Pars interarticularis injury in elite athletes - The role of imaging in diagnosis and management.

Injuries of the lumbar neural arch, in particular the pars interarticularis, are widely considered to be due to abnormal bone stress secondary to repetitive loading/shearing, and are a common pathology and a main cause of lower back pain in elite athletes across a range of sports. Medical imaging plays a pivotal role in the diagnosis, monitoring and prognostication of neural arch injury. Early detection is highly desirable in the young elite athlete, as early injuries have been shown to require shorter recovery time and have a higher potential of full healing, whilst accurate grading of injury allows appropriate rehabilitation planning. Various imaging modalities are used in the diagnosis and management of pars stress injury, each with their strengths and weaknesses. There is currently a lack of general consensus over the most appropriate imaging pathway for neural arch injury in this specific group of patients. In this review article, we present an overview of neural arch injury, the various imaging modalities used and their imaging appearances with a brief pictorial review, and a proposed imaging algorithm with special considerations in the young elite athletes.

Muscle pyruvate availability can limit the flux, but not activation, of the pyruvate dehydrogenase complex during submaximal exercise in humans.

While lowering muscle glycogen availability to an extent that would reduce muscle pyruvate formation during intense exercise, we investigated the importance of muscle pyruvate availability to pyruvate dehydrogenase complex (PDC) activation during intense exercise in human skeletal muscle. The present study demonstrated that regardless of whether pre-exercise muscle glycogen content was at a habitual resting concentration (412 +/- 30 mmol (kg dry muscle)(-1)) or depleted (60 +/- 3 mmol (kg dry muscle)(-1)), the increase in PDC activation from its resting value (5.46 +/- 0.96 and 3.67 +/- 0.34 nmol acetyl-CoA min(-1) (mg protein)(-1), respectively) during 10 min of exercise at 75% of the maximum rate of oxygen consumption (VO2max) (delta12.82 +/- 1.72 and delta13.24 +/- 1.42 nmol acetyl-CoA min(-1) (mg protein)(-1), respectively) was the same, despite pyruvate accumulation during exercise being 3-fold lower in the glycogen depleted state (delta0.34 +/- 0.04 and delta0.11 +/- 0.06 mmol (kg dry muscle)(-1), P < 0.001). However, as a result of the reduction in pyruvate availability, calculated flux through the PDC reaction was at least 2-fold lower in the glycogen depleted state compared with normal (21.81 +/- 2.62 and 9.41 +/- 0.63 nmol acetyl-CoA min(-1) (mg protein)(-1), respectively; P < 0.001). It is therefore pertinent to conclude that whilst muscle pyruvate availability appears to be important to the rate of flux through the PDC reaction during in vivo contraction, it is not of primary importance to the control of PDC activation under these conditions, which is probably principally regulated by muscle calcium availability. The proposed central role of pyruvate in muscle PDC activation during in vivo contraction may therefore have been over stated.