The insular cortex has been implicated as a region of cortical cardiovascular control, yet its role during exercise remains undefined. The purpose of the present investigation was to determine whether the insular cortex was activated during volitional dynamic exercise and to evaluate further its role as a site for regulation of autonomic activity. Eight subjects were studied during voluntary active cycling and passively induced cycling. Additionally, four of the subjects underwent passive movement combined with electrical stimulation of the legs. Increases in regional cerebral blood flow (rCBF) distribution were determined for each individual using single‐photon emission‐computed tomography (SPECT) co‐registered with magnetic resonance (MR) images to define exact anatomical sites of cerebral activation during each condition. The rCBF significantly increased in the left insula during active, but not passive cycling. There were no significant changes in rCBF for the right insula. Also, the magnitude of rCBF increase for leg primary motor areas was significantly greater for both active cycling and passive cycling combined with electrical stimulation compared with passive cycling alone. These findings provide the first evidence of insular activation during dynamic exercise in humans, suggesting that the left insular cortex may serve as a site for cortical regulation of cardiac autonomic (parasympathetic) activity. Additionally, findings during passive cycling with electrical stimulation support the role of leg muscle afferent input towards the full activation of leg motor areas.

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R-R interval (RRI) changes were recorded from 15 healthy volunteers in response to volitional unloaded cycling and passively induced cycling (PC). PC was also combined with electrical stimulation (n = 5) to increase muscle mechanoreceptor activation. The electrocardiogram and leg electromyographic activity were continuously sampled by computer at 1,000 Hz, and an electronic trigger was used to designate the instant of pedal movement within an RRI. Changes in RRI were expressed as the difference of the interval in which the trigger was activated (onset RRI) and the average of resting intervals (4-8 intervals). Volitional unloaded cycling produced the greatest decrease in the onset RRI [907 +/- 11 (SE) to 855 +/- 10 ms; -5.4 +/- 0.4%; P < 0.01] when movement was initiated within the first one-third of the interval. A shortening of the onset RRI was also detected when trigger activation occurred in the last one-third of the interval (906 +/- 12 to 875 +/- 11 ms; -3.1 +/- 0.4%; P < 0.01). There were no significant effects of PC alone on the onset RRI. However, PC+electrical stimulation shortened the onset RRI (906 +/- 12 to 883 +/- 11 ms; -2.5 +/- 0.2%; P < 0.05) but only when the movement was initiated within the first one-third of the interval.(ABSTRACT TRUNCATED AT 250 WORDS)

The hemodynamic effects of reducing venous return were assessed beat by beat at the onset of upright dynamic exercise. Mean arterial pressure (MAP), heart rate, and left ventricular end-systolic (ESV) and end-diastolic volumes (EDV; two-dimensional echocardiography) were measured in 10 healthy men during 20-s trials of upright cycling (30 W; 60 rpm). Exercise was performed either with or without venous occlusion of the legs (bilateral thigh cuffs inflated to 100 mmHg) in a random order. Without venous occlusion, MAP and cardiac output (CO) increased, and total peripheral resistance (TPR) decreased (P < 0.05) during the first approximately 10 beats after the onset of exercise. Initially, the CO response was accounted for by a rapid heart rate acceleration and, after approximately 15 cardiac cycles, by an increase in stroke volume, which occurred with a decrease in ESV and no change in EDV. With venous occlusion, EDV decreased and stroke volume did not rise during exercise. Thus the CO response was blunted by venous occlusion and MAP did not increase initially. However, after approximately 13 heart beats, MAP increased with no change in TPR. These findings suggest that compensatory mechanisms can elicit an increase in MAP at the onset of mild upright cycling when the CO response is blunted by reducing venous return.