The growth hormone (growth hormone, GH) is an important regulator of metabolism and plays a crucial role in the growth and development of our organism. GH is secreted in a pulsatile manner and the frequency of the peaks is influenced by numerous factors such as nutrition, sleep, exercise, stress and fasting.
In turn, GH synthesis and secretion are stimulated by the hypothalamic hormone GHRH (literally GH-releasing hormone) and ghrelin secreted mainly by the stomach, while hypothalamic somatostatin and insulin-like growth factor 1 (IGF- 1), whose production is stimulated by GH, are the main inhibitors of GH.
Muscle metabolism and effects of GH on muscle
The endocrine system is an essential regulator of muscle metabolism in both physiological and pathological conditions. Hormones such as GH and androgens are the main regulators of muscle metabolism; these hormones, in fact, act as anabolic factors – that is, they contribute to the synthesis and formation of complex molecules – and are important regulators of muscle mass. On the contrary, glucocorticoids have catabolic effects – that is, they demolish complex molecules – and induce the elimination of muscle proteins.
Regardless of the indirect anabolic effect of GH due to IGF-1, GH is also able to bind directly to a receptor found in myocytes – the cells of muscle tissue – thus activating specific enzymes (called Janus kinase 2 or JAK2). Testosterone Cypionate prescribed by the physicians for the bone and muscle development. You can find more details here https://hghtherapydoctor.us/product/watson-testosterone-cypionate/
Skeletal muscle is the main component of lean mass. Adults with GH deficiency may have reduced lean body mass compared to healthy individuals. Initial studies, supported by later research, suggest that this reduction is about 7-8%, corresponding to about 4 kg of lean tissue. The demonstrated changes in lean body mass in GH-deficient adults are also associated with a mild to moderate reduction in muscle strength.
Examination of the contractile properties of muscles in GH-deficient patients revealed that their muscles are significantly “faster”, suggesting an increase in the percentage of type II fibers – those muscle fibers capable of rapid contraction. However, studies of quadriceps muscle fiber morphology in GH-deficient adults found no difference between these patients and healthy subjects.
Due to the pulsatile secretion of GH, it is not easy to determine the changes in GH secretion in muscle atrophy induced by various conditions. However, even at a young age, GH deficiency syndrome and hypogonadism are associated with lower muscle mass, muscle strength and reduced physical performance, compared to healthy controls.
Finally, the so-called somatopause can occur in old age, which is one of the endocrine changes associated with aging, a stage in which there is a significant decline in plasma concentrations of GH and IGF-1. This decrease in GH secretion contributes to sarcopenia, or the loss of muscle mass.
Skeletal metabolism and effects of GH on bones
Both GH and IGF-1 have different effects on the skeleton throughout the life span, influencing bone formation and resorption.
In fact, GH is able to directly stimulate osteoblastogenesis – that is the production of osteoblasts, one of the four types of bone cells – and bone formation. Furthermore, osteoblasts produce and secrete IGF-1 under stimulation of parathyroid hormone (PTH). GH and IGF-1 stimulate linear growth, ie the increase in height in children, by acting on the growth plate. The “growth plate” is a thin layer of cartilage found in most bones, including long bones and vertebrae. In the “growth plate”, the chondrocytes, or cells of the cartilage tissue, proliferate and secrete the extracellular matrix (substance between the cells) of the cartilage. These processes generate new cartilage tissue, which is subsequently remodeled into bone. The net result is that new bone is progressively created on the “growth plate”, causing the bones to grow. GH acts precisely on the growth plate to stimulate the formation of new bone both through the increase of circulating IGF-1 and also locally.
