Female athletes typically have a slightly higher resting HR and a lower systolic BP than male athletes. With exercise, female athletes exhibit a lower absolute change in their systolic BP.

While males typically have larger hearts at baseline, both males and female athletes demonstrate physiologic cardiac hypertrophy in response to training.

The mechanism for hypertrophy may be different in females compared with testosterone-driven muscle hypertrophy in males. Females have a higher Ca ²⁺ /calmodulin-dependent kinase (CaMK) and protein kinase B/glycogen synthase kinase-3-beta (AKT/GSK-3) pathway signaling as well as increased fatty acid metabolism, which may contribute more to female-specific physiologic cardiac hypertrophy.

Pathologic cardiac hypertrophy and arrhythmias are less common in female athletes and considered secondary to estrogen’s protective cardiac effects against harmful remodeling.

Gender differences in cardiac functioning and contribution to maximal oxygen consumption (VO ₂ max) may be more related to the larger size of male hearts that have greater stroke volume compared with smaller female hearts.

Beginning at around 2 years of age, male lungs are larger than female lungs even when normalized to height/length.

Females have smaller lung volumes and lower expiratory flow rates compared with males. In addition, with regard to total lung volumes, females have considerably smaller airways, which can contribute to expiratory flow limitations.

On approaching maximal exercise, females increase their end expiratory lung volumes back toward resting, hyperinflating their lungs in response to these expiratory flow limitations. Simultaneously, higher end inspiratory lung volumes are required to maintain tidal volume. Ultimately, the intensity of breathing is greater in females, approximately twice as high at maximal exercise.

The prevalence of arterial oxyhemoglobin desaturation is higher in females than in males owing to smaller lung volumes, smaller airways, lower resting diffusion capacity, and lower maximal expiratory flow rates.

Moreover, females experience less exercise-induced diaphragmatic fatigue.

17 β-estradiol promotes lipid oxidation during endurance exercise, and female athletes have been shown to have a greater dependence on lipid oxidation during endurance events. In addition, 17 β-estradiol promotes hepatic glycogen sparing.

This enhanced capacity of lipid oxidation, as well as a greater ability to maintain plasma glucose, may account for the ability of female athletes to outperform male athletes at very high distances.

Females have a lower leucine oxidation rate at rest and during exercise, which accounts for their lower protein requirements.

There is some evidence that female athletes do not obtain the same benefits from traditional carbohydrate loading compared with male athletes, and in fact need to ingest a proportionally higher amount of carbohydrates in order to gain the same effects.

Lower ferritin and total body iron tends to be associated with higher oxidative stress. Female athletes are frequently shown to have higher levels of reactive oxygen metabolites and lower iron stores than their male counterparts.

Throughout the menstrual cycle, from early follicular phase to luteal phase, total body water in females can increase by as much as 2 L. Females have been shown to have lower urine osmolality than do males at rest, with daily activities and with exercise, most likely owing to differences in arginine vasopressin (AVP) concentrations.

In a study of endurance cyclists matched for BMI and performance, no differences were observed in the ratings of thirst and thermal sensation or the rate of perceived exertion; however, marked differences were noted in terms of female cyclists having a greater total fluid intake, greater percentage of change in body mass, lower urine specific gravity of urine, and lighter color of urine.

Female athletes do not sweat as much as male athletes do, but they sweat over a greater proportion of their body. In general, studies have shown that females tend to overconsume water in relation to their body size and metabolic rate.

A study evaluating the relationship between blood lactate and cortical excitability during exercise revealed that females exhibited a significantly greater improvement in excitability of the primary motor cortex in response to increased lactate levels; this was attributed to the excitatory role of estrogens on the cerebral cortex.

Female athletes have been shown to have a similar composition of muscle fibers and enzymatic activity as their male counterparts do when involved with similar sports and activities; however, female muscle fibers are smaller.

Female athletes are able to achieve significant strength gains with training, but they cannot achieve the same strength levels or hypertrophy as a similarly sized and trained male athlete owing to the difference in testosterone.

Before puberty, both boys and girls have similar strength and joint laxity. At puberty, estrogen contributes to increased joint laxity in girls, while testosterone contributes to muscle hypertrophy in boys.

Certain studies have shown lower collagen synthesis in tendons of combined oral contraceptive users, although not all studies have reported differences in tendon properties across the menstrual cycle.

Some of the increased injury risk seen in female athletes after the age of puberty is attributed to lax joints and strength imbalance caused by these hormonal changes.

The incidence of gastrointestinal symptoms and complaints is higher in female endurance athletes.

In addition, studies have revealed a higher incidence of gastrointestinal ischemia in female athletes than in male athletes; however, the underlying pathophysiology remains unknown.

Low EA occurs when daily caloric intake does not meet the caloric expenditure needs of a female athlete. EA is the energy available for daily physiologic functioning after the body has used energy for exercise.

Reduction in total EA results in adaptations over time to conserve energy. Chronic reduction in EA can lead to suppression of metabolic and menstrual hormones.

In studies controlling for exercise levels, low EA alone is enough to cause amenorrhea, while restoration of the energy balance by meeting caloric needs is able to restore ovulation.

Reduction in the total available energy in terms of caloric intake may be intentional or unintentional. Female athletes may not be aware that increased activity levels require increased caloric intake and may inadvertently find themselves with low EA.

Low EA may also be the result of eating disorder concerns (for more information on eating disorders, see Chapter 27 : Eating Disorders in Athletes).

As caloric demands increase with activity, female athletes need to balance their EA by increasing caloric consumption.

Low EA leads to lower levels of menstrual hormones, which leads to menstrual dysfunction.

Menstrual dysfunction begins with suppression of progesterone levels resulting in a luteal phase that is <11 days.

Functional hypothalamic amenorrhea occurs when there is a disruption in gonadotropin-releasing hormone pulsatility; this disruption leads to decreased follicle stimulating hormone and luteinizing hormone levels and ultimately suppression of estrogen levels.

Menstrual dysfunction due to low EA has been studied and can be reversed with restoration of appropriate energy balance.

Suppression of menstrual hormones causes low BMD due to decrease in estrogen, androgens, insulin-like growth factor 1 (IGF-1), and growth hormone. Each of these hormones plays a role in increased bone deposition.

Reduction of caloric intake resulting in low EA further reduces BMD by restricting available nutritional resources to build new bone.

90% of peak BMD is achieved by the age of 18 years. Adolescence is a critical age for achieving optimum BMD. Disruptions in bone mass accrual during this critical time period can have lasting consequences.

American College of Sports Medicine (ACSM) defines low BMD as a Z score of <−1.0 in female athletes playing weight-bearing sports.

Low BMD places the athlete at a higher risk of stress injury.

Low BMD has been studied and shown to be reversible with restoration of EA.

The goal of screening is to identify athletes that have the triad, hopefully in the earliest stages, and intervene for treatment as well as to prevent future complications.

As EA has a substantial effect on the other two components of the triad, one may choose to focus on screening for EA or eating disorders during a female athlete’s preparticipation examination. Validated screening tools for EA and eating disorders include the Low Energy Availability in Females Questionnaire (LEAF-Q), Female Athlete Screening Tool (FAST), Brief Eating Disorders in Athletes Questionnaire (BEDA-Q), and the Athletic Milieu Direct Questionnaire (AMDQ).

The Female Athlete Triad Coalition suggests screening for the triad during the preparticipation examination (see Box 12.2 ). Most questions are incorporated into the AAP- and AAFP-recommended preparticipation forms.

Box 12.2

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