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In this paper, we review the effects of caffeine on muscle strength and provide suggestions for caffeine supplementation in powerlifting competitions. The currently available studies indicate that caffeine ingestion may enhance strength in two powerlifting competition events, the squat and the bench press. For the deadlift, the same might be expected even though studies directly using this event are lacking. Optimal doses of caffeine are likely in the range from 2 to 6 mg·kg−1, and are highly individual. When using caffeine-containing capsules, 60 minutes pre-exercise seems to be a good timing of caffeine consumption. For other sources such as caffeinated chewing gum, a shorter period (5 to 10 min) from consumption to the start of the exercise seems to be effective. For shorter duration powerlifting competitions (e.g., 2 hours), one pre-competition dose of caffeine could be sufficient for acute performance-enhancing effects that might be maintained across all three events. For longer duration competitions (with longer rest periods between one repetition maximum attempts), there might be a benefit to repeated dosing with caffeine; for example, ingesting smaller doses of caffeine before each attempt or event. During training, powerlifters may consider ingesting caffeine only before the training sessions with the highest intensity. This approach might eliminate the attenuation of caffeine’s effects associated with chronic caffeine ingestion and would help in maximizing performance benefits from acute caffeine ingestion at the competition. Nonetheless, withdrawal from caffeine (e.g., no caffeine intake seven days before competition) does not seem necessary and may have some indirect negative effects.

Effects of resistance training on muscle strength and hypertrophy are well established in adults and younger elderly. However, less is currently known about these effects in the very elderly (i.e., 75 years of age and older). To examine the effects of resistance training on muscle size and strength in very elderly individuals. Randomized controlled studies that explored the effects of resistance training in very elderly on muscle strength, handgrip strength, whole-muscle hypertrophy, and/or muscle fiber hypertrophy were included in the review. Meta-analyses of effect sizes (ESs) were used to analyze the data. Twenty-two studies were included in the review. The meta-analysis found a significant effect of resistance training on muscle strength in the very elderly [difference in ES = 0.97; 95% confidence interval (CI) 0.50, 1.44; p = 0.001]. In a subgroup analysis that included only the oldest-old participants (80 + years of age), there was a significant effect of resistance training on muscle strength (difference in ES = 1.28; 95% CI 0.28, 2.29; p = 0.020). For handgrip strength, we found no significant difference between resistance training and control groups (difference in ES = 0.26; 95% CI − 0.02, 0.54; p = 0.064). For whole-muscle hypertrophy, there was a significant effect of resistance training in the very elderly (difference in ES = 0 30; 95% CI 0.10, 0.50; p = 0.013). We found no significant difference in muscle fiber hypertrophy between resistance training and control groups (difference in ES = 0.33; 95% CI − 0.67, 1.33; p = 0.266). There were minimal reports of adverse events associated with the training programs in the included studies. We found that very elderly can increase muscle strength and muscle size by participating in resistance training programs. Resistance training was found to be an effective way to improve muscle strength even among the oldest-old.

Purpose We aimed to perform a systematic review and meta-analysis of the effects of training to muscle failure or non-failure on muscular strength and hypertrophy. Methods Meta-analyses of effect sizes (ESs) explored the effects of training to failure vs. non-failure on strength and hypertrophy. Subgroup meta-analyses explored potential moderating effects of variables such as training status (trained vs. untrained), training volume (volume equated vs. volume non-equated), body region (upper vs. lower), exercise selection (multi- vs. single-joint exercises (only for strength)), and study design (independent vs. dependent groups). Results Fifteen studies were included in the review. All studies included young adults as participants. Meta-analysis indicated no significant difference between the training conditions for muscular strength (ES = –0.09; 95% confidence interval (95%CI): –0.22 to 0.05) and for hypertrophy (ES = 0.22; 95%CI: –0.11 to 0.55). Subgroup analyses that stratified the studies according to body region, exercise selection, or study design showed no significant differences between training conditions. In studies that did not equate training volume between the groups, the analysis showed significant favoring of non-failure training on strength gains (ES = –0.32; 95%CI: –0.57 to –0.07). In the subgroup analysis for resistance-trained individuals, the analysis showed a significant effect of training to failure for muscle hypertrophy (ES = 0.15; 95%CI: 0.03–0.26). Conclusion Training to muscle failure does not seem to be required for gains in strength and muscle size. However, training in this manner does not seem to have detrimental effects on these adaptations, either. More studies should be conducted among older adults and highly trained individuals to improve the generalizability of these findings.

