Skeletal muscle contains intramyocellular lipid droplets within the cytoplasm of myocytes as well as intermuscular adipocytes. These depots exhibit physiological and pathological variation which has been revealed with the advent of diagnostic imaging approaches: magnetic resonance (MR) imaging, MR spectroscopy and computed tomography (CT). CT uses computer-processed X-rays and is now being applied in muscle physiology research. The purpose of this review is to present CT methodologies and summarize factors that influence muscle radiation attenuation, a parameter which is inversely related to muscle fat content. Pre-defined radiation attenuation ranges are used to demarcate intermuscular adipose tissue [from −190 to −30 Hounsfield units (HU)] and muscle (−29 HU to +150 HU). Within the latter range, the mean muscle radiation attenuation [muscle (radio) density] is reported. Inconsistent criteria for the upper and lower HU cut-offs used to characterize muscle attenuation limit comparisons between investigations. This area of research would benefit from standardized criteria for reporting muscle attenuation. Available evidence suggests that muscle attenuation is plastic with physiological variation induced by the process of ageing, as well as by aerobic training, which probably reflects accumulation of lipids to fuel aerobic work. Pathological variation in muscle attenuation reflects excess fat deposition in the tissue and is observed in people with obesity, diabetes type II, myositis, osteoarthritis, spinal stenosis and cancer. A poor prognosis and different types of morbidity are predicted by the presence of reduced mean muscle attenuation values in patients with these conditions; however, the biological features of muscle with these characteristics require further investigation.

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The main purpose of this review is to discuss associations between within-litter variation in birth weight, and preweaning survival and postnatal growth in the pig, as the basis for suggesting that the developmental competence of pigs born, as well as the size of the litter, need critical consideration. Extremes of intrauterine growth retardation (IUGR) occur within a discrete subset of fetuses, substantially smaller than their littermates and commonly described as runt piglets. The lower preweaning growth of runt pigs cannot be entirely explained based on their lower birth weight, nor do they show full postnatal compensatory growth. Interestingly, this more complex reprogramming of development in runt pigs can already be identified by d 27 to 35 of gestation. Recently, we reported more universal IUGR effects in commercial dam-line sows, as an indirect response to selection for increased litter size. High ovulation rates (>30 ovulations) in a proportion of greater parity sows are associated with increased numbers of conceptuses surviving to d 30 of gestation, resulting in detrimental effects on placental development of uterine crowding in the early postimplantation period. In turn, this limits nutrient availability to the embryo during a critical period of myogenesis. Consequently, although a reduction in the number of conceptuses occurs by d 50, placental development in the surviving fetuses remains compromised, resulting in IUGR and reduced numbers of muscle fibers at d 90 and at birth, in all surviving littermates. These effects of uterine crowding on fetal and postnatal development are analogous to the detrimental effects of nutritional restriction in gestating sows on fetal myogenesis, birth weight, and postnatal growth. The incompatibility between increased numbers of conceptuses surviving to the postimplantation period, in the absence of increased uterine capacity, offers a biological explanation for increased variability in birth weight and postnatal growth performance reported in greater parity sows. We conclude that a strategy of introducing hyperprolific females into the breeding nucleus, as a means of increasing the numbers of pigs born, needs to be critically evaluated in the context of the overall efficiency of pork production.

The present study investigated motor unit (MU) loss in a murine model of familial amyotrophic lateral sclerosis (ALS). The fast-twitch tibialis anterior (TA) and medial gastrocnemius (MG) muscles of transgenic SOD1G93A and SOD1 WT mice were studied during the presymptomatic phase of disease progression at 60 days of age. Whole muscle maximum isometric twitch and tetanic forces were 80% lower (P < 0.01) in the TA muscles of SOD1 G93A compared to SOD1 WT mice. Enumeration of total MU numbers within TA muscles showed a 60% reduction (P < 0.01) within SOD1 G93A mice (38 ± 7) compared with SOD1 WT controls (95 ± 12); this was attributed to a lower proportion of the most forceful fast-fatigable (FF) MU in SOD1 G93A mice, as seen by a significant (P < 0.01) leftward shift in the cumulative frequency histogram of single MU forces. Similar patterns of MU loss and corresponding decreases in isometric twitch force were observed in the MG. Immunocytochemical analyses of the entire cross-sectional area (CSA) of serial sections of TA muscles stained with anti-neural cell adhesion molecule (NCAM) and various monoclonal antibodies for myosin heavy chain (MHC) isoforms showed respective 65% (P < 0.01) and 28% (P < 0.05) decreases in the number of innervated IIB and IID/X muscle fibres in SOD1 G93A , which paralleled the 60% decrease (P < 0.01) in the force generating capacity of individual fibres. The loss of fast MUs was partially compensated by activity-dependent fast-to-slower fibre type transitions, as determined by increases (P < 0.04) in the CSA and proportion of IIA fibres (from 4% to 14%) and IID/X fibres (from 31% to 39%), and decreases (P < 0.001) in the CSA and proportion of type IIB fibres (from 65% to 44%). We conclude that preferential loss of IIB fibres is incomplete at 60 days of age, and is consistent with a selective albeit gradual loss of FF MUs that is not fully compensated by sprouting of the remaining motoneurons that innervate type IIA or IID/X muscle fibres. Our findings indicate that disease progression in fast-twitch muscles of SOD1 G93A