scholarly journals Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise

2003 ◽  
Vol 94 (4) ◽  
pp. 1501-1507 ◽  
Author(s):  
Jamie S. M. Pringle ◽  
Jonathan H. Doust ◽  
Helen Carter ◽  
Keith Tolfrey ◽  
Andrew M. Jones

We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O2 uptake (V˙o 2) slow component during heavy-cycle exercise. Ten subjects (mean ± SD, age 26 ± 4 yr, body mass 71.5 ± 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peakV˙o 2, and the baseline power output was adjusted to account for differences in the O2 cost of unloaded pedaling. The gain of the V˙o 2primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean ± SE, 10.6 ± 0.3, 9.5 ± 0.2, and 8.9 ± 0.4 ml · min−1 · W−1, respectively; P < 0.05). The amplitude of theV˙o 2 slow component was significantly greater at 115 rpm (328 ± 29 ml/min) compared with 35 rpm (109 ± 30 ml/min) and 75 rpm (202 ± 38 ml/min) ( P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 ± 0.2 mM) and 75 rpm (2.8 ± 0.3 mM) compared with 35 rpm (1.7 ± 0.4 mM) ( P < 0.05). These data indicate that pedal rate influences V˙o 2 kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.

2006 ◽  
Vol 101 (5) ◽  
pp. 1320-1327 ◽  
Author(s):  
Mark Burnley ◽  
Jonathan H. Doust ◽  
Andrew M. Jones

Prior heavy exercise markedly alters the O2 uptake (V̇o2) response to subsequent heavy exercise. However, the time required for V̇o2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the V̇o2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second V̇o2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary V̇o2 time constant (from 25.9 ± 4.7 s to 23.9 ± 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary V̇o2 amplitude (from 2.42 ± 0.39 to 2.53 ± 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the V̇o2 slow component (from 0.44 ± 0.13 to 0.21 ± 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20–45 min, but not after 60 min, of recovery. The increase in the primary V̇o2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 ± 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20–60 min of recovery. The priming effect of prior heavy exercise on the V̇o2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.


2004 ◽  
Vol 29 (2) ◽  
pp. 146-156 ◽  
Author(s):  
Xavier Nesi ◽  
Laurent Bosquet ◽  
Serge Berthoin ◽  
Jeanne Dekerle ◽  
Patrick Pelayo

The aim of this study was to evaluate the effect of a 15% increase in preferred pedal rate (PPR) on both time to exhaustion and pulmonary O2 uptake [Formula: see text] response during heavy exercise. Seven competitive cyclists underwent two constant-power tests (CPT) at a power output that theoretically requires 50% of the difference in [Formula: see text] between the second ventilatory threshold and [Formula: see text]max (PΔ50). Each cyclist cycled a CPT at PPR (CPTPPR) and a CPT at +15% of PPR (CPT+15%) in a randomized order. The average PPR value was 94 ± 4 rpm, and time to exhaustion was significantly longer in CPTPPR compared with CPT+15% (465 ± 139 vs. 303 ± 42 s, respectively; p = 0.01). A significant decrease in [Formula: see text] values in the first minutes of exercise and a significant increase in [Formula: see text] slow component was reported in CPT+15% compared with CPTPPR. These data indicate that the increase of 15% PPR was associated with a decrease in exercise tolerance and a specific [Formula: see text] response, presumably due to an increase of negative muscular work, internal work, and an altering of motor unit recruitment patterns. Key words: aerobic demand, cadence, cyclists, exercise tolerance, pedaling frequency


2002 ◽  
Vol 92 (6) ◽  
pp. 2571-2577 ◽  
Author(s):  
Andrew M. Jones ◽  
Helen Carter ◽  
Jamie S. M. Pringle ◽  
Iain T. Campbell

The purpose of this study was to test the effect of oral creatine (Cr) supplementation on pulmonary oxygen uptake (V˙o 2) kinetics during moderate [below ventilatory threshold (VT)] and heavy (above VT) submaximal cycle exercise. Nine subjects (7 men; means ± SD: age 28 ± 3 yr, body mass 73.2 ± 5.6 kg, maximalV˙o 2 46.4 ± 8.0 ml · kg−1 · min−1) volunteered to participate in this study. Subjects performed transitions of 6-min duration from unloaded cycling to moderate (80% VT; 8–12 repeats) and heavy exercise (50% change; i.e., halfway between VT and maximal V˙o 2; 4–6 repeats), both in the control condition and after Cr loading, in a crossover design. The Cr loading regimen involved oral consumption of 20 g/day of Cr monohydrate for 5 days, followed by a maintenance dose of 5 g/day thereafter. V˙o 2 was measured breath by breath and modeled by using two (moderate) or three (heavy) exponential terms. For moderate exercise, there were no differences in the parameters of the V˙o 2 kinetic response between control and Cr-loaded conditions. For heavy exercise, the time-based parameters of the V˙o 2response were unchanged, but the amplitude of the primary component was significantly reduced with Cr loading (means ± SE: control 2.00 ± 0.12 l/min; Cr loaded 1.92 ± 0.10 l/min; P < 0.05) as was the end-exerciseV˙o 2 (control 2.19 ± 0.13 l/min; Cr loaded 2.12 ± 0.14 l/min; P < 0.05). The magnitude of the reduction in submaximalV˙o 2 with Cr loading was significantly correlated with the percentage of type II fibers in the vastus lateralis ( r = 0.87; P < 0.01; n = 7), indicating that the effect might be related to changes in motor unit recruitment patterns or the volume of muscle activated.


