EXERCISE AND GROWTH
Cooper, D. M. (1994). Evidence for and mechanisms of exercise modulation of growth--an overview. Medicine and Science in Exercise and Sports, 26(6), 733-740.
The "anabolic effects" of exercise are defined as constructive or biosynthetic metabolic processes involved in tissue adaptation to physical activity. A sizable anabolic stimulus arises from the relatively modest physical activity of daily living. Excessive training may have adverse effects (it has been reported that a reduction of growth potential occurs in female gymnasts engaged in intense training).
Naturally occurring levels of physical activity, energy expenditure, and muscle strength exhibit some of their most rapid increases during childhood and puberty. Most children pass through activity phases that far exceed those of adults, and some biologically essential, minimal threshold of activity is reached by the vast majority of healthy children. The effects of exercise on somatic growth become important only if a child's level of activity (possibly due to social, psychological, or disease causes) falls below this biological threshold.
Exercise modulation of growth does not imply that increasing levels of physical activity will increase somatic growth in healthy children. Increases in heart mass or skeletal muscle mitochondrial density may have little impact on overall body size. Conflicting results have been obtained from studies done to test the effect of training on growth rates in children.
It may be useful to focus on exercise anabolic effects in terms of cardiorespiratory adaptation rather than somatic growth. There is evidence that an integrated cardiorespiratory and muscular response to exercise may be modulated by childhood patterns of physical activity and exercise. The time to respond to the onset of exercise and to recover is faster in children than in adults. These responses are also faster in lean children than those who are obese. This suggests that CO2 transport from cells to the lungs is delayed by the high solubility of CO2 in adipose tissue. This may also explain the differences in CO2 transport dynamics between adults and children since adiposity increases with age in adults. Children also work less efficiently in terms of oxygen cost of exercise than do adults.
Patterns of physical activity during childhood may affect the incidence and morbidity of disease later in life.
Peripheral mechanisms of exercise stimulation. Energy generated by exercise is transformed into signals that stimulate cellular anabolism at the site of the exercise. Physical stretch profoundly influences endothelial cell orientation and actin cytoskeleton organization. In exercising muscle, PO2 and pH are low and lactate concentrations are high. Similar conditions can be found in the interior milieu of wounds. The healing wound is characterized by new capillary and collagen formation which suggests that there is a parallel between wound healing and exercise-induced anabolism.
Central mechanisms. Physical activity is a naturally occurring stimulator of growth hormone (hGH) release into the circulation. hGH induces tissue production of IGF-1 (insulin-like growth factor 1) and elevations in serum IGF-1. An hypothesis exists that exercise induced hGH release is partly responsible--directly or indirectly--for anabolic effects of exercise. hGH plays an important role in anabolic effects of exercise, but the mechanism of regulation is not known. The role of the pattern of physical activity in the adult or developing child may prove to be particularly important. hGH given in pulses results in more and better growth than when it is given continuously. Thus, the body has a mechanism that pulses hGH rather than continuously introducing it into the system. It is intriguing to note that activity patterns in children are characterized by bursts of exercise, perhaps being a pattern that optimizes the anabolic effects of exercise in the growing child.
Both hGH -dependent and hGH -independent pathways likely exist and link exercise with tissue anabolism.
Nutritional factors. One possible mechanism that effects exercise-stimulated hGH release is diet. Glucose ingestion leads to hyperglycemia that inhibits hGH release. Meals high in fat could inhibit pituitary hGH release either by the direct effect of free fatty acids on the pituitary, or might cause release of gastric and pancreatic somatostatin. A single high-fat meal prior to exercise can interfere with performance and prolong the period of recovery.
Structure-function interactions. The athlete's heart is more massive in both absolute and normalized to body weight terms.
The combination of a high-fat diet and inactivity contributes to the development of obesity, hypercholesterolemia, hypertension, and coronary artery disease.
One could argue that there is no need in healthy children to attempt to impose patterns of physical activity since the natural inclination of children is to be active (they maximize the anabolic effects of exercise).
The use of growth promoting agents may have different long-term
physiological consequences in children compared with adults.
Drug use touted to boost body height, strength, and athletic prowess
in normal children and young adults should be construed as being
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