It'd be funny to have two groups divided between back squats or deadlifts and see what happens...
Interesting. I've seen that the doggcrapp method can get some pertty impressive results, but its nice to see some science back up the philosophy of slow eccentrics.
-Guarner and Malagelada, "Gut flora in health and disease"Quote:
Anaerobic metabolism of peptides and proteins (putrefaction) by the microflora also produces short-chain fatty acids but, at the same time, it generates a series of potentially toxic substances including ammonia, amines, phenols, thiols, and indols.
Well, so much for yogurt enemas... (Thanks to Jack for the review)
An interesting tidbit on cellulose digestibility...
-Cummings, "Cellulose and the human gut"Quote:
Balance studies in humans where intake of dietary cellulose and faecal excretion have been measured and the source of cellulose was commonly eaten foods, such as fruit and vegetables and refined cereals, cellulose digestibility was of the order of 70-80%.5 These and other reports have not unnaturally led to the study of cellulose metabolism in man in more detail, using purified forms of cellulose. Such preparations of cellulose have very different physical properties from the cellulose present in the plant cell wall and so lead to conflicting views of the role of cellulose in the gut. For example, in the work of Van Soest's group10 11 in which healthy volunteers were fed controlled diets with the addition of cellulose from either cabbage, bran, or a purified cellulose (Solka Floc), average cellulose digestibility was 74% on the control diet, 75% in the cabbage, about 53% in the bran but only 25% from the Solka Floc. Moreover, the purified cellulose depressed the breakdown of other cell wall polysaccharides and reduced cellulose digestion in the subjects when they were changed to other diets. The capacity of colonic microorganisms to digest cellulose in vitro was also tested and in these studies the purified cellulose was virtually indigestible, while that from cabbage was extensively degraded. Similar findings were reported in 1936 by Williams and Olmsted' who fed three medical students cellulose from a wide range of food sources and observed that while 60-70% from carrot and cabbage was digested only 0-10% of a purified cellulose was broken down and 3-25% from cotton seed hulls.
Given that this review is from '84, when the concept of resistant starch was relatively novel, I wonder if anyone's since figured out where exactly this variance is coming from?
Oh, and guess what arrived today?
Each bag is five pounds, for a total of thirty pounds of milk protein isolate. But who's that lonely fellow over on the right?
Edit: The image is a bit blurry. Summary:
Whey Protein Isolate Cold Filtration 75%
Hydrolyzed Whey Protein High Grade 25%
Premium Dutch Chocolate Fudge $0.75/lb
Protease Enzyme Complex: $0.70/lb
That little number worked out to $10.07/lb plus shipping and tax. Not bad.
Potential research questions...
-Presumably follistatin increases the nitrogen balance of affected cells (skeletal muscle). Could this lead to amino acid/protein deficits in unaffected cells (heart muscle, organs, etc.)?
-The absence of uncontrolled, indefinite growth implies a negative feedback loop. Does this loop involve upregulation of myostatin production, and could this have detrimental effects on other cells?
-What is the loading requirement for an eccentric movement to induce stretch hypertrophy, and is this requirement proportional to the peak eccentric force developed by a rested muscle, or does it decrease as the muscle fatigues and/or acquires damage?
And back to the micro-scale, because that's how I roll.
-Friden, "Changes in human skeletal muscle induced by long-term eccentric exercise"Quote:
The fine structure of muscle fibres from m. vastus lateralis of nine healthy males (mean age 26 years) was investigated. Four individuals constituted non-exercised controls while five subjects participated in a two-months eccentric muscular training program. Specimens from the controls showed a well-preserved, regular myofibrillar band pattern while changes in the myofibrillar architecture were constantly found in specimens taken after the training program. These changes consisted of Z-band alterations, Z-bands being out of register, extra sarcomeres, Z-band extensions and bisected Z-bands. Between the separated Z-band halves, thin and thick myofilaments as well as abundant glycogen particles and/or ribosomes, were observed. Type-2 (fast-twitch) fibres were predominantly affected. Contrary to the controls the trained individuals constantly showed a greater variation in sarcomere lengths in Type-2 fibres than in Type-1 fibres. It is concluded that muscular work of high tension can induce fine-structural alterations. When repeated over a long period of time, extreme tension demands seem to initiate reorganization in the muscle fibres, predominantly in the, ultrastructurally defined, Type-2 fibres. This adaptation probably results in a better stretchability of the muscle fibres, reduces the risk for mechanical damage and brings about an optimal overlap between actin and myosin filaments.
-McCully, "Detection of muscle injury in humans with 31-P magnetic resonance spectroscopy"Quote:
Strenuous exercise can result in muscle injury that may persist for 2 weeks. Our purpose was to determine if muscle injury can be detected with 31-P magnetic resonance spectroscopy. Normal subjects performed repeated lengthening contractions with either arms or legs designed to result in mild muscle injury. One hour after the arm exercise, there was a significant increase in the inorganic phosphate to phosphocreatine ratio (Pi/PCr), with the maximum increase in Pi/PCr occurring 1 day postexercise (0.12 +/- 0.01 to 0.21 +/- 0.05). Pi/PCr remained elevated for 3-10 days. Similar results were seen following the leg exercise protocol. ATP/(Pi + PCr) decreased in all the arm exercised subjects. Exercise protocols that did not contain lengthening contractions did not result in changes of Pi/PCr or ATP/(Pi + PCr). Patients with various neuromuscular diseases with evidence of muscle damage (elevated CK, muscle soreness, and histopathological findings) also showed increased Pi/PCr at rest. We conclude that elevated Pi/PCr at rest can reflect nonspecific muscle damage in normal and diseased subjects.
If the inorganic phosphate/phosphocreatine ratio is a reliable characteristic of stretch-induced hypertrophy, we could measure it non-invasively. That's a big if, though.
Long-time readers may remember this caffeine-head trauma post. Well, here's a follow-up to explain the why...
-Addicott et al., "The effect of daily caffeine use on cerebral blood flow: How much caffeine can we tolerate?"Quote:
Caffeine is a commonly used neurostimulant that also produces cerebral vasoconstriction by antagonizing adenosine receptors. Chronic caffeine use results in an adaptation of the vascular adenosine receptor system presumably to compensate for the vasoconstrictive effects of caffeine. We investigated the effects of caffeine on cerebral blood flow (CBF) in increasing levels of chronic caffeine use. Low (mean = 45 mg/day), moderate (mean = 405 mg/day), and high (mean = 950 mg/day) caffeine users underwent quantitative perfusion magnetic resonance imaging on four separate occasions: twice in a caffeine abstinent state (abstained state) and twice in a caffeinated state following their normal caffeine use (native state). In each state, there were two drug conditions: participants received either caffeine (250 mg) or placebo. Gray matter CBF was tested with repeated-measures analysis of variance using caffeine use as a between-subjects factor, and correlational analyses were conducted between CBF and caffeine use. Caffeine reduced CBF by an average of 27% across both caffeine states. In the abstained placebo condition, moderate and high users had similarly greater CBF than low users; but in the native placebo condition, the high users had a trend towards less CBF than the low and moderate users. Our results suggest a limited ability of the cerebrovascular adenosine system to compensate for high amounts of daily caffeine use.
Reduced bloodflow? What does that remind us of? Perhaps the energy crisis discussed in this post?
This ‘‘hypermetabolism’’ occurs in the setting of diminished cerebral blood flow, and the disparity between glucose supply and demand triggers a cellular energy crisis.