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Effect of Leg Blood Flow Restriction during Cycling on Cerebral Perfusion: Role of Carbon Dioxide
Author(s) -
Prodel Eliza,
Balanos George M.,
Braz Igor D.,
Nobrega Antonio C. L.,
Vianna Lauro C.,
Fisher James P.
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.1289.1
Subject(s) - hyperventilation , cerebral blood flow , medicine , cardiology , perfusion , cycling , middle cerebral artery , hemodynamics , blood flow , blood pressure , cerebral perfusion pressure , anesthesia , ischemia , archaeology , history
Exercise with blood flow restriction (BFR) enhances skeletal muscle metabolite accumulation and has been used to stimulate training‐induced improvements in strength and endurance, but the consequences for the cerebral circulation are unknown. The activation of group III and IV skeletal muscle afferents by exercise‐induced metabolites (muscle metaboreflex) has been suggested to increase cerebral perfusion during exercise. However, this may be masked by a hyperventilation related decrease in the partial pressure of arterial carbon dioxide (indexed by partial pressure of end‐tidal carbon dioxide; P ET CO 2 ). We sought to determine how muscle metaboreflex activation with BFR affects cerebral blood flow and whether this is secondary to confounding changes in P ET CO 2 . In 11 healthy male participants (age 25±4 years; height 180±1 cm; weight 71±7 kg; mean±SD) we measured middle cerebral artery mean blood velocity (MCA V m ), internal carotid artery blood flow (ICA Q ) and P ET CO 2 , during leg cycling exercise under free‐flow conditions (target heart rate at 120 bpm) and with BFR. Trials were conducted where P ET CO 2 was permitted to fluctuate spontaneously (control) and where P ET CO 2 was clamped at 1 mmHg above resting levels. In the control trial, P ET CO 2 was slightly increased from rest during leg cycling (Δ2.2±0.3 mmHg; P<0.05) and significantly decreased during exercise with BFR (Δ‐4.8±0.9 mmHg; P<0.05). P ET CO 2 remained unchanged throughout the clamp trial. Leg cycling under free‐flow conditions evoked similar increases in MCA V m during the control (Δ6.5±1.8 cm.s −1 ) and P ET CO 2 clamp (Δ6.8±2.4 cm.s −1 ) trials (P<0.05 vs. rest). During exercise with BFR a further increase in MCA V m was noted in the P ET CO 2 clamp trial (Δ5.9±1.4 cm.s −1 ; P<0.05 vs. rest and free‐flow exercise), but not in the control trial. In both trials, ICA Q was not significantly changed from rest during leg cycling under free‐flow conditions (control Δ‐3.5±10.31 ml.min −1 ; P ET CO 2 clamp Δ7.2±7.41 ml.min −1 ; P>0.05 vs. rest). During exercise with BFR, ICA Q was significantly increased when P ET CO 2 was clamped (Δ27.2±6.6 ml.min −1 ; P<0.05 vs. rest), but was decreased in the control trial (Δ‐22.7±12.1 ml.min −1 ; P<0.05 vs. rest). In conclusion, enhanced muscle metaboreflex activation with leg BFR during cycling increases cerebral blood flow, but only when P ET CO 2 is maintained at resting levels. Support or Funding Information This study was supported by Coordination for the Improvement of Higher Education Personnel (CAPES‐Brazil) through the program Science without Borders.