Ischemic preconditioning reduces hemodynamic response during metaboreflex activation

Abstract

Ischemic preconditioning (IP) has been shown to improve exercise performance and to delay fatigue. However, the precise mechanisms through which IP operates remain elusive. It has been hypothesized that IP lowers the sensation of fatigue by reducing the discharge of group III and IV nerve endings, which also regulate hemodynamics during the metaboreflex. We hypothesized that IP reduces the blood pressure response during the metaboreflex. Fourteen healthy males (age between 25 and 48 yr) participated in this study. They underwent the following randomly assigned protocol: postexercise muscle ischemia (PEMI) test, during which the metaboreflex was elicited after dynamic handgrip; control exercise recovery session (CER) test; and PEMI after IP (IP-PEMI) test. IP was obtained by occluding forearm circulation for three cycles of 5 min spaced by 5 min of reperfusion. Hemodynamics were evaluated by echocardiography and impedance cardiography. The main results were that after IP the mean arterial pressure response was reduced compared with the PEMI test (means ± SD +3.37 ± 6.41 vs. +9.16 ± 7.09 mmHg, respectively). This was the consequence of an impaired venous return that impaired the stroke volume during the IP-PEMI more than during the PEMI test (-1.43 ± 15.35 vs. +10.28 ± 10.479 ml, respectively). It was concluded that during the metaboreflex, IP affects hemodynamics mainly because it impairs the capacity to augment venous return and to recruit the cardiac preload reserve. It was hypothesized that this is the consequence of an increased nitric oxide production, which reduces the possibility to constrict venous capacity vessels.

Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men

“…Our findings during PECO are in contrast with a prior observation following rhythmic handgrip exercise (Mulliri et al. ), which demonstrated a blunted pressor response secondary to reductions in stroke volume and cardiac preload, as well as an increase in total vascular resistance. The reductions in stroke volume and mean arterial pressure may have unloaded the cardiopulmonary or arterial baroreflex, increasing peripheral vasoconstrictor outflow (MSNA) (Floras et al.…”

“…) and explaining the rise in total vascular resistance (Mulliri et al. ). The mechanisms responsible for a reduction in stroke volume or cardiac preload following IPC are not clear but have been suggested to involve nitric oxide‐mediated venodilation (Mulliri et al.…”

“…The mechanisms responsible for a reduction in stroke volume or cardiac preload following IPC are not clear but have been suggested to involve nitric oxide‐mediated venodilation (Mulliri et al. ). IPC has been shown to increase nitric oxide bioavailability (Costa et al.…”

“…In contrast, IPC was reported recently to increase systemic vascular resistance during post‐exercise circulatory occlusion (PECO) (Mulliri et al. ), a technique commonly used to isolate the influence of the muscle metaboreflex (Mitchell et al. ; Victor et al.…”

Effects of Six Months Training on Physical Capacity and Metaboreflex Activity in Patients with Multiple Sclerosis

“…It has been hypothesized that the discharges of afferent group III and IV nerve endings in the muscle, which are responsible for the metaboreflex eliciting, are at least in part also responsible for the sensation of fatigue. Feedback from these nervous afferents potentially inhibits central motor drive and facilitates central fatigue, thereby limiting exercise performance (Amann et al, 2008; Mulliri et al, 2016). Thus, fatigue may be hypothetically related to the level of metaboreflex activation.…”