Thursday, March 12, 2009

An Important Lesson and Performance Research for March: Protein Synthesis part 1

Greetings from screwball weather Minnesota. It has been stupid cold the past few days (stupid cold= below zero temps in the AM).

Yesterday the sun was out in the evening and I could not take being inside any more. So I did some deadlifts and KB snatches (Tactical Strength Challenge prep) in my garage with the door open so I could see the sun. The garage temp dropped to 17 F then, so I must either be a) nuts b) completely sun deprived or most like c) both. Nothing like seeing your breath.

In this issue
  • What can we learn from caterpillars?
  • More research on muscle protein synthesis (aka building muscle)
I need to thank my buddy Craig Keaton at The Movement in TX for sending this one along. If you are in Texas, get your butt over to his place and tell him I sent ya (I get paid nothing for sending clients to him).

Don't Follow The Follower

Processionary caterpillars travel in long, undulating lines, one creature behind the other. Jean Hanri Fabre, the French entomologist, once lead a group of these caterpillars onto the rim of a large flowerpot so that the leader of the procession found himself nose to tail with the last caterpillar in the procession, forming a circle without end or beginning.

Through sheer force of habit and, of course, instinct, the ring of caterpillars circled the flowerpot for seven days and seven nights, until they died from exhaustion and starvation. An ample supply of food was close at hand and plainly visible, but it was outside the range of the circle, so the caterpillars continued along the beaten path.

People often behave in a similar way. Habit patterns and ways of thinking become deeply established, and it seems easier and more comforting to follow them than to cope with change, even when that change may represent freedom, achievement, and success.

Earl Nightingale
From The Essence of Success
Don't Follow The Follower

On to the studies!

Cardioprotection requires taking out the trash.

Gottlieb RA, Finley KD, Mentzer RM Jr. The BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA, 92182-4650, USA,

Autophagy is a critical cellular housekeeping process that is essential for removal of damaged or unwanted organelles and protein aggregates. Under conditions of starvation, it is also a mechanism to break down proteins to generate amino acids for synthesis of new and more urgently needed proteins. In the heart, autophagy is upregulated by starvation, reactive oxygen species, hypoxia, exercise, and ischemic preconditioning, the latter a well-known potent cardioprotective phenomenon.

The observation that upregulation of autophagy confers protection against ischemia/reperfusion injury and inhibition of autophagy is associated with a loss of cardioprotection conferred by pharmacological conditioning suggests that the pathway plays a key role in enhancing the heart's tolerance to ischemia. While many of the antecedent signaling pathways of preconditioning are well-defined, the mechanisms by which preconditioning and autophagy converge to protect the heart are unknown.

CONCLUSION: In this review we discuss mechanisms that potentially underlie the linkage between cardioprotection and autophagy in the heart.

My Notes:
Ischemic (meaning no oxygen) preconditioning helps protect the heart. This process involves stopping blood (and therefore oxygen) to the heart for a very SHORT period of time. If that process goes on too long it becomes bad and is known as a heart atack (MI for you geeks).
I wonder if this happens in skeletal muscle also? Does the "pump" you get from lifting (which is cutting down on some blood flow to the muscle during contraction) help protect muscles long term?

AMPK in contraction-regulation of skeletal muscle metabolism: necessary and/or sufficient?

Jensen TE, Wojtaszewski JF, Richter EA. Molecular Physiology Group, Copenhagen Muscle Research Centre, Section of Human Physiology, Department of Exercise and Sport Sciences, University of Copenhagen, Denmark.

In skeletal muscle, the contraction-activated heterotrimeric 5' AMP-activated protein kinase (AMPK) protein is proposed to regulate the balance between anabolic and catabolic processes by increasing substrate uptake and turnover in addition to regulating the transcription of proteins involved in mitochondrial biogenesis and other aspects of promoting an oxidative muscle phenotype.

Here, the current knowledge on expression of AMPK subunits in human quadriceps muscle and evidence from rodent studies suggesting distinct AMPK subunit expression-pattern in different muscle types is reviewed. Then, the intensity and time-dependence of AMPK-activation in human quadriceps and rodent muscle is evaluated. Subsequently, a major part of this review critically examines the evidence supporting a necessary and/or sufficient role of AMPK in a broad spectrum of skeletal muscle contraction-relevant processes.

CONCLUSION: These include glucose uptake, glycogen synthesis, post-exercise insulin-sensitivity, fatty acid uptake, intramuscular triacylglyceride hydrolysis, fatty acid oxidation, suppression of protein synthesis, proteolysis, autophagy and transcriptional regulation of genes relevant to promoting an oxidative phenotype.

My Notes: Sounds like a pretty important process if it is involved in all of that stuff. Think of AMPK as a "metabolic fuel gage"--just like the fuel gage on your car. Another new study related to this published just days ago in Nature below

AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity

And the last one for today, but it is a good one.

Differential stimulation of myofibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and after resistance exercise.

Moore DR, Tang JE, Burd NA, Rerecich T, Tarnopolsky MA, Phillips SM. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.

We aimed to determine whether there is a differential stimulation of the contractile myofibrillar and the cellular sarcoplasmic proteins after ingestion of protein and how this is affected by resistance exercise. Fasted (FAST) muscle protein synthesis was measured in seven healthy young men with a primed constant infusion of L-[ring-(13)C(6)]phenylalanine. Participants then performed an intense bout of unilateral resistance exercise followed by the consumption of 25 g of whey protein to maximally stimulate protein synthesis. In the rested (FED) leg myofibrillar (MYO) protein synthesis was elevated (P <> 0.05).

In contrast, MYO protein synthesis in the exercised (FED-EX) leg was stimulated above FAST at 1, 3 and 5 h (approximately 100, 216, and 229%, respectively; P < style="font-weight: bold;">

CONCLUSION: In conclusion, myofibrillar and sarcoplasmic protein synthesis are similarly, but transiently, stimulated with protein feeding. In contrast, resistance exercise rapidly stimulates and sustains the synthesis of only the myofibrillar protein fraction after protein ingestion. These data highlight the importance of measuring the synthetic response of specific muscle protein fractions when examining the effects of exercise and nutrition.

My Notes: Protein has effects just by itself to build bigger muscles, as does resistance training (weight lifting). The logical conclusion is

Protein + Heavy Weights= More muscle!

Rock on
Mike T Nelson