4/27/2010 1:10am, #381
As someone (I think it was Scott Able) once said, 'it's not bags of apples people wolf down when they're sitting at home lonely'. Or something to that effect.
4/27/2010 1:13am, #382
4/27/2010 3:35am, #383
But I want to get the most out of the exercise. Encouraging fat just seems like a waste of time.
Having said this, I've not had sweets or dessert in six months. Only in April have I had a month off, for a few ice creams and a cookie or two.
4/27/2010 3:37am, #384
4/28/2010 10:54pm, #385
We've got a live one!
... Approximately 18, 42, and 90 h after cessation of training, GLUT-4 protein concentration and 2-[1,2-3H]deoxy-D-glucose transport in the presence of a maximally stimulating concentration of insulin (2 mU/ml) were examined by using incubated epitrochlearis muscle preparation. Swimming training increased GLUT-4 protein concentration and insulin responsiveness by 87 and 85%, respectively, relative to age-matched controls when examined 18 h after training. Forty-two hours after training, GLUT-4 protein concentration and insulin responsiveness were still higher by 52 and 51%, respectively, in muscle from trained rats compared with control. GLUT-4 protein concentration and insulin responsiveness in trained muscle returned to sedentary control level within 90 h after training. We conclude that 1) the change in insulin responsiveness during detraining is directly related to muscle GLUT-4 protein content, and 2) consequently, the greater the increase in GLUT-4 protein content that is induced by training, the longer an effect on insulin responsiveness persists after the training.
4/28/2010 11:22pm, #386
Also, for the next time the subject of aerobic/anaerobic transitions come up:
Figure 2 and 5 of Weyand and Bundle, "Energetics of high-speed running: integrating classical theory and contemporary observations"
... current understanding of the biochemistry of exercise has made it clear that there is not a "threshold" where a shift from "aerobic" to "anaerobic" metabolism occurs.[20-22] Rather, at high rates of energy requirements, substrate level phosphorylation (ATP production via glycolysis, creatine kinase, adenylate kinase, and succinyl-CoA synthetase) plays an increasingly important role in supplying ATP for contractile function, even though the rate of energy supply via oxidative phosphorylation is not exceeded.[23,24] As opposed to a shift from oxidative to glycolytic pathways, the lactate threshold during progressive exercise protocols is due to (a) the energetics of substrate utilization, which by mass action lead to an increased rate of pyruvate production and thus inevitably result in lactate production as both a product of glycolysis and for direct oxidation via the lactate shuttle; (b) an increased rate of glycolytic flux as exercise intensity increases; and (c) the efficiency of lactate clearance mechanisms.[25,26] Hence, from an organ-systems perspective, the rise in blood lactate provides useful information on compensatory mechanisms possessed by sets of distributed, but interrelated, functions. It must also be recognized that maximal or near-maximal levels of oxidative flux continue during exercise at intensities that equal or even exceed maximal oxygen uptake.
4/29/2010 12:13am, #387
And while I'm at it, a bit on adiponectin.
Adipose tissue is a hormonally active tissue, producing adipocytokines which may influence activity of other tissues. Adiponectin, abundantly present in the plasma increases insulin sensitivity by stimulating fatty acid oxidation, decreases plasma triglycerides and improves glucose metabolism. Adiponectin levels are inversely related to the degree of adiposity....
The mechanism responsible for the control of Apn synthesis has not been determined in detail so far. The expression and secretion of Apn from adipocytes are reduced significantly by TNF-α (Fasshauer et al. 2002a,b). TNF-α is one of the candidate molecules responsible for causing insulin resistance. The recent study has shown that insulin reduces the level of Apn mRNA in a dose- and time-dependent fashion (Fasshauer et al. 2002a,b). Also β-adrenergic agonists (Zhang et al. 2002) and glucocorticoid are reported to inhibit Apn gene expression and secretion, suggesting that decreased Apn production could play a role in catecholamine- or glucocorticoid-induced insulin resistance. Finally, the stomach-derived peptide, ghrelin, inhibits Apn gene expression (Ott et al. 2002)....
Sounds pretty important.
6/01/2010 2:20pm, #388
Having regained possession of my blender, my cunning plan was to mix up a bunch of servings of chocolate milk protein isolate + whipping cream shakes at once, then fridge the pitcher and drink straight from it through the day.
Russ: "Why not add a bit of guar gum to thicken things up?"
Russ's blender: *squeals and makes burning smell*
I want a meaner blender. Actually, what I really want is a slow-cooker. Anyone got brand/model recommendations? My last one leaked moisture out the top so everything got dried out.
I put in a big-ass order with TrueProtein... some post-workout protein (80/20 WPC/hydrolyzed), some fish oil, and some alpha-lipoic acid caps (remind me to post more about this later). If my volume was sufficient to justify carbohydrate intake, I'd be set for killer insulin sensitivity.
6/01/2010 7:51pm, #389
- Join Date
- Jul 2005
If I had a choice, I'd get one of the newer ones with the locking spill proof lid. Transporting soup in it turned into a disaster on the front floor of the car. :/
6/01/2010 7:56pm, #390
Rival Crock-Pot 5-Quart Round Smart-Pot Programmable Slow Cooker" (see the picture of what it looked like after it finished cooking).