Growth Hormone and Tendon and Ligament Injuries: Does it Work? by Jerry Brainum 12/25

 

 

Among bodybuilders and fitness influencers, human growth hormone has achieved near-mythical status as a muscle-building powerhouse. But Stuart Phillips, a muscle metabolism researcher at McMaster University, is calling foul on this widespread belief. In a pointed social media intervention, Phillips challenged the fitness community's fundamental assumption about GH.

His argument hinges on a simple question: If growth hormone truly builds muscle, what would we see in people with abnormal GH levels? The answer is revealing. People with growth hormone deficiency often develop dwarfism, but they typically show no signs of muscle wasting—their muscles are proportionally normal. Conversely, those with excess GH develop acromegaly, a condition characterized by enlarged hands, feet, and facial features due to overdeveloped connective tissue, rather than increased muscularity.

"Stop writing and saying that GH stimulates muscle growth," Phillips concluded bluntly. "It does not." The hormone stimulates collagen synthesis—the protein that makes up tendons, ligaments, and skin—but doesn't trigger the muscle protein synthesis that actually enlarges muscle fibers.

Phillips' conclusion—drawn from controlled laboratory studies—may not capture the full complexity of how growth hormone behaves in the extreme pharmacological context of elite bodybuilding. When combined with supraphysiological doses of anabolic steroids and insulin, GH may play a contributory role in muscle growth, though isolating its specific effect remains challenging.

The circumstantial evidence is striking. Following the widespread adoption of the "anabolic triumvirate" in the early 1990s, competitive bodybuilders began achieving physiques that surpassed those of previous generations. Competitors like Ronnie Coleman appeared onstage at contest weights exceeding 300 pounds with single-digit body fat percentages—sizes previously considered physiologically impossible.

However, these dramatic gains came with equally dramatic side effects. Many of these athletes developed severe abdominal distension despite maintaining extremely low body fat levels. Six-time Mr. Olympia Dorian Yates, competing later in his career, exhibited this characteristic protrusion, which he attributed to his use of insulin alongside growth hormone and anabolic steroids. 

The mechanism behind this distension remains a topic of debate. Insulin and GH both promote cell growth—potentially enlarging visceral organs, including the intestines, liver, and heart. Whether these same mechanisms contribute to skeletal muscle hypertrophy in this context, or whether the observed muscle growth stems primarily from the concurrent use of anabolic steroids, remains an open question that controlled research has yet to answer definitively.

Phillips also overlooked what happens when GH is provided to those who are clinically deficient in the hormone. A seminal study of GH published in 1990 involved providing GH to men shown to be GH-deficient. Within a short time after starting GH replacement therapy, all the men showed beneficial changes in body . . .