15 not then-Ir .n which energy can be converted into offspring, but the number of ol up. u tunities to mate with fecund females. This may seem a rather crass hlJlI ment, but it is a generalization that is fundamental to male reprntlut lI\- physiology. Among the consequences that follow from this basic- dill. l E puberty and reaches adult levels within a dle age, when it begins to decline in : flystemsuiUnlike female fecundity, - urehe until the mid—twenties and t i the mid'thirties, male fecundity rises . ing adolescence and then appears to cillly possible. The logic behind this the much hig : dearly in terms of her own growth, survival and, ultimately. - I'cpnuluctive success if she begins to when young even if upporlunities are rare. Simil THE BODY BUILDERS 25? ence in constraints on male and female reproductive success are three that shape male fecundity in patterns distinctly different from those of female fecundity. [T he first consequence is the fact that males produce a prodigious andunearly continuous supply of gametes. ceed a reproductive rate of one litter a Males, however, lows. In order t Female mammals cannot ex— t a time, even theoretically. can sire numerous overlapping litters. ifopportunity al- o realize such opportunities, gametes must always be available. Only when it can safely be assumed that infecund, as in the nonbreecling seasons of some specie duction suspended in healthy adult males. Even when sUCCessful mating is low, the cost all females are 5, is sperm pro— the chance of a of missing that opportunity when it comes along is likely to be greater than the cost of maintaining the nec— essary sperm supply. Even in a species like humans that breeds year- round, an individual female’s reproductive lifetime is normally com- posed of alternating fecund and infecund intervals. Fecundity in human males, by contrast, is normally continuous and uninterrupted. A second consequence is related to the first. Male gamete produc— tion shows little variation with age other than that associated with gent cral physiological senescence. In humans, gamete production begins at few years. It is sustained at adolescence until late mid- parallel with other physiological which increases gradually from men- hen begins a steady decline as early as more abruptly to a peak value dur' be sustained as long as physiologi— difference in age patterns is tied to her energetic costs of reproduction for females than for Males and the associated trade—offs. that level in healthy individuals from early Whereas a young female may pay her lifetime reproduce too rapidly too soon, the Illule pays little cost for maintaining his physiological potential to mate arly. at older ag‘s fe- l THE soot BUiLnERs 258 males face tradeoffs between the benefits of additional offspring and the costs of additional reproduction in terms of their ability to survive and invest in offspring already born. As noted above, with Increasing age the optimum balance may well shift for females in favor of lowedr fe— cundity. In males, however, the physiological costs of late age repro uc' tion are unlikely to mount at anything near the female rate, whlle the benefits to lifetime reproductive success of fathering offspring late III life, especially if the mother is relatively young, remain nearly constant. A third consequence also follows from the low direct energetic cosl of reproduction for malesfMale fecundity shows nothlng like the exqui- site sensitivity to energetic conditions that female fecundity shows. Studies of male marathon runners show no significant differences In sperm count, for example, between them and nonathletic men. hior air increases in athletic training regimes associated with reductions In sperm production indices within individual mengsevete undernutii tion, severe enough to threaten survival, can result In Interrupted spei III production. At such extremes even marginal energetic savlngs may con tribute to survival. But under the range of conditions humans normally face, including a broad range of energetic conditions, the cost of main taining sperm production is relatively small. Even If limited eneiml availability reduces the probability that any offspring conceived wrml. survive and flourish. the cost of making the attempt does not fall on lin- male.;A female can actually lower her lifetime reproductive success lit trying to reproduce under such circumstances, since substantial ‘illlll and energy may be lost in an unsuccessful attempt. A male Idoes noi have to pay the same costs of failure. One might. argue that In a pan bonded species a male largely shares the reproductive success oi lir- mate. Therefore he would also share the costs of impregnating her qu-I: the probability of a successful outcome are low. But if his fecundity “'Il'll to be suppressed, he would also lose all possibility of impregnating oi I- 1 females as well. Even if such opportunities make only marginal t‘lllllll butions to a male's lifetime reproductive success, there would still lu- an advantage for a male to sustain his fecundity under conditions Il'i.i| § - I ‘ ‘ i ‘ ‘- ‘ ates ‘Ili siolo' In I: an I lower his mate's fecundity. He can rely on his in i y Ly I illty and its ecolog THE BODY BUILDERS ZSQJ her fecundity under stressful energetic conditions while maintaining his own fecundity in order to be able to take advanta ge of mating opportu— nities with other females. is the implied measure. Certainly anything that interrupts sperm pro— duction brings male fecundity to zero, but the significance of quantitav tive variation in sperm count is less clear. In clinical terms, sperm counts above 15,000 or 20,000 per milliliter of semen are considered “normal.” There is little evidence that variation in sperm count above such a threshold increases a man’s chance of fathering children, even though sperm counts can range to concentrations of 250,000,000 per milliliter or more. Perhaps the significance ofsueh variation is not man. lfest in a monogamously mated couple trying to conceive. Perhaps, as with the fecundity of young adolescent males, the value of high sperm counts is more obvious when mating is more opportunistic. if, for exam- ple, it could be demonstrated for humans, mestie mammals, rate as it has been for many do. that a higher sperm count is associated with a higher of fertile matings, then the question of variation in male fecun— ical correlates Would need to be reexamined. Theo- ht expect that at some point, however low the cost of sperm production, that cost could outweigh the diminishing tit/ed from increasing sperm counts. An o lion might be affected by emerge Very I‘soft" retically one mig returns do. ptimum level ofsperm produc— tic conditions, but it might also be a optimum, where large differences in sperm production make only small differences in fecundity. Although we cannot be sure, this description appears to fit what we know about normal variation in hu— miiii sperm counts, with variation at the high end having little obvious relationship to male fecundity. - lilillU OF CHOICE If the relationship between gamete production and fecundity is tenuous in men, the relationship between testicular hormone production and fe' i‘illiilily is even more so. Tesiosierone is necessary to maintain sperm THE BODY BUILDER.k THE BODY BUILDERS 261 260 ._. I production, but quantitative variation in testosterone levels within the very broad range of values recognized as normal does not appear to be .. related to quantitative variation in sperm production, e1ther between men or within individuals. iYet testosterone levels do show predictable patterns of variation that seem to require some functional explanation. 