Effect of creatine supplementation during resistance training on lean tissue mass and muscular strength in older adults: a meta-analysis

To estimate the healthcare costs of sarcopenia in the United States and to examine the effect that a reduced sarcopenia prevalence would have on healthcare expenditures. Cross-sectional surveys. Nationally representative surveys using data from the U.S. Census, Third National Health and Nutrition Examination Survey, and National Medical Care and Utilization Expenditure Survey. Representative samples of U.S. adults aged 60 and older. The healthcare costs of sarcopenia were estimated based on the effect of sarcopenia on increasing physical disability risk in older persons. In the first step, the healthcare cost of disability in older Americans was estimated from national surveys. In the second step, the proportion of the disability cost due to sarcopenia (population-attributable risk) was calculated to determine the healthcare costs of sarcopenia. These calculations relied upon previously published relative risk values for disability in sarcopenic individuals and sarcopenia prevalence rates in the older population. The estimated direct healthcare cost attributable to sarcopenia in the United States in 2000 was $18.5 billion ($10.8 billion in men, $7.7 billion in women), which represented about 1.5% of total healthcare expenditures for that year. A sensitivity analysis indicated that the costs could be as low as $11.8 billion and as high as $26.2 billion. The excess healthcare expenditures were $860 for every sarcopenic man and $933 for every sarcopenic woman. A 10% reduction in sarcopenia prevalence would result in savings of $1.1 billion (dollars adjusted to 2000 rate) per year in U.S. healthcare costs. Sarcopenia imposes a significant but modifiable economic burden on government-reimbursed healthcare services in the United States. Because the number of older Americans is increasing, the economic costs of sarcopenia will escalate unless effective public health campaigns aimed at reducing the occurrence of sarcopenia are implemented.

This study determined the decline in oxidative capacity per volume of human vastus lateralis muscle between nine adult (mean age 38.8 years) and 40 elderly (mean age 68.8 years) human subjects (age range 25-80 years). We based our oxidative capacity estimates on the kinetics of changes in creatine phosphate content ([PCr]) during recovery from exercise as measured by (31)P magnetic resonance (MR) spectroscopy. A matched muscle biopsy sample permitted determination of mitochondrial volume density and the contribution of the loss of mitochondrial content to the decline in oxidative capacity with age. The maximal oxidative phosphorylation rate or oxidative capacity was estimated from the PCr recovery rate constant (k(PCr)) and the [PCr] in accordance with a simple electrical circuit model of mitochondrial respiratory control. Oxidative capacity was 50 % lower in the elderly vs. the adult group (0.61 +/- 0.04 vs. 1.16 +/- 0.147 mM ATP s(-1)). Mitochondrial volume density was significantly lower in elderly compared with adult muscle (2.9 +/- 0.15 vs. 3.6 +/- 0.11 %). In addition, the oxidative capacity per mitochondrial volume (0.22 +/- 0.042 vs. 0.32 +/- 0.015 mM ATP (s %)(-1)) was reduced in elderly vs. adult subjects. This study showed that elderly subjects had nearly 50 % lower oxidative capacity per volume of muscle than adult subjects. The cellular basis of this drop was a reduction in mitochondrial content, as well as a lower oxidative capacity of the mitochondria with age.

Adult skeletal muscle can regenerate in response to muscle damage. This ability is conferred by the presence of myogenic stem cells called satellite cells. In response to stimuli such as injury or exercise, these cells become activated and express myogenic regulatory factors (MRFs), i.e., transcription factors of the myogenic lineage including Myf5, MyoD, myogenin, and Mrf4 to proliferate and differentiate into myofibers. The MRF family of proteins controls the transcription of important muscle-specific proteins such as myosin heavy chain and muscle creatine kinase. Different growth factors are secreted during muscle repair among which insulin-like growth factors (IGFs) are the only ones that promote both muscle cell proliferation and differentiation and that play a key role in muscle regeneration and hypertrophy. Different isoforms of IGFs are expressed during muscle repair: IGF-IEa, IGF-IEb, or IGF-IEc (also known as mechano growth factor, MGF) and IGF-II. MGF is expressed first and is observed in satellite cells and in proliferating myoblasts whereas IGF-Ia and IGF-II expression occurs at the state of muscle fiber formation. Interestingly, several studies report the induction of MRFs in response to IGFs stimulation. Inversely, IGFs expression may also be regulated by MRFs. Various mechanisms are proposed to support these interactions. In this review, we describe the general process of muscle hypertrophy and regeneration and decipher the interactions between the two groups of factors involved in the process.