Format

Send to

Choose Destination
Eur J Appl Physiol. 2004 Aug;92(4-5):399-406.

Neuromuscular adaptations in human muscle following low intensity resistance training with vascular occlusion.

Author information

1
Department of Kinesiology, Exercise and Metabolism Research Group, McMaster University, 1280 Main St. W., Hamilton, Ontario, L8S 4K1, Canada.

Abstract

Low-intensity (approximately 50% of a single repetition maximum-1 RM) resistance training combined with vascular occlusion results in increases in muscle strength and cross-sectional area [Takarada et al. (2002) Eur J Appl Physiol 86:308-331]. The mechanisms responsible for this hypertrophy and strength gain remain elusive and no study has assessed the contribution of neuromuscular adaptations to these strength gains. We examined the effect of low-intensity training (8 weeks of unilateral elbow flexion at 50% 1 RM) both with (OCC) and without vascular occlusion (CON) on neuromuscular changes in the elbow flexors of eight previously untrained men [19.5 (0.4) years]. Following training, maximal voluntary dynamic strength increased (P<0.05) in OCC (22%) and CON (23%); however, isometric maximal voluntary contraction (MVC) strength increased in OCC only (8.3%, P<0.05). Motor unit activation, assessed by interpolated twitch, was high (approximately 98%) in OCC and CON both pre- and post-training. Evoked resting twitch torque decreased 21% in OCC (P<0.05) but was not altered in CON. Training resulted in a reduction in the twitch:MVC ratio in OCC only (29%, P<0.01). Post-activation potentiation (PAP) significantly increased by 51% in OCC (P<0.05) and was not changed in CON. We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength and causes changes in indices of neuromuscular function, such as depressed resting twitch torque and enhanced PAP.

PMID:
15205956
DOI:
10.1007/s00421-004-1072-y
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center