'Free testosterone levels decline steadily with age, for example, and are consistently lower in men from traditional societies and rural communi- ties in the developing world than among populations from developed countries. Although not as acutely responsive to moderate variation in energy balance and flux as female ovarian steroid levels, testosterone levels do seem to respond to long»lasting energetic conditions. Yet ll testosterone levels themselves have no clear relationship to male fecun dity, where do we look for a functional explanation of these patterns oi variation? We noted above that the basic constraints on male and female i'e productive success are quite different. Because females carry the enel getic burden of reproduction, female reproductive success 13 pfll'I‘IHIIIV limited by the availability of energy and the necessary time consumed by the process. Male reproductive success, by contrast, is primarily lun ited not by male fecundity but by mating opportunities-Energy can sI Ill be important for male reproductive success, but not the same way II is for females. If female reproductive physiology in mammals can In- crudely characterized as a system for turning energy into offspring, mult- rcproductive physiology can be crudely characterized as a system IIII turning energy into mating opportunities. It is in the management “I this system that the functional significance of testosterone variallun seems to lie,‘ There are two basic channels by which testosterone helps to man age the rate at which energy is converted into mating opportunitie- through its effects on behavior and through its effects on metabolism Steroids as a class of hormones are particularly suited to influence ln havior owing to their ability to pass through cell membranes. This ml i.- bility allows them to go where larger molecules like protems L‘illlllul across the blood-brain barrierI for instance. This barrier is composed of basement membrane that separates the brain and cerebrospinal fluid from the circulatory system. It allows the chemical milieu of the brain to be carefully controlled, but it also seals off the brain from many of the chemical signals that originate elsewhere in the body. The peripheral signal molecules that can most reliably reach the central nervous system are the steroids. Not only do they reach the brain, but it is clear the brain is listening. Many parts of the brain, especially in the limbic sys' tem and hypothalamus—areas of the brain concerned with the regular tion of emotional and appetitive behavior and with the regulation of the anterior pituitary gland and all its downstream target tissues—are densely endowed with steroid receptors. Radioactiver labeled steroids, injected into an animal's peripheral circulation, can soon be found bound to these central nervous system receptors. Among the most obvious effects of gonadal steroids on the brain are their influences on reproductive behavior. Injecting an ovariectomiaed female rat with estradiol will elicit stereotypical behavior patterns that invite copulation from a male. Injecting a castrated male songbird with I testosterone will elicit the singing associated with mate attraction and territorial defense. Numerous other examples can be cited to illustrate the same basic point. The behavioral effects of gonadal steroids help to coordinate reproductive behavior with reproductive condition. Ania mills do not typically display adult reproductive behavior patterns until reproductive maturation raises circulating steroid levels. In seasonally breeding species it is the renewal of gonadal activity (often linked to photoperiod or some other signal of the approach of appropriate breedv lng conditions) that stimulates the renewal of reproductive behavior.'_ We humans are, of course, complicated creatures, and the number Of influences on our behavior are legion. Yet it is hard for even the most Ilniial or biased observer to doubt the influence of gonadal steroid pro— duction on human reproductive behavior. Something transforms not only Ihe bodies but the predilections of adolescents, and something else flools our sexual ardor with advancing age. Colloquially, parents refer to Il‘Ir influence ol“'r:lging hormones” on their teenagers, and pharmaceu— fli'ul i'imlpallies Imlt Ilie lmost ro lagging sex lives of hormone replace: 262 THE BODY BUILDERS ment therapies for both men and women. But more direct evidence also exists to substantiate the claim that steroids affect several important as pects of human sexual behavior, and that these links are particularly im' portant for males. I The traditional experiment used to demonstrate the influence of testosterone on male libido in experimental animals involves castration followed by exogenous testosterone replacement. Castrated male rats, for example, are much less likely than intact males to attempt copula' tion with a female in estrus. When given increasing doses of exoge- nous testosterone, castrated rats show an increasing probability of mat-- ing until at quasi-normal testosterone levels the castrated animals are just as likely as the intact ones to try to mate. This is not an experiment that is likely to pass the scrutiny ofa Human Subjects Review Commil tee, or to draw many human volunteers if it did. Involuntary castration has been used, of course, to reduce the libido of slaves, prisoners, and the mentally retarded in different. cultures at different times, and the 1m- of chemical castration in the sentencing of repeated sexual offender-- has been debated recently in our own society. But experiments very- close to the rat experiments have, in fact, recently been conducted in the course of attempts to develop effective chemical contraception i: u men. One of the prime obstacles to the development of a male “coon-.