Priming Exercise Research Articles

Reduction of V̇O2 slow component by priming exercise: novel mechanistic insights from time-resolved near-infrared spectroscopy.

Novel time-resolved near-infrared spectroscopy (TR-NIRS), with adipose tissue thickness correction, was used to test the hypotheses that heavy priming exercise reduces the V̇O2 slow component (V̇O2SC) (1) by elevating microvascular [Hb] volume at multiple sites within the quadriceps femoris (2) rather than reducing the heterogeneity of muscle deoxygenation kinetics. Twelve subjects completed two 6-min bouts of heavy work rate exercise, separated by 6 min of unloaded cycling. Priming exercise induced faster overall V̇O2 kinetics consequent to a substantial reduction in the V̇O2SC (0.27 ± 0.12 vs. 0.11 ± 0.09 L·min−1, P < 0.05) with an unchanged primary V̇O2 time constant. An increased baseline for the primed bout [total (Hb + Mb)] (197.5 ± 21.6 vs. 210.7 ± 22.5 μmol L−1, P < 0.01), reflecting increased microvascular [Hb] volume, correlated significantly with the V̇O2SC reduction. At multiple sites within the quadriceps femoris, priming exercise reduced the baseline and slowed the increase in [deoxy (Hb + Mb)]. Changes in the intersite coefficient of variation in the time delay and time constant of [deoxy (Hb + Mb)] during the second bout were not correlated with the V̇O2SC reduction. These results support a mechanistic link between priming exercise-induced increase in muscle [Hb] volume and the reduced V̇O2SC that serves to speed overall V̇O2 kinetics. However, reduction in the heterogeneity of muscle deoxygenation kinetics does not appear to be an obligatory feature of the priming response.

A Comparison of Different Modes of Morning Priming Exercise on Afternoon Performance

Purpose: To assess the effects of different modes of morning (AM) exercise on afternoon (PM) performance and salivary hormone responses in professional rugby union players. Methods: On 4 occasions (randomized, crossover design), 15 professional rugby players provided AM (~8 AM) and PM (~2 PM) saliva samples before PM assessments of countermovement-jump height, reaction time, and repeated-sprint ability. Control (passive rest), weights (bench press: 5 × 10 repetitions, 75% 1-repetition maximum, 90-s intraset recovery), cycling (6 × 6-s maximal sprint cycling, 7.5% body mass load, 54-s intraset recovery), and running (6 × 40-m maximal sprints, 20-s intraset recovery) interventions preceded (~5 h) PM testing. Results: PM sprint performance improved (P < .05) after weights (>0.15 ± 0.19 s, >2.04% ± 2.46%) and running (>0.15 ± 0.17 s, >2.12% ± 2.22%) but not cycling (P > .05). PM jump height increased after cycling (0.012 ± 0.009 m, 2.31% ± 1.76%, P < .001) and running (0.020 ± 0.009 m, 3.90% ± 1.79%, P < .001) but not weights (P = .936). Reaction time remained unchanged between trials (P = .379). Relative to control (131 ± 21 pg/mL), PM testosterone was greater in weights (21 ± 23 pg/mL, 17% ± 18%, P = .002) and running (28 ± 26 pg/mL, 22% ± 20%, P = .001) but not cycling (P = .072). Salivary cortisol was unaffected by AM exercise (P = .540). Conclusions: All modes of AM exercise improved at least 1 marker of PM performance, but running appeared the most beneficial to professional rugby union players. A rationale therefore exists for preceding PM competition with AM exercise.

