The results have important positive implications for future studies that focus on the activation of trunk muscles by demonstrating the feasibility of collecting comprehensive electromyographic data during this standardized task in healthy older adults.
Our research groups have contributed to the field of muscle aging by demonstrating that specific aspects of the excitation-contraction coupling (ECC) process are compromised with age [ 11, 12].
In 1986, the Weintraub laboratory [ 9] laid the groundwork for muscle cell reprogramming by demonstrating that somatic cells could be induced to adopt a skeletal muscle cell fate in vitro, through overexpression of the skeletal muscle master regulator gene, MyoD.
15 The only study that compared the effect of adding NMES to an exercise program supports our present findings by demonstrating muscle strength improvement in both groups, with no additive effect of NMES.
The present study aimed to overcome these limitations by demonstrating mobilization of muscle cells into a target-specific site for in situ muscle regeneration.
Gene-clustering approaches supported the above hypothesis by demonstrating that muscles from T2DM patients display downregulation of lipid oxidation and mitochondrial metabolism genes (Mootha et al, 2003; Patti et al, 2003).
Diagnosis is determined by demonstrating that the exercising muscles do not produce lactic acid as they should.
Inclusion criteria for eligibility were the following: age 8 to 80 years, genetic confirmation of DMD, BMD, carriership or sarcoglycanopathy by DNA analysis or muscle biopsy demonstrating absent, reduced or abnormal dystrophin or sarcogycan on immunohistochemical and/or immunobiochemical analysis.
However, histological analyses of muscle revealed vast regeneration of muscle fibers in limb muscles, demonstrated by the presence of small fibers with centrally located nuclei (Fig. 6A).
Akt is sufficient to induce muscle hypertrophy as demonstrated by muscle-specific expression of a constitutively active form of Akt [3].