Oriented fibres and materials based on orientated fibres have great potential for use in tissue engineering for tissues, where the arrangement of extracellular matrix is fundamental. The drawing method is based on mechanical pulling of a polymer solution out of its base droplet, resulting in a solidified fibre of determined geometrical characteristics. A new machine designed for lab scale drawing was invented enabling a repeatable quality of drawing conditions. The results demonstrate that it is possible to influence and define the fibre diameter and its distribution. From the in vitro experiments, it is evident that the aligned fibres guide the cell growth in the direction of the fibres. Moreover, the prepared fibres were functionalised with polypyrrole as an example of their versatility. These features make drawing an easy and suitable tool for the fabrication of scaffolds with a precise structure for tissues, e.g. nerve tissue.

Purpose: To explore the effects of 3 doses of caffeine on muscle strength and muscle endurance. Methods: Twenty-eight resistance-trained men completed the testing sessions under 5 conditions: no-placebo control, placebo control, and with caffeine doses of 2, 4, and 6 mg·kg−1. Muscle strength was assessed using the 1-repetition-maximum test; muscle endurance was assessed by having the participants perform a maximal number of repetitions with 60% 1-repetition maximum. Results: In comparison with both control conditions, only a caffeine dose of 2 mg·kg−1 enhanced lower-body strength (d = 0.13–0.15). In comparison with the no-placebo control condition, caffeine doses of 4 and 6 mg·kg−1 enhanced upper-body strength (d = 0.07–0.09) with a significant linear trend for the effectiveness of different doses of caffeine (P = .020). Compared with both control conditions, all 3 caffeine doses enhanced lower-body muscle endurance (d = 0.46–0.68). For upper-body muscle endurance, this study did not find significant effects of caffeine. Conclusions: This study revealed a linear trend between the dose of caffeine and its effects on upper-body strength. The study found no clear association between the dose of caffeine and the magnitude of its ergogenic effects on lower-body strength and muscle endurance. From a practical standpoint, the magnitude of caffeine’s effects on strength is of questionable relevance. A low dose of caffeine (2 mg·kg−1)—for an 80-kg individual, the dose of caffeine in 1–2 cups of coffee—may produce substantial improvements in lower-body muscle endurance with the magnitude of the effect being similar to that attained using higher doses of caffeine.

Purpose: To examine the acute effects of 3 doses of caffeine on upper- and lower-body ballistic exercise performance and to explore if habitual caffeine intake affects the acute effects of caffeine ingestion on ballistic exercise performance. Methods: Twenty recreationally active male participants completed medicine-ball-throw and vertical-jump tests under 4 experimental conditions (placebo and 2, 4, and 6 mg·kg−1 of caffeine). Results: One-way repeated-measures analysis of variance (ANOVA) with subsequent post hoc analyses indicated that performance in the medicine-ball-throw test improved, compared with placebo, only with a 6 mg·kg−1 dose of caffeine (P = .032). Effect size, calculated as the mean difference between the 2 measurements divided by the pooled SD, amounted to 0.29 (+3.7%). For the vertical-jump test, all 3 caffeine doses were effective (compared with placebo) for acute increases in performance (P values .022–.044, effect sizes 0.35–0.42, percentage changes +3.7% to +4.1%). A 2-way repeated-measures ANOVA indicated that there was no significant group × condition interaction effect, suggesting comparable responses between low (≤100 mg·d−1) and moderate to high (>100 mg·d−1) caffeine users to the experimental conditions. Conclusion: Caffeine doses of 2, 4, and 6 mg·kg−1 seem to be effective for acute enhancements in lower-body ballistic exercise performance in recreationally trained male individuals. For the upper-body ballistic exercise performance, only a caffeine dose of 6 mg·kg−1 seems to be effective. The acute effects of caffeine ingestion do not seem to be affected by habitual caffeine intake; however, this requires further exploration.