The Positive Effects of Priming Exercise on Oxygen Uptake Kinetics and High-Intensity Exercise Performance Are Not Magnified by a Fast-Start Pacing Strategy in Trained Cyclists

The purpose of this study was to determine both the independent and additive effects of prior heavy-intensity exercise and pacing strategies on the VO2 kinetics and performance during high-intensity exercise. Fourteen endurance cyclists (VO2max = 62.8±8.5 mL.kg−1.min−1) volunteered to participate in the present study with the following protocols: 1) incremental test to determine lactate threshold and VO2max; 2) four maximal constant-load tests to estimate critical power; 3) six bouts of exercise, using a fast-start (FS), even-start (ES) or slow-start (SS) pacing strategy, with and without a preceding heavy-intensity exercise session (i.e., 90% critical power). In all conditions, the subjects completed an all-out sprint during the final 60 s of the test as a measure of the performance. For the control condition, the mean response time was significantly shorter (p<0.001) for FS (27±4 s) than for ES (32±5 s) and SS (32±6 s). After the prior exercise, the mean response time was not significantly different among the paced conditions (FS = 24±5 s; ES = 25±5 s; SS = 26±5 s). The end-sprint performance (i.e., mean power output) was only improved (∼3.2%, p<0.01) by prior exercise. Thus, in trained endurance cyclists, an FS pacing strategy does not magnify the positive effects of priming exercise on the overall VO2 kinetics and short-term high-intensity performance.

Warm-up with a weighted vest improves running performance via leg stiffness and running economy

To determine the effects of "strides" with a weighted-vest during a warm-up on endurance performance and its potential neuromuscular and metabolic mediators. A bout of resistance exercise can enhance subsequent high-intensity performance, but little is known about such priming exercise for endurance performance. A crossover with 5-7 days between an experimental and control trial was performed by 11 well-trained distance runners. Each trial was preceded by a warm-up consisting of a 10-min self-paced jog, a 5-min submaximal run to determine running economy, and six 10-s strides with or without a weighted-vest (20% of body mass). After a 10-min recovery period, runners performed a series of jumps to determine leg stiffness and other neuromuscular characteristics, another 5-min submaximal run, and an incremental treadmill test to determine peak running speed. Clinical and non-clinical forms of magnitude-based inference were used to assess outcomes. Correlations and linear regression were used to assess relationships between performance and underlying measures. The weighted-vest condition resulted in a very-large enhancement of peak running speed (2.9%; 90% confidence limits ±0.8%), a moderate increase in leg stiffness (20.4%; ±4.2%) and a large improvement in running economy (6.0%; ±1.6%); there were also small-moderate clear reductions in cardiorespiratory measures. Relationships between change scores showed that changes in leg stiffness could explain all the improvements in performance and economy. Strides with a weighted-vest have a priming effect on leg stiffness and running economy. It is postulated the associated major effect on peak treadmill running speed will translate into enhancement of competitive endurance performance.

The effect of priming exercise on O2 uptake kinetics, muscle O2 delivery and utilization, muscle activity, and exercise tolerance in boys

This study used priming exercise in young boys to investigate (i) how muscle oxygen delivery and oxygen utilization, and muscle activity modulate oxygen uptake kinetics during exercise; and (ii) whether the accelerated oxygen uptake kinetics following priming exercise can improve exercise tolerance. Seven boys that were aged 11.3 ± 1.6 years completed either a single bout (bout 1) or repeated bouts with 6 min of recovery (bout 2) of very heavy-intensity cycling exercise. During the tests oxygen uptake, muscle oxygenation, muscle electrical activity and exercise tolerance were measured. Priming exercise most likely shortened the oxygen uptake mean response time (change, ±90% confidence limits; -8.0 s, ±3.0), possibly increased the phase II oxygen uptake amplitude (0.11 L·min(-1), ±0.09) and very likely reduced the oxygen uptake slow component amplitude (-0.08 L·min(-1), ±0.07). Priming resulted in a likely reduction in integrated electromyography (-24% baseline, ±21% and -25% baseline, ±19) and a very likely reduction in Δ deoxyhaemoglobin/Δoxygen uptake (-0.16, ±0.11 and -0.09, ±0.05) over the phase II and slow component portions of the oxygen uptake response, respectively. A correlation was present between the change in tissue oxygenation index during bout 2 and the change in the phase II (r = -0.72, likely negative) and slow component (r = 0.72, likely positive) oxygen uptake amplitudes following priming exercise, but not for muscle activity. Exercise tolerance was likely reduced (change -177 s, ±180) following priming exercise. The altered phase II and slow component oxygen uptake amplitudes in boys following priming exercise are linked to an improved localised matching of muscle oxygen delivery to oxygen uptake and not muscle electrical activity. Despite more rapid oxygen uptake kinetics following priming exercise, exercise tolerance was not enhanced.

