The first study is very cool since it was actually conducted in a "fed" state. Most studies are done after an overnight fast. This is good since it eliminates many other variables and allows the researchers to focus in on exactly what they are studying! The downside, is that this does not related to the real world most of the time. Ideally you want to be eating smaller meals through out the day; so most of the time you are then in a "fed" state (some times too often for most if you look around!).
So the big question as of late--does the use of protein and carbohydrates help us add muscle in a fed state?
This brand new study looked at a carbohydrate and a carbohydrate + protein group, given PRE and DURING resistance training (weight training).
The results showed that the inclusion of protein was beneficial to help increase protein synthesis (add more muscle).
The downside is that we don't know how MUCH muscle/strength can be gained from this method, based only on this study (other studies show protein and carbs are helpful). It does add to the evidence that protein and carbs around your training time EVEN when NOT fasted is beneficial! Order me up a protein carb shake and hit the weights.
For those uber geeks, here are a few more details.
The subjects were active but it does not say much else. They were lean with around 12% bodyfat done by underwater weighing. The carb mix was 50% glucose and 50% maltodextrin, the protein was Pepto Pro which is a casein hydrolyse protein. Treatment was randomized and double blind. Exercise was started 3 hours after the last meal. Whole body protein metabolism was measured by phenylalanine flux. Not sure who sponsored it, but AK Kies is a researcher for DSM Food Specialties (who make Pepto Pro).
Protein coingestion stimulates muscle protein synthesis during resistance-type exercise.
Beelen M, Koopman R, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, van Loon LJ. Department of Human Movement Sciences, Maastricht University, 6200 MD Maastricht, The Netherlands. Milou.Beelen@BW.unimaas.nl In contrast to the effect of nutritional intervention on postexercise muscle protein synthesis, little is known about the potential to modulate protein synthesis during exercise. This study investigates the effect of protein coingestion with carbohydrate on muscle protein synthesis during resistance-type exercise. Ten healthy males were studied in the evening after they consumed a standardized diet throughout the day. Subjects participated in two experiments in which they ingested either carbohydrate or carbohydrate with protein during a 2-h resistance exercise session. Subjects received a bolus of test drink before and every 15 min during exercise, providing 0.15 g x kg(-1) x h(-1) carbohydrate with (CHO + PRO) or without (CHO) 0.15 g x kg(-1) x h(-1) protein hydrolysate. Continuous intravenous infusions with l-[ring-(13)C(6)]phenylalanine and l-[ring-(2)H(2)]tyrosine were applied, and blood and muscle biopsies were collected to assess whole body and muscle protein synthesis rates during exercise. Protein coingestion lowered whole body protein breakdown rates by 8.4 +/- 3.6% (P = 0.066), compared with the ingestion of carbohydrate only, and augmented protein oxidation and synthesis rates by 77 +/- 17 and 33 +/- 3%, respectively (P < style="font-weight: bold;">
Conclusion: Even in a fed state, protein coingestion stimulates whole body and muscle protein synthesis rates during resistance-type exercise.
Discovery of aminoquinolines as a new class of potent inhibitors of heat shock protein 90 (Hsp90): Synthesis, biology, and molecular modeling.
Ganesh T, Min J, Thepchatri P, Du Y, Li L, Lewis I, Wilson L, Fu H, Chiosis G, Dingledine R, Liotta D, Snyder JP, Sun A. Chemical Biology Discovery Center, 1510 Clifton Road, Emory University, Atlanta, GA 30322, USA. The molecular chaperone Hsp90 plays important roles in maintaining malignant phenotypes. Recent studies suggest that Hsp90 exerts high-affinity interactions with multiple oncoproteins, which are essential for the growth of tumor cells. As a result, research has focused on finding Hsp90 probes as potential and selective anticancer agents. In a high-throughput screening exercise, we identified quinoline 7 as a moderate inhibitor of Hsp90. Further hit identification, SAR studies, and biological investigation revealed several synthetic analogs in this series with micromolar activities in both fluorescent polarization (FP) assay and a cell-based Western blot (WB) assay.
Conclusion: These compounds represent a new class of Hsp90 inhibitors with simple chemical structures.
Type 1 diabetes: can exercise impair the autoimmune event? The L-arginine/glutamine coupling hypothesis.
Krause Mda S, de Bittencourt PI Jr. Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, School of Physical Education, Porto Alegre, RS, Brazil. Prevention of type 1 diabetes mellitus (T1DM) requires early intervention in the autoimmune process directed against beta-cells of the pancreatic islets of Langerhans, which is believed to result from a disorder of immunoregulation. According to this concept, a T-helper lymphocyte of type 1 (Th1) subset of T-lymphocytes and their cytokine products, the type 1 cytokines [e.g. interleukin 2 (IL-2), interferon gamma (IFN-gamma) and tumour necrosis factor beta (TNF-beta)] prevail over immunoregulatory (anti-inflammatory) Th2 subset and its cytokine products, i.e. type 2 cytokines (e.g. IL-4, IL-6 and IL-10). This allows type 1 cytokines to initiate a cascade of immune/inflammatory processes in the islet (insulitis), culminating in beta-cell destruction. Activation of sympathetic-corticotropin-releasing hormone (CRH) axis by psychological stress induces specifically Th1 cell overactivity that determines enhanced glutamine utilization and consequent poor L-arginine supply for nitric oxide (NO)-assisted insulin secretion. This determines the shift of intraislet glutamate metabolism from the synthesis of glutathione (GSH) to that of L-arginine, leading to a redox imbalance that activates nuclear factor kappaB exacerbating inflammation and NO-mediated cytotoxicity. Physical exercise is capable of inducing changes in the pattern of cytokine production and release towards type 2 class and to normalize the glutamine supply to the circulation, which reduces the need for glutamate, whose metabolic fate may be restored in the direction of GSH synthesis and antioxidant defence. Also, the 70-kDa heat shock protein (hsp70), which is immunoregulatory, may modulate exercise-induced anti-inflammation.
Conclusion: We envisage how exercise can intervene in the mechanisms involved in the autoimmune process against beta-cells and how novel therapeutic approaches may be inferred from these observations.