The poster I presented at the 2007 BSRA conference was detailing recent research I have carried out on the effects of glutamine supplementation during sepsis. Sepsis occurs frequently in critically ill humans and animals. Cells and tissues of patients with sepsis are exposed to an inflammatory process including systemic pro- and anti-inflammatory cytokines and the increased generation of oxidants, resulting in profound tissue degeneration, particularly of skeletal muscle. During sepsis, skeletal muscle is lost at a rate of 2-4% per day and the ability to withstand and recover from a septic insult is dependent on available muscle mass. By the age of 70, up to 40% of skeletal muscle has undergone atrophy. This has profound consequences on recovery from sepsis in the elderly population. Mechanisms by which severe tissue degradation during sepsis occurs are little understood and optimal therapies remain elusive.
Skeletal muscle adapts following stress by the rapid increased content of HSPs. This increase in HSP content provides protection against subsequent damage and facilitates protein synthesis and tissue regeneration. In the aged population, this adaptation is diminished, and we hypothesise that this inability to produce HSPs plays a major role in the poor function of muscles of older individuals during and following sepsis.
During sepsis, the free glutamine pool in muscle of ICU patients falls by 75%. Glutamine supplementation improves survival of ICU patients but the mechanisms of this protection remain uncertain. Work in a rat sepsis model has confirmed that glutamine infusions preserve the ability of muscles to induce HSPs during sepsis and this is associated with a striking preservation of the ability of muscle to contract. If mobilisation of cellular defence mechanisms such as HSPs are crucial and can be facilitated with glutamine supplementation, mechanisms leading to atrophy and damage may be modified resulting in increased survival of ICU patients, in particular elderly patients.
The recent BSRA annual conference at the University of Liverpool brought together some of the worlds leading scientists in ageing to discuss their latest research in this important area. Professor Holly Van Remmen from the University of Texas Health Science Centre presented work that demonstrated a role for mitochondrial oxidative stress in the age related loss of skeletal muscle mass and function. Professor Van Remmen showed that mice lacking CuZnSOD show an accelerated age-related loss of muscle mass, suggesting a role for superoxide toxicity in muscle atrophy. In addition, muscle mitochondria ROS production in these animals is increased over 100% in 20 month compared to 5 month old mice along with a greater than 50% loss in muscle mass compared to a 3-fold increase in old vs young wild type mice, associated with a 30% loss in muscle mass. I found this presentation of particular interest as it focuses on areas of research similar to my current research. The Lord Cohen Medal Lecture presented by Professor Raymond Tallis from the University Of Manchester was an excellent presentation and a particular highlight for myself. The presentation titled Ageing research: Makropoulitan and other reflections, focussed on the ultimate practical aim of research into ageing by finding means of extending life by preventing, arresting or reversing the ageing process.
In addition to the excellent presentations there was a wide variety of outstanding poster presentations. This meeting allowed scientists to chat and exchange ideas in this important field of research.