Prof. Mike J. Rennie
Q Question. A Answer
Q. Mike, you had retired at the Postgraduate Medical School in Derby. What are you doing now? Are you still actively involved in research projects?
A. I hated being forced to retire – I was a month too old in August 2011 to benefit from new UK Gov regulations which would have forced the admin myrmidons to allow me to work for another two years.
It took me a while to adapt - not a good time. I keep busy by doing ad hoc jobs as a consultant to a number of universities (recently about the REF). I never get asked to meetings or to act as an external examiner and I get few requests to review grants or papers, though they do dribble along.
I also teach for the Open University – two second level 8 month courses, one on practical science in modern biology and another on sports conditioning and professional development. All on-line using tremendous presentation and conferencing tools.
I am a member of a DoH expert committee on mutagenesis in food and consumer products (as a lay member).
I continue to edit two journals on intensive care: the British Journal of Intensive Care and International Journal of Intensive Care. I also do freelance journalism and hope to increase my training/consultant activities as a grant doctor and publication (abstracts, papers, presentations) tutor for postgrad students.
My ex-colleagues are still getting round to producing paper drafts of work now completed, which we started a few years ago. I still can make some input here but only in correcting the drafts. Probably a few more yet to appear such as one where we explore the importance of microcirculation and muscle anabolism.
On a personal basis , I’ve recently made efforts to adopt a healthier lifestyle, and I have a wide range of cultural interests (and four grandchildren) which keep me sane.
Q. Looking back, what is your most important paper that you have published and why do you rank it your as your most important paper?
A. Oooh! Very hard to say. I was very proud of the early J Physiol paper on metabolic and hormonal changes during exercise which was undercited but rather novel in its scope.
The work I did with John Holloszy at WUMS St Louis on fat versus CHO (Biochem J, AJP) was highly cited but some found the results controversial.
I was very proud to be associated with influential work on stable isotope tracing of AA metabolism and muscle protein turnover in people: at rest with and without feeding, and the effects of exercise and Duchenne muscular dystrophy. These were published in FASEB J, Nature and Science. Great colleagues and good fortune helped tremendously.
This started an avalanche of work by others in this area and I produced quite a few papers showing that in many slow wasting conditions (including aging) depressed muscle protein synthesis was the major driver of wasting. This has continued to annoy many pacman enthusiasts... Of course its different in fast wasting.
The work I did with some great graduate students and postdocs in Dundee on muscle AA transport was interesting but turned out to be negative in demonstrating that transport is very unlikely to be a process regulating muscle anabolism (or catabolism) or fuel use.
Recent papers on insulin action and effects of PUFA were very satisfying.
The concept of anabolic resistance has been well received and so has the work on dose response and time dependency of anabolism after feeding are highlights of the last period when I felt my enthusiasm and insights were at a height. Sadly curtailed by crappy administrators.
Q. In the field of human skeletal muscle research, what is the most important paper where you were not involved and why do you rank it as the most important one?
A. I can’t think of single papers but the increase of the understanding of satellite cells will turn out to have been very important, as will the work just starting by others on epigenetic effects of training.
Q. Correct me if I am wrong but you frequently highlight (and data support that of course) that anabolic/mTOR signalling and protein synthesis do not always/rarely match in human muscle. Yet, rapamycin blocks amino acid and resistance exercise-induced increases in protein synthesis in human muscle and something must connect anabolic stimuli to protein synthesis. What is your current take on all of this?
A. Biology is full of examples of redundancy of pathways and also examples in which existence of a pathway does not mean that the pathway is important in regulation. One problem of the use of westerns and mRNA blots is that their interpretation ignores the fact that these are Vmax measures and not point of time activitity.
Q. Your have done a lot of research on sarcopenia and other forms of atrophy. Based on this what is your current practical recommendation for people with sarcopenia?
A. Choose your parents!
Q. Do you expect truly novel treatments to emerge in the next 20 years and if you had a guess what was the nature of these treatments?
A. There have been lots of false starts. I will be very interested to see if antibody based inhibition of catabolic proteins or receptors have any use. I doubt they will in ageing but might for cancer and critical care though the indications are equivocal. Drugs like SARMs look promising. HMB turns out to be interesting. I was sceptical for years but Phil Atherton has nailed its effects in stimulating MPS. And PUFA effects: fascinating.... anti-inflammatory or what? Puzzling.
Q. Do you have top tips for young researchers who wish to become active in the area of human skeletal muscle research?
A. First choose a good smart mentor who is interested in bright young people, who publishes prolifically, who has a well set up lab, and who gets grants to support novelty. I had two: John Holloszy and Richard Edwards. Be open to advice from clever colleagues at home and abroad and collaborate widely. Don’t follow fashion but use it to gain insights on stuff to avoid; anybody can think up an obvious hypothesis but then think “if that is true, then what...?”