- ceptive pill" has been the link between testosterone and libido. [In easiest way to interrupt sperm production pharmacologically is to elilm nate or drastically reduce testicular testosterone production. This l1:l.‘- .: number of undesirable side effects, however, including the loss of Iihith -. which would of course undermine the entire marketing value of Ilu product. The idea, after all, is to enjoy sex without risk of concept it -u. not to induce celibacy. Recently research has focused on ways to slml down sperm production and then exogenoust replace testostcronr h- support normal libido. The first part of the goal—shutting oil sprou- production—mis achieved by administering a long—acting UnRH alt-Iliu- As discussed previously, such analogs mask the natural pulsatilitr ul GnRH that is necessary for normal release of pituitary golmtlotrol-m 'I'HE soot BUHJ‘JERS 263 Without LH to support Leydig cell function and FSH to support Sertoli cell function, both testosterone production and sperm production come to a halt. It takes some weeks for all residual sperm to be eliminated from the testes and epidydimus, after which continued administration of the GnRH analog keeps gonadal function suppressed. Then exov genoth testosterone is introduced, either through injection or trans- dermally from a patch worn on the skin. With appropriate controls, it is possible to study the relationship between the level of testosterone re— placement and various measures of male libido, such as frequency of erections, sexual fantasies, masturbation, or intercourse. All of these show progressive responses to increasing testosterone doses until at HOP mal testosterone levels the experimental subjects are no longer distin- guishable from controls. There is no evidence that supranormal levels of testosterone produce exaggerated libido, however. Many factors may play a role in establishing an individual's sex drive as well as the transla— tion of that drive into behavior. What the testosterone replacement studies do suggest is that testosterone is necessary to support normal male libido. Interestingly, there is also compelling evidence that androgens are involved in supporting female libido as well. In women the major source of androgens is the adrenal gland, the gland that is also responsible for producing cortisol. Women who suffer from adrenal insufficiency are often treated with exogenous cortisol, but not exogenous androgens. When androgens are added to the treatment regime, the reported fre— quencies of sexual fantasy, activity, and pleasure all rise compared to the frequencies reported by controls treated with a placebo. Hormone re- placement therapy for postmenopausal women usually involves exoge' nous estrogens and progesterone. But when androgens are added to that regime similar increases in reported frequencies of sexual fantasy, activ- ity, and satisfaction are recorded. As illuminating as these cases of androgen replacement are in dem' onstraring the role of androgens in supporting the libido of both sexes, they nevertheless represent abnormal situations. It is much more dif— llL‘llll to determine whether normal variation in male testosterone lev— 264 THE BODY BUILIWI-Ia els. either between or within individuals, is associated with variation in libido. Low testosterone levels associated with dramatic energetic stress. such as starvation or the combination of dietary restriction and intents: exercise experienced by varsity wrestlers during training, are often assi- ciated with reports of low libido. But there are many other physiological changes confounded in these situations which make it difficult to con fidently attribute the changes in libido to the effects of testosterotu alone. One famous anecdotal account relating to this issue was pul- lishcd anonymously in the prestigious journal Nature in 1970. A Sillile male researcher who was engaged in research on the Isle of Rhurn nil the Scottish coast for extended periods made a habit of collecting all In-. beard shavings from his electric razor each day and weighing them. The. measure of daily beard growth provided him with a crude bioassay oi hr. own testosterone levels. The report in Nature presented these data plt It ted day by day. Also indicated on the graph were the periods duritw which the researcher left the island to enjoy the companionship of in. female partner on the mainland. The sinusoidal pattern of the hennl growth data lends itself to interpretation as a graph of libido, lowest in. mediater after the researcher returned from the mainland and ruin]- steadily in anticipation of the next visit. Libido is not the only behavioral attribute that is credited to the m tion of testosterone. however. Aggressiveness seems to be associnh .I with testosterone as well. Again the evidence is most convincing in :n u mals. Castration has been used to reduce the aggressiveness of domesti- animals for millennia. Testosterone replacement studies like those til. -I above show that restoring the testosterone levels of castrated male [.It'. increases the probability that they will fight with other males in prt in u tion to the close of hormone received. Demonstrating similar effects in humans, however. is more difficult. ,In the testosterone replaceIm-nt studies conducted in conjunction with the effort to develop a tonic: ceptive for males, subjects did not report any noticeable change in tin n subjective sense of aggressiveness or anger. Geriatric patients wltu t. ceive testosterone supplements to aid in the maintenance of I‘llllSt‘lt‘ l|-. THE BODY BUILDERS 265 Sue report increases in positive feelings and elevations of mood, not any increase in irritability or tendency toward aggression. It is possible, though, that we are searching under the wrong street lamp. it may be that testosterone contributes to a different set of behavv iorai attributes, one that can result in aggression under certain circum- stances, perhaps more reliably in some species than in others, but that does not necessarily produce aggression in the absence of suitable provo— cation. it may simply be the dramatic nature of animal aggression and Its unmistakable reduction following castration that attracted the atten- tion of researchers and the label of a testosterone-mediated behaviordln fact, in humans available data do suggest a relationship between testos— tcrone and something more like self-confidence or social assertiveness. I For instance, in a study of male testosterone levels and occupations, James Dabbs of the University of Georgia and his colleagues found that while professional football players have higher testosterone levels than ministers, professional actors' levels are higher still! Cause and effect are ' difficult to determine in a study of this kind, but high testosterone levels have repeatedly been associated with occupations and lifestyles that in~ volve risk'taking and assertiveness in social situations.