Igor A. Fernandes

Remote ischemic preconditioning delays fatigue development during handgrip exercise

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.

Preserved flow-mediated dilation but delayed time-to-peak diameter in individuals with metabolic syndrome.

Inconsistent evidences of the metabolic syndrome (MetS) impact on vascular reactivity raise questions on flow‐mediated dilation (FMD) discriminatory power for disturbances induced by this clustering of risk factors. Previous reports, however, suggest that covariates such as the follow‐up of the artery diameter changes, the arterial size and shear stress affect FMD responses and consequently its discriminatory power for distinctive clinical profiles.

Intrathecal fentanyl abolishes the exaggerated blood pressure response to cycling in hypertensive men

The increase in blood pressure observed during physical activities is exaggerated in patients with hypertension, exposing them to a higher cardiovascular risk. Neural signals from the skeletal muscles appear to be overactive, resulting in this abnormal response in hypertensive patients. In the present study, we tested whether the attenuation of these neural signals in hypertensive patients could normalize their abnormal increase in blood pressure during physical activity. Attenuation of the neural signals from the leg muscles with intrathecal fentanyl injection reduced the blood pressure of hypertensive men during cycling exercise to a level comparable to that of normotensive men. Skeletal muscle afferent overactivity causes the abnormal cardiovascular response to exercise and was reverted in this experimental model, appearing as potential target for treatment.

Aerobic exercise acutely prevents the endothelial dysfunction induced by mental stress among subjects with metabolic syndrome: the role of shear rate

Mental stress induces transient endothelial dysfunction, which is an important finding for subjects at cardiometabolic risk. Thus, we tested whether aerobic exercise prevents this dysfunction among subjects with metabolic syndrome (MetS) and whether an increase in shear rate during exercise plays a role in this phenomenon. Subjects with MetS participated in two protocols. In protocol 1 (n = 16), endothelial function was assessed using brachial artery flow-mediated dilation (FMD). Subjects then underwent a mental stress test followed by either 40 min of leg cycling or rest across two randomized sessions. FMD was assessed again at 30 and 60 min after exercise or rest, with a second mental stress test in between. Mental stress reduced FMD at 30 and 60 min after the rest session (baseline: 7.7 ± 0.4%, 30 min: 5.4 ± 0.5%, and 60 min: 3.9 ± 0.5%, P < 0.05 vs. baseline), whereas exercise prevented this reduction (baseline: 7.5 ± 0.4%, 30 min: 7.2 ± 0.7%, and 60 min: 8.7 ± 0.8%, P > 0.05 vs. baseline). Protocol 2 (n = 5) was similar to protocol 1 except that the first period of mental stress was followed by either exercise in which the brachial artery shear rate was attenuated via forearm cuff inflation or exercise without a cuff. Noncuffed exercise prevented the reduction in FMD (baseline: 7.5 ± 0.7%, 30 min: 7.0 ± 0.7%, and 60 min: 8.7 ± 0.8%, P > 0.05 vs. baseline), whereas cuffed exercise failed to prevent this reduction (baseline: 7.5 ± 0.6%, 30 min: 5.4 ± 0.8%, and 60 min: 4.1 ± 0.9%, P < 0.05 vs. baseline). In conclusion, exercise prevented mental stress-induced endothelial dysfunction among subjects with MetS, and an increase in shear rate during exercise mediated this effect.

Diving and Exercise: The interaction of trigeminal receptors and muscle metaboreceptors on muscle sympathetic nerve activity in humans

Swimming involves muscular activity and submersion, creating a conflict of autonomic reflexes elicited by the trigeminal receptors and skeletal muscle afferents. We sought to determine the autonomic cardiovascular responses to separate and concurrent stimulation of the trigeminal cutaneous receptors and metabolically sensitive skeletal muscle afferents (muscle metaboreflex). In eight healthy men (30 ± 2 yr) muscle sympathetic nerve activity (MSNA; microneurography), mean arterial pressure (MAP; Finometer), femoral artery blood flow (duplex Doppler ultrasonography), and femoral vascular conductance (femoral artery blood flow/MAP) were assessed during the following three experimental conditions: 1) facial cooling (trigeminal nerve stimulation), 2) postexercise ischemia (PEI; muscle metaboreflex activation) following isometric handgrip, and 3) trigeminal nerve stimulation with concurrent PEI. Trigeminal nerve stimulation produced significant increases in MSNA total activity (Δ347 ± 167%) and MAP (Δ21 ± 5%) and a reduction in femoral artery vascular conductance (Δ-17 ± 9%). PEI also evoked significant increases in MSNA total activity (Δ234 ± 83%) and MAP (Δ36 ± 4%) and a slight nonsignificant reduction in femoral artery vascular conductance (Δ-9 ± 12%). Trigeminal nerve stimulation with concurrent PEI evoked changes in MSNA total activity (Δ341 ± 96%), MAP (Δ39 ± 4%), and femoral artery vascular conductance (Δ-20 ± 9%) that were similar to those evoked by either separate trigeminal nerve stimulation or separate PEI. Thus, excitatory inputs from the trigeminal nerve and metabolically sensitive skeletal muscle afferents do not summate algebraically in eliciting a MSNA and cardiovascular response but rather exhibit synaptic occlusion, suggesting a high degree of convergent inputs on output neurons.

Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise.

Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (-9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: -0.8 ± 0.8 vs. ipsilateral: -2.6 ± 1.3 ml·min(-1)·mmHg(-1), P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced (P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: -0.4 ± 0.7 vs. ipsilateral: -0.4 ± 1.0 ml·min(-1)·mmHg(-1), P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.

Welcome the carotid chemoreflex to the ‘neural control of the circulation during exercise’ club

Chemoreceptors in the brain (central chemoreceptors) and in the carotid sinus (peripheral chemoreceptors) are known to exert powerful influence over autonomic control during exposure to hypercapnia and hypoxia, respectively. However, the contributionofchemoreceptorstotheautonomic response to exercise, and thus its influence on the cardiovascular response to exercise, has not received much attention. Stickland et al. (2007) showed for the first time that the inhibition of carotid chemoreceptors by closed-carotid infusion of dopamine or hyperoxic Ringer solution at rest did not change blood flow and conductance in the hindlimb of healthy dogs, but caused an immediate vasodilatory response in the hindlimb of dogs with heart failure. During mild exercise, inhibitionofcarotidchemoreceptorscaused vasodilatation in the hindlimb of both healthy dogs and dogs with heart failure. In addition, it was shown that this response was entirely attributed to a decrease in the sympathetic restraint of skeletal muscle blood flow during exercise, since the vasodilatory response was abolished after infusion of an alpha adrenergic blocker (phentolamine) both in healthy dogs and in dogs with heart failure. Thereafter,Sticklandetal.(2008)elegantly translated these findings to exercising healthy humans. They showed that the transient inhibition of the carotid chemoreceptors by inhalation of hyperoxic gas during dynamic handgrip exercise reduced muscle sympathetic nerve activity (MSNA) by approximately 35%, while the transient stimulation of the carotid chemoreceptors by inhalation of hypoxic gas increased MSNA with a similar time delay to that obtained with carotid chemoreceptors inhibition via hyperoxia. Hence, these results highlighted the important role of the carotid chemoreflex in regulating the sympathoexcitation during exercise in healthy humans. Nonetheless, at this point, it was not known if the carotid chemoreceptors indeed influence skeletal muscle bloodflowandvascularconductanceduring exercise in humans.

Heterogeneity of rectus femoris muscle architectural adaptations after two different 14-week resistance training programmes

This study aimed to determine the architectural changes of rectus femoris muscle at distinctive sites of the thigh length after two different 14‐week resistance training programmes.

Oscillatory blood pressure response to the onset of cycling exercise in men: role of group III/IV muscle afferents

What is the central question of this study? Neural feedback from group III/IV muscle afferents has a key role in regulation of cardiovascular responses to exercise. Blood pressure oscillates in the first seconds of dynamic exercise, but the contribution of muscle afferent feedback to this pattern is unclear. What is the main finding and its importance? We demonstrate that attenuation of group III/IV muscle afferent feedback by spinal fentanyl impairs the pressor response after 10 s of moderate leg cycling exercise, but this afferent feedback does not appear to be necessary for induction of the oscillatory pattern of blood pressure at the onset of exercise.

Reduced arterial vasodilatation in response to hypoxia impairs cerebral and peripheral oxygen delivery in hypertensive men

Hypoxaemia evokes a repertoire of homeostatic adjustments that maintain oxygen supply to organs and tissues including the brain and skeletal muscles. Because hypertensive patients have impaired endothelial‐dependent vasodilatation and an increased sympathetic response to arterial oxygen desaturation, we investigated whether hypertension impairs isocapnic hypoxia‐induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. In middle‐aged hypertensive men, vertebral and femoral artery blood flow do not increase in response to isocapnic hypoxia, limiting brain and peripheral hyperaemia and oxygen supply. Increased chemoreflex‐induced sympathetic activation impairs skeletal muscle perfusion and oxygen supply, whereas an attenuation of local vasodilatory signalling in the posterior cerebrovasculature reduced brain hyperperfusion of hypertensive middle‐aged men in response to isocapnic hypoxia.