News & Views from the Editor-in-Chief - L. Bruce Gladden
There are many fine papers in this month's issue, but I am directing attention to three of them. First, in their review, Grassi et al. summarize their work dealing with functional evaluation of exercise tolerance in patients with metabolic myopathies (McArdle disease, mitochondrial myopathies), rare diseases characterized by derangements of glycogen metabolism or mitochondrial function. These patients represent types of "human knockout" models, and offer unique opportunities to investigate physiological mechanisms. Methods developed in the field of exercise physiology were applied to these patients, within a translational approach bringing basic science "to the bed of the patient." General message of the review: physiology is the essential link between genes, molecules, and clinical care. The "–omics" world may identify concepts and mechanisms, but only physiology can give a meaning to these findings within the general picture of a human body, healthy or ill.
Second, Routledge and colleagues investigated the validity of an ultrasound method for the assessment of muscle glycogen during a rugby league match and in a controlled laboratory setting. In study 1, rugby league match play decreased muscle glycogen concentration in 14 professional players by approximately 50% (muscle biopsy) although no change was observed in the ultrasound score. In study 2, the authors used a laboratory cycling protocol to deplete muscle glycogen in 16 males followed by 36 h of a high- or low-carbohydrate diet. Despite differences between high (531 ± 129 mmol·kg-1 dw) and low (252 ± 64 mmol·kg-1 dw) glycogen concentrations via muscle biopsy, there was no difference in ultrasound scores (56 ± 7, 54 ± 6, respectively). These data demonstrate that ultrasound is not valid for measurement of muscle glycogen within the physiological range (i.e., 200–500 mmol·kg-1 dw) that is applicable to exercise-induced utilization and postexercise glycogen resynthesis.
Finally, Salomoni et al. assessed whether the presence of pain affects movement performance and muscle activation strategy when learning a novel motor task. Using systematic force field perturbations during rapid arm-reaching movements, they found that pain reduced the initial rate of learning and modified the motor strategy used to adapt to the force field perturbation. Remarkably, motor strategies developed in the presence of pain were sustained when the same motor task was repeated after complete resolution of the painful stimulus. These results suggest that learning in the presence of pain may underpin the development of suboptimal motor strategies. There are potentially critical implications if this effect applies to learning motor skills in sport and rehabilitation.
L. Bruce Gladden
School of Kinesiology