Influence of oxygen uptake kinetics on physical performance in youth soccer

Purpose: To examine the relationship between oxygen uptake kinetics (VO2 kinetics) and physical measures associated with soccer match-play, within a group of highly trained youth soccer players. Methods: Seventeen highly trained youth soccer players (age: 13.3 ± 0.4 yr, self-assessed Tanner Stage: 3 ± 1) volunteered for the study. Players initially completed an incremental treadmill protocol to exhaustion, to establish gaseous exchange threshold (GET) and VO2max (59.1 ± 5.4 mL.kg-1.min-1). On subsequent visits players completed a step transition protocol from, rest–moderate intensity exercise, followed by an immediate transition from moderate–severe intensity exercise (moderate: 95%GET, severe: 60%∆), during which VO2 kinetics were determined. Physical soccer-based performance was assessed using a maximal Yo-Yo Intermittent Recovery test level 1 (Yo-Yo IR1) and via GPS derived measures of physical soccer performance during soccer match-play, 3 2 x 20min, 11 v 11 matches, to gain measures of physical performance during soccer match-play. Results: Partial correlations revealed significant inverse relationships between the unloaded to moderate transition time constant (tau) and: Yo-Yo IR1 performance (r = -0.58, P = 0.02) and GPS variables (Total distance (TD): r = - 0.64, P = 0.007, High speed running (HSR): r = - 0.64, P = 0.008, High speed running efforts (HSReff): r = - 0.66, P = 0.005). Conclusion: Measures of VO2 kinetics are related to physical measures associated with soccer match-play and could potentially be used to distinguish between those of superior physical performance, within a group of highly-trained youth soccer players

Effects of power variation on cycle performance during simulated hilly time-trials

It has previously been shown that cyclists are unable to maintain a constant power output during cycle time-trials on hilly courses. The purpose of the present study is therefore to quantify these effects of power variation using a mathematical model of cycling performance. A hypothetical cyclist (body mass: 70 kg, bicycle mass: 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance was modelled over three hypothetical 40-km courses, comprising repeated 2.5-km sections of uphill and downhill with gradients of 1%, 3%, and 6%, respectively. Amplitude (5–15%) and distance (0.31–20.00 km) of variation were modelled over a range of mean power outputs (200–600 W) and compared to sustaining a constant power. Power variation was typically detrimental to performance; these effects were augmented as the amplitude of variation and severity of gradient increased. Varying power every 1.25 km was most detrimental to performance; at a mean power of 200 W, performance was impaired by 43.90 s (±15% variation, 6% gradient). However at the steepest gradients, the effect of power variation was relatively independent of the distance of variation. In contrast, varying power in parallel with changes in gradient improved performance by 188.89 s (±15% variation, 6% gradient) at 200 W. The present data demonstrate that during hilly time-trials, power variation that does not occur in parallel with changes in gradient is detrimental to performance, especially at steeper gradients. These adverse effects are substantially larger than those previously observed during flat, windless time-trials

Effect of Ischemic Preconditioning (IPC) on Recovery of Exercise Performance Following a Bout of Exercise to Volitional Exhaustion

The purpose of the present study was to investigate the effect of ischemic preconditioning (IPC) on the recovery of exercise performance following maximal, incremental exercise. A total of 13 healthy males volunteered to participate, undertaking three experimental trials involving a constant work-rate bout of severe intensity exercise undertaken to the limit of tolerance that was preceded by a 40-min recovery period consequent to a maximal, incremental exercise test. During the recovery period, participants underwent IPC at 220 mmHg, sham IPC (SHAM; 20 mmHg), and passive rest (CON). Exercise tolerance time was higher following IPC as compared to SHAM and CON {199 ± 36 (CON) vs. 203 ± 35 (SHAM) vs. 219 ± 34 (IPC), p = 0.03}. This effect was accompanied by a tendency toward an augmented increase in blood lactate from rest to exercise in IPC compared to SHAM and CON (p = 0.08). There was no effect of IPC on oxygen uptake kinetics or muscle oxygenation as indicated via near-infrared spectroscopy. IPC may therefore have the capacity to augment recovery from prior maximal exercise, but this does not appear to be due to enhancements to oxygen uptake kinetics or muscle oxygenatio