Background Currently, there are inconsistencies in the body of evidence for the effects of resistance and aerobic training on skeletal muscle hypertrophy. Objective We aimed to systematically review and meta-analyze current evidence on the differences in hypertrophic adaptation to aerobic and resistance training, and to discuss potential reasons for the disparities noted in the literature. Methods The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed for this review. The Downs and Black checklist was used for the assessment of methodological quality of the included studies. A random-effects meta- analysis was employed. In total, three analyses were performed: (1) for whole-muscle knee extensor data ; (2) for type I fiber cross- sectional area ; and (3) for type II fiber cross-sectional area. Results The final number of included studies in the present review is 21. All studies were of good or moderate methodological quality. The meta-analysis for whole-muscle hypertrophy resulted in a significant pooled difference (p < 0.001) in responses between the aerobic training and resistance training interventions. The pooled Hedge’s g, favoring resistance over aerobic training, was 0.66 (95% confidence interval 0.41–90 ; I2 = 0%). The meta-analysis for type I fiber cross-sectional area data resulted in a significant pooled difference (p < 0.001) between the aerobic training and resistance training groups. The pooled Hedge’s g, favoring resistance training over aerobic training, was 0.99 (95% confidence interval 0.44–1.54 ; I2 = 24%). The meta-analysis of type II fiber cross- sectional area data resulted in a significant pooled difference (p < 0.001) between the aerobic training and resistance training groups. The pooled Hedge’s g, favoring resistance training over aerobic training, was 1.44 (95% confidence interval 0.93–1.95 ; I2 = 8%). Conclusions The results of this systematic review and meta-analysis suggest that single- mode aerobic training does not promote the same skeletal muscle hypertrophy as resistance training. This finding was consistent with measurements of muscle hypertrophy both at the whole-muscle and myofiber levels. While these results are specific to the knee extensor musculature, it can be hypothesized that similar results would be seen for other muscle groups as well.

Neurofibromatosis type 1 (NF1) or von Recklinghausen's disease is one of the most common autosomal dominant inherited diseases in humans with an estimated birth incidence of 1/2500 and a disease prevalence of 1/3000-4000 (1). NF1 gene is located on the pericentromeric region of chromosome 17q11.2 (2). It is a megagene, spaning 350 kb of genomic DNA and consisting of 60 exons encoding an 11-13 kb GTPase activating protein – neurofibromin of 2818 amino acids (3,4). The mutation rate for NF1 gene is high. A half of all NF1 cases are familial, while the other half is caused by a new mutation (5). Genetic molecular testing confirms the disease’s existence but has no predictive value for its severity and course. In the past thirty years, the diagnosis of NF1 was made using a set of clinical criteria developed by the National Institutes of Health Consensus Conference, so called NIH diagnostic criteria (6). The diagnosis of NF1 is based on the presence of two or more of the following: 1) six or more cafe au lait macules, the greatest diameter of which is more than 0.5 cm in prepubertal patients and more than 1.5 cm in postpubertal patients; 2) two or more neurofibromas of any type, or one plexiform neurofibroma; 3) freckling in the axillary or inguinal region; 4) optic glioma; 5) two or more Lisch nodules; 6) a distinctive osseous lesion such as sphenoid dysplasia or pseudarthrosis; 7) a first-degree relative with NF1 according to the preceding criteria. However, the diagnosis cannot always be made in all children using the above mentioned criteria, especially in early childhood when the penetration of NF1 gene in usually not complete (7,8). The cranial magnetic resonance imaging (MRI) is the best method for showing many features of NF1, including optic pathway gliomas, brain tumors of various locations, brain stem tumors, and orbital neurofibromas. Most frequent brain changes in children with NF1 are areas of increased T2-weighted signal intensity – T2-hyperintensities or “unidentified bright objects,” as they usually cannot be visualized using T1-weighted imaging. T2-hyperintensities are age-related findings on MRI and have been observed in 43%-93% of children who suffer from NF1 (9-11). These lesions do not exert mass effect, contrast enhancement, or surrounding edema. They are most commonly found in the basal ganglia, thalamus, cerebellum, and brainstem (12). Former research on multiple T2-hyperintensities on brain MRI in children as diagnostic criterion for NF1 was contradictory and scarce (13-17). The aim of this cross-sectional study was to determine the prevalence, number, and location of multiple (≥2) brain T2-hyperintensities on MRI, and their correlation with age in children with NF1. A further aim was to determine the indicators of diagnostic accuracy of T2-hyperintensities in children of different ages, especially in the early age (from 2 to 7 years) when the NF1 gene penetration is still not completed.

