Figure 1.
Example of muscle spindle discharge locked to the arterial pulsations.
This afferent responded with one single spike at the early part of the upbeat of pulse wave and about ∼250 ms following R-wave in ECG signal. Note also muscle sympathetic burst activity in nerve signal.
Figure 2.
Pulse-wave driven muscle spindles.
Each panel shows post stimulus time histogram at the bottom and raster sweeps of single cardiac cycles on top. A–C, Afferents typically responded with one single spike phase-locked to the cardiac cycle. D–F, Afferents responding with two spikes at the time corresponding to the pulse wave upbeat. A third spike corresponding to the time of dicrotic notch is generated by afferents depicted in E and F (see also B&D). Each bar indicates total count of spikes falling within corresponding 0.02 s time bin. Each dot in raster plot indicates one spike.
Figure 3.
Phase-locking and resetting of ongoing muscle spindle discharge.
For further details see text and legend of Fig. 2.
Figure 4.
Examples of R-wave triggered discharge rate averages in pulse-wave modulated muscle spindles.
Panels on the left (A–E) illustrate five afferents showing positive peak (excitatory response to the upbeat of pulse wave). Panels on the right (F–J) show five afferents displaying an initial negative peak (inhibitory effect). Discharge rate modulation is expressed as % difference from mean discharge rate. Time elapsed after R-wave is shown on the x-axis. Text box indicates the relative amount of variance explained by arterial pulsations (EV). Black thick lines represent averages. Gray thin lines show overlay of individual discharge rate traces in every cardiac cycle.
Figure 5.
Examples of spectral analyses for the same ten afferents illustrated in figure 4 A–J, respectively.
The gray shaded area shows the distribution of spectral power represented as a percentage of total power. Mean heart rate (HR) is indicated by the left dashed vertical line and numeric value. The right dashed vertical line indicates the frequency twice that of the heart rate. The thin black line indicates the 95% confidence interval, determined using the surrogate power spectrum distribution.
Figure 6.
Principal component analysis (PCA) of 55 spontaneously active afferents in control (resting) conditions.
Top panels display the first principal component of the time-domain analysis (explained variance = 48%), i.e. R-wave triggered discharge rate averages, extracting the modulation pattern common across afferents. Panel A shows the projection of the data with characteristic regions that are stable (p<0.01) across recordings depicted in gray. The time axis is normalized to the average RR-interval for each afferent before performing PCA. Panel B shows the histogram of the eigenvector coefficients representing the strength of this pattern in each afferent. Afferents with significant pulse wave modulation are depicted in black, non-significant afferents in grey. Lower panels display the first principal component of the frequency-domain analysis (explained variance = 43%), representing the common power spectrum across afferents (Panel C). The frequency axis is normalized to the average heart rate for each afferent before performing PCA. Panels D shows the histogram of the corresponding eigenvector coefficients.
Figure 7.
Comparison of R-wave triggered discharge rate averages between different physiological conditions.
Modulation of discharge rate is normalized to the variance in discharge rate over the whole recording and plotted as a function of time, measured from the R-wave of ECG signal. Afferents are grouped according to whether the initial modulatory peak in response to the upbeat of the pulse wave is positive (graphs in left column) or negative (graphs in right column), as revealed by the sign of the eigenvector coefficient (Fig. 6B). A & B, changes in discharge rate modulation during inspiratory-capacity apnoea. C & D, changes in discharge rate modulation during muscle pain. E & F, changes in discharge rate modulation during skin pain. G & H, discharge rate modulation during active voluntary contraction.