Beschreibung:
<jats:sec><jats:title>Introduction</jats:title><jats:p>Age related declines in oxidative metabolic capacity have been attributed to slowing of O<jats:sub>2</jats:sub> delivery and utilization. While these declines are pronounced in postmenopausal women, it is unclear how these changes compare with age‐matched men. This study aimed to phenotype adjustments of muscle oxy‐ and‐ deoxygenation during transitions of low intensity fixed‐load exercise in postmenopausal women and age‐matched men.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Healthy postmenopausal women (PW) and men (M) (N = 7 and 6; age 57 ± 7 and 61 ± 10 years; BMI 26 ± 2 and 27 ± 4 kg/m<jats:sup>2</jats:sup>, respectively, all <jats:italic>P</jats:italic>>0.05) completed 3 identical 8 min transients of fixed pedal rate (=35) and load (=20W) ergometry wearing bilateral thigh cuffs. After 5 min of rest, exercise began with 3 min without thigh cuff inflation followed by 5 min of exercise+cuff inflation at 90 mm Hg (to provoke locomotor congestion). Deoxy (HHb)‐ and total (Hb<jats:sub>tot</jats:sub>)‐ hemoglobin were measured by near‐infrared spectroscopy (NIRS) at the right calf. Data were sampled at 1 s intervals and ensemble averaged across 3 transients and binned to 10 s epochs for each participant prior to mono‐exponential modeling: Y<jats:sub>B</jats:sub> + A [1 − e<jats:sup>−(t‐TD)/τ</jats:sup>]; where Y<jats:sub>B</jats:sub> = baseline value of Y for the 30 s prior to the step transition; τ = time constant; A = asymptote; TD = time delay. Mean response time (MRT) = TD + τ. Kinetics were modelled for the transition from exercise without to exercise+cuff inflation.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Following the exercise on‐transient, TD was 9±4 vs. 7±3 s (P=0.35) and 8±4 vs. 6±3 s (P=0.28) for PW vs. M prior to the rise in ΔHHb or ΔHb<jats:sub>tot</jats:sub>, respectively. For PW vs. M, the A representing the rise in ΔHHb was 8±7 vs. 15±7 μM (P=0.04) and for ΔHb<jats:sub>tot</jats:sub> it was 13±8 vs. 18±8 μM (P=0.17), respectively. The kinetics of HHb following the exercise+cuff onset were similar for PW and M (τ=53±38 vs. 34±9 s, respectively, P=0.36) as well as for Hb<jats:sub>tot</jats:sub> (τ=43±29 vs. 29±16 s, respectively, P=0.43). The overall time course for the change in HHb (MRT=62±35 vs. 41±8 s, P=0.27) or Hb<jats:sub>tot</jats:sub> (MRT=51±27 vs. 35±14 s, P=0.31) did not differ for PW and M, respectively.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Despite age‐matched men demonstrating greater ΔHHb compared with PW, these data do not support the hypothesis that following exercise onset, the rate of locomotor hemodynamic adjustment and O<jats:sub>2</jats:sub> extraction for a given metabolic demand differ between these groups. Thus, as opposed to gross factors of blood flow and O<jats:sub>2</jats:sub> delivery, effects such as slowing of the rate of activation and/or processes regulating oxidative phosphorylation and mitochondrial respiration may play a stronger role in explaining differences in oxidative metabolic capacity between PW and M.</jats:p><jats:p><jats:bold>Support or Funding Information</jats:bold></jats:p><jats:p>Funding for this work was supported by National Institutes of Health [RO1‐HL126638 to TPO]; and American Heart Association [16POST30260021 to EHV] and National Institutes of Health [HL138814 to EHV].</jats:p><jats:p>This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in <jats:italic>The FASEB Journal</jats:italic>.</jats:p></jats:sec>