Impact of supine exercise on muscle deoxygenation kinetics heterogeneity: mechanistic insights into slow pulmonary oxygen uptake dynamics

Abstract

Oxygen uptake (VO2) kinetics are slowed in the supine (S) position due to impaired muscle O2 delivery (QO2), however, these conclusions are predicated on single-site measurements in superficial muscle using continuous-wave near-infrared spectroscopy (NIRS). This study aimed to determine the impact of body position (i.e. upright U vs. S) on deep and superficial muscle deoxygenation (deoxy[heme]) using time-resolved (TR-) NIRS, and how these relate to slowed pulmonary VO2 kinetics. 17 healthy men completed constant power tests during 1) S heavy intensity exercise; and 2) U exercise at the same absolute work rate, with a subset of 10 completing additional tests at the same relative work rate as S. Pulmonary VO2 was measured breath-by-breath and, deoxy- and total[heme] were resolved via TR-NIRS in the superficial and deep vastus lateralis and superficial rectus femoris. The fundamental phase VO2 time constant was increased during S compared to U (S: 36±10 vs. U: 27±8 s, P<0.001). The deoxy[heme] amplitude (S: 25-28 vs. U: 13-18 µM, P<0.05) and total[heme] amplitude (S: 17-20 vs. U: 9-16µM, P<0.05) were greater in S compared to U and were consistent for the same absolute (above data) and relative work rates (n=10, all P<0.05). The greater deoxy- and total[heme] amplitudes in S vs. U supports that reduced perfusive QO2 in S, even within deep muscle, necessitated a greater reliance on fractional O2 extraction and diffusive QO2. The slower VO2 kinetics in S vs. U demonstrates that, ultimately, these adaptations were insufficient to prevent impairments in whole-body oxidative metabolism.

Impact of supine versus upright exercise on muscle deoxygenation heterogeneity during ramp incremental cycling is site specific

“…Hence, the greater ability of the VLd to defend Q O 2 /VO 2 against changes in perfusion pressure induced by the supine position may be related to this muscle region consisting of a greater proportion of highly oxidative type I fibers with greater rates of blood flow, a higher pressure head for bloodto-myocyte O 2 flux, and greater vasodilatory control sensitivity (Behnke et al 2003;Laughlin et al 2012;McDonough et al 2005). The present findings are in contradiction with our recent finding of an increased muscle deoxy[heme] amplitude in the VLd during heavy supine constant work rate exercise (Goulding et al 2020b). One explanation for this discrepancy may be the fact that muscle deoxy[heme] kinetics are slower during supine compared to upright exercise (Goulding et al 2020b), and hence the non-steady-state conditions of ramp exercise in the present study may not have allowed sufficient time for steady-state Q O 2 /VO 2 reductions to become manifest in the VLd (Boone et al 2010).…”

“…The aim of the present study was, therefore, to examine the influence of posture (i.e., supine vs. upright) on the muscle deoxy[heme], total[heme] (i.e., deoxy-+ oxygenated[heme]), and muscle activation (assessed via EMG) responses to ramp exercise and their heterogeneity within and among the locomotor muscles. In accordance with our recent study (Goulding et al 2020b), we hypothesized that supine exercise would: 1) increase the absolute values and slopes of the deoxy[heme] responses to exercise; and 2) that this profile would be invariant across muscles and exercise intensities. In assessing multiple sites using combined high-precision TR-NIRS and EMG measurements, we sought to gain insight into the physiological mechanisms underpinning earlier task failure during supine ramp exercise.…”

“…Our recent findings of increased amplitude of the deoxy[heme] in the supine position in response to heavyintensity, constant-work rate exercise in both deep and superficial muscle suggest that the impairment in Q O 2 /V O 2 brought about by the supine intervention is apparent across the exercising muscle mass (Goulding et al 2020b). However, it remains unknown to what extent these effects differ as a function of exercise intensity and/or fiber type.…”

“…Indeed, capillary red blood cell velocity increases more with contractions in less oxidative rat muscles (Dawson et al 1987) and faster red blood cell velocity is associated with a higher capillary hematocrit (Kindig et al 2002). We have previously demonstrated that the RFs is more dependent on O 2 extraction for a given degree of muscle activation when compared to the VLs (Goulding et al 2020b), consistent with what would be expected in a muscle consisting of a greater proportion of higher-order, less oxidative fibers (Dahmane et al 2005;Johnson et al 1973). Therefore, the findings in the RFs herein might reflect that which would be expected from the recruitment of a muscle comprised of a greater proportion of type II muscle fibers that are inherently more sensitive to reductions in muscle perfusion pressure (i.e., closer to their respective O 2 delivery "tipping points"; DiMenna et al 2010b; Goulding et al 2020a, b;Poole et al 2007Poole et al , 2008Poole and Jones 2012), such as that brought about by supine exercise.…”

High-intensity exercise impairs extradiaphragmatic respiratory muscle perfusion in patients with COPD

“…We used continuous wave (CW) near-infrared spectrometers (spatial resolved spectroscopy [SRS], Hamamatsu photonics), where the light source is of constant intensity, and providing changes in superficial muscle haeme components from an arbitrary baseline (10). Recently more advanced near-infrared spectrometers incorporating time-domain technology can provide deeper muscle NIRS readings and absolute concentrations of the heme components in tissues of interest (10,30,43,67). However, NIRS devices based on CW technology are the only commercial instruments with the capacity to simultaneously measure tissue haeme variables and ICG concentrations for the calculation of tissue perfusion.…”