Time of day effects on the regulation of food consumption after activation of health goals

Previous research has found that while self-regulation is a resource that can be depleted, enhanced motivation to do so can help people successfully self-regulate. The aim of this research was to determine whether activating health goals—either via laboratory priming techniques or via advertisements—can help people regulate food intake later in the day, when self-regulation resources are typically depleted. In two experimental studies, participants completed goal activation tasks in the morning or in the afternoon while they had a snack food (M&M’s candies) available for consumption. In study 1, 121 participants viewed television shows with either healthy food ads, indulgent food ads, or non-food ads embedded within the program. In study 2, 149 participants completed a supraliminal but nonconscious goal priming exercise, in which they searched for health, indulgence, or control words in a puzzle. In both studies, activation of health goals led to decreased consumption of the snack food in the afternoon. In contrast, activation of health goals did not change consumption in the morning, when self-regulatory resources are typically high, due to replenishment after rest. These results suggest that activating health goals—either via classic laboratory goal-priming paradigms or via “real world primes,” such as ads for healthy foods—helps people to overcome failures in curbing food consumption due to depleted self-regulatory resources later in the day.

Prolonged moderate-intensity exercise oxygen uptake response following heavy-intensity priming exercise with short- and longer-term recovery

This study examines the effects of recovery duration following heavy-intensity "priming" exercise (Hvy) on pulmonary oxygen (O2) uptake (V̇O2p) during subsequent prolonged moderate-intensity exercise (Mod). Nine participants (6 men and 3 women) (27 ± 7 years) each completed 3 repetitions of 2 continuous Mod 1-Hvy-Mod 2 leg-cycling protocols in which Mod 2 lasted 30 min, but was preceded by a recovery duration of either 6 (R6) or 20 (R20) min at 20 W following Hvy; in each case, Mod 1 and Hvy lasted 6 min and were preceded by 6 min at 20 W. V̇O2p, heart rate (HR), and near-infrared spectroscopy (NIRS)-derived muscle deoxygenation ([HHb]) responses were modeled as a monoexponential; additionally, 60-s averages were computed every 6 min in Mod 1 and Mod 2. V̇O2p was elevated (p < 0.05) throughout Mod 2 compared with Mod 1 in both R6 and R20 (by -82 mL·min(-1) or ∼5.0%); this occurred despite a complete recovery of baseline V̇O2p (V̇O2pBsln) following R20. HR and minute ventilation (V̇E), but not [HHb], were also elevated throughout Mod 2. The phase II time constant for V̇O2p (τV̇O2p) was reduced in Mod 2 (22 s (Mod 1), 19 s (Mod 2); p < 0.05), as was the "overshoot" in the normalized [HHb]/O2 uptake ratio (p < 0.05). This study shows that V̇O2p was elevated during Mod following Hvy, regardless of recovery duration; however, a determining role for V̇O2pBsln is precluded. Furthermore, neither V̇O2p, HR, nor V̇E showed any evidence of a readjustment back to no-Hvy conditions during prolonged Mod (p > 0.05). Lastly, regardless of recovery duration, τV̇O2p was reduced to a similar extent with Hvy, likely resulting from an improved matching of local muscle O2 delivery to O2 utilization.

