Premium
Effects of Ischemic Preconditioning on Neural and Hemodynamic Responses to Muscle Metaboreflex Activation
Author(s) -
Incognito Anthony,
Doherty Connor,
Lee Jordan,
Millar Philip
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1289.9
Subject(s) - medicine , microneurography , cardiology , isometric exercise , blood pressure , heart rate , anesthesia , stroke volume , hemodynamics , cuff , baroreflex , surgery
Ischemic preconditioning (IPC), the exposure to brief intermittent periods of circulatory occlusion, has been demonstrated to reduce submaximal lactate accumulation and improve exercise performance. Lactic acid is a potent stimulator of the muscle metaboreflex, which results in increased efferent sympathetic outflow to skeletal muscle. We tested the hypothesis that IPC would attenuate the neural (muscle sympathetic nerve activity (MSNA)) and hemodynamic response to activation of the muscle metaboreflex during post‐exercise circulatory occlusion (PECO). In a randomized‐controlled design, 17 healthy young (24±3 yrs), normotensive (107±7/64±5 mmHg) men were allocated to IPC (n=10) or sham‐IPC (n=7) treatment groups. IPC and sham‐IPC treatments consisted of 3 cycles of 5 min cuff inflation at 200 mmHg or 20 mmHg, respectively, each followed by a 5 min cuff deflation. Continuous measurements of MSNA (microneurography), blood pressure, heart rate, stroke volume, cardiac output and total peripheral resistance were collected at rest and during 2 min of isometric handgrip (IHG) at 30% of maximal voluntary contraction followed by 3 min of PECO, before and after an acute bout of IPC or sham‐IPC. Compared to baseline, MSNA burst frequency increased during IHG and PECO (both p<0.01) but was unchanged following IPC (IHG Δ9±10 vs. Δ10±7; PECO Δ7±11 vs. Δ8±7 bursts/min) or sham‐IPC (IHG: Δ5±2 vs. Δ5±3; PECO: Δ5±2 vs. Δ3±6 bursts/min). Systolic and diastolic blood pressure were increased during IHG and PECO (both p<0.01) but unchanged following IPC (IHG Δ23±13/17±9 vs. Δ21±10/16±7; PECO Δ19±14/11±7 vs. Δ18±15/11±8 mmHg) or sham‐IPC (IHG: Δ15±8/12±6 vs. Δ16±5/11±4; PECO Δ11±7/8±5 vs. Δ10±6/5±4 mmHg). Heart rate was increased during IHG (p<0.01) but not PECO and unchanged following IPC (IHG Δ18±11 vs. Δ19±12; PECO Δ5±7 vs. Δ6±8 bpm) or sham‐IPC (IHG: Δ15±9 vs. Δ13±8; PECO: Δ3±5 vs. Δ0±5 bursts/min). Similarly, stroke volume, cardiac output, and total peripheral resistance responses were unchanged by IPC or sham‐IPC (p>0.05). These findings suggest that IPC is not capable of modulating the efferent sympathetic or hemodynamic responses during exercise or muscle metaboreflex activation. The mechanisms responsible for improvements in exercise capacity and time‐trial performance following IPC require further investigation but are unlikely neurogenic. Support or Funding Information Canadian Institutes of Health Research (CIHR), National Science and Engineering Research Council (NSERC)