___lt is easy to Imagine that self-confidence and social assertiveness could lead to higher rates of aggression if the provocation is there. A bolder, more Confident individual might be less likely to back down under a threat from another individual, and might even be more likely to engage in be. l'mvior that another could perceive as threatening in turn. in colloquial terms this kind of behavior is often associated with maleness and even mule genitals. in American slang, a man with this set of characteristics might be described as “having balls," or an action that requires the ex- pression of these traits as one that "takes balls.” Similar expressions oc— Car in many languages. But not all bold and assertive men are aggres- Ith‘, nor are all aggressive men naturally bold and assertive. Human aggression rises from the confluence of many physiological, psychologi— mi, and sociological springs. Self—confidence and assertiveness, however, are characteristics that 266 THE BODY BUILDERS can easily be associated with what in primate behavior studies goes by the name of social dominance. Dominance relationships among pri- mates that live in social groups can usually be discerned from patterns of dyadic behavior that may or may not involve aggression. Dominance may be established between two males by the outcome of one or more aggressive encounters, and it may later be contested or even reversed by new aggression. But the majority of dyadic encounters between males reveal the relationship by the ability of the dominant male to asserl himself and cause the subordinate male to retreat. The dominant male may assert himself at a food source, or claim proximity to a female, on simply approach a subordinate male and cause him to yield his sitting places'When the testosterone levels of monkeys are studied, the more dominant animals tend to have higher testosterone levels, although the correlation may not be perfect. Changes in dominance rank, howevel. are regularly accompanied by changes in testosterone levels in the same direction: the animal who goes up in rank goes up in testosterone while the animal who sinks in rank sinks in androgen level as well. In experi mental situations where previously unacquainted male macaques an- caged together, they quickly work out a dominant'subordinate relation ship, with the subordinate animal undergoing a significant decrease in testosterone level and the dominant animal a significant increase. Sim: lar patterns have also been observed among wild chimpanzees, our C11 in est primate relatives, when dominance relationships change within .. group. _ Changes in testosterone levels of a comparable kind can be ob served in human males following dyadic competitions in which there r. a clear winner and loser. The first demonstration of this phenomenon was by a Harvard undergraduate. Michael Elias, using as subjects llu members of the varsity wrestling team. He persuaded several memln-e of the team to allow him to draw samples of their blood immediately In- fore their matches, and again immediately after and an hour after II:- matches. Testosterone levels tended to be higher in all the wrestlers m. mediater after their matches compared to their pre-match baseline». In part this can be attributed to the physical exertion of wrestling. wlw l. THE BODY HL‘ILIHERS 267 tends to shunt blood away from the liver and to temporarily reduce the rate at which hormones are removed from the circulation. However, the wrestlers who won their matches showed significantly greater increases than those who lost, and an hour after the match the losers' levels were significantly below their preamatch baselines while the winners' were still above theirs. Elias suggested that these different testosterone pat« terns were responses to the psychological impact of winning or losing. This result has been confirmed and extended in numerous subse— quent studies. many of which have sought to rule out possible alterna' ' live interpretations. For instance, it was pointed out that varsity wres- tlers are often well acquainted with their opponents. either by prior experience or by reputation. Perhaps the losers expected to lose and hence didn't try as hard as they might have. Perhaps differences in lev— t'ls of physical exertion often distinguish winners from losers and are also correlaled with Ieslosterone changes. The same qualitative results l | L268 THE aonv BUILDER.“- are obtained, however, even when wrestlers are matched against oppo- nents they have never encountered or heard of. Nor is the phenome- non limited to contests involving physical exertion. Tournament chess matches also produce testosterone declines in the losers and rises in the winners. Even spectators, if sufficiently bound up in the vicarious expe- rience of their team’s fate, have been found to display similar changes in testosterone levels.'_Comparable changes have not been demonstrated in female competitors despite several investigations, a fact which simul- taneously implicates testicular production as the source of the differ ences in males and undermines the possibility that they derive from changes in clearance rates ofcirculating hormones due to physical exer tion. In one study, which involved collecting saliva samples from wres tiers every fifteen minutes after a match, the pulses of testosterone thal are a recognizable reflection of testicular production ceased for several hours in the losers while continuing in the winners. This finding sug gests that the divergence in testosterone levels between the contestani-. may be caused as much by the agony of defeat as by the thrill ofvictory In this study the testosterone levels of winners and losers were onu- more indistinguishable three hours after the match. Recreational com petition may have the advantage of transient effects. In a social situa tion such as a primate group where the same competitors may poreii tially renew their contest at any time, the effects may be longer lasting. ’In the case of the outcome of human contests or primate donu nance interactions, testosterone levels appear to be consequences of In- havior, not antecedents. It is possible, of course, that testosterone um be both and thereby help provide a loop by which past experience :il fects future behavior. In a primate group, for example, it may be adap tive for an animal that suffers repeated defeats in agonistic encounter. to adopt a less bold attitude, to assert himself less and give way to di um nant animals more readily. If conditions change, however, and the salni animal experiences a higher frequency of victories in unavoidable :lllt'l cations, it may be to his