EFFECT OF HYPEROXIA ON CRITICAL POWER AND V ̇O2 KINETICS DURING UPRIGHT CYCLING

Introduction/Purpose: Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance, however its physiological determinants are incompletely understood. The present study determined the impact of hyperoxia on CP, the time constant of phase II pulmonary oxygen uptake kinetics (τ_V ̇ O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in 9 healthy men performing upright cycle ergometry. Methods: CP was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via 4 severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, τ_V ̇ O2 and the time constant of muscle deoxyhaemoglobin kinetics (τ[HHb]), alongside absolute concentrations of muscle oxyhaemoglobin ([HbO2]), were determined. Results: CP was greater (hyperoxia: 216 ± 30 vs. normoxia: 197 ± 29W; P < 0.001) whereas W’ was reduced (hyperoxia: 15.4 ± 5.2 kJ, normoxia: 17.5 ± 4.3 W; P = 0.037) in hyperoxia compared to normoxia. τ_V ̇ O2 (hyperoxia: 35 ± 12 vs normoxia: 33 ± 10 s; P = 0.33) and τ[HHb] (hyperoxia: 11 ± 5 vs. normoxia: 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO2] during exercise was greater in hyperoxia compared to normoxia (hyperoxia: 73 ± 20 vs. normoxia: 66 ± 15 μM; P = 0.001). Conclusion: This study provides novel insights into the physiological determinants of CP and by extension, exercise tolerance. Microvascular oxygenation and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter τ_V ̇ O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, i.e. CP

Prior exercise speeds pulmonary oxygen uptake kinetics and increases critical power during supine but not upright cycling

Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance and is related to the time constant of phase II pulmonary oxygen uptake kinetics (τV̇O2). To test the hypothesis that this relationship is causal we determined the impact of prior exercise (“priming”) on CP and τV̇O2 in the upright and supine positions. 17 healthy men were assigned to either upright or supine exercise groups, whereby CP, τV̇O2 and muscle deoxyhaemoglobin kinetics (τ[HHb]) were determined via constant-power tests to exhaustion at four work-rates with (primed) and without (control) priming exercise at ∼31%Δ. During supine exercise, priming reduced τV̇O2 (control: 54 ± 18 vs. primed: 39 ± 11 s; P < 0.001), increased τ[HHb] (control: 8 ± 4 vs. primed: 12 ± 4 s; P = 0.003) and increased CP (control: 177 ± 31 vs. primed: 185 ± 30 W, P = 0.006) compared to control. However, priming exercise had no effect on τV̇O2 (control: 37 ± 12 vs. primed: 35 ± 8 s; P = 0.82), τ[HHb] (CON: 10 ± 5 s vs. PRI: 14 ± 10; P = 0.10), or CP (control: 235 ± 42 vs. primed: 232 ± 35 W; P = 0.57) during upright exercise. The concomitant reduction of τV̇O2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τV̇O2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability

Bi-exponential modelling of W ′ reconstitution kinetics in trained cyclists

From Springer Nature via Jisc Publications RouterHistory: received 2021-06-21, accepted 2021-12-10, registration 2021-12-11, pub-electronic 2021-12-18, online 2021-12-18, pub-print 2022-03Publication status: PublishedAbstract: Purpose: The aim of this study was to investigate the individual W′ reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal mathematical model to describe W′ reconstitution. Methods: Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; V˙O2max 58.6 ± 7.1 mL kg min−1) completed three incremental ramps (20 W min−1) to the limit of tolerance with varying recovery durations (15–360 s) on 5–9 occasions. W′ reconstitution was measured following the first and second recovery periods against which mono-exponential and bi-exponential models were compared with adjusted R2 and bias-corrected Akaike information criterion (AICc). Results: A bi-exponential model outperformed the mono-exponential model of W′ reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adjR2 = 0.999) for the first recovery when optimised with parameters of fast component (FC) amplitude = 50.67%; slow component (SC) amplitude = 49.33%; time constant (τ)FC = 21.5 s; τSC = 388 s. Following the second recovery, W′ reconstitution reduced by 9.1 ± 7.3%, at 180 s and 8.2 ± 9.8% at 240 s resulting in an increase in the modelled τSC to 716 s with τFC unchanged. Individual bi-exponential models also fit well (adjR2 = 0.978 ± 0.017) with large individual parameter variations (FC amplitude 47.7 ± 17.8%; first recovery: (τ)FC = 22.0 ± 11.8 s; (τ)SC = 377 ± 100 s; second recovery: (τ)FC = 16.3.0 ± 6.6 s; (τ)SC = 549 ± 226 s). Conclusions: W′ reconstitution kinetics were best described by a bi-exponential model consisting of distinct fast and slow phases. The amplitudes of the FC and SC remained unchanged with repeated bouts, with a slowing of W′ reconstitution confined to an increase in the time constant of the slow component

