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imported_dkm1987
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Clustering is effective if used for their purpose. Reduced peripheral fatique management, coupled with increased tension and maintenance of TUT.[b said:Quote[/b] (Actarus @ July 30 2005,6:15)]clustering is not effective :
My point.[b said:Quote[/b] ]Results: Measurements of blood lactate and serum hormone concentrations after the NR and WR regimens showed that the NR regimen induced strong lactate, growth hormone (GH), epinephrine (E), and norepinephrine (NE) responses
Also from Br J Sports Med2002;36:370–374
[b said:Quote[/b] ]Methods: Twenty three healthy adults (18–29 years of age; eight women) were assigned to either a high fatigue protocol (HF: four sets of 10 repetitions with 30 seconds rest between sets) to maximise metabolic stress or a low fatigue protocol (LF: 40 repetitions with 30 seconds between each repetition) to minimise changes. Subjects lifted on average 73% of their 1 repetition maximum through the full range of knee extension with both legs, three times a week. Quadriceps isometric strength of each leg was measured at a knee joint angle of 1.57 rad (90°), and a Cybex 340 isokinetic dynamometer was used to measure the angle-torque and torque-velocity relations of the non-dominant leg.
Results: At the mid-point of the training, the HF group had 50% greater gains in isometric strength, although this was not significant (4.5 weeks: HF, 13.3 (4.4)%; LF, 8.9 (3.6)%). This rate of increase was not sustained by the HF group, and after nine weeks of training all the strength measurements
showed similar improvements for both groups (isometric strength: HF, 18.2 (3.9)%; LF, 14.5 (4.0)%).
The strength gains were limited to the longer muscle lengths despite training over the full range of movement.
Also look at
"Recent Advances in the Understanding of Skeletal Muscle Fatigue"
and
J Appl Physiol 96: 218–225, 2004.
[b said:Quote[/b] ]With the current activity-rest intervals within and between bouts, it was found that MVCs induced both peripheral (16.2%) and central fatigue (12.6%), with only peripheral fatigue being correlated to the decrease in plantar flexor strength.
also
From Annu. Rev. Physiol. 2004. 66:799–828
[b said:Quote[/b] ]In contrast, an increased energy demand (reflected by lowered ATP/ADP ratio, higher AMP, and lower creatine phosphate concentrations) leads to a depression of protein synthesis (85). A recently discovered interaction between AMPK and PKB-mTOR signaling in muscle has provided a possible mechanism for this effect:
AMPK is activated by AMP and inhibited by ATP and creatine phosphate and is involved in the regulation of numerous cellular functions such as mitochondrial biogenesis and fuel metabolism (18, 86). Treatment of rats with the AMPK-activator, AICAR, resulted in a reduction in skeletal muscle protein synthesis.
This was accompanied by a decreased activation of PKB-mTOR and its downstream targets p70S6k and 4E-BP1 (87).