High-intensity interval training (HIIT) increases insulin-like growth factor-I (IGF-I) in sedentary aging men but not masters’ athletes: an observational study

Introduction: The aim of this investigation was to examine the impact high-intensity interval training (HIIT) on serum insulin-like growth factor-I (IGF-I) in active compared with sedentary aging men.

Methods: 22 lifetime sedentary (SED; 62?±?2 years) and 17 masters’ athletes (LEX; 60?±?5 years) were recruited to the study. As HIIT requires preconditioning exercise in sedentary cohorts, the study required three assessment phases; enrollment (phase A), following preconditioning exercise (phase B), and post-HIIT (phase C). Serum IGF-I was determined by electrochemiluminescent immunoassay.

Results: IGF-I was higher in LEX compared to SED at baseline (p?=?0.007, Cohen’s d?=?0.91), and phase B (p?=?0.083, Cohen’s d?=?0.59), with only a small difference at C (p?=?0.291, Cohen’s d?=?0.35). SED experienced a small increase in IGF-I following preconditioning from 13.1?±?4.7 to 14.2?±?6.0?μg·dl^?1 (p?=?0.376, Cohen’s d?=?0.22), followed by a larger increase post-HIIT (16.9?±?4.4?μg·dl^?1), which was significantly elevated compared with baseline (p?=?0.002, Cohen’s d?=?0.85), and post-preconditioning (p?=?0.005, Cohen’s d?=?0.51). LEX experienced a trivial changes in IGF-I from A to B (18.2?±?6.4 to 17.2?±?3.7?μg·dl^?1 [p?=?0.538, Cohen’s d?=?0.19]), and a small change post-HIIT (18.4?±?4.1?μg·dl^?1 [p?=?0.283, Cohen’s d?=?0.31]). Small increases were observed in fat-free mass in both groups following HIIT (p?d?=?0.32–0.45).

Conclusions: In conclusion, HIIT with preconditioning exercise abrogates the age associated difference in IGF-I between SED and LEX, and induces small improvements in fat-free mass in both SED and LEX.     

The insulin-like growth factor-I receptor: Implications for the aging process

Aging is associated with decreased levels of growth hormone and both circulating and local levels of insulin-like growth factor-I (IGF-I). The decline in IGF-I has been postulated to be important in both physiological aging and pathological states that are seen with aging. In parallel, inappropriate apoptosis is thought to play a role in some of these same processes. In experimental models, IGF-I signalling through the IGF-I receptor confers a protective effect from apoptosis. This review summarizes the results of studies documenting the IGF-I anti-apoptotic effect in neuronal model systems. The known downstream signalling cascades that mediate this signal are beginning to be elucidated; these include MAP kinase and Akt. In addition, IGF-I prevents the reduction of anti-apoptotic proteins of the bcl-2 family induced by hyperosmotic conditions in cultured neuronal cells. IGF-I has been shown to positively impact on tau, the microtubule-associated protein, possibly preventing the degradation of proteins that are associated with the neurofibrils seen in Alzheimer's disease. All of the studies to date support the hypothesis that appropriately high levels of IGF-I signalling prevent some of the processes associated with aging.