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The article reports on the influenza A (H1N1) virus which was first observed in the U.S. and Mexico in 2009. The virus was imported into New Zealand by a group of high school students returning from Mexico in April 2009. The students went through isolation quarantine which was conducted by government and health officials and other medical groups. The officials are closely monitoring the influenza A H1N1 virus to check if it would spread further to other countries.

It has become clear that circadian clocks in peripheral tissues play important functions. Disruption of the circadian clock in skeletal muscle, for example, results in insulin resistance, sarcomere disorganization, and muscle weakness 1 . Interestingly, cavefish, which exhibit a disrupted central clock, exhibit similar muscle phenotypes 2 , 3 , 4 , raising the question of whether they are caused by alterations to central or peripheral clocks. Here, we demonstrate a loss in clock function in the skeletal muscle of the Mexican Cavefish Astyanax mexicanus that is associated with reduced rhythmicity of a large number of genes and disrupted nocturnal protein catabolism. Some of the identified genes are associated with metabolic dysfunction in humans., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Physical inactivity is a scourge to human health, promoting metabolic disease and muscle wasting. Interestingly, multiple ecological niches have relaxed investment into physical activity, providing an evolutionary perspective into the effect of adaptive physical inactivity on tissue homeostasis. One such example, the Mexican cavefish Astyanax mexicanus, has lost moderate-to-vigorous activity following cave colonization, reaching basal swim speeds ~3.7-fold slower than their river-dwelling counterpart. This change in behavior is accompanied by a marked shift in body composition, decreasing total muscle mass and increasing fat mass. This shift persisted at the single muscle fiber level via increased lipid and sugar accumulation at the expense of myofibrillar volume. Transcriptomic analysis of laboratory-reared and wild-caught cavefish indicated that this shift is driven by increased expression of pparγ -the master regulator of adipogenesis-with a simultaneous decrease in fast myosin heavy chain expression. Ex vivo and in vivo analysis confirmed that these investment strategies come with a functional trade-off, decreasing cavefish muscle fiber shortening velocity, time to maximal force, and ultimately maximal swimming speed. Despite this, cavefish displayed a striking degree of muscular endurance, reaching maximal swim speeds ~3.5-fold faster than their basal swim speeds. Multi-omic analysis suggested metabolic reprogramming, specifically phosphorylation of Pgm1-Threonine 19, as a key component enhancing cavefish glycogen metabolism and sustained muscle contraction. Collectively, we reveal broad skeletal muscle changes following cave colonization, displaying an adaptive skeletal muscle phenotype reminiscent to mammalian disuse and high-fat models while simultaneously maintaining a unique capacity for sustained muscle contraction via enhanced glycogen metabolism.