Abstract

Previously we observed dissociation of skeletal muscle activation and force recovery following sustained maximal voluntary isometric contractions (MVIC). Fatigue was specifically related to reduced muscle activation within bouts; yet, incomplete recovery of force between bouts occurred with maximal muscle activation, suggesting interference in excitation-contraction coupling. PURPOSE: to investigate time-dependency of nervous system recovery following MVIC. METHODS: Men (n=29) performed two bouts (B1, B2) of sustained handgrip MVIC preceded/followed by 10-min recovery periods. Force (dynamometer) and surface EMG (sEMG) from the brachioradialis (BR), flexor carpi radialis (FCR), flexor carpi ulnaris (FCU), and flexor digitorum profundus (FDP) were collected continuously (1000 Hz) during bouts. sEMG signals were band pass filtered, rectified, and integrated (iEMG), then normalized (nEMG) to initial B1 iEMG. Force and sEMG were analyzed at 0.5 second intervals every 15 seconds. RESULTS: Recovery (B2 initial force >90% of B1) response fell into two groups; recovered (R, n=13) and not recovered (NR; n=16). Force decreased similarly in B1 (R: 77%; NR: 78%) and B2 (R: 79%; NR: 80%), yet initial B2 force was less (22%) than B1 in NR. Fatigue progressed in two-phases; B1 fast-phase decreased more rapidly with slow phase inflection occurring earlier (60 sec; 35% initial force) in R compared to NR (90 sec; 26% initial force). In R, B2 had a similar rate of decline in force and inflection (60 sec; 32% initial force). NR B2 showed a similar rate of decline in force, but inflection occurred sooner (75 sec) at the same level of initial B1 force (22%). Muscle activation (iEMG) during B1 was reduced similarly in R and NR (R: BR: 68%; FCR: 63%; FCU: 73%; FDP: 75%; NR: BR: 61%; FCR: 67%; FCU: 43%; FDP: 57%). During B2, R and NR showed similar decreases as B1, but all muscles except FCR showed lower initial B2 muscle activation compared to B1. CONCLUSIONS: Fatigue manifested in two phases; fast and slow. Recovery of force following sustained MVIC appears to be related to initial rate of decline of force (fast phase) with earlier onset of phase two. Earlier onset of phase shift may be related to changes in external compressive force and blood flow through the muscle, reducing metabolic perturbation and reflex inhibition of activation.

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