The field of pediatric exercise physiology is still an emerging science. Biological maturation and large variations in morphology of this group raise challenges in studying and describing physiologic responses in children and adolescents. Because of this variability, chronologic age is not a reliable means of comparison. Tanner staging has merit clinically, but not shown to be as reliable in exercise physiology. There is a lack of means to standardize measures for size and development. There are ethical aspects, which makes research in this population more challenging than its adult counterpart. Studies need to be appropriately designed with clear benefit outweighing risk in this vulnerable population. In fact, actual long-term risk of type of exercise may not be completely known.

The adolescent period appears to be unique because of the impact of the changing hormone milieu which is occurring. Prior to this period, the child’s growth is largely driven by growth hormones. During pubertal growth, reproductive hormones come into play. This change affects not only growth and development, but physiologic responses as well (Figure 4-1).

A clear understanding of factors that promote growth itself is lacking. However, physical development of organ systems such as the cardiac, ventilatory, and musculoskeletal are considered the driving force of physiologic improvement of performance and capacity in children. Acute and chronic exercise may stimulate growth factors by impacting binding proteins and receptor sites. Growth factor variations with exercise may be associated with nutritional variation resulting in biological markers of overuse.

Increased sex hormones present in puberty leads to a variety of changes in physiologic functioning that impact exercise performance. Exercise training has been associated with an inhibition of hypothalamic–pituitary–gonadal axis. This impact of regular exercise on reproductive functioning may be mediated by nutritional state, caloric balance, body composition, or some combination of these. Regular vigorous exercise has been shown to slow linear growth in gymnasts only. While the significance of this inhibition of hormones is not completely understood, low estrogen levels may have a long-term effect on bone development.

Metabolic pathways in response to activity are thought to vary with development of children. Anaerobic glycolysis progressively rises as children age, whereas aerobic metabolic capacity declines. These changes progress steadily throughout childhood without significant influence of puberty. The relationship of this phenomenon to body size mimics the pattern seen in adults.1

Exercise responses in children are often compared to adults based on current understanding of adult exercise physiology. There are variations in responses between these two groups. Some of this variation is present despite normalization for size. A summary of physiologic responses for children is listed in Table 4-1.

In spite of challenges in testing physiologic factors, studies have monitored responses to acute exercise. Many protocols exist for testing aerobic and anaerobic fitness. No single method is considered best. Exercise testing is limited by heterogeneity of techniques. Variations in physiologic responses to treadmill activity versus cycle ergometer have been described. Further, minute oxygen consumption (Vo2) is not directly related to treadmill grade and speed in children as is the case in adults.2 Lack of biomechanical familiarity with the treadmill may lead to metabolic inefficiencies. Also, relative perceived exertion scales do not correlate with exercise intensity in children, as they do in adults. Children do appear to recover faster from physical activity compared to adults. This faster recovery for children may be related to lower power generation.

Cardiovascular Responses

Maximal oxygen uptake (Vo2max) is a function of several body systems. Vo2max increases concomitantly with growth in children until age 18 in boys and age 14 in girls (Figure 4-2). Until age 12, absolute Vo2max values increase at the same rate in both genders, although boys have higher values as early as age 5. These values were significantly in excess of those recorded for average adult population. Bar-Or found that values in boys remained stable for ages 6 to 17, values in girls were less than those in boys and remain stable until age 11 or 12, then decline each year thereafter.1 Children between ages 6 and17 showed a mean anaerobic threshold of 58% Vo2max. For college age males, the mean was 58.6% Vo2max. Adult males had a mean of 49% to 63% Vo2max, and adult women had a mean of 50% to 60%.

The pattern of relative magnitude of cardiovascular response to progressive and sustained dynamic exercise appears to be qualitatively similar between adults and children. With Vo2max and anaerobic threshold as indicators of cardiovascular potential in childhood, these appear equal to that of adults. Stroke volume is increased in exercising children to match cardiac output to size and meet metabolic demands. At rest, heart rate accounts for matching metabolic demands. Heart rate response to maximal exercise is protocol dependent.

Resting heart rate declines during the course of childhood. Stroke volume increases in proportion to left ventricular size. While maximum heart rate remains constant during childhood, stoke volume during maximal exercise increases in proportion to body size and left ventricle size. Therefore, stoke volume serves as the determinant of increase in maximal cardiac output in the growing child.

Maximal cardiac output increases in proportion to Vo2 in absolute values. Vo2max remains stable during childhood. In females, maximal cardiac output may decline in relation to weight. Cardiac output in children is dependent on cardiac function. Circulatory adaptations to increased work are not affected by maturation. Myocardial oxygen uptake relative to heart mass at rest remains constant. Myocardial contractility is independent of age and maturation. Myocardial oxygen uptake during maximal exercise increases, as children grow, because of a rise in systolic blood pressure. Maximal oxygen consumption may be moderately heredity related, but left ventricle size is minimally influenced by genetics. No maturational changes occur in exercise myocardial function during childhood.

Maturational changes do not appear to affect myocardial performance or cardiac loading. Maximal stroke volume changes with age are a direct result of increased left ventricular chamber size. These changes are in direct relationship to body dimension. With aging, heart rate decreases because of intrinsic sinus node maturation. Resting cardiac output and Vo2max increase in absolute values but decline relative to body mass. Peripheral factors also play a role in meeting the demands of exercise. Arteriolar dilation in active muscle tissues will deliver increased blood flow to active muscle. The pumping action of the skeletal muscle will also augment the flow as well.

During submaximal activity, walking or running economy improves throughout childhood. Though the cause is unclear, this relationship holds for scaling for size. Improved coordination, substrate utilization, or elastic recoil forces may play a role. With increasing age in childhood, Vo2max at a given work intensity will decline. Endurance performance also improves with aging.

Cardiovascular responses to resistance exercise in children are similar to those in adults. Both systolic and diastolic blood pressures rise. Heart rate and cardiac output show limited changes. While the acute response to high-intensity physical activity is qualitatively similar to adults, there are quantitative differences. Children and adolescents have higher heart rates, a higher arterial-venous oxygen (a-vo2) difference, lower diastolic and systolic blood pressures, lower stroke volume, and lower cardiac output for any given level of Vo2max.

Ventilatory Responses

Much as there are similar qualitative responses of the cardiovascular system to exercise between children and adults, there are likewise similar patterns of responses in the ventilatory system. In response to the acute exercise bout, ventilation increases in children as in adults, however prepubertal children demonstrate certain anatomic and functional characteristics.

Childhood ventilatory responses to exercise include lower relative tidal volumes, higher breathing rates, higher ventilation rates (Ve), and higher ventilatory equivalents (Ve/Vo2) compared to adults. Thus, children have relative inefficiency in breathing compared to adults. However, children demonstrate more than adequate Vo2max and anaerobic threshold levels relative to body size, and qualitatively similar hemodynamic and ventilatory responses to acute exercise.

Children hyperventilate during exercise resulting in an increased ratio of minute ventilation to oxygen consumption at all intensities. Arterial concentration of carbon dioxide (PCO2) is lower. This results in greater pH at maximal exercise in children. Thus, ventilatory compensation appears exaggerated in the face of less lactate production. There is no understanding of these variations in children. This hyperventilatory response is less obvious as children grow, possibly owing to hormonal influence of puberty. Children breathe more rapidly and with greater frequency in relation to a given tidal volume. Less lung compliance and greater airway resistance in children may explain this response. In spite of this, normal arterial oxygenation is maintained at maximal exercise.