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During puberty in females, follicle-stimulating hormone and luteinizing hormone cause estrogen production from the ovaries, which in turn instigates pelvis broadening, increased bone growth, targeted fat depot sites, and breast development. However, puberty in males is the result of these hormones causing testosterone production from the testes, which upregulates bone formation and muscle mass as well as increases erythropoietin production from the kidneys. One can infer why sexually divergent responses to exercise are present for both cardiovascular and skeletal muscle systems in the human body. Perhaps the greatest impact of sex differences in exercise responses may be seen in a population of individuals with chronic diseases (i.e., hypertension), since exercise may be as beneficial to a particular sex as pharmacological interventions (or even more). This entry presents some of the recent data detailing sex differences in response to acute and chronic resistance and cardiovascular exercise. Because cardiovascular disease (CVD) is associated with the greatest morbidity and mortality worldwide and there are sex differences in the treatment of the disease, the entry also delves into the effects of exercise on resting hemodynamics and vascular responsiveness in a hypertensive cohort.

Muscle Responses

In relation to acute exercise, males and females exhibit similar mechanisms of motor control and similar muscle quality and show no difference in lower body muscle strength when it is expressed relative to body weight. However, women have been shown to possess less upper body strength than their male counterparts. Yet women show greater resistance to fatiguing contractions, which may in part be the result of increased muscle blood flow during contraction and the differential responses in muscle metabolism between males and females. Since women have less muscle mass, the muscle contraction may not occlude blood flow, thus enabling the muscle to maintain the exercise longer than in males. Another potential mechanism may be a difference in motor unit discharge rate as women have greater recruitment synergism and relative muscle activation of the muscle compartment than age-matched men and a lower rating of perceived exertion during the task. In relation to muscle mass, older women may show a blunted response to hypertrophic resistance training that may be related to an attenuation of protein synthesis. Further data to support this evidence suggest that women have decreased muscle protein synthesis following the ingestion of a meal. However, even though women have less muscle mass on average, they still show considerable strength gains following a progressive resistance training regimen. On the whole, women show greater fatigue resistance to acute exercise; however, they exhibit a resistance to skeletal muscle hypertrophy via an attenuation of protein synthesis with resistance training compared with men.

Cardiovascular Responses

Women are consistently improving their world records in events that are related to cardiovascular fitness (e.g., track and field and marathoning), thereby decreasing the time gap between sexes. The cardiovascular responses to acute exercise show dissimilarities that are mostly reflective of stature and mass differences between the sexes. Women show higher heart rates yet similar cardiac output responses at relative and absolute submaximal loads, respectively. Women show no difference in maximal heart rates; however, they have a lower stroke volume due to the sheer size of the heart. On average, women have lower hemoglobin content and less potential for increasing the arterial to venous oxygen difference. These factors along with the fact that women have more sex-specific body fat storage translate into a Vo2max (maximal oxygen uptake) that is 70% to 75% that of their male counterparts.

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