Noninvasive estimation of microvascular O2 provision during exercise on-transients in healthy young males

Two methods for estimating changes in microvascular O2 delivery during the on-transient of exercise were evaluated. They were tested to assess the role of the adjustment of the estimated microvascular O2 delivery in the speeding of Vo2 kinetics during a Mod1-Hvy-Mod2 protocol (Mod, moderate-intensity exercise; Hvy, heavy-intensity "priming" exercise), in which Mod2 is preceded by a bout of Hvy. Mod pulmonary Vo2 (Vo(2p)) and deoxy-hemoglobin [HHb] data were collected in 12 males (23 ± 3 yr); response profiles were fit with a monoexponential. Signals were also 1) scaled to a relative % of the response (0-100%) to calculate the [HHb]/Vo2 ratio for each individual and 2) rearranged in the Fick equation for estimation of capillary blood flow (Q(cap)). A transient [HHb]/Vo2 "overshoot" observed in Mod1 (1.06 ± 0.05; P < 0.05) was absent during Mod2 (1.01 ± 0.06; P > 0.05); reductions in the [HHb]/Vo2 ratio (Mod1 - Mod2) were related to reductions in phase II τVo(2p) (r = 0.82; P < 0.05). For Q(cap), a near-exponential response was observed in 8/12 subjects in Mod1 and only in 4/12 subjects in Mod2. The Q(cap) profile was shown to be highly dependent on the [HHb] baseline-to-amplitude ratio. Thus, accurate and physiologically consistent estimations of Q(cap) were not possible in most cases. This study confirmed that priming exercise results in an improved O2 delivery as shown by the decreased [HHb]/Vo2) ratio that was related to the smaller τVo2 in Mod2. Additionally, this study suggested that Q(cap) analysis may not be valid and should be interpreted with caution when assessing microvascular delivery of O2.

New insights in paediatric exercise metabolism

Abstract Research in paediatric exercise metabolism has been constrained by being unable to interrogate muscle in vivo . Conventionally, research has been limited to the estimation of muscle metabolism from observations of blood and respiratory gases during maximal or steady state exercise and the analysis of a few muscle biopsies taken at rest or post-exercise. The purpose of this paper is to review how the introduction of 31 P-magnetic resonance spectroscopy and breath-by-breath oxygen uptake kinetics studies has contributed to current understanding of exercise metabolism during growth and maturation. Methodologically robust studies using 31 P-magnetic resonance spectroscopy and oxygen uptake kinetics with children are sparse and some data are in conflict. However, it can be concluded that children respond to exercise with enhanced oxygen utilization within the myocyte compared with adults and that their responses are consistent with a greater recruitment of type I muscle fibres. Changes in muscle metabolism are age, maturation- and sex-related and dependent on the intensity of the exercise challenge. The introduction of experimental models such as “priming exercise” and “work-to-work” transitions provide intriguing avenues of research into the mechanisms underpinning exercise metabolism during growth and maturation.

Effects of priming exercise on the speed of adjustment of muscle oxidative metabolism at the onset of moderate-intensity step transitions in older adults

Aging is associated with a functional decline of the oxidative metabolism due to progressive limitations of both O(2) delivery and utilization. Priming exercise (PE) increases the speed of adjustment of oxidative metabolism during successive moderate-intensity transitions. We tested the hypothesis that such improvement is due to a better matching of O(2) delivery to utilization within the working muscles. In 21 healthy older adults (65.7 ± 5 yr), we measured contemporaneously noninvasive indexes of the overall speed of adjustment of the oxidative metabolism (i.e., pulmonary Vo(2) kinetics), of the bulk O(2) delivery (i.e., cardiac output), and of the rate of muscle deoxygenation (i.e., deoxygenated hemoglobin, HHb) during moderate-intensity step transitions, either with (ModB) or without (ModA) prior PE. The local matching of O(2) delivery to utilization was evaluated by the ΔHHb/ΔVo(2) ratio index. The overall speed of adjustment of the Vo(2) kinetics was significantly increased in ModB compared with ModA (P < 0.05). On the contrary, the kinetics of cardiac output was unaffected by PE. At the muscle level, ModB was associated with a significant reduction of the "overshoot" in the ΔHHb/ΔVo(2) ratio compared with ModA (P < 0.05), suggesting an improved O(2) delivery. Our data are compatible with the hypothesis that, in older adults, PE, prior to moderate-intensity exercise, beneficially affects the speed of adjustment of oxidative metabolism due to an acute improvement of the local matching of O(2) delivery to utilization.

