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In addition, GH stimulates the IRS1/Akt (Costoya et al., 1999; Consitt et al., 2017) and mitogen-activated protein kinase (MAPK) pathways which are thought to be the main pathways contributing to GH/IGF-1-induced muscle hypertrophy via p42/p44 and p38 pathways (Consitt et al., 2017) (Figure 1). Thus, while GH is a positive regulator of extracellular matrix (ECM) synthesis (Kragstrup et al., 2011) which is important in morphogenesis (Rozario and DeSimone, 2010), there is still debate surrounding its role in the regulation of muscle mass in adults; however what may be key is the lack of effect on muscle function regardless of its impact on growth pathways and MPS. In younger adults, exercise-induced GH release is relatively non-specific occurring in response to both RE and aerobic exercise (e.g., 60% VO2 max) (Godfrey et al., 2003). Given that estrogen stimulates post-RE myogenesis, decreased estrogen levels in post-menopausal women may be a contributing factor to the development of sarcopenia, diminishing the rate of muscle repair and adaptive capacity in older women (Thomas et al., 2010). HSPs act as an index of cellular damage and activate inflammatory cell populations (e.g., neutrophils and macrophages) thereby regulating the extent of inflammatory responses after muscle injury (Senf et al., 2013). Oestrogens are steroid hormones, primarily produced in the ovaries from testosterone via an aromatase enzyme, of which women have four times the amount compared with men, until the menopause (Hansen and Kjaer, 2014). Anabolic effects of AR and testosterone upregulation after RE occur through a combination of both genomic i.e., transcriptional capacity, and non-genomic i.e., translational efficiency, pathways (Kraemer et al., 2020).
In its binary form, IGF-I circulates with one of seven binding proteins whereas in its ternary form, IGF-I circulates with IGFBP-3 and its acid labile subunit (ALS). Finally, how the various splice variants and aggregates of GH are integrated within the larger web of hormonal and molecular signaling remains to be seen as various studies continue to unravel the complex nature of homeostatic regulation with acute exercise and chronic exercise adaptations. This is reflected in its close associations of blood lactate, that when lactate is elevated beyond the anaerobic threshold or is dramatically elevated with a resistance training workout, IGH is highly responsive (134, 142–145). It becomes apparent that understanding the role(s) of GH in responding to exercise stress and adapting to exercise training is still in its embryonic stage. While the GH responses to exercise has been characterized for decades understanding the many selective roles in metabolism and other physiological mechanisms related to acute homeostasis and repair and remodeling of tissues remain needed (94, 132–136). Chemical reduction of culture media from type II, but not type I, somatotrophs increases immunoreactivity (5X vs. 1.3X, respectively). But most important exercise-induced changes in GH bioactivity were experienced after 6 months of training (6 × 10 squat at 80% of 1 RM with 2 min rest between sets).
Circadian patterning and newly discovered variants of glucocorticoid isoforms largely dictate glucocorticoid sensitivity and catabolic, muscle sparing, or pathological influence. Growth hormones exhibit differential influences depending on the "type" of the hormone being assayed and the magnitude of the physiological stress. In fact, intermittent administration of glucocorticoids appears to promote sarcolemmal repair and muscle recovery from injury (232) and muscle performance (233). A peripheral clock system is present in a human adrenocortical cells where periodic oscillations of clock genes are influenced by glucocorticoids, mainly through GRα (230). Yet, glucocorticoid resistance may also be acquired and localized to the sites of inflammation (169) with pathological conditions (224).
— Tissue growth and regeneration is dependent primarily on the hGH/IGF-1 axis, whose mechanism of response to exercise is yet to be fully understood. In this study, after the wrestling training, cortisol level was found to have increased statistically significantly. — Cortisol is a catabolic hormone released from the adrenal cortex in response to emotional and/or physical stress; it enhances protein breakdown and inhibits its synthesis.
DNA binding domains and ligand binding domains between the AR and GR are 79 and 50% homologous. Non-genomic signaling occurs rapidly within seconds to minutes, much faster than classic genomic signaling which takes hours, and requires constant presence of androgens to maintain intracellular signaling. Thus, the RT stimulus is critical to activation of muscle tissue and the role of androgens in enhanced neural drive warrants further study. The androgen/AR complex serves as a transcription factor leading to protein synthesis with the help of co-activator proteins. However, RT studies in younger men and women show no changes in muscle T or steroidogenic enzymes (17, 31). These conflicting results demonstrate the complexity of hormonal responses and the likelihood several factors are contributing to the response.
IGF-1 binds to IGF-1R’s on skeletal muscle and signals for hypertrophy technically I think it’s a combination of hypertrophy and hyperplasia. Also, RE-induced IGF1-Akt activation phosphorylates AS160 (Akt substrate of 160 kDa) resulting in enhanced GLUT4 translocation and glucose uptake, reflecting the mediator role of IGF-1 in glycaemic control via insulin-IGF-1-Akt pathway activation in muscle (Kido et al., 2016). Similar to GH, IGF-1 alone stimulates the IRS1/Akt (Costoya et al., 1999; Consitt et al., 2017) and mitogen-activated protein kinase (MAPK) pathways which are thought to be main pathways contributing to GH/IGF-1-induced muscle hypertrophy (Consitt et al., 2017). In addition, IGFBPs are important in potentiating IGF-1 anabolic signaling. Indeed, circulating IGF-1 levels have even been shown to decrease during periods of active muscle building, likely due to a redistribution of IGF-1 from the circulation into the muscle (Arnarson et al., 2015). Like testosterone levels, older adults experience a lower basal level of IGF-1 (the so-called somatopause which refers to the diminishment of the GH-IGF-1 system) which attenuates post-RE levels of IGF-1 (Kraemer et al., 1999).
The actions of IGF-I are regulated by a family of binding proteins (IGFBPs 1–6), which can either stimulate or inhibit biological action depending on binding. All aspects from production, release, transportation, and tissue uptake to intracellular signaling affect the cell signaling and communication that govern basic activities of cells and coordinate all cellular actions. Hormones are largely responsible for the integrated communication network responsible for modulating cellular signaling for protein synthesis (165). The diurnal variations in the glucocorticoid receptor may serve to coordinate the reactivity of the target cells to cortisol (231).
Future trials are needed to clarify the effects of the oestrogens on muscle biology under different conditions e.g., phase of menstrual cycle, pre or post-menopause, and the response to nutrition (fasting/feeding) and exercise training (Hansen, 2018). For example, low estrogen in the early follicular stage, may negatively affect RE-induced increases in estrogen levels (Hansen et al., 2012), while, in the luteal phase where circulating progesterone is relatively high, may also counteract the sensitizing effects of estrogen on muscle impairing any benefit of acute RE-induced during these phases (Hansen, 2018). Conversely, impaired testosterone responsiveness to RE in older adults, likely attenuates the AR response, due to lack of testosterone mediated AR increases, and subsequently, limits muscle mass gains with RET.
It is possible that increased muscle steroidogenesis may be a mechanism to help counteract T reductions in older men undergoing RT but less likely in healthy, young men. The increased DHT and FT were related to increased isokinetic strength, muscle CSA, and power (30). This enzyme is present in skeletal muscle and circulating DHT can diffuse into muscle cells and bind to ARs with higher affinity than T.
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