[Steven, please post a summary of any feedback that isn't sent directly to the list--otherwise this posting amounts to an ad for your blog. -Will]

Colleagues,

 

I'm pasting a response from a member of another group (Supertraining) that may be of interest. Apologies for any formatting errors. For dual group members, here's the URL for that post:

 

Regards,

 

-----------------

Jamie Carruthers wrote:

 

IMO the taper period should be highly "neural" i.e., high intensity and specific. The below was submitted some years ago by Loren Chiu:

> The IIx "overshoot" phenomenon observed with periods of detraining
> could simply be those fibers returning to their "default" states.
> The question is, does the MHC conversion provide a physiological
> reason for the observed loss of speed-strength characteristics
after
> periods of heavy strength training?

Loren wrote:
Unlikely. Research we presented at the 2002 NSCA conference indicated
that decreases in speed and power related variables during high
relative intensity overtraining were unrelated to changes in MHC
expression. The abstracts are available online for NSCA members (Fry
et al. and Schilling et al.).

Also see Chiu and Barnes in the latest Strength and Conditioning* *
Journal Myosin heavy chain expression appears to become fairly stable
following a prolonged period of training, and is thus a general
fitness characteristic.
Changes in speed and power related variables tend to occur as an
acute response or short-term adaptation making these a function of
fitness and/or fatigue after-effects. ""

**The brief, infrequent imposition of high-intensity training may
maintain or increase the specific fitness after-effects without
substantially affecting fatigue after-effects (16, 43, 64).
Therefore, this period is more than simply removing the fatigue after-
effect;
this period also maximizes the magnitude of the fitness after effect.
Thus, rather than taper, a more appropriate term for this phase of
training may be ramping.

============ ========= =====

Muscle and Performance Adaptations to High-Load Resistance Exercise
Overtraining

B.K. Schilling, A.C. Fry, L.Z.F. Chiu, E. Bernard, S.T. Belzer, and
L.W.

To examine the contributing physiological mechanisms to high-load
resistance exercise overtraining, 16 moderately weight trained males
(MEAN 6 SD; age 5 20.2 6 1.9 yrs; height 5 179.7 6 8.0 cm; weight 5
77.7 6 9.4 kg) performed 2 weeks of either a high load weight
training protocol designed to induce 1 repetition maximum (1-RM)
strength decrements (HL; n 5 8), or a normal weight training protocol
designed to maintain 1-RM strength (CON; n 5 8). After 3 weeks of
normal training to familiarize the subjects with the exercise device,
the HL group performed 10 3 1 at 100% 1-RM load daily (high load
phase) on a squat simulating machine (Tru-Squat; Southern
Xercise, Cleveland, TN), while the CON group lifted 2/wk using 50%–
70% 1-RM loads.

Test batteries were administered before (pre) and after (post) the 2-
week high load training phase. Tests included muscle biopsies from
the vastus lateralis m. that were analyzed for relative myosin heavy
chain expression (% MHC) using SDS-PAGE. Performance measures
included training-specific 1-RM strength, isometric force and EMG
variables during knee extension exercise, and various vertical jump
parameters. The high intensity phase induced an overtrained state in
the HL group based on the significant (p 5 0.03) decrease in 1 RM
levels on the squat machine (HL group, max 1 RM 5 159.3 6 10.1, last
1 RM 5 51.4 6 9.9; CON group, max 1 RM 5 146.0 6 12.9, last 1 RM 5
144.9 6 13.3). No changes in % MHC expression were observed for the
HL group (pre %I 5 14.4 6 4.2, post %I 5 15.5 6 3.7, p 5 0.341; pre
IIa 5 58.5 6 4.8, post %IIa 5 59.0 6 4.2, p 5 0.327; pre %IIb 5 26.4
6 3.4, post %IIb 5 25.4 6 3.5, p 5 0.717) or the CON group (pre %I 5
12.1 6 1.6, post %I 5 12.0 6 1.7; pre %IIa 5 63.4 6 2.7, post %IIa 5
59.7 6 3.1; pre %IIb 5 24.4 6 2.3, post %IIb 5 28.3 6 3.7). In
addition, no significant changes (p . 0.05) were observed for any of
the isometric and EMG variables, or any vertical jump variable for
either group.

These data suggest that the decreases in training-specific strength
were not due to alterations in contractile protein expression (i.e.,
MHC). Furthermore, in this case high load overtraining does not
affect measures of voluntary isometric force and EMG characteristics
and VJ performance.