2010 ◽  
Vol 35 (2) ◽  
pp. 142-150 ◽  
Author(s):  
Martin Buchheit ◽  
Pascale Duché ◽  
Paul B. Laursen ◽  
Sébastien Ratel

The aim of the present study was to determine whether differences in age-related heart rate recovery (HRR) kinetics were associated with differences in power output, blood lactate concentration ([La]b), and acidosis among children, adolescents, and adults. Ten prepubertal boys (aged 9.6 ± 0.7 years), 6 pubertal boys (aged 15.2 ± 0.8 years), and 7 men (aged 20.4 ± 1.0 years) performed 10 repeated 10-s all-out cycling sprints, interspersed with 5-min passive recovery intervals. Mean power output (MPO) was measured during each sprint, and HRR, [La]b, and acidosis (pHb) were determined immediately after each sprint. Children displayed a shorter time constant of the primary component of HRR than adolescents and adults (17.5 ± 4.1 vs. 38.0 ± 5.3 and 36.9 ± 4.9 s, p < 0.001 for both), but no difference was observed between adolescents and adults (p = 1.00). MPO, [La]b, and pHb were also lower in children compared with the other 2 groups (p < 0.001 for both). When data were pooled, HRR was significantly correlated with MPO (r = 0.48, p < 0.001), [La]b (r = 0.58, p < 0.001), and pHb (r = –0.60, p < 0.001). Covarying for MPO, [La]b, or pHb abolished the between-group differences in HRR (p = 0.42, p = 0.19, and p = 0.16, respectively). Anaerobic glycolytic contribution and power output explained a significant portion of the HRR variance following high-intensity intermittent exercise. The faster HRR kinetic observed in children appears to be related, at least in part, to their lower work rate and inherent lack of anaerobic metabolic capacity.


2004 ◽  
Vol 97 (4) ◽  
pp. 1227-1236 ◽  
Author(s):  
Daryl P. Wilkerson ◽  
Katrien Koppo ◽  
Thomas J. Barstow ◽  
Andrew M. Jones

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (V̇o2) kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to V̇o2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to ∼105% of the predetermined V̇o2 peak, separated by 3 × 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means ± SD: MAX1: 1.3 ± 0.4 mM vs. MAX2: 7.7 ± 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in V̇o2 was not significantly different between the two conditions (MAX1: 33.8 ± 5.5 s vs. MAX2: 33.2 ± 7.7 s). Rather, the asymptotic “gain” of the primary V̇o2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 ± 0.9 ml·min−1·W−1 vs. MAX2: 9.0 ± 0.7 ml·min−1·W−1; P < 0.05), such that V̇o2 was projecting to a higher “steady-state” amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component V̇o2 response but does increase the amplitude to which V̇o2 may rise following the onset of perimaximal-intensity cycle exercise.


2021 ◽  
Vol 11 (8) ◽  
pp. 3624
Author(s):  
Aurelio Trofè ◽  
Milena Raffi ◽  
David Muehsam ◽  
Andrea Meoni ◽  
Francesco Campa ◽  
...  

Pulsed electromagnetic fields (PEMFs) are used as non-invasive tools to enhance microcirculation and tissue oxygenation, with a modulatory influence on the microvasculature. This study aimed to measure the acute effect of PEMF on muscle oxygenation and its influence on pulmonary oxygen kinetics during exercise. Eighteen male cyclists performed, on different days, a constant-load exercise in both active (ON) and inactive (OFF) PEMF stimulations while deoxyhemoglobin and pulmonary oxygen kinetics, total oxygenation index, and blood lactate were collected. PEMF enhanced muscle oxygenation, with higher values of deoxyhemoglobin both at the primary component and at the steady-state level. Moreover, PEMF accelerated deoxyhemoglobin on-transition kinetic, with a shorter time delay, time constant, and mean response time than the OFF condition. Lactate concentration was higher during stimulation. No differences were found for total oxygenation index and pulmonary oxygen kinetics. Local application of a precise PEMF stimulation can increase the rate of the muscle O2 extraction and utilization. These changes were not accompanied by faster oxygen kinetics, reduced oxygen slow component, or reduced blood lactate level. It seems that oxygen consumption is more influenced by exercise involving large muscle mass like cycling, whereas PEMF might only act at the local level.