advantage—particularly in terms of :IL‘L‘L'M in food and mates—to be bolder and more assertive. Shifts in testosti-roiu levels may help to adjust these underlying behavioral tendencies with THE BODY BUILDERS 269 out predetermining an animal’s response to any particular situation. Similarly in humans, testosterone changes may reinforce the shifts in selfaconfidenee that can follow significant defeats and victories. There is already speculation that this phenomenon may contribute to slumps and streaks in athletic performance. It is tantalizing to imagine that tesv tosterone responses may play a similar role in the social World of human males as well, where competition may be more subtle but just as intense as in the wrestling ring. BE ALL THAT YOU CAN BE In addition to the behavioral effects of testosterone that may he of im- portance to male reproduction and the direct physiological effect of supporting sperm production, testosterone also has important physiw logical effects in promoting the production of muscle mass. This effect of testosterone has gained a certain notoriety through the use and mis- use of anabolic steroids by athletes. Testosterone is the original anabolic steroid (anabolism being the term for "building up" molecules, as op. posed to catabolism, the term for “breaking down" molecules). Testos‘ terone has been used directly as an anabolic hormone to promote mus- cle development in both male and female athletes and body builders. It has also been used to help geriatric patients maintain muscle mass and the strength and balance that come with it. Other anabolic steroids have been developed synthetically in an attempt to maximize muscle. promoting effects while minimizing other masculinizing effects, as well its to avoid detection in sports where steroid use is illegal. Controversies surrounding the use of anabolic steroids by athletes, especially in sports iiuch as track and professional football where they are prohibited, have surfaced repeatedly. The East German women’s Olympic team was criti— cited by other nations for using them, Ben johnson was stripped of his Olympic gold medal for steroid use, and Mark McGwire drew censure when he acknowledged that he had regularly used andtostcnedione, a Weak androgen of debatable effect, during his record—breaking home run season. Few knowledgeable observers doubt that National Foot— lmll League linemen regularly use anabolic. steroids to achieve bulk, | i no Il|l- "not mm III-11'. strength, and speed. Nor is there much doubt of their regular use in sports where they are not regulated, such as professional wrestling aml body building. Testosterone supports muscle building by promoting the uptake oi glucose and amino acids by muscle cells and their use in producing structural protein. This action can be contrasted with the action ol estradiol in promoting the uptake of glucose by fat cells. Prior to puberty boys and girls have quite similar amounts of muscle and fat on their bodies. But at puberty rising levels of the dominant gonadal steroids, testosterone boys, estradiol in girls, send their metabolisms in differ- ent directions._Boys continue to accumulate fat in absolute terms, it ecological circumstances allow, fat that they need to ensure their own survival in case of insufficient food. But excess energy is primarily di- rccted toward muscle growth. Girls continue to build muscle as they grow, but excess energy is primarily directed toward storage as fat. The resulting divergence of body composition is a consequence of both of these processes. In absolute terms, the average adult male carries a simi» lar amount of fat on his body as the average adult female, but his muscle mass may be twice as great. His frame is also larger on average. But even when we correct for differences in overall size, the large difference in body composition between males and females is more a function of dif— ferences in muscle mass than of differences in fat mass. The importance of testosterone in mediating changes in muscle mass can be vividly demonstrated by data derived from studies in which researchers used GnRH analogs to halt endogenous testicular hormone production and then later replaced the testosterone exogenously. Men who are deprived of their own endogenous testosterone in this way show decreases in protein production and protein turnover and loss of muscle mass and strength. At the same time, they show increases in fat deposition. Replacing the testosterone reverses these effects and leads to increases in muscle mass and strength. Similarly, exogenous supplementation of testosterone levels in older men leads to increases in muscle mass and strength and decreases in fat mass. Of course, testosterone alone doesn’t produce muscle. Two other el— IIII- 1mm I\I!I| III lr'. ."(I emcnts are important. Energy must be available to convert into muscle, and the muscle lnust. be used. A man who is starving will begin to catabolize his own skeletal muscle as a source of amino acids and energy to stay alive. In order to add to one’s muscle mass there must be energy available to devote to the task after other metabolic demands are met. Not only does muscle require energy to build, unlike fat it requires en; ergy to maintain as well. Skeletal muscle can account for 20 percent or more of a man’s basal metabolic budget, which is not a trivial fraction. Ounce for ounce, muscle is not as expensive to maintain as some other metabolically active tissues, such as brain, liver, or kidney, but it is more expensive to maintain than inert tissues such as bone or fat and some metabolically active tissues such as skin. More important, it is the meta! bolically active tissue that is most expendable and adjustable. It is not very feasiblew—nor would it be adaptive——to reduce one’s brain size or kidney size or skin coverage to cut metabolic costs if energy is in short supply. It is, however, possible to reduce muscle mass under adverse conr ditions and to build it up again under favorable ones. The mechanisms that link muscle anabolism to energy availability are simple. Muscle cells take up glucose in response to insulin secretion, which in turn is determined by energy availability. Testosterone acts to enhance this process, in part by contributing to the expression of insulin receptors by the muscle cells. Flexibility in muscle mass and its consequences for the overall met- abolic budget relate to the other requirement for building muscle: the muscle must be used. lfyou are planning to take anabolic steroids regu~ larly and then sit back and wait for your biceps to bulge, you are in for a disappointment. You still have to go to the gym and do biceps curls if you want results. Use of the muscle stimulates the production of the en— zyme systems necessary