Human and economic impacts of natural disasters: can we trust the global data?

Reliable and complete data held in disaster databases are imperative to inform effective disaster preparedness and mitigation policies. Nonetheless, disaster databases are highly prone to missingness. In this article, we conduct a missing data diagnosis of the widely-cited, global disaster database, the Emergency Events Database (EM-DAT) to identify the extent and potential determinants of missing data within EM-DAT. In addition, through a review of prominent empirical literature, we contextualise how missing data within EM-DAT has been handled previously. A large proportion of missing data was identified for disasters attributed to natural hazards occurring between 1990 and 2020, particularly on the economic losses. The year the disaster occurred, income-classification of the affected country and disaster type were all significant predictors of missingness for key human and economic loss variables. Accordingly, data are unlikely to be missing completely at random. Advanced statistical methods to handle missing data are thus warranted when analysing disaster data to minimise the risk of biasing statistical inferences and to ensure global disaster data can be trusted.

Biomarkers associated with lower limb muscle function in individuals with sarcopenia: a systematic review.

Lower limb muscle dysfunction is a key driver for impaired physical capacity and frailty status, both characteristics of sarcopenia. Sarcopenia is the key pathway between frailty and disability. Identifying biological markers for early diagnosis, treatment, and prevention may be key to early intervention and prevention of disability particularly mobility issues. To identify biological markers associated with lower limb muscle (dys)function in adults with sarcopenia, a systematic literature search was conducted in AMED, CINAHL, Cochrane Library, EMBASE, Medline, PubMed, Scopus, SPORTDiscus, and Web of Science databases from inception to 17 November 2021. Title, abstract, and full-text screening, data extraction, and methodological quality assessment were performed by two reviewers independently and verified by a third reviewer. Depending on available data, associations are reported as either Pearson's correlations, regression R2 or partial R2 , P value, and sample size (n). Twenty eligible studies including 3306 participants were included (females: 79%, males: 15%, unreported: 6%; mean age ranged from 53 to 92 years) with 36% in a distinct sarcopenic subgroup (females: 73%, males: 19%, unreported: 8%; mean age range 55-92 years). A total of 119 biomarkers were reported, categorized into: genetic and microRNAs (n = 64), oxidative stress (n = 10), energy metabolism (n = 18), inflammation (n = 7), enzyme (n = 4), hormone (n = 7), bone (n = 3), vitamin (n = 2), and cytokine (n = 4) markers) and seven lower limb muscle measures predominately focused on strength. Seven studies reported associations between lower limb muscle measures including (e.g. power, force, and torque) and biomarkers. In individuals with sarcopenia, muscle strength was positively associated with free testosterone (r = 0.40, P = 0.01; n = 46). In analysis with combined sarcopenic and non-sarcopenic individuals, muscle strength was positively associated with combined genetic and methylation score (partial R2  = 0.122, P = 0.03; n = 48) and negatively associated with sarcopenia-driven methylation score (partial R2  = 0.401, P < 0.01; n = 48). Biomarkers related to genetics (R2  = 0.001-0.014, partial R2  = 0.013-0.122, P > 0.05; n = 48), oxidative stress (r = 0.061, P > 0.05; n ≥ 77), hormone (r = 0.01, ρ = 0.052 p > 0.05, n ≥ 46) and combined protein, oxidative stress, muscle performance, and hormones (R2  = 22.0, P > 0.05; n ≥ 82) did not report significant associations with lower limb muscle strength. Several biomarkers demonstrated associations with lower limb muscle dysfunction. The current literature remains difficult to draw clear conclusions on the relationship between biomarkers and lower limb muscle dysfunction in adults with sarcopenia. Heterogeneity of biomarkers and lower limb muscle function precluded direct comparison. Use of international classification of sarcopenia and a set of core standardized outcome measures should be adopted to aid future investigation and recommendations to be made.

Carnosine in health and disease.

