Of bears, frogs, meat, mice and men: complexity of factors affecting skeletal muscle mass and fat

Abstract

Extreme loss of skeletal muscle mass (atrophy) occurs in human muscles that are not used. In striking contrast, skeletal muscles do not rapidly waste away in hibernating mammals such as bears, or aestivating frogs, subjected to many months of inactivity and starvation. What factors regulate skeletal muscle mass and what mechanisms protect against muscle atrophy in some species? Severe atrophy also occurs with ageing and there is much clinical interest in reducing such loss of muscle mass and strength (sarcopenia). In the meat industry, a key aim is optimizing the control of skeletal muscle growth and meat quality. The impaired response of muscle to insulin resulting in diabetes, that is a consequence of the metabolic impact of increasing obesity and fat deposition in humans, is also of increasing clinical concern. Intensive research in these fields, combined with mouse models, is reviewed with respect to the molecular control of muscle growth (myogenesis) and atrophy/hypertrophy and fat deposition (adipogenesis) in skeletal muscle, with a focus on IGF-1/insulin signaling.

Each to their own: skeletal muscles of different function use different biochemical strategies during aestivation at high temperature

“…This disparity in results is likely due to differences in the specific antioxidants used, the ratio of the magnitude of oxidative stress (threshold level) to the magnitude of the administered antioxidant, the particular muscle tested, different conditions of disuse and combinations thereof. Dormant animals undergo much less MDA than is seen in artificially immobilised laboratory model organisms (McDonagh et al, 2004;Shavlakadze and Grounds, 2006). Naturally prolonged muscular disuse, as occurs during dormancy in a number of animals, also involves a substantial depression of oxygen consumption and whole-animal metabolic systems with a coordinated reduction in both protein synthesis and protein degradation (Storey and Storey, 1990).…”

Cellular senescence in human myoblasts is overcome by human telomerase reverse transcriptase and cyclin‐dependent kinase 4: consequences in aging muscle and therapeutic strategies for muscular dystrophies

“…Aging muscle is characterized by progressive muscle weakness and atrophy (Shavlakadze & Grounds, 2006) as well as by a slower regenerative capacity (Mouly et al ., 2005a). At least two factors may be linked to the regenerative capacity of skeletal muscle: (i) the number of progenitor cells, for example satellite cells, which decreases with age in both rodents and humans, and (ii) their proliferative potential, which is limited in humans by cellular senescence, triggered by excessive telomere shortening (Renault et al ., 2002;Wright & Shay, 2002).…”

Mammalian hibernation: differential gene expression and novel application of epigenetic controls

“…The focus of the present article is mammalian hibernation, a seasonal state characterized by prolonged periods of deep torpor where metabolic rate can plunge to less than 5% of the normal resting rate. Hibernation is the most extreme example of hypometabolism among mammalian species and the lessons learned from studies of the regulation of hibernation have multiple potential applications to human biology and medicine, addressing concerns such as ischemia resistance, hypothermic organ preservation, prevention of muscle atrophy, and even the development of inducible torpor as an aid to long term space flight (Storey, 2004;Lee and Hallenbeck, 2006;Shavlakadze and Grounds, 2006). Another form of mammalian hypometabolism is daily torpor, a common phenomenon that is characterized by a much shallower reduction of core body temperature (Tb) and a much shorter time frame (hours instead of days) (Geiser, 2004).…”