Effects of prior heavy-intensity exercise on oxygen uptake and muscle deoxygenation kinetics of a subsequent heavy-intensity cycling and knee-extension exercise

This study examined the effects of prior heavy-intensity exercise on the adjustment of pulmonary oxygen uptake (VO(2p)) and muscle deoxygenation Δ[HHb] during the transition to subsequent heavy-intensity cycling (CE) or knee-extension (KE) exercise. Nine young adults (aged 24 ± 5 years) performed 4 repetitions of repeated bouts of heavy-intensity exercise separated by light-intensity CE and KE, which included 6 min of baseline exercise, a 6-min step of heavy-intensity exercise (H1), 6-min recovery, and a 6-min step of heavy-intensity exercise (H2). Exercise was performed at 50 r·min(-1) or contractions per minute per leg. Oxygen uptake (VO(2)) mean response time was ∼20% faster (p < 0.05) during H2 compared with H1 in both modalities. Phase 2 time constants (τ) were not different between heavy bouts of CE (H1, 29.6 ± 6.5 s; H2, 28.0 ± 4.6 s) or KE exercise (H1, 31.6 ± 6.7 s; H2, 29.8 ± 5.6 s). The VO(2) slow component amplitude was lower (p < 0.05) in H2 in both modalities (CE, 0.19 ± 0.06 L·min(-1); KE, 0.12 ± 0.07 L·min(-1)) compared with H1 (CE, 0.29 ± 0.09 L·min(-1); KE, 0.18 ± 0.07 L·min(-1)), with the contribution of the slow component to the total VO(2) response reduced (p < 0.05) in H2 during both exercise modes. The effective τHHb was similar between bouts for CE (H1, 18.2 ± 3.0 s; H2, 18.0 ± 3.6 s) and KE exercise (H1, 26.0 ± 7.0 s; H2, 24.0 ± 5.8 s). The ΔHHb slow component was reduced during H2 in both CE and KE (p < 0.05). In conclusion, phase 2 VO(2p) was unchanged with priming exercise; however, a faster mean response time of VO(2p) during the heavy-intensity exercise preceded by a priming heavy-intensity exercise was attributed to a smaller slow component and reduced muscle deoxygenation indicative of improved muscle O(2) delivery during the second bout of exercise.

Regulation of V̇o2 kinetics by O2 delivery: insights from acute hypoxia and heavy-intensity priming exercise in young men

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity "priming" exercise (Hvy) on pulmonary O(2) uptake (Vo(2p)) kinetics during moderate-intensity exercise (Mod). Breath-by-breath Vo(2p) and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O(2) (Fi(O(2))) = 15%, Mod 2 + Hypo] or "sham" (Fi(O(2)) = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient Vo(2p) and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0-100%), the signals were time-aligned, and the individual [HHb]-to-Vo(2) ratio was calculated. Compared with control (Mod 1), τVo(2p) and the O(2) deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced (P < 0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased (P < 0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τVo(2p) was increased (30 ± 8 s, P < 0.05), yet O(2) deficit was unaffected (643 ± 193 ml, P > 0.05). The modest "overshoot" in the [HHb]-to-Vo(2) ratio (reflecting an O(2) delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P = 0.13). The present data do not support an "O(2) delivery-independent" speeding of τVo(2p) following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O(2) delivery likely governs the rate of adjustment of Vo(2) at τVo(2p) greater than ∼20 s.

Slow Component of V˙O2 Kinetics

The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.

