A raised metabolic rate slows pulmonary O₂uptake kinetics on transition to moderate-intensity exercise in humans independently of work rate

Abstract

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary O 2 uptake (V O 2 ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV O 2 using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O 2 uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and lung τV O 2 was assessed by computer simulations. The τV O 2 in R2 (32 ± 9 s) was not different (P > 0.05) from S2 (30 ± 10 s), but both were greater (P < 0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowedV O 2 kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV O 2 predicted by simulations: S1 = R2 < S2). These data therefore suggest that the dynamics of muscle O 2 consumption are slowed when exercise is initiated from a less favourable energetic state.

Inorganic nitrate supplementation improves muscle oxygenation, O2uptake kinetics, and exercise tolerance at high but not low pedal rates

“…It is also possible that the higher baseline metabolic rate evoked by the higher pedal cadence was responsible for the effects of BR at 115 rpm, but not 35 rpm, in this study (12). Bowen et al (9) suggested that elevating metabolic rate during cycling exercise negatively impacted the intramuscular energy state leading to slower phase II V O 2 kinetics. Since NO 3 Ϫ supplementation has been shown to blunt intramuscular adenosine diphosphate and inorganic phosphate accumulation, and phosphocreatine utilization during exercise (3), the faster V O 2 kinetics and improved exercise tolerance in 115-BR might be linked to an improved intramuscular energy state, regardless of muscle fiber recruitment patterns, in the higher cadence condition.…”

“…The slower phase II V O 2 kinetics at the higher pedal cadence might also reflect increased fast-twitch fiber recruitment (7), because fasttwitch fibers are believed to exhibit slower V O 2 kinetics (17,40). Alternatively, the higher baseline metabolic rate that is elicited by cycling at a higher pedal cadence might have slowed phase II V O 2 kinetics because of the altered energetic state (9,12). Although our recent study indicated that supplementation with BR speeded V O 2 kinetics in the upper step of a double step test, where a greater proportional recruitment of type II muscle fibers would be expected (38,39), muscle fiber recruitment patterns were not directly addressed in that study (11).…”

Pulmonary O2 uptake kinetics during moderate-intensity exercise transitions initiated from low versus elevated metabolic rates: insights from manipulations in cadence

“…Within the context of the double-step model, several mechanisms have been proposed to explain the slower V O 2p kinetics in the US including: O 2 delivery limitations due to slowed heart rate and conduit artery blood flow responses (Hughson and Morrissey 1982;MacPhee et al 2005); progressive recruitment of less energetically efficient muscle fibers (Brittain et al 2001); and a reduction in the intracellular energy state consequent to an elevated pre-transition work and/or metabolic rate (Bowen et al 2011). Recently, Bowen et al (2011) attempted to resolve the influences of these mechanisms using both the doublestep exercise model and two separate single-step transitions from 20 W to 90 % θ L separated by either 30 s (i.e., partial recovery) or 12 min (i.e., complete recovery) baseline cycling.…”

“…Recently, it was shown that the adjustment of V O 2p in response to a given increase in work rate (WR) within the moderate-intensity domain displays dynamic nonlinearities such that the rate of adjustment (as given by the time constant, τV O 2p ) and the amplitude (as given by the V O 2p gain, ΔV O 2p /ΔWR) of the fundamental component of the V O 2p response are greater when exercise is initiated from an elevated baseline WR and/or metabolic rate (Bowen et al 2011;Brittain et al 2001;Hughson and Morrissey 1982;MacPhee et al 2005;Spencer et al 2011;Williams et al 2013). Utilizing a constant-load double-step exercise model whereby the moderate-intensity domain was bisected into two identical step-WR increments (between 20 W and 90 % θ L ), Brittain et al (2001) observed an ~15 s greater phase II V O 2p time constant (τV O 2p ) during transitions initiated from a raised (US; ~40 s) compared to a lower (LS; ~25 s) baseline WR and metabolic rate, as well as a greater phase II V O 2p gain (ΔV O 2pSS /ΔWR; 11.9 vs. 10.6 ml min −1 W −1 ).…”

The Complex Reality of VO2 Kinetics to Steady State: Reassessment of the Models Used to Quantify and Interpret VO2 Kinetics, Steady State, and Time to Steady State

“…There have been numerous studies comparing V O2 kinetics of moderate, heavy, and severe exercise following transitions from a baseline intensity above rest or an unloaded output, or from prior priming exercise (Hughson & Morrissey, 1982;Di Prampero et al, 1989;MacDonald et al, 1997;Burnley et al, 2002;Ferguson et al, 2007;DiMenna et al, 2009;DiMenna et al, 2010;Bowen et al, 2011;Cleland et al, 2012;Spencer et al, 2013). Of these, Hughson and Morrissey (1982) Hughson and Morrissey (1982) studied the V O2 kinetics of six healthy untrained subjects completing two cycle ergometer protocols.…”