Objective Neurofibromatosis 1 (NF1) is autosomal dominant inherited disorder often difficult to diagnose in children besause of its age-dependent presentation. The early diagnosis using National Intitutes of Health (so called NIH-criteria) cannot be made on the basis of routine clinical and ophthalmological examinations in all children, especially in patients of early age and in sporadic cases. T2-hyperintensities on brain MRI has been suggested as a new diagnostic sign. The aim of this study was to compare the degree of diagnostic accuracy T2-hyperintensity versus diagnostic accuracy NIH diagnostic changes. Methods We performed a cross-sectional study of 162 children with NF1 from Croatian Neurofibromatosis Association Database and 163 control children between the ages of 2 and 18 years who underwent brain MRI during twenty year period. In this study we used the basic reference standard – NIH diagnostic criteria for NF1 to determine or exclude a definitive clinical diagnosis of NF1. Results Multiple T2-hyperintensities on brain MRI had excellent diagnostic accuracy with the area under the ROC curve of 0.849, estimated on the whole group subjects aged 2–18 years. The diagnostic accuracy of T2-hyperintensities for NF1 were highest in the youngest age (2–8 years). At that age diagnostic accuracy of multiple T2-hyperintensities was significantly higher than diagnostic accuracy of majority of NIH-diagnostic signs – neurofibromas, freckling in the axillary or inguinal region, Lisch nodules, optic gliomas, a distinctive osseous lesions (p Conclusion Significant higher levels of multiple T2-hyperintensities in comparison to most of the NIH diagnostic criteria, especially in the early children's age, confirm of justifiableness of their inclusion in the major NF1 diagnostic criteria and the need to revise the current NIH diagnostic criteria NF1 in children.