2006 ◽  
Vol 31 (5) ◽  
pp. 612-620 ◽  
Author(s):  
Lixin Wang ◽  
Takahiro Yoshikawa ◽  
Taketaka Hara ◽  
Hayato Nakao ◽  
Takashi Suzuki ◽  
...  

Various near-infrared spectroscopy (NIRS) variables have been used to estimate muscle lactate threshold (LT), but no study has determined which common NIRS variable best reflects muscle estimated LT. Establishing the inflection point of 2 regression lines for deoxyhaemoglobin (ΔHHbi.p.), oxyhaemoglobin (ΔO2Hbi.p.), and tissue oxygenation index (TOIi.p.), as well as for blood lactate concentration, we then investigated the relationships between NIRS variables and ventilatory threshold (VT), LT, or maximal tissue hemoglobin index (nTHImax) during incremental cycling exercise. ΔHHbi.p. and TOIi.p. could be determined for all 15 subjects, but ΔO2Hbi.p. was determined for only 11 subjects. The mean absolute values for the 2 measurable slopes of the 2 continuous linear regression lines exhibited increased changes in 3 NIRS variables. The workload and VO2 at ΔO2Hbi.p. and nTHImax were greater than those at VT, LT, ΔHHbi.p., and TOIi.p.. For workload and VO2, ΔHHbi.p. was correlated with VT and LT, whereas ΔO2Hbi.p. was correlated with nTHImax, and TOIi.p. with VT and nTHImax. These findings indicate that ΔO2Hb strongly corresponds with local perfusion, and TOI corresponds with both local perfusion and deoxygenation, but that ΔHHb can exactly determine deoxygenation changes and reflect O2 metabolic dynamics. The finding of strongest correlations between ΔHHb and VT or LT indicates that ΔHHb is the best variable for muscle LT estimation.


2016 ◽  
Vol 53 (1) ◽  
pp. 179-187 ◽  
Author(s):  
José Vilaça-Alves ◽  
Nuno Miguel Freitas ◽  
Francisco José Saavedra ◽  
Christopher B. Scott ◽  
Victor Machado dos Reis ◽  
...  

AbstractThe aim of this study was to compare the values of oxygen uptake (VO2) during and after strength training exercises (STe) and ergometer exercises (Ee), matched for intensity and exercise time. Eight men (24 ± 2.33 years) performed upper and lower body cycling Ee at the individual’s ventilatory threshold (VE/VCO2). The STe session included half squats and the bench press which were performed with a load at the individual blood lactate concentration of 4 mmol/l. Both sessions lasted 30 minutes, alternating 50 seconds of effort with a 10 second transition time between upper and lower body work. The averaged overall VO2 between sessions was significantly higher for Ee (24.96 ± 3.6 ml·kg·min-1) compared to STe (21.66 ± 1.77 ml·kg·min-1) (p = 0.035), but this difference was only seen for the first 20 minutes of exercise. Absolute VO2 values between sessions did not reveal differences. There were more statistically greater values in Ee compared to STe, regarding VO2 of lower limbs (25.44 ± 3.84 ml·kg·min-1 versus 21.83 ± 2·24 ml·kg·min-1; p = 0.038) and upper limbs (24.49 ± 3.84 ml·kg·min-1 versus 21.54 ± 1.77 ml·kg·min-1; p = 0.047). There were further significant differences regarding the moment effect (p<0.0001) of both STe and Ee sessions. With respect to the moment × session effect, only VO2 5 minutes into recovery showed significant differences (p = 0.017). In conclusion, although significant increases in VO2 were seen following Ee compared to STe, it appears that the load/intensity, and not the material/equipment used for the execution of an exercise, are variables that best influence oxygen uptake.


2005 ◽  
Vol 288 (1) ◽  
pp. R212-R220 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Tomoyuki Shiojiri ◽  
Narihiko Kondo ◽  
Yoshiyuki Fukuba ◽  
...  

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O2 uptake (pV̇o2) kinetics and 2) to characterize the muscle blood flow, muscle V̇o2 (mV̇o2), and pV̇o2 kinetics during KE to investigate the rate-limiting factor(s) of pV̇o2 on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pV̇o2 during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mV̇o2 at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pV̇o2 for both moderate and heavy exercise was higher during KE (∼12 ml·W−1·min−1) compared with CE (∼10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mV̇o2 during heavy KE [25.8 ± 9.0 s (SD)] was not significantly different from that of the phase II pV̇o2. Moreover, the slow component of pV̇o2 evident for the heavy KE reflected the gradual increase in mV̇o2. The initial LBF kinetics after onset of KE were significantly faster than the phase II pV̇o2 kinetics (moderate: time constant LBF = 8.0 ± 3.5 s, pV̇o2 = 32.7 ± 5.6 s, P < 0.05; heavy: LBF = 9.7 ± 2.0 s, pV̇o2 = 29.9 ± 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pV̇o2. These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pV̇o2, consistent with an intramuscular limitation to V̇o2 kinetics, i.e., a microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia.


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