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1

Discuss the key methodology used by Atherton (2005) in rodents to look at selective activation??

Low frequency stimulation was used to mimic endurance exercise - isometric contractions at 50hz and 10hz with a 10ms duration, continuously for 3h.

High frequency stimulation to mimic res ex - isometric contractions involving 10 sets of 6 reps at 50hz and 100hz with a 7ms delay on contractions - 3 seconds in length with 10 sec recovery, 1 min rest between sets.

2

Discuss the LFS results from Atherton (2005)??

In LFS, a preferential increase in AMPK phosphorylation and PGC-1a gene expression was seen in skeletal muscle.

AMPK thr172 was sig higher post and 3h post in LFS compared to HFS, PGC-1a just sig higher post

3

Discuss the HFS results from Atherton et al (2005)???

In HFS, a preferential increase in mTORC1 and S6K1 phosphorylation in skeletal muscle can be seen.
- mTORser2448 was significantly higher post in HFS compared to LFS
- s6kthr389 was sig higher post and 3h post in HFS compared to LFS

HFS increases myofibrillar/sarcoplasmic protein synthesis in SM (FSR significantly higher in HFS than LFS and control)

The authors proposed an AMPK-PKB switch that regulates the divergent adaptive response to LFS and HFS.

4

Wilkinson et al (2008) looked at the differential effects of res and endurance exercise in the fed state on signalling muscle phosphorylation and PS in human skeletal muscle. What did they find??

Found a preferential increase in myofibrillar FSR in the trained and untrained state post-ex.
Also found an increase in mitochondrial FSR following endurance exercise in both the trained and untrained.

In contrast to Atherton (2005), there was no difference in AMPK phosphorylation between the two groups.
Only difference was AKT phosphorylation was seen post training in the trained RES ex group (0hr post)
Only difference observed in S6K1 phosphorylation was observed in untrained individuals in the resistance exercise group (4hours post)

5

Discuss the key concurrent training paper from Hickson (1980)?? - methodology

Strength group: 5 leg session a week for 10 weeks, 80% 1RM with 3 min recovery

Endurance group: 6 sessions a week for 10 weeks, cycling intervals and continuous running training.

Strength + endurance (2h recovery between them)

6

Discuss the key concurrent training paper from Hickson (1980)?? - results

Strength increases linearly in strength group. In concomitant group, it tapered off at around 7 weeks. In endurance group it barely improved.

Cycling work (kj)'was higher in endurance than concomitant.
Endurance and concomitant training improved Vo2 max in both cycling and running tests whereas res ex did not.

At the upper limits, aerobic training interferes with further strength increases.

7

Discuss Bylund-Fellenius et al (1984)??

Showed that protein synthesis is lower after contraction when muscle energy stays is reduced .

When looking at recovery in gastroc and TA with low perfusion, protein synthesis fails to reach normal levels.

8

Discuss Bolster et al (2002)??

Showed that the AMPK activator AICAR (mimics AMP) reduces protein synthesis and mTORC1 activity in rat skeletal muscle.

MPS, mTORser2448 phosphorylation and s6K1thr389 (significant) were all lower for AICAR compared to control. See paper fro exact significances as not clear.

9

Discuss Thomson et al (2008)???

Looked at phosphorylation of AMPKthr172 in the extensor digitorum longus muscle for saline or AICAR treated rats immediately post contraction.

AICAR stimulation was significantly higher than AICAR control immediately after stim/20 min post stim and 40 min post stim.
S6K1thr389 phosphorylation non existent in control post stim, and significantly higher in saline compared to AICAR group.

10

Discuss Chen et al (2003)???

Found AMPK activity and signalling in skeletal muscle is dependent on ex intensity and energy status.

3 ways to activate AMPK :- 1. Decrease ATP content 2.increase AMP content 3.deplete glycogen stores

11

What did Camera et al (2012) find??

Found low muscle glycogen concentration does not suppress the anabolic response to resistance exercise.

Showed no difference in myofibrillar FSR between placebo or nutrient (500ml) or between normal and low.
Also no differences in S6K1thr389 and rps6ser235/6 phosphorylation.

Concluded that glycogen depletion has no effect on acute FSR post res ex and thereby questioning the role of energy depletion on PS.

12

Apro et al (2013) looked at if endurance exercise blocks the beneficial signalling effects of RE. What did they find ??

Suggests that MTORC1 related signalling may be suppressed at later timepoints when endurance exercise is performed immediately after RE
- showed a blunted S6k1thr389 phosphorylation in resistance and endurance compared to just resistance.

13

Donges et al (2012) looked at middle aged untrained subjects, discuss the design??

Subjects completed 3 exercise trials each separated by 1wk.
RE - 8 sets of 8 reps of leg ext @70%1RM.
AE - 40 mins of cycling at 55% peak aerobic power
CE - completed 50% of both trials immediately after one another

14

Discuss Donges (2012) results ??

CE results in an amplified myofibrillar FSR in contrast to aerobic ex which has no effect on myo FSR.
Mitochondrial FSR is sensitive to all conditions.
The ratio of phosphorylated to total protein content for rpS6ser235/236mwas significantly higher 1h post for RE.

15

Discuss Babcock et al (2012)??

Building from O'Connor and Paulath (2007) who discussed the importance of satellite cells and their role in driving the latter stages of hypertrophy, Babcock found concurrent exercise and aerobic exercise interferes with the satellite cell response to acute resistance exercise.