As a athlete, incorporating a growth hormone-like Ipamorelin is extremely beneficial. Not only in the development of lean muscle tissue and muscle mass, but also in the decreased recovery time you are going to experience after each workout. You can workout more, you can workout and lift harder, and you can increase your level of exertion at the gym to experience the greatest gains, as your body is going to heal much faster than it would without the growth hormone.
Background: The human growth hormone (hGH) has properties making it a potential candidate to treat obesity, however safety issues limit its long-term use. AOD9604 is a peptide fragment of the C-terminus of hGH (Tyr-hGH177-191), which harbors the fat reducing activity of hGH, without its negative effects. In this paper the safety data of AOD9604 obtained in clinical trials are summarized.
I'm new to the forum and there is some great information here that I need to do more reading on. I've been taking Ipam and ModGrf 1-29 for at least 2yrs now. The first thing I noticed is that I have good quality sleep. I have difficulty sleeping and staying asleep. I take these peps 20min before I go to bed and get a good deep sleep for at least most of the night. I take them before doing my morning cardio, after my workout (afternoon) and before I go to bed. I've read if you take it before your morning cardio it releases more FFA to burn during your session. After the workout to aid in recovery. Before bed to aid in a deeper sleep. It is important when you take them. Dont eat before morning cardio...no carbs/sugary drinks...3hrs should have passed before taking another shot and do not eat before 15-20min after taking the peps. The reason (I've read) to wait these times is to take them while your insulin levels are low. High Insulin levels will minimize the pulsation of the GH. The phrase I've read is to try to keep "insulin quiet" to maximize the pulse of GH. Ipam can work by itself but if taken with ModGrf 1-29 it will magnify the GH Pulse. ModGrf is useless by itself. I've read that there is a saturation dose, so more is not better. 200mcg for each should do the job. Since synthetic GH shuts down natural production, these peps stimulate the pituitary to pulse more natural GH. To get the maximum effect of syn GH, you would also take the shot at the same time discussed above. Once again, this is what I've read and the protocol that I've followed. The results arent like AAS (nothing is!) but it is a good way to feel better since I cant take TRT. (trying to have kids) I also travel with the peps bc I value the sleep that I get from it.
IGF-1 also increases the activity of muscle protein synthesis and the activity of muscle stem cells (also called satellite cells) for repair of damaged muscle. This is probably why intense weight training is one primary stimulus for a natural release of IGF-1 in muscle. As a matter of fact, exercise researchers have found that systemic IGF-1 normally produced in the liver isn’t even required for this type of muscle repair, as other IGF-1 forms produced by your own muscles during and post-exercise allows for adequate muscle tissue repair.
Resting plasma concentrations (mean±SEM) of mature ANP and Nt‐proANP were 14±2 pg/mL and 4±0.6 pg/mL at baseline. After gastric bypass surgery, the resting plasma concentrations rose to 24±5 pg/mL and 7±0.7 pg/mL for ANP and Nt‐proANP (increased by 23% and 43%), respectively (P=0.016 and 0.008). Absolute concentrations of ANP and Nt‐proANP were higher in individuals after bypass surgery at all acute time points during and after administration of intravenous saline (Figure 1A and 1B; P<0.001). A secondary analysis, adjusted for age, sex, and mean arterial pressure yielded similar results.
A synthetic analogue (AOD9604) of the lipolytic domain of human growth hormone (hGH) has been studied for its metabolic actions in obese Zucker rats. Daily treatment with an oral dose of AOD9604 of 500 microg/kg body weight for 19 days reduced over 50% (15.8 +/- 0.6 vs. 35.6 +/- 0.8 g) body weight gain of the animals in comparison with the control. The adipose tissues of the AOD9604--treated animals were found to have an increase in lipolytic activity. In contrast to chronic treatment with intact hGH, chronic treatment with AOD9604 showed no adverse effect on insulin sensitivity of the animals, as demonstrated with euglycemic clamp techniques. The results in the present study suggest that the analogue of the hGH lipolytic domain may have the potential to be developed into an orally usable and safe therapeutic agent for obesity.
Other studies have had similar results with regards to the effect of collagen supplementation in helping to promote fullness. One study consisted of 24 healthy adults testing the satiety effects of various protein supplements. The subjects had two breakfast meals with specific types of protein in each: one meal had alpha-lactalbumin, gelatin, or gelatin + tryptophan (TRP) (Breakfast 1) and the other meal contained casein, soy, whey, or whey + glycomacropeptide (GMP) (Breakfast 2). The study found that Breakfast 1, which included gelatin (collagen), was 40% more satiating than Breakfast 2, which did not contain gelatin or collagen. Additionally, the participants who ate Breakfast 1 with gelatin ended up consuming less calories for lunch. Researchers concluded that gelatin increases satiety, which can lead to subsequent reduced energy intake, thereby promoting weight loss (2).
Natriuretic peptide measurements were tested for normality and were logarithmically transformed for analysis. We used paired t tests to examine the change in BMI, blood pressure, and natriuretic peptides before and after surgery. Mixed effect models using all non‐missing data from 18 study subjects were used to assess the effects of surgery and intravenous saline and their interaction on plasma Nt‐proANP, Nt‐proBNP, and mature ANP and BNP levels, as well as echocardiographic measures. To account for repeated measures for each subject, a spatial power structure for ANP. Nt‐proANP, BNP, and Nt‐proBNP, and a completely general (unstructured) covariance matrix for echocardiographic outcomes were used. None of the interactions terms were significant and P values reported are based on models without interaction. A secondary analysis after covariate adjustment for age, sex, and blood pressure was also performed. All analyses were conducted using SAS (Cary, NC). A two‐sided P<0.05 was considered statistically significant for the primary outcome.
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