Carnosine was originally discovered in skeletal muscle, where it exists in larger amounts than in other tissues. The majority of research into the physiological roles of carnosine have been conducted on skeletal muscle. Given this and the potential for muscle carnosine content to be increased with supplementation, there is now a large body of research examining the ergogenic effects (or otherwise) of carnosine. More recent research, however, points towards a potential for carnosine to exert a wider range of physiological effects in other tissues, including the brain, heart, pancreas, kidney and cancer cells. Taken together, this is suggestive of a potential for carnosine to have therapeutic benefits in health and disease, although this is by no means without complication. Herein, we will provide a review of the current literature relating to the potential therapeutic effects of carnosine in health and disease.

ß-alanine supplementation improves in-vivo fresh and fatigued skeletal muscle relaxation speed.

PURPOSE: In fresh muscle, supplementation with the rate-limiting precursor of carnosine, ß-alanine (BA), results in a decline in muscle half-relaxation time (HRT) potentially via alterations to calcium (Ca2+) handling. Accumulation of hydrogen cation (H+) has been shown to impact Ca2+ signalling during muscular contraction, carnosine has the potential to serve as a cytoplasmic regulator of Ca2+ and H+ coupling, since it binds to both ions. The present study examined the effect of BA supplementation on intrinsic in-vivo isometric knee extensor force production and muscle contractility in both fresh and fatigued human skeletal muscle assessed during voluntary and electrically evoked (nerve and superficial muscle stimulation) contractions. METHODS: Twenty-three males completed two experimental sessions, pre- and post- 28 day supplementation with 6.4 g.day-1 of BA (n = 12) or placebo (PLA; n = 11). Isometric force was recorded during a series of voluntary and electrically evoked knee extensor contractions. RESULTS: BA supplementation had no effect on voluntary or electrically evoked isometric force production, or twitch electromechanical delay and time-to-peak tension. There was a significant decline in muscle HRT in fresh and fatigued muscle conditions during both resting (3 ± 13%; 19 ± 26%) and potentiated (1 ± 15%; 2 ± 20%) twitch contractions. CONCLUSIONS: The mechanism for reduced HRT in fresh and fatigued skeletal muscle following BA supplementation is unclear. Due to the importance of muscle relaxation on total energy consumption, especially during short, repeated contractions, BA supplementation may prove to be beneficial in minimising contractile slowing induced by fatigue. TRIAL REGISTRATION: The trial is registered with Clinicaltrials.gov, ID number NCT02819505.

Dose-Response of Sodium Bicarbonate Ingestion Highlights Individuality in Time Course of Blood Analyte Responses.

To defend against hydrogen cation accumulation and muscle fatigue during exercise, sodium bicarbonate (NaHCO3) ingestion is commonplace. The individualized dose-response relationship between NaHCO3 ingestion and blood biochemistry is unclear. The present study investigated the bicarbonate, pH, base excess and sodium responses to NaHCO3 ingestion. Sixteen healthy males (23 ± 2 years; 78.6 ± 15.1 kg) attended three randomized order-balanced, nonblinded sessions, ingesting a single dose of either 0.1, 0.2 or 0.3 g·kg-1BM of NaHCO3 (Intralabs, UK). Fingertip capillary blood was obtained at baseline and every 10 min for 1 hr, then every 15 min for a further 2 hr. There was a significant main effect of both time and condition for all assessed blood analytes (p ≤ .001). Blood analyte responses were significantly lower following 0.1 g·kg-1BM compared with 0.2 g·kg-1BM; bicarbonate concentrations and base excess were highest following ingestion of 0.3 g·kg-1BM (p ≤ .01). Bicarbonate concentrations and pH significantly increased from baseline following all doses; the higher the dose the greater the increase. Large interindividual variability was shown in the magnitude of the increase in bicarbonate concentrations following each dose (+2.0-5; +5.1-8.1; and +6.0-12.3 mmol·L-1 for 0.1, 0.2 and 0.3 g·kg-1BM) and in the range of time to peak concentrations (30-150; 40-165; and 75-180 min for 0.1, 0.2 and 0.3 g·kg-1BM). The variability in bicarbonate responses was not affected by normalization to body mass. These results challenge current practices relating to NaHCO3 supplementation and clearly show the need for athletes to individualize their ingestion protocol and trial varying dosages before competition.