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Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.

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Creatine (Cr) is essential in safeguarding ATP levels and in moving ATP from its production site (mitochondria) to the cytoplasmic regions where it is used. Moreover, it has effects unrelated to energy metabolism, such as free radical scavenging, antiapoptotic action, and protection against excitotoxicity. Recent research has studied Cr-derived compounds (Cr benzyl ester and phos-pho-Cr-magnesium complex) that reproduce the neuroprotective effects of Cr while better crossing the neuronal plasma membrane and, hopefully, the blood-brain barrier (BBB). Intracellular levels of Cr can be increased by incubation with Cr or some of its derivatives, and this increase is protective against anoxic or ischemic damage. A large amount of experimental evidence shows that pretreatment with Cr is capable of reducing the damage induced by ischemia or anoxia in both heart and brain, and that such treatment may also be useful even after stroke or myocardial infarction (MI) has already occurred. Cr has been safely administered to patients affected by several neurological diseases, yet it has never been tested in human brain ischemia, the condition where its rationale is strongest. Phosphocreatine (PCr) has been administered after human MI, where it proved to be safe and probably helpful. Cr should be tested in the prophylactic protection against human brain ischemia and either Cr or PCr should be further tested in MI. Moreover, Cr- or PCr-derived drugs should be developed in order to overcome these molecules' limitations in crossing the BBB and the cell plasma membrane.

The present study aimed to evaluate the effects of two types of 9-month adapted physical activity (APA) program, based on a muscle reinforcement training and a postural training, respectively, on muscle mass, muscle strength, and static balance in moderate sarcopenic older women. The diagnosis of sarcopenia was done in accordance with measurable variables and cut-off points suggested by the European Working Group on Sarcopenia in Older People (EWGSOP). Seventy-two participants were randomly assigned to two groups: the muscle reinforcement training group (RESISTANCE) (n=35; 69.9 ± 2.7 years) and the postural training group (POSTURAL) (n=37; 70.0±2.8 years). Body composition, muscle mass, skeletal muscle mass index (SMI), and handgrip strength (HGS) were evaluated for sarcopenia assessment, whereas Sway Path, Sway Area, Stay Time, and Spatial Distance were evaluated for static balance assessment. Sixty-six participants completed the study (RESISTANCE group: n=33; POSTURAL group: n=33). Significant increases of muscle mass, SMI, and handgrip strength values were found in the RESISTANCE group, after muscle reinforcement program. No significant differences appeared in the POSTURAL group, after postural training. Furthermore, RESISTANCE group showed significant improvements in static balance parameters, whereas no significant differences appeared in the POSTURAL group. On the whole, the results of this study suggest that the APA program based on muscle reinforcement applied on moderate sarcopenic older women was able to significantly improve muscle mass and muscle strength, and it was also more effective than the applied postural protocol in determining positive effects on static balance.

Some derivatives more lipophylic than creatine, thus theoretically being capable to better cross the blood-brain barrier, were studied for their protective effect in mouse hippocampal slices. We found that N-amidino-piperidine is harmful to brain tissue, and that phosphocreatine is ineffective. Creatine, creatine-Mg-complex (acetate) and phosphocreatine-Mg-complex (acetate) increased the latency to population spike disappearance during anoxia. Creatine and creatine-Mg-complex (acetate) also increased the latency of anoxic depolarization, while the delay induced by phosphocreatine-Mg-complex (acetate) was of borderline significance (P = 0.056). Phosphocreatine-Mg-complex (acetate) significantly reduced neuronal hyperexcitability during anoxia, an effect that no other compound (including creatine itself) showed. For all parameters except reduced hyperexcitability the effects statistically correlated with tissue levels of creatine or phosphocreatine. Summing up, exogenous phosphocreatine and N-amidino piperidine are not useful for brain protection, while chelates of both creatine and phosphocreatine do replicate some of the known protective effects of creatine. In addition, phosphocreatine-Mg-complex (acetate) also reduced neuronal hyperexcitability during anoxia.

Given the wide variety of conditioning program trainings employed, the present study compared the catabolic effects induced by CrossFit® and resistance training in moderately trained subjects. Twenty males joined either the CrossFit® group (n = 10; 30 min/day of “workout of the day”) or the resistance training (RT) group (n = 10; 30 min/day of resistance exercises) thrice a week, for 8 weeks. Salivary levels of cortisol, interleukin 1-beta (IL-1β), and uric acid were assessed via enzyme-linked immunosorbent assays before (PRE) and 30-min after (POST) SESSION 1 and SESSION 24. Variables’ percentual changes were computed as (POST-PRE)/PRE*100 in each session (Δ%). CrossFit® acutely increased cortisol levels in both sessions, with a significant decrease in Δ%cortisol from SESSION 1 to 24. In the RT group, cortisol values decreased in both sessions, only acutely. A significant decrease in IL-1β levels was registered acutely in both groups, in both sessions, whereas Δ%IL-1β was not different between the two groups. While uric acid levels increased in both groups acutely, a chronic downregulation of Δ%uric acid, from SESSION 1 to 24, was appreciated for the RT group only. Overall, CrossFit® appeared to induce more intense effects than the RT program as to the investigated catabolic responses.