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End‐exercise ΔHHb/ΔVO 2 and post‐exercise local oxygen availability in relation to exercise intensity
Author(s) -
Stöcker F.,
Von Oldershausen C.,
Paternoster F. K.,
Schulz T.,
Oberhoffer R.
Publication year - 2017
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1111/cpf.12314
Subject(s) - medicine , vo2 max , exercise intensity , cardiology , physical exercise , incremental exercise , perfusion , intensity (physics) , microcirculation , vastus lateralis muscle , oxygen , heart rate , chemistry , skeletal muscle , blood pressure , physics , quantum mechanics , organic chemistry
Summary Increased local blood supply is thought to be one of the mechanisms underlying oxidative adaptations to interval training regimes. The relationship of exercise intensity with local blood supply and oxygen availability has not been sufficiently evaluated yet. The aim of this study was to examine the effect of six different intensities (40–90% peak oxygen uptake, VO 2peak ) on relative changes in oxygenated, deoxygenated and total haemoglobin (ΔO 2 Hb, Δ HH b, Δ TH b) concentration after exercise as well as end‐exercise Δ HH b/Δ VO 2 as a marker for microvascular O 2 distribution. Seventeen male subjects performed an experimental protocol consisting of 3 min cycling bouts at each exercise intensity in randomized order, separated by 5 min rests. ΔO 2 Hb and Δ HH b were monitored with near‐infrared spectroscopy of the vastus lateralis muscle, and VO 2 was assessed. Δ HH b/Δ VO 2 increased significantly from 40% to 60% VO 2 peak and decreased from 60% to 90% VO 2 peak. Post‐exercise Δ TH b and ΔO 2 Hb showed an overshoot in relation to pre‐exercise values, which was equal after 40–60% VO 2peak and rose significantly thereafter. A plateau was reached following exercise at ≥80% VO 2peak . The results suggest that there is an increasing mismatch of local O 2 delivery and utilization during exercise up to 60% VO 2peak . This insufficient local O 2 distribution is progressively improved above that intensity. Further, exercise intensities of ≥80% VO 2peak induce highest local post‐exercise O 2 availability. These effects are likely due to improved microvascular perfusion by enhanced vasodilation, which could be mediated by higher lactate production and the accompanying acidosis.