During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discussed.
Ischemic preconditioning (IPC) of one or two limbs improves performance of exercise that recruits the same limb(s). However, it is unclear whether IPC application to another limb than that in exercise is also effective and which mechanisms are involved. We investigated the effect of remote IPC (RIPC) on muscle fatigue, time to task failure, forearm hemodynamics, and deoxygenation during handgrip exercise. Thirteen men underwent RIPC in the lower limbs or a control intervention (CON), in random order, and then performed a constant load rhythmic handgrip protocol until task failure. Rates of contraction and relaxation (ΔForce/ΔTime) were used as indices of fatigue. Brachial artery blood flow and conductance, besides forearm microvascular deoxygenation, were assessed during exercise. RIPC attenuated the slowing of contraction and relaxation throughout exercise (P < 0.05 vs CON) and increased time to task failure by 11.2% (95% confidence interval: 0.7-21.7%, P <0.05 vs CON). There was no significant difference in blood flow, conductance, and deoxygenation between conditions throughout exercise (P > 0.05). In conclusion, RIPC applied to the lower limbs delayed the development of fatigue during handgrip exercise, prolonged time to task failure, but was not accompanied by changes in forearm hemodynamics and deoxygenation.
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.
OBJECTIVE -We measured plasma markers of endothelial dysfunction, vascular inflammation, and pro-coagulation in obese Hispanic/Latino children and adolescents with normal glucose tolerance and determined their relationship to body composition and indexes of glucose and lipid metabolism.
RESEARCH DESIGN AND METHODS-A total of 38 lean or obese Hispanic children and adolescents (10 -18 years of age) were selected. The overweight group (n ϭ 21) had a BMI Ͼ85th percentile for their age and sex, and the lean group (n ϭ 17) had a BMI between the 25th and 50th percentiles. Studies included an oral glucose tolerance test, measurements of plasma glucose and lipids, several markers of endothelial function and inflammation, and determination of body composition by dual X-ray absorptiometry.RESULTS -The obese group had higher systolic blood pressure and plasma triglycerides and was more insulin resistant than the lean group. The obese group also had higher plasma soluble intercellular adhesion molecule (259.5 Ϯ 60.0 vs. 223.2 Ϯ 47.5 ng/ml, P ϭ 0.047), tumor necrosis factor-␣ (2.57 Ϯ 1.1 vs. 1.74 Ϯ 0.6 pg/ml, P ϭ 0.008), high-sensitivity C-reactive protein (2.0 vs. 0.13 mg/l, P Ͻ 0.0001), plasminogen-activated inhibitor-1 (47.0 Ϯ 35.7 vs. 12.0 Ϯ 5.2 ng/ml, P Ͻ 0.0001), tissue plasminogen activator (6.1 Ϯ 1.9 vs. 4.1 Ϯ 0.8 ng/ml, P ϭ 0.001), and white blood cell count (6.9 vs. 5.3 ϫ 10 3 , P ϭ 0.031) and lower levels of adiponectin (8.7 Ϯ 3.3 vs. 12.6 Ϯ 5.2 g/ml, P ϭ 0.022). No significant differences were observed for soluble vascular cell adhesion molecule or interleukin-6. CONCLUSIONS -Overweight Hispanic children and adolescents with normal glucose tolerance exhibit increased plasma markers of endothelial dysfunction and subclinical inflammation in association with obesity and insulin resistance. These abnormalities may predispose them to the development of type 2 diabetes and cardiovascular disease.
Two autonomic tests which evaluate cardiac vagal activity, the respiratory sinus arrhythmia and the newer 4-second exercise test, have been compared. From electrocardiograph tracings, respiratory sinus arrhythmia was quantified by the ratio between the longest R-R interval during expiration and the shortest one during inspiration (E/I ratio), and the 4-second exercise test by the ratio between the last R-R interval before and the shortest one during exercise (B/C ratio). In 29 healthy subjects there was a correlation (R = 0.60, p less than 0.05) between the responses to the two tests. In a group of six healthy subjects the same tests were performed after autonomic blockade with intravenous atropine and/or propranolol. The heart rate rise during the 4-second exercise test was nearly abolished by atropine (mean +/- SD) (B/C: control = 1.53/0.33; after atropine = 1.04/0.03), whereas RSA was diminished to a lesser extent (E/I: control = 1.59/0.24; after atropine = 1.13/0.07). beta-adrenoceptor blockade did not affect the test ratios (after propranolol: B/C = 1.51/0.33 and E/I = 1.45/0.14). Successive tests during the following hour after atropine infusion showed a somewhat faster recovery of the respiratory sinus arrhythmia than the heart rate acceleration induced by the 4-second exercise test (p less than 0.05). We conclude that there may be some difference in the mechanisms which contribute to the heart rate changes in these two autonomic cardiovascular tests; these remain to be clarified. The 4-second exercise test may be an alternative to the respiratory sinus arrhythmia test in the non-invasive evaluation of cardiac parasympathetic activity.
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