Getting comfortable with a steady running routine is definitely something to be proud of, but when you're on that cardio grind day-in and day-out, you might be ready to change things up and take on a new challenge. Time to throw some strength training into the mix. It can be a little intimidating at first if you don't know where the hell to start, but understanding the basics can help you feel confident in your refreshed fitness routine.
A study showed that 100mg/kg creatine monohydrate daily over four months supplemented by boys with DMD is able to enhance handgrip strength in the dominant hand only (less than 10% increase) and increase whole-body lean mass. While the trend toward whole body strength reduction seen in placebo was ablated and there was no interaction with corticosteroids, this study failed to find an influence on activities of daily living or lung function. Elsewhere in children not on corticosteroids with DMD, supplementation of 5g creatine for eight weeks was confirmed to increase muscular phosphocreatine content and according to a manual muscle test (MMT) there was a significant improvement in muscular function relative to placebo, with more parents reporting benefit with creatine (53.8%) relative to placebo (14%).
One study investigating the effects of creatine supplementation on people with osteoarthritis undergoing knee arthroplasty (surgical procedure for osteoarthritis), who received creatine at 10g daily for 10 days prior to surgery and 5g daily for a month afterward, failed to find benefit with supplementation. This study failed to find any differences in muscular creatine stores or weight changes.
In regard to bioenergetics, phosphorylated cyclocreatine appears to have less affinity for the creatine kinase enzyme than phosphorylated creatine in terms of donating the high energy phosphate group (about 160-fold less affinity) despite the process of receiving phosphorylation being similar. When fed to chickens, phosphorylated cyclocreatine can accumulate up to 60mM in skeletal muscle, which suggests a sequestering of phosphate groups before equilibrium is reached. Cyclocreatine still has the capacity to donate phosphate, however, as beta-adrenergic stimulated skeletal muscle (which depletes ATP and glycogen) exhibits an attenuation of glycogen depletion (indicative of preservation of ATP) with phosphocreatine.
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.