to build more contractile fibers and other func- tional elements of the muscle cell. Testosterone enhances this response but it can’t create the response where it doesn’t exist. Disuse of a muscle will send things in the other direction, causing atrophy of muscle tissue and loss of strength. Even the most muscular man will find his leg mus- cles wither appreciably if he has his leg in a cast for a month or more. I ."U IIII- liiiil‘i' I'llIII I'I I" The anabolic response of muscles to habitual use is muscle spei'iiii :I-. well. Exercising the biceps will not produce massive quadriceps. Wliwl chair marathoners simultaneously illustrate the effects of use and dismi- Their upper bodies are typically heavily muscled while their leg l'i'lllfit'lt". have often atrophied completer owing to disuse resulting from par:in sis. The body seems to adjust muscle mass rather naturally to meei llu' demands of habitual use. "Use it or lose it" is a principle that applii-u nicely to muscle in the interests of metabolic economy. Alas, if only ilu- same principle applied to fat! Testosterone, then, does not cause muscle to grow by itself. It en hances the body’s ability to accomplish this task when conditions illl' right, when energy is available, and when habitual use indicates that additional muscle mass would be functional. When men are matched for diet and exercise but given different doses of exogenous testosterone, higher testosterone results in faster muscle growth and greater eventqu muscle size. Differences in absolute testosterone levels between individ ual men do not always predict muscularity, however, since testosterone alone does not determine muscle growth. Men may differ in their exei' cise habits, their diets, or even their normal testosterone receptor den- sity in muscle tissue. As in the winners and losers of wrestling matches discussed abOve, the changes in level within individuals are of greater significance than the absolute levels. Large differences in absolute levels of testosterone, such as that between males and females, clearly make :i difference, however. Yet while the average difference in muscle mass between males and females is not particularly controversial, the functional reasons for the difference are more likely to be. One common assumption is that males are biologically endowed with a greater propensity to accumulate mus cle mass because the tasks they perform under the traditional sexual di» vision of labor require more strength. They must perform the heavy work, it is argued, while women are responsible for lighter work such as child care and food preparation. If such a division of labor has been typ— ical of human societies for the majority of our evolutionary history, the argument continues, men will have been selected for greater muscle I | ."!i l H”. Ilil'lll‘f lilJII 11! It'- mass. This characterization of the traditional division of labor often seems bizarre to those who have spent time with hunter'gatherers or subsistence agriculturalists. For example, Lese men in the Ituri Forest are responsible for clearing new gardens for planting, an activity that re- ' ~ ar, quires strenuous labor for several weeks. During the rest of the ye however, they can often be found resting in their hammocks while their wives carry firewood and water weighing nearly as much as themselves for long distances. Moreover, to the extent that labor tasks are’divide between the sexes on the basis of the strength required, it is as likely for such division to be the result of differences in muscle mass as it is for it to be the cause. ‘ I y perhaps the most telling observation is that differences inymus» cle mass are typical of many species where sexual division of labor is not an issue. In many other primates, for example, including common chimv panzees (Pan troglodytes), gorillas, baboons, and macaques, males hive significantly more muscle mass than females. Features of this type, c at: acteristic of one sex but not the other, are often the result of sexual se~ lectiori; these features contribute to the ability of individuals to curl:— pete with members of its own sex for opportunities to mate with L e opposite sex. The feature may be used to attract mates, like the ela‘oaf rate tail display of the peacock, or to fight with rivals, like the antlers o the deer. Very often both functions are served, since the other sex may find features attractive that provide the bearer with a competitive ad— vantage in direct struggle with members of its own sex. in cases of sex: ual selection among mammals it is most often males that are competing for access to females for the reasons discussed above, and primates are no exception. The muscle mass of males and the formidable canine teeth they often bear are used primarily in confrontations with conspev cific males, confrontations that can at times result in death. The keener the rivalry for mating the more exaggerated the development of these primary weapons. Where the rivalry is relaxed by eci'ilogical circum' ' - ’ ' cus stances, as among the pygmy chimpanzees, or bonobos (l an‘pams ), sexual dimorphism in muscle mass is also dramatically reduced.“ it is likely that the sexual dimorphism in muscle mass displayed by 274 THE BODY BUILDERS humans is one more example of sexual selection for competitive ability visva'vis other males. Perhaps males do not often come to blows over their prospective mates in the modern world (though this may happen more than we realize, as homicide statistics suggest), and perhaps women do not necessarily find muscular male physiques attractive (though the film and advertising industries are betting otherwise). It is easy to imagine, however, that physical strength may well have been important for male social dominance and mating opportunity in our evolutionary past, as it apparently is for our primate relatives in the present. MAKING AN EFFORT In previous chapters I have argued that variation in ovarian function helps to modulate female reproductive effort in humans, using the term “reproductive effort” in its technical sense. In females, reproductive el fort primarily takes the form of physiological investment of time and energy in the production and nursing of offspring. A similar argumenl can be made that variation in testicular function helps to regulate l'l'lilli' reproductive effort. For males, reproductive effort primarily takes the- form of the investment of time and energy in gaining mating opportunl ties. Some of this investment is behavioral, some physiological. Teslm terone contributes to both pathways by helping to modulate libido, or the motivation to pursue mating opportunities; by promoting self~cou fidence and the social assertiveness necessary to compete effectively lur mating