Growth Hormone (GH), IGF-1 & Exercise Interactions - Science Report

Growth hormone is a potent stimulus for increasing IGF-1 synthesis in the liver and muscles. Since intense heavy weight training, as practiced by most competitive bodybuilders, can promote increased GH secretion, does it also lead to higher levels of IGF-1?

Increased IGF-1 provides a definite advantage to body-builders seeking increased muscle size, because most scientists consider IGF-1 to be more anabolic than growth hormone itself.

Taking forms of growth hormone, like Humatropin, results in an increased blood level of IGF-1 within 12 to 24 hours following injection. So it would seem likely that under the aegis of intense exercise - a known - GH stimulator - IGF-1 levels would also likely rise.

A study published in the Journal of Applied Physiology (1995;79:1310-1315), however, refutes this notion. Using a group of seven experienced lifters, the study tested the GH/IGF-1 response of individuals to heavy weight training. The lifters followed a routine that worked all major muscle groups. As expected, they experienced an increased growth-hormone response after the workout.

However, the GH increase did not translate into increased IGF-1 secretion. The researchers checked for increased IGF-1 within 24 hours of the workout span during which IGF-1 theoretically should have peaked in response to the increased GH secretion triggered by the workout. But it didn't.

One explanation for this paradox involves the normal response pattern of GH after exercise. Unlike GH that has been injected, the natural secretion of GH is based on a feedback mechanism linking blood to the pituitary gland, the site of GH production. In short, when levels of GH increase in the blood, the increase is monitored by the pituitary, which responds by producing less GH- Because the GH level is now lowered, IGF-1 production is also curtailed. This contrasts with the exogenous administration of GH, where a higher blood level of GH for a longer time does promote IGF-1 release several hours later!

Another possible explanation is that the subjects, being experienced weight trainers, already produced great amounts of IGF-1, which may play a role in the repair of muscle fiber after intense exercise. Under this scenario, the subjects may have been used to the type of training involved in the study, which would have limited the subsequent release of IGF-1.

This theory is buttressed by the fact that the men also showed low blood levels of the enzyme creatine kinase, which is an indicator of muscle damage. Thus, their workouts didn't dam- age their muscles significantly enough to foster an IGF-1 repair response above normal.

The primary conclusion of this study is that IGF-1 may be independent of growth hormone.