MASA syndrome (OMIM 303350) is a rare X-linked recessive neurologic disorder, also called CRASH syndrome, spastic paraplegia 1 and Gareis-Mason syndrome. The acronym MASA describes four major signs: Mental retardation, Aphasia, Shuffl ing gait and Adducted thumbs. A more suitable name for this syndrome is L1 syndrome because the disorder has been associated with mutations in the neuronal cell adhesion molecule L1 (L1CAM) gene. The syndrome has severe symptoms in males, while females are carriers because only one X chromosome is aff ected. The aim of this report is to show similarities and diff erences in clinical manifestations between twins with the L1CAM gene mutation and to emphasize the importance of genetic counseling. Our patients were dizygotic twins born prematurely at 35 weeks of gestation. Pregnancy was complicated with early bleeding and gestational diabetes. Immediately after birth, hypertonia of lower extremities was observed in both twins. Sixteen-year clinical follow up showed spastic paraparetic form with shuffl ing gait, clumsiness, delayed speech development, lower intellectual functioning at the level of mild to moderate mental retardation, primary nocturnal enuresis, behavioral and sleep disorder (more pronounced in the second twin). Magnetic resonance imaging of the brain showed complete agenesis of the corpus callosum, complete lack of the anterior commissure, and internal hydrocephalus. Electroencephalograms showed nonspecifi c slower dysrhythmic changes. Kidney ultrasound showed mild dilatation in the channel system of both kidneys in both twins. Ophthalmologic examination was normal. Molecular genetic testing identifi ed homozygous intron 26 L1CAM gene IVS26-12G→A mutation in both twins. The mother is carrier of the same heterozygous mutations. In conclusion, our patients, fraternal twins, show similar clinical changes typical of the MASA syndrome. After identifying the specifi c genetic mutations, this family has become eligible for genetic counseling and informative for prenatal diagnosis., Sindrom MASA (OMIM 303350), nazvan još i CRASH sindrom, nasljedna spastička paraplegija 1 i Gareis-Masonov sindrom, je X-vezana, recesivno naslijedna bolest. Akronim „MASA“ opisuje četiri glavna klinička znaka - mentalnu retardaciju, afaziju, poremećaj hoda (shuffl ing gait ), pri čemu bolesnik hoda vrlo sporo, povlači stopala, a ne odiže ih od podloge i aducirane palčeve. Pogodniji naziv za ovaj sindrom je „L1 sindrom“. Ovo odstupanje je povezano s mutacijom gena L1CAM. Budući da je zahvaćen samo jedan X kromosom , u ovom sindromu nalazimo umjerene do teške simptome u muškaraca, dok su žene prenositeljice. Cilj ovog rada je pokazati sličnosti i razlike kliničkih manifestacija u blizanaca s mutacijom gena L1CAM i istaknuti važnost genetičke obrade bolesnika za genetsko savjetovanje obitelji. Naši bolesnici, dvojajčani blizanci, rođeni prijevemeno u 35. tjednu gestacije. Trudnoća je komplicirana ranim krvarenjem i gestacijskim dijabetesom. Neposredno nakon rođenja uočen je hipertonus donjih ekstremiteta u oba blizanca. U tijeku šesnaestogodišnjeg praćenja u kliničkom statusu pokazali su motoričko odstupanje u vidu spastičkog paraparetskog obrasca hoda, nespretnost, usporen razvoj govora, intelektualno funkcioniranje na razini blaže do umjerene mentalne retardacije, primarnu noćnu enurezu, poremećaj ponašanja i spavanja (više izražene u drugog blizanca). MRI mozga blizanaca pokazao je kompletnu ageneziju korpusa kalozuma, kompletni nedostatak prednje komisure i interni hidrocefalus. U EEG-u su, uz spori osnovni ritam, registrirane dizritmične promjene. Ultrazvuk bubrega blizanaca pokazao je umjerenu dilataciju kanalnog sustava oba bubrega. Oftalmološki pregled je bio uredan. Molekularnim genetičkim testiranjem utvrđeno je da su blizanci homozigotni nositelji mutacije IVS26-12G → A u intronu 26 L1CAM gena. Majka je heterozigotna nositeljica iste mutacije. Naši bolesnici, dvojajčani blizanci, pokazali su slične kliničke značajke tipične za sindrom MASA. Nakon utvrđivanja specifi čne genske mutacije ova obitelj postala je podobna za genetsko savjetovanje i informativna za prenatalnu dijagnostiku.