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

COPD patients have reduced muscle glutamate which may contribute to an impaired response of oxidative metabolism to exercise. We hypothesised that prior glutamine supplementation would enhance View the MathML source peak, View the MathML source at lactate threshold and speed pulmonary oxygen uptake kinetics in COPD. 13 patients (9 males, age 66 ± 5 years, mean ± SD) with severe COPD (mean FEV1 0.88 ± 0.23 l, 33 ± 7% predicted) performed on separate days ramp cycle-ergometry (5–10 W min−1) to volitional exhaustion and subsequently square-wave transitions to 80% estimated lactate threshold (LT) following consumption of either placebo (CON) or 0.125 g kg bm−1 of glutamine (GLN) in 5 ml kg bm−1 placebo. Oral glutamine had no effect on peak or View the MathML source at LT, {View the MathML source peak: CON = 0.70 ± 0.1 l min−1 vs. GLN = 0.73 ± 0.2 l min−1; LT: CON = 0.57 ± 0.1 l min−1 vs. GLN = 0.54 ± 0.1 l min−1} or View the MathML source kinetics {tau: CON = 68 ± 22 s vs. GLN = 68 ± 16 s}. Ingestion of glutamine before exercise did not improve indices of oxidative metabolism in this patient group

Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee-extension

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with (31)P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n = 14). Unlocalized (31)P spectra were collected from the quadriceps throughout using a dual-tuned ((1)H and (31)P) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min(-1)) or change in [PCr] (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min(-1); each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min(-1) (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P < 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min(-1), or 26 ± 30%; P < 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r(2) = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O)

LIMITATIONS TO EXERCISE TOLERANCE IN TYPE 1 DIABETES: THE ROLE OF PULMONARY OXYGEN UPTAKE KINETICS AND PRIMING EXERCISE

We compared the time constant (τ_V ̇ O2) of the fundamental phase of pulmonary oxygen uptake (V ̇O2) kinetics between young adult males with type 1 diabetes and healthy controls. We also assessed the impact of priming exercise on τ_V ̇ O2, critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. 17 males with type 1 diabetes and 17 healthy male controls performed moderate-intensity exercise to determine τ_V ̇ O2. A subset of 7 participants with type 1 diabetes performed an additional eight visits, whereby critical power, τ_V ̇ O2 and muscle deoxyhaemoglobin + myoglobin ([HHb+Mb]; via near-infrared spectroscopy) kinetics (described by a time constant, τ[HHb+Mb]) were determined with (PRI) and without (CON) a prior 6-minute bout of heavy exercise. τ_V ̇ O2 was greater in participants with type 1 diabetes compared to controls (type 1 diabetes: 50±13 vs. control: 32±12 s; P<0.001). Critical power was greater in PRI compared to CON (PRI: 161±25 W vs. CON: 149±22 W; P<0.001), whereas τ_V ̇ O2 (PRI: 36±15 vs. CON: 50±21 s; P=0.006) and τ[HHb+Mb] (PRI: 10±5 vs. CON: 17±11 s; P=0.037) were reduced in PRI compared to CON. Type 1 diabetes patients showed slower pulmonary V ̇O2 kinetics when compared to controls; priming exercise speeded V ̇O2 and [HHb + Mb] kinetics, and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterisation of the power-duration relationship in type 1 diabetes, and the first experimental evidence that τ_V ̇ O2 is an independent determinant of critical power in this population

Medium chain triglycerides with a C8:C10 ratio of 30:70 enhances cognitive performance and mitigates the cognitive decline associated with prolonged exercise in young and healthy adults

Introduction: Prolonged exercise has been linked to a decline in cognitive function due to a variety of factors, such as a drop in oxygen in the prefrontal cortex and an increase in stress hormones and neurotransmitters. Medium chain triglycerides (MCTs) may possibly offset this decline as they provide energy for the brain via both direct and indirect pathways, alongside promoting chronic physiological adaptations within the brain. Methods: Participants were divided into two groups; MCT (n = 9) and Placebo (n = 10). The MCT gels contained 6g of MCT with a C8:C10 ratio of 30:70, whereas the placebo gels contained carbohydrates of similar calorific value to the MCT gels. Participants visited the laboratory on three occasions (familiarisation/fitness test, pre-supplementation, post-supplementation), during which they performed a battery of cognitive tasks assessing domains such as processing speed, working memory, selective attention, decision making and coordination, before and after a prolonged bout of exercise (60 mins at 90% gas exchange threshold (GET). A 2-week supplementation period between visits 2 and 3 involved the ingestion of 2 gels per day. Results: Exercise resulted in detriments in most cognitive tasks pre-supplementation for both groups, and post-supplementation for the Placebo group (main effect ps .05). Furthermore, MCT supplementation enhanced before-exercise cognitive performance and in some measures, such as working memory, this was maintained after-exercise (interaction effect ps> .05). Conclusions: Chronic MCT supplementation enhanced before-exercise cognitive performance and offset the cognitive decline caused by a prolonged bout of exercise. In some cases, improvements in before-exercise cognitive performance were maintained after-exercise