Effects of Transitioning from Un‐Occluded to Occluded Hyperbolic Submaximal Exercise on VO2 Mean Response Time and Oxygen Deficit

Abstract

IntroductionAdditional oxygen uptake (VO2) beyond muscle oxygen (O2) utilization rates may coincide with exercise at or above the lactate threshold, which may be illustrated using a Phase II to III two‐exponential on‐transient VO2 kinetics model. This is expected to prolong mean response time (MRT) to VO2 steady‐state commensurate with increased O2deficit (O2def), which suggests reduced energy efficiency. Several factors may provoke metabolic acidosis during ergometry including exaggerated pedal frequency related to greater recruitment of type II muscle fibers. Also unclear is whether locomotor subsystolic regional circulatory occlusion (SubRCO), used to study group III/IV afferents during ergometry, accelerates metabolic acidosis due to influences on arterial‐to‐venous gradients. Thus, this study aimed to test the hypothesis that the transition from exercise without SubRCO to with SubRCO during fixed high rate pedaling leads to a Phase III rise in on‐transient VO2 kinetics and, hence, augmented MRT and O2def during hyperbolic submaximal exercise.MethodsHealthy adults (N = 15, 53% male; age 36 ± 17 years; BMI 24 ± 4 kg/m2) completed 2 study visits of 3 identical sessions of fixed‐load (20W) ergometry at fixed pedal rates of 35 or 100 rpm (randomized). Sessions began with 5 min of rest, followed by 3 min of exercise without SubRCO, and immediately transitioning to a 5 min period of exercise+SubRCO at 90 mm Hg bilateral‐thigh cuff inflation pressure. A metabolic system integrated with gas mass‐spectrometry was used to measure breath‐by‐breath VO2. Data were linearly interpolated to 1 sec intervals and ensemble averaged across 3 sessions/day for each participant prior to modeling. Models included: single exponential, VO2REST + A [1 − e−(t‐TD)/τ]; two exponential, VO2REST + A [1 − e−(t‐TD)/τ] + A2 [1 − e−(t‐TD2)/τ2]; O2def, [A • 8 min] − ∫ VO2dt; MRT, τ + TD; where τ = time constant; A = asymptote; TD = time delay; ∫ VO2dt = integral of actual VO2 across 8 min.ResultsSingle vs two exponential model sums of squares were similar within sessions of 35 (0.05 ± 0.03 vs 0.05 ± 0.03, P = 0.15) and 100 rpm (0.15 ± 0.07 vs 0.14 ± 0.07, P = 0.59), respectively; suggesting an absent Phase III response. Thus, MRT and O2def were derived using single exponential models beginning at t = 0. At 35 rpm, MRT = 56 ± 22 sec, and O2def = 0.36 ± 0.13 L; which differed significantly from 100 rpm, MRT = 43 ± 13 sec, and O2def = 0.70 ± 0.21 L (all P<0.05).ConclusionsWhile these observations demonstrate shortened MRT but increased O2def in high versus low pedaling, these data do not suggest locomotor SubRCO provokes worsening of these parameters relating to marked dissociation between VO2 and muscle O2 utilization rates during low intensity ergometry in healthy adults. Similarly, although O2def demonstrates sensitivity to pedal rate, an absent Phase III rise in VO2 commensurate with a shortened MRT during high rate pedaling does not suggest an uncoupling of pulmonary and muscle O2 increases from early to end‐exercise in healthy adults.Support or Funding InformationNHLBI RO1 HL126638; AHA 16POST30260021