Neurofibromatoza tip 1 (NF1) jedna je od najčešćih autosomno dominantnih genetskih bolesti koja se očituje brojnim manifestacijama različitih organskih sustava. U ovom radu raspravlja se o učestalosti, kliničkom ispoljavanju i općim preporukama za liječenje brojnih promjena i komplikacija perifernog i središnjeg živčanog sustava u djece s NF-om1. Najčešći neurološki poremećaji NF-a1 u djetinjstvu su kognitivni deficiti i specifični poremećaji učenja (i do 80%). Periferni kutani /subkutani neurofibromi obično se javljaju u pubertetskom razdoblju, a pleksiformni neurofibromi kao prirođene lezije mogu prvih godina života biti nezamijećeni. Učestalost malignih tumora ovojnica perifernih živaca (neurofibrosarkoma ) u NF-u1 je veća nego u općoj populaciji – procjenjuje se na 2%-5%. Najčešće promjene mozga su multipli T2-hiperintenziteti prikazani na MRI-u mozga, od 43% do 93%, ovisno o dobi. Lokalizirani su najčešće u bazalnim ganglijima, moždanom deblu i malom mozgu. Njihov klinički značaj je nepoznat, pa odatle i naziv „neidentificirani svijetleći objekti“. Optički gliomi (pilocitički astrocitomi) najčešći su tumori mozga u djece s NF-om1. Njihova učestalost procjenjuje se na oko 20%. Drugi po učestalosti su tumori moždanog debla. Najčešći uzrok hipertenzivnog hidrocefalusa u djece s NF-om1 je stenoza akvedukta. Liječenje neuroloških komplikacija u djece s NF-om1 ne razlikuje se od istovrsnih neuroloških promjena u djece koja nemaju NF1., Neurofibromatosis type 1 (NF1) is one of the most common autosomal dominant genetic diseases with a variety of changes and complications of the peripheral and central nervous system. In this article we discuss the prevalence, clinical manifestations and general recommendations for the treatment of children with NF1. The most common neurological disturbances in NF during childhood are cognitive deficits and specific learning difficulties (up to 80 %). Peripheral cutaneous /subcutaneous neurofibromas are usually present in puberty, while plexiform neurofibromas, as inherited lesions in the first years of life, could remain unrecognized. Incidence of malignant peripheral nerve sheath tumors (neurofibrosarcomas) is higher in NF1 than in the general population, with an estimated value of 2%-5%. The most common brain changes are multiple T2-hyperintensities presented in 43% to 93% of children with NF1 age dependent. They are usually localized in basal ganglia, brainstem and cerebellum. Their clinical importance is still unknown which is why they are called „unidentified bright objects“. Visual pathway gliomas (pilocytic astrocytomas) are the most common brain tumors in children with NF1 with the prevalence of 20%. Second in the range are the brainstem tumors. Aqueductal stenosis is the most common reason for hypertensive hydrocephalus in children with NF1. The medical treatment of neurological complications in children with NF1 does not differ from the treatment of equivalent neurological changes in children without NF1.

Neurofibromatosis type 2 (NF2) is an autosomal dominant disease that predisposes to bilateral vestibular schwannomas (neurinomas), other central and peripheral nervous system tumours (multiple meningeomas and neurofibromas) and ocular abnormalities (cataract). The NF2 tumour suppresor gene is localised on chromosome 22q12 and encodes protein called schwannomin or merlin which is related to a family of cytoskeleton-to-membrane proteins linkers ERM (ezrin-radixin-moesin proteins). About 50% of all cases are new germline mutations, although about 20% of apparently sporadic cases represent somatic mosaicism. The majority of observed germline NF2 mutations are point mutations which result in schwannomin with an altered or absent C-terminal domain. NF2 has a variable clinical presentation, with two basic types: severe type having early onset and progressive growth of tumors and the milder type having later onset and less aggressive course. The genotype-phenotype correlations indicate a greater variability of clinical disease expression. In this paper we discuss the epidemiology, genetic and clinical characteristics, diagnostic criteria, investigations, screening for risk persons and recommendations for care and therapy of patients with NF2.