Another part of training isn't just doing the exercises, it's resting between the exercises. This comes with experience, but the general rule is, the higher the reps, the shorter the rest. So, if you're doing 15 reps, you might rest about 30 to 60 seconds between exercises. If you're lifting very heavy, say 4 to 6 reps, you may need up to two or more minutes.
Creatine is normally metabolized into creatinine (note the difference in spelling), which is eliminated by the kidneys under normal conditions. When the kidneys fail and cannot clear the blood as effectively, many metabolites get “backlogged” in the blood. Creatinine is easy to measure and as such it is a biomarker of kidney damage. If serum creatinine levels are elevated, the doctor may suspect some kidney damage. Low-dose creatine (≤5 g/day) may not cause alterations in this biomarker in otherwise normal adults but high doses of supplemental creatine may cause a false positive (an increase in creatinine, due to creatine turning into creatinine, which does not signify kidney damage) and is a diagnostic error. Most studies, however, have noted only a small increase in creatinine levels even with doses ≈20 g/day.
Beach muscles and Olympic lifts draw more attention. But the many little stabilizer muscles around your shoulders, hips, and midsection — collectively the core — provide a strong foundation. Challenging the stability and mobility of these key muscles with medicine balls, physioballs, mini-bands, and rotational movements (lifting, chopping) pays huge dividends.
Studies of so-called "smart drugs" have also been taken out of context. Some "smart" nutrients, available over the counter, are marketed as a way to "increase mental focus and concentration during training." The problem is that the studies they're based upon involved either animals or people with brain pathology. In normal people the effects of smart drugs remain unproven, except anecdotally.
In general, muscle content of creatine tends to be elevated to 15-20% above baseline (more than 20mM increase) in response to oral supplementation. People who get a sufficiently high influx of creatine are known as responders. A phenomena known as “creatine nonresponse” occurs when people have less than a 10mM influx of creatine into muscle after prolonged supplementation. Quasi-responders (10-20mM increase) also exist. Nonresponse is thought to explain instances where people do not benefit from creatine supplementation in trials, since some trials that find no significant effect do find one when only investigating people with high creatine responsiveness. There are clear differences between those who respond and those who do not, in regard to physical performance. People who are creatine responsive tend to be younger, have higher muscle mass and type II muscle fiber content, but this has no correlation with dietary protein intake.
Several review studies assessing the safety of creatine supplementation tend to make note of increases in formaldehyde and possible carcinogenic results. Specifically, creatine is metabolized into an intermediate called methylamine, which can be converted to formaldehyde by the SSAO enzyme. An increase in urinary formaldehyde has been noted in youth given 21g of creatine for one week, during which both methylamine (820% increase) and formaldehyde (350%) were increased, relative to control. However, a more prolonged study using 300mg/kg (loading dose of around 20g) in adults for ten weeks failed to replicate these effects.
Increasing creatine levels in skeletal muscle to 687% of baseline (0.5mM creatine, thought to be equivalent to 5g creatine) doesn’t seem to per se increase glucose uptake, but increases glucose oxidation (140% of baseline) which is due to a two-fold increase in the activity of α1 and α2 subunits of AMPK, a potency comparable to 1mM of the reference drug AICAR. Glucose uptake associated with AMPK has indeed been noted in diabetic people who are undergoing physical exercise and in contracting skeletal muscle cells, but according to rat and in vitro studies of cells not being contracted, this is not a per se effect of non-exercising tissue but an augmentation of exercise-induced glucose uptake.
Due to the growing concerns of the high cost, health consequences, and illegal nature of some steroids, many organizations have formed in response and have deemed themselves "natural" bodybuilding competitions. In addition to the concerns noted, many promoters of bodybuilding have sought to shed the "freakish" perception that the general public has of bodybuilding and have successfully introduced a more mainstream audience to the sport of bodybuilding by including competitors whose physiques appear much more attainable and realistic.
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter. In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency. More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources is the major source of neural creatine. However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded. These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.