Effects of Priming Exercise on V˙O2 Kinetics and the Power-Duration Relationship

This study aimed to investigate the influence of prior heavy- and severe-intensity exercise on the oxygen uptake (V·O₂) kinetics and the power-duration relationship. Ten cyclists performed 13 exercise tests during a 4-wk period, consisting of a ramp test to determine the gas exchange threshold (GET) and the peak V·O₂, followed by a series of square-wave tests to exhaustion under three conditions: no prior exercise (control), prior heavy exercise (6 min at a work rate above GET but below critical power [CP)], and prior severe exercise (6 min at a work rate above the CP). Pulmonary gas exchange was measured throughout the exhaustive exercise bouts and the parameters of the power-duration relationship (CP and the curvature constant, W') were determined from the linear work-time model. Prior heavy exercise increased the amplitude of the primary V·O₂ response (by ∼ 0.19 ± 0.28 L·min(-1), P = 0.001), reduced the V·O₂ slow component trajectory (by 0.04 ± 0.09 L·min(-2), P = 0.002), and increased the time to exhaustion (by ∼ 52 ± 92 s, P = 0.005). The CP was unchanged (control vs prior heavy: 284 ± 47 vs 283 ± 44 W; 95% confidence interval, -7 to 5 W), whereas the W' was increased by heavy-intensity priming (16.0 ± 4.8 vs 18.7 ± 4.8 kJ; 95% confidence interval, 0.3-5.2 kJ). Severe-intensity exercise had a similar effect on the V·O₂ kinetics but had no effect on the time to exhaustion, the CP (275 ± 45 W), or the W' (16.7 ± 4.7 kJ). Prior heavy-intensity exercise primes the V·O₂ kinetics and increases the amount of work that can be performed above the CP.

Speeding of V̇o2 kinetics during moderate-intensity exercise subsequent to heavy-intensity exercise is associated with improved local O2 distribution

The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II V(O(2p)) during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity "priming" exercise. Moderate intensity V(O(2p)) and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). V(O(2p)) was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. V(O(2p)) and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0-100%). The Δ[HHb]/Vo(2) ratio for each individual (reflecting the local matching of O(2) delivery to O(2) utilization) was calculated as the average Δ[HHb]/Vo(2) response from 20 s to 120 s during the exercise on-transient. Phase II τV(O(2p)) was reduced in Mod 2 compared with Mod 1 (P < 0.05). The effective τ'Δ[HHb] remained the same in Mod 1 and Mod 2 (P > 0.05). During Mod 1, there was an "overshoot" in the Δ[HHb]/Vo(2) ratio (1.08; P < 0.05) that was not present during Mod 2 (1.01; P > 0.05). There was a positive correlation between the reduction in the Δ[HHb]/Vo(2) ratio and the smaller τV(O(2p)) from Mod 1 to Mod 2 (r = 0.78; P < 0.05). This study showed that a smaller τV(O(2p)) during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O(2) delivery during the on-transient of exercise, as suggested by a smaller Δ[HHb]/Vo(2) ratio.

Influence of priming exercise on muscle deoxy[Hb + Mb] during ramp cycle exercise

The aim of the present study was to gain better insight into the mechanisms underpinning the sigmoid pattern of deoxy[Hb + Mb] during incremental exercise by assessing the changes in the profile following prior high-intensity exercise. Ten physically active students performed two incremental ramp (25 W min(-1)) exercises (AL and LL, respectively) preceded on one occasion by incremental arm (10 W min(-1)) and on another occasion by incremental leg exercise (25 W min(-1)), which served as the reference test (RT). Deoxy[Hb + Mb] was measured by means of near-infrared spectroscopy and surface EMG was recorded at the Vastus Lateralis throughout the exercises. Deoxy[Hb + Mb], integrated EMG and Median Power Frequency (MdPF) were expressed as a function of work rate (W) and compared between the exercises. During RT and AL deoxy[Hb + Mb] followed a sigmoid increase as a function of work rate. However, during LL deoxy[Hb + Mb] increased immediately from the onset of the ramp exercise and thus no longer followed a sigmoid pattern. This different pattern in deoxy[Hb + Mb] was accompanied by a steeper slope of the iEMG/W-relationship below the GET (LL: 0.89 ± 0.11% W(-1); RT: 0.74 ± 0.08% W(-1); AL: 0.72 ± 0.10% W(-1)) and a more pronounced decrease in MdPF in LL (17.2 ± 4.5%) compared to RT (5.0 ± 2.1%) and AL (3.9 ± 3.2%). It was observed that the sigmoid pattern of deoxy[Hb + Mb] was disturbed when the ramp exercise was preceded by priming leg exercise. Since the differences in deoxy[Hb + Mb] were accompanied by differences in EMG it can be suggested that muscle fibre recruitment is an important underlying mechanism for the pattern of deoxy[Hb + Mb] during ramp exercise.

