Abstract
We quantified the relationship between the change in post-contraction blood flow with motor unit firing rates and metrics of fatigue during intermittent, sub-maximal fatiguing contractions of the knee extensor muscles after stroke. Ten chronic stroke survivors (>1-year post-stroke) and nine controls participated. Throughout fatiguing contractions, the discharge timings of individual motor units were identified by decomposition of high-density surface EMG signals. After five consecutive contractions, a blood flow measurement through the femoral artery was obtained using an ultrasound machine and probe designed for vascular measurements. There was a greater increase of motor unit firing rates from the beginning of the fatigue protocol to the end of the fatigue protocol for the control group compared to the stroke group (14.97 ± 3.78% vs. 1.99 ± 11.90%, p = 0.023). While blood flow increased with fatigue for both groups (p = 0.003), the magnitude of post-contraction blood flow was significantly greater for the control group compared to the stroke group (p = 0.004). We found that despite the lower magnitude of muscle perfusion through the femoral artery in the stroke group, blood flow has a greater impact on peripheral fatigue for the control group; however, we observed a significant correlation between change in blood flow and motor unit firing rate modulation (r2 = 0.654, p = 0.004) during fatigue in the stroke group and not the control group (r2 = 0.024, p < 0.768). Taken together, this data showed a disruption between motor unit firing rates and post-contraction blood flow in the stroke group, suggesting that there may be a disruption to common inputs to both the reticular system and the corticospinal tract. This study provides novel insights in the relationship between the hyperemic response to exercise and motor unit firing behavior for post-stroke force production and may provide new approaches for recovery by improving both blood flow and muscle activation simultaneously.
Highlights
In addition to baseline weakness, individuals with stroke can have decreased ability to generate on-going sub-maximal forces during activities, such as walking, that require repeated activation of muscles and this can limit function
A significant interaction effect was observed in the voluntary activation measurement between the control and stroke groups [F(1,17) = 24.9, p < 0.001] as the individuals with stroke had a larger decrease in the voluntary activation from the first cycle to the last cycle of the fatigue protocol (93.6 ± 4.5% to 75.4 ± 10.5, p < 0.001) (Figure 3A)
(Figure 5); (2) greater increases in blood flow related to longer task duration for the control group but not the stroke group (Figure 6); and (3) changes in motor unit firing rates correlated with changes in blood flow for people with stroke (Figure 9)
Summary
In addition to baseline weakness, individuals with stroke can have decreased ability to generate on-going sub-maximal forces during activities, such as walking, that require repeated activation of muscles and this can limit function. Based on studies showing decreased excitability in descending motor pathways, it is not surprising that recent evidence suggests that in people with stroke, central fatigue is a more significant contributor to fatigability of the paretic leg muscles than for the non-paretic legs and healthy controls (Riley and Bilodeau, 2002; Hu et al, 2006; Klein et al, 2010; Knorr et al, 2011; Hyngstrom et al, 2012; Bowden et al, 2014; Rybar et al, 2014; Kuhnen et al, 2015; McManus et al, 2017) These studies attribute force generating deficits to baseline reductions in cortical commands, but they do not consider the impact of the build-up of metabolic by-products on muscle function that could contribute to increased fatigability of limb muscles
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