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Do Transitioned Athletes Compete at an Advantage or Disadvantage

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<strong>Tr<strong>an</strong>sitioned</strong> <strong>Athletes</strong> <strong>an</strong>d Competition 10<br />

glycogen utiliz<strong>at</strong>ion will be seen. Additionally, these studies suggest th<strong>at</strong> <strong>at</strong> the level of substr<strong>at</strong>e<br />

utiliz<strong>at</strong>ion E2 has a gre<strong>at</strong>er impact on CHO, as opposed to lipid, metabolism.<br />

Estrogen also acts as <strong>an</strong> <strong>an</strong>ti-oxid<strong>an</strong>t, <strong>at</strong>tenu<strong>at</strong>ing exercise-induced oxid<strong>at</strong>ive stress <strong>an</strong>d<br />

inflamm<strong>at</strong>ion (54, 84). Acute bouts of exercise increase reactive oxygen species production in<br />

hum<strong>an</strong>s (1, 24, 74). Increases in reactive oxygen species production leads to oxid<strong>at</strong>ive stress <strong>an</strong>d<br />

c<strong>an</strong> result in oxid<strong>at</strong>ive damage in muscle <strong>an</strong>d blood (1, 10, 55, 74, 97). Oxid<strong>an</strong>t induced muscle<br />

damage c<strong>an</strong> decrease muscle function <strong>an</strong>d result in muscle s<strong>or</strong>eness (24, 62) <strong>an</strong>d may also result<br />

in muscle f<strong>at</strong>igue (4), decreasing perf<strong>or</strong>m<strong>an</strong>ce capacity. In various cell lines, E2 inhibits reactive<br />

oxygen species gener<strong>at</strong>ion by inhibiting NADPH oxidase enzyme activity (50, 91). Similar<br />

effects of E2 to inhibit reactive oxygen species production have been found in <strong>an</strong>imal models as<br />

well (21, 32, 50, 54). However, acute increases in reactive oxygen species production during<br />

exercise stimul<strong>at</strong>e gene tr<strong>an</strong>scription to increase <strong>an</strong>tioxid<strong>an</strong>t enzyme content (77). In fact, despite<br />

acute bouts of exercise increasing reactive oxygen species production, trained individuals have<br />

lower levels of oxid<strong>at</strong>ive stress <strong>an</strong>d higher levels of <strong>an</strong>tioxid<strong>an</strong>t enzymes (14, 23, 59) as<br />

compared with their sedentary counterparts. These findings c<strong>an</strong> be interpreted in two ways. First,<br />

if estrogen acts to <strong>at</strong>tenu<strong>at</strong>e reactive oxygen species production, perhaps the oxid<strong>an</strong>t effect of <strong>an</strong><br />

acute bout of exercise is lower in women, as compared with men, resulting in lower muscle<br />

damage <strong>an</strong>d s<strong>or</strong>eness. On the other h<strong>an</strong>d, the effect of estrogen to <strong>at</strong>tenu<strong>at</strong>e reactive oxygen<br />

species production during exercise may result in a smaller adapt<strong>at</strong>ion to repe<strong>at</strong>ed bouts of<br />

exercise (i.e. endur<strong>an</strong>ce training) in women. Thus, estrogen plays <strong>an</strong> imp<strong>or</strong>t<strong>an</strong>t role in the<br />

regul<strong>at</strong>ion of substr<strong>at</strong>e metabolism during exercise as well as the oxid<strong>at</strong>ive stress response to<br />

exercise.<br />

5.0 H<strong>or</strong>mone Levels in <strong>Tr<strong>an</strong>sitioned</strong> Men <strong>an</strong>d Women Compared with Physically B<strong>or</strong>n Men<br />

<strong>an</strong>d Women<br />

The typical sex h<strong>or</strong>mone concentr<strong>at</strong>ions in tr<strong>an</strong>sitioned men <strong>an</strong>d women, as well as those<br />

from physically b<strong>or</strong>n men <strong>an</strong>d women are presented in table 3. When comparing the values,<br />

physically b<strong>or</strong>n women <strong>an</strong>d tr<strong>an</strong>sitioned women have very similar concentr<strong>at</strong>ions of both<br />

testosterone <strong>an</strong>d estrogen. However, tr<strong>an</strong>sitioned men appear to have higher estrogen <strong>an</strong>d<br />

Table 3: Testosterone <strong>an</strong>d estrogen concentr<strong>at</strong>ions in tr<strong>an</strong>sitioned men <strong>an</strong>d women as compared<br />

with physically b<strong>or</strong>n men <strong>an</strong>d women.<br />

Testosterone<br />

(nmol/L)<br />

Estrogen<br />

(pmol/L)<br />

Physically b<strong>or</strong>n men 22 + 6 96 + 12<br />

<strong>Tr<strong>an</strong>sitioned</strong> men 31 + 11 134 + 35<br />

Physically b<strong>or</strong>n women 1.6 + 0.6 161 + 55<br />

<strong>Tr<strong>an</strong>sitioned</strong> women 1.0 + 0.0 175 + 37<br />

D<strong>at</strong>a are me<strong>an</strong>s + SEM. D<strong>at</strong>a from Elbers et al. Am J Physiol Endocrinol Metab,<br />

1999; 276:E317-E325.<br />

testosterone concentr<strong>at</strong>ions as compared with physically b<strong>or</strong>n men. This is intriguing as it<br />

suggests th<strong>at</strong> tr<strong>an</strong>sitioned men may experience perf<strong>or</strong>m<strong>an</strong>ce benefits from higher levels of both<br />

testosterone (muscle strength <strong>an</strong>d mass) <strong>an</strong>d estrogen (increased reli<strong>an</strong>ce on lipid st<strong>or</strong>es during

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