Priming Exercise Induced Attenuation Of VO2 Slow Component Is Associated With Changes In Muscle EMG Activity

Priming Exercise Induced Attenuation Of VO2 Slow Component Is Associated With Changes In Muscle EMG Activity

O2uptake and blood pressure regulation at the onset of exercise: interaction of circadian rhythm and priming exercise

Circadian rhythm has an influence on several physiological functions that contribute to athletic performance. We tested the hypothesis that circadian rhythm would affect blood pressure (BP) responses but not O(2) uptake (Vo(2)) kinetics during the transitions to moderate and heavy cycling exercises. Nine male athletes (peak Vo(2): 60.5 ± 3.2 ml·kg(-1)·min(-1)) performed multiple rides of two different cycling protocols involving sequences of 6-min bouts at moderate or heavy intensities interspersed by a 20-W baseline in the morning (7 AM) and evening (5 PM). Breath-by-breath Vo(2) and beat-by-beat BP estimated by finger cuff plethysmography were measured simultaneously throughout the protocols. Circadian rhythm did not affect Vo(2) onset kinetics determined from the phase II time constant (τ(2)) during either moderate or heavy exercise bouts with no prior priming exercise (τ(2) moderate exercise: morning 22.5 ± 4.6 s vs. evening 22.2 ± 4.6 s and τ(2) heavy exercise: morning 26.0 ± 2.7 s vs. evening 26.2 ± 2.6 s, P > 0.05). Priming exercise induced the same robust acceleration in Vo(2) kinetics during subsequent moderate and heavy exercise in the morning and evening. A novel finding was an overshoot in BP (estimated from finger cuff plethysmography) in the first minutes of each moderate and heavy exercise bout. After the initial overshoot, BP declined in association with increased skin blood flow between the third and sixth minute of the exercise bout. Priming exercise showed a greater effect in modulating the BP responses in the evening. These findings suggest that circadian rhythm interacts with priming exercise to lower BP during exercise after an initial overshoot with a greater influence in the evening associated with increased skin blood flow.

The influence of priming exercise on oxygen uptake, cardiac output, and muscle oxygenation kinetics during very heavy-intensity exercise in 9- to 13-yr-old boys

The present study examined the effect of priming exercise on O(2) uptake (Vo(2)) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O(2) delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II Vo(2) tau, 3) elevate the phase II Vo(2) total amplitude, and 4) reduce the magnitude of the Vo(2) slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests Vo(2), muscle oxygenation (near infrared spectroscopy), and cardiac output (Q) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q at baseline and throughout the second exercise bout. The phase II Vo(2) tau was not altered by priming exercise (bout 1: 22 + or - 7 s vs. bout 2: 20 + or - 4 s; P = 0.30). However, the time constant describing the entire Vo(2) response from start to end of exercise was accelerated (bout 1: 43 + or - 8 s vs. bout 2: 36 + or - 5 s; P = 0.002) due to an increased total phase II Vo(2) amplitude (bout 1: 1.73 + or - 0.33 l/min vs. bout 2: 1.80 + or - 0.59 l/min; P = 0.002) and a reduced Vo(2) slow component amplitude (bout 1: 0.18 + or - 0.08 l/min vs. bout 2: 0.12 + or - 0.09 l/min; P = 0.048). These results suggest that phase II Vo(2) