PHYSIOLOGY

Physiology of Exercise



Physiology of Exercise

An important role for endogenous growth hormone (GH) in the physiology of exercise was first proposed more than 40 years ago when it was observed that increased circulating GH levels in response to exercise were followed by an increase in circulating free fatty acids. Hunter et al. hypothesised that through its lipolytic effect, GH could increase the availability to exercising muscle of oxidisable fat, potentially conserving glycogen stores and prolonging the ability to exercise. Other mechanisms through which GH could influence exercise performance increase increased delivery of glucose and oxygen, increased muscle strength, changes in body composition and more efficient thermoregulation.

Useful information can also be obtained from normal subjects by studying the effects of agents that suppress GH secretion and more indirectly by correlating the GH response to exercise with metabolic changes during exercise. Finally, we will also consider how supraphysiologic GH levels influences GH performance. This can be done by studying the effects of endogenous supraphysiologic GH production in the pathophysiologic model of acromegaly, or by studying the effects of supraphysiologic GH administration to normal subjects and to athletes. This is important in determining whether self-administration of GH by athletes is likely to improve performance.

The GH response to exercise

Exercise is the most potent physiologic stimulus to GH release. GH levels start to increase 10-20 min after the onset of exercise, peak either at the end or shortly after exercise and remain elevated for up to 2 h following exercise. The neuroendocrine pathways through which GH secretion is regulated during exercise are complex and poorly understood, but there is evidence that adrenergic, cholinergic and opioid pathways are involved. The physiologic mechanisms through which GH secretion increases during exercise are not known, but changes in body temperature, blood lactate levels  and pH have all been postulated.

Supporting a role of body temperature is the observation that the GH response to exercise is greatly attenuated during exercise in cold conditions and is proportional to core temperature. Against an effect of lactate are the observations that infusion of sodium l-lactate does not increase GH secretion [18] (although this experimental model differs significantly from an exercise -induced metabolic acidosis), and furthermore there is a linear increase in GH secretion with increased exercise intensity that can be observed before the lactate threshold is reached. There is little data concerning the effect of pH although one study has demonstrated reduced GH secretion in response to exercise following alkali infusion.

 Exercise exerts acute effects on other components of the GH/IGF-I axis. GH-binding protein (GHBP), total IGF-I, IGFBP-3, and acid-labile subunit (ALS) increase slightly during exercise, while IGFBP-1 increases following exercise and free IGF-I does not appear to change during or following exercise.

These observations are not altered following adjustment for changes in hydration status during exercise. IGF-I, IGFBP-3 and ALS circulate as a ternary complex and the observation that all three components increase in parallel with no change in free IGF-I, suggests that these effects occur due to mobilization of preformed intact ...