It’s true—your genes can play a role when it comes to building muscle. In general, there are two types of muscle fibers: Type I, which are slow twitch, and Type II, which are fast twitch. Depending on which you have more of, you may have an easier or harder time gaining muscle. “Fast twitch muscle fibers are two times as thick as slow twitch muscle fibers, lending to the overall thickness of the muscle without any activity,” explains Lovitt. “Those people with a genetic predisposition of a high percentage of these fibers can increase muscle size very easily while the people with a higher percentage of slow twitch muscle fibers have to work really hard to put on mass.” It’s the reason why a world-class sprinter genetically has more fast twitch muscle fibers than a world-class marathoner—it comes down to what we’re born with.
Naturo Nitro Creatine Chrome could be an interesting choice for women. It’s actually magnesium creatine chelate, a type of creatine that may help to improve performance without increasing water weight. We don’t have a lot of studies on it just yet, but the research we do have suggests it could potentially be a good choice for women who want to improve performance without experiencing the “bloat” of regular creatine.
In a sample of people with colorectal cancer given creatine supplementation for 8 weeks to assess its interactions with chemotherapy, creatine failed to benefit muscle function or quality of life. Benefits were observed in body cell mass and phase angle (indicative of cellular viability), but only in the subsample with less aggressive chemotherapy.
In patients with DM1 given a short loading phase (10.6g for ten days) followed by a 5.3g maintenance for the remainder of an 8-week trial noted that supplementation resulted in a minor improvement in strength (statistical significance only occurred since placebo deteriorated) and no significant difference was noted in self-reported perceived benefits. Maintaining a 5g dosage for four months also failed to significantly improve physical performance (handgrip strength and functional tests) in people with DM1, possible related to a failure to increase muscular phosphocreatine concentrations.
Minor liver lesions (grade I, no grade II or III, pathology not indicative of toxicity) have been studied in SOD1 G93A transgenic mice (a research model for amyotrophic lateral sclerosis or ALS, but used in this study to assess a state of chronic pro-oxidative stress) for 159 days with 2% of feed intake and in CD-1 rats (seen as normal) over 56 days with 0.025-0.5mg/kg in CD-1 mice, although in Sprague-Dawley rats (normal controls) there were no significant differences noted even after 2% of feed intake for 365 days. These observations appear to be due to the strain of the rodents used, and human studies on amyotrophic lateral sclerosis (ALS; what the SOD1 G93A transgenic mice are thought to represent) lasting from nine to sixteen months with subjects supplementing with up to 10g of creatine daily have failed to find any abnormalities in serum biomarkers of liver or kidney health.
It is known that intracellular energy depletion (assessed by a depletion of ATP) stimulates AMPK activity in order to normalize the AMP:ATP ratio, and when activated AMPK (active in states of low cellular energy and colocalizes with creatine kinase in muscle tissue) appears to inhibit creatine kinase via phosphorylation (preserving phosphocreatine stores but attenuating the rate that creatine buffers ATP). While phosphocreatine technically inhibits AMPK, this does not occur in the presence of creatine at a 2:1 ratio. It seems that if the ratio of phosphocreatine:creatine increases (indicative of excess cellular energy status) that AMPK activity is then attenuated, since when a cell is in a high energy status, there is less AMP to directly activate AMPK.