opportunities with other males; and by helping to build most I: mass, which enhances male competitive ability. Increases in tesroin-i one within an individual appear to enhance all these elements of malt reproductive effort, while decreases lower them. Sperm production It mains largely unaffected since it is not the capacity for fertilization rim is costly or limiting in terms of male reproductive success, but rallu I gaining the opportunity to mate. - In the light of this understanding of testosterone and its eflei-Is. u- can examine patterns of variation in male testicular function aan Ilu u relationship to ecological and constitutional factors. We should ooh n THE BODY BUILDERS 2'25] the outset that that there is tremendous variation between individuals in testosterone levels, as much as a tenfold range, all of which is consid— ered “normal.” As with the variation in sperm counts noted above, the significance of these baseline individual differences in testosterone is not clear. Clinical research tends to treat variation in this broad “nor. mal’I range as inconsequential, concerning itself only with “abnormal” testosterone levels. From this perspective there is little notable varia: tion in testicular function among populations of healthy males since there is little variation in the frequency of abnormal testosterone read— ings. Among twenty'nine Lese and Efe males from the lturi Forest, for example, only one had a testosterone level that fell below the normal range. As a group, however, the lturi males had average testosterone levels that were significantly lower than males of similar age in Boston had. These differences were particularly great in the morning, when tes- tosterone levels tend to be high. Studies of a number of traditional soci- eties, including Tamang and Kami men in Nepal, IKung men in Bot- swana, Turkana men in Kenya, Aymara men in Bolivia, and Ache men in Paraguay, also document testosterone levels that are significantly lower on average than observed among populations in developed coun— tries, although the majority of individuals in all these populations fall within the “normal” range. As with ovarian function in Women, then, testicular function in men, indexed by testosterone levels, appears sus— ceptible of quantitative variation that is not pathological. Testicular function can be higher or lower, not just on or off. The causes of this quantitative variation in average testosterone levels between populations are more difficult to determine. Variation in energy expenditure does not seem to be associated with reduced testos- terone levels. Indeed, given the role of testosterone in supporting in- creases in muscle mass it would be odd if increases in habitual muscle rise resulted in lower testosterone. Neither does moderate variation in energy balance appear to lower testosterone levels. Among the Lese, for instance, the seasonal weight loss that produces significant changes in female ovarian function doesn‘t appear to have a similar effect on male Ivslostt'rooe levels. Nor do 'lbmang males in Nepal show any correla— 276 THE soot BUILDERS tion between testosterone levels and energy balance comparable to the variation in ovarian function documented among Tamang women. Chronic energy shortage lnay be a different. matter, however. All the populations mentioned above that have low average testosterone levels compared to Western populations also show evidence of chronic energy shortage both in terms of low levels of stored fat and in terms of their short stature as gauged by international growth standards. It would make sense, physiologically, for testosterone to correlate with long— term but not shortrterm energetic conditions._Short—term variation in energy availability may result in mobilization or storage of fat in males as i1 does in females. It would not be very adaptive to meet with such short term variation by alternately breaking down and building up muscle. Not only is it a much more expensive process, metabolically, than thr- drawing down and building up of fat reserves, but it also has appreciable effects on physical performance. Longer-term energy shortage. on 1hr other hand, may require a lowering of metabolic expenditures. Rr ducing muscle mass may be a step toward meeting such challenger. Long—term positive energy balance may similarly provide an opporlu nity to increase muscle mass and competitive ability. By this logic Ira tosterone should not show the sensitivity to acute energetic condition. that female ovarian function displays, but should track longerrterm i'll ergetic conditions instead, Whether we should also expect permanent developmental effect s oi energetic conditions on testicular function similar to those postulalul for ovarian function in females is less clear. For females, we noted ilm the metabolic costs of reproduction remain fairly inflexible. A sumll woman must invest nearly as much in the gestation and nursing ol In I offspring as a large woman, although these costs may represent a gram I fraction of her total metabolic budget. Chronic energy shortage dial in sults in small adult stature may require women to space births mum widely to maintain long-term energy balance and optimize their l'l'|IlH ductive effort. Therefore we expect chronic energetic conditions 1|..u result in slow growth and late maturation also to result in lower :I\"l‘| .l|'- female fecundity and ovarian function. In males the situation may lu somewhat different. Smaller adult stature may allow a male to maintain a higher percentage of muscle under conditions of energy shortage. A smaller man may be able to support more muscle than can a taller man under the same energy budget, and the same absolute amount of muscle will be a greater proportion of total mass on a smaller man. Reducing adult statute under conditions of chronic energy shortage may be part of an overall somatic strategy that allows a man to optimize his reproduc- tive effort as well as his survival. Age patterns of testicular function appear to be quite different from age patterns of ovarian function. For one thing, there is no equivalent to menopause in men. We noted in the previous chapter that female menopause is a consequence of a finite supply of oocytes. Male spera matocytes are continuously replenished by mitosis from the germinal epithelium of the semeniferous tubules, so there is no inevitable mov ment at which the supply runs out. That is not to say that testicular function shows no effects of age. Virtually every index of testicular func- tion declines with age in older men: sperm counts, sperm motility, res- tosterone levels, and, most notoriously, the ability to achieve and main— tain an erection. Many of the indiecs of testicular function that decline with age ap- pear to be correlated with general health and physiological robustness. [In this respect declining testicular function looks very much like an. other manifestation of general senescence. Men who remain healthy and physically vigorous into old age are more likely to maintain tes' ticular function at higher levels than men whose general health den clines more rapidly. Given this fact, it has been difficult to determine whether there is any underlying age-related decline in testicular func' tion that is independent of general senescence as the decline of ovarian function prior to menopause appears to be in women. Testosterone is a promising index of testicular function to assessI since the relevant data are easier to collect from large random samples than data on sperm count or potency, for example. There are problems to overcome with testosterone as well, however. For one thing, total testosterone, the illmsnrement usually made in blood, may be misleading since it com: THE aonr BUILDERS 27? 278 THE BODY BUILnERs bines a measure of free, biologically active hormone with a measure of protein'bound, inactive hormone. Salivary testosterone provides a very good index of free testosterone since only free testosterone passes through cell membranes to enter the saliva. and since it does so in near perfect equilibrium with free testos: terone levels in the blood. Levels of salivary testosterone in samples of men from the Boston area screened only to exclude illness or steroid medication decline quite steadily, nearly linearly in fact, from early adulthood on. The range of individual variability is, as noted previously. quite high, but the downward trend is highly significant and quite steep. Levels of salivary testosterone at the age of sixty are on average less than half of the levels at age thirty. In part this decline may reflecl changes in the ratio of bound to free testosterone. But. the frequency ol testosterone pulses declines with age as well, Suggesting that testoster- one production is also reduced. Salivary testosterone generally appears to decline quite linearly with age in other populations as well, although the slope of the declim- can vary a great deal. In some populations, however, the slope is so Hal that the decline is no longer significant. When this occurs it appears Io be associated with low testosterone levels in young adulthood, not high levels in old age. The Ache in Paraguay and the Tamang in Nepal cs hibit this pattern, for example. Comparing the age patterns of testosm one for Ache, Tamang, Lese, and Boston men indicates that the higlu-I the early adult testosterone level, the steeper the decline with age. Tlu: suggests that the decline in testosterone is more a function of variation in youth than variation in old age. Testosterone levels in older men LIII' much the same regardless of the population from which they are drawn Rather it seems that early maturing populations may reach levels oi II". tosterone early in adulthood that are difficult to Sustain. It remains nu clear whether the linear decline from such high early adult levels is in fact inevitable, or is merely a correlate of declining physical :u-Iivm with age in Western populations. Thinking about testosterone in terms of the regulation of |Il:llt‘ u productive effort may shed some light on the question of male “mull: THl—I sour BUILDERS 2?9 and reproductive maturation left unresolved a few chapters earlier. Prer sumably there is no fixed critical size for males to attain to be reproduc— tively successful. Other things being equal, bigger is better if bigger translates into superior competitive ability. Environmental constraints in terms of chronic energy availability, however, mean that bigger is not always better. For given environmental circumstances there is an opti' mal size allowing enough muscle to be maintained to enhance competi- tive ability without too great a sacrifice of survival probability. It is in a male's favor to grow as quickly as can be managed to this size and then to stop, putting available metabolic energy into muscle mass and the be— havioral components of reproductive effort. Under more stringent envi— ronmental conditions growth will be slower and final adult size smaller. Under more favorable conditions growth will be faster and final adult size greater. Because males are trying to be “as big as possible” rather than "big enough'I they grow for a longer time than females, two to three years longer on average, before shifting metabolic res0urces from growth to reproduction. Male stature is also more environmentally vari— able than female stature. Under the conditions of virtually unlimited energy availability that privileged populations enjoy in the modern world, growth appears to reach the limits of its flexibility. If, however, men were still to compete physically for mating opportunities, the stage would be set for the evolution of even greater male size and strength. There is much more that we need to know about the ecology of testicular function. But what we do know of that ecology seems to make sense as a mechanism to modulate male reproductive effort. The key is to realize that male reproductive success is tied to competition for mat— lug opportunities. Testosterone can be understood as a major regulator of male reproductive effort since it helps to modulate the motivation to ' Heel: mating opportunities (libido), the motivation to compete socially ' with other males (self—confidence and social assertiveness), and the al— luml ion of somatic resources to make such competitive engagement ef— lvrlive (muscle mass). Chronically favorable energetic circumstances I'lillauee all of these through raising testosterone levels, whereas I‘luonic energy shorl'ag‘ reduces them. Peak reproductive effort, as re— I I 280 THE BODY BUILDER'- flected in peak testosterone levels. occurs soon after the attainment cal physical maturity and declines as physical vigor declines. Other things being equal, young men have higher testosterone (and hence are ex peeted to have greater reproductive effort) that older men; men under chronically favorable energetic circumstances have higher testosterom- than men under unfavorable circumstances; healthy, vigorous men how- higher testosterone than do sick, inactive men. In general, however, ii“ men maintain sperm production as long as possible through all but trult T H E O W ‘ life-threatening emergencies, since the energetic requirements of sun J U R N E Y A N D T H E P R O C E b 5 I O N taining fecundity are so low. Hope, it seems, dies hard in the gonads ml the human male. ...
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ellison_chapter - I I) SAY THAT MEN AND WOMEN differ in...

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