fourth set of LL-BFR, this effect rapidly recovered
upon reperfusion at 2 minutes post-exercise. Further,
Cook (2013) found no change in central activation
post-exercise between HL, LL-BFR or LL conditions.
This outcome would explain the lack of change seen
at 60 minutes post-exercise in the present study.
Together, with the results mentioned previously,
evidence suggests that the decrement in
neuromuscular performance observed in the present
study is due to peripheral fatigue, as opposed to
central factors.
In conclusion, HL and CBFR squat exercise
appears to impair neuromuscular performance to a
similar extent at 1-hour post-exercise despite the
reduced mechanical stress and total training volume
completed in the CBFR condition. The impairment in
performance was due to peripheral factors as
voluntary activation of the knee extensors remained
unchanged following exercise. Further research
should seek to extend the timeline of neuromuscular
performance recovery past 60 minutes to determine if
differences exist between HL and CBFR.
Furthermore, whether the equivalent acute
neuromuscular responses between HL and CBFR
exercise translate to similar chronic hypertrophic
changes should be evaluated, as LL-BFR training
may serve as a strategy to manage total training stress
and chronic fatigue during busy periods of training
and competition.
ACKNOWLEDGEMENTS
This work is supported by the Queensland Academy
of Sport’s Sport Performance Innovation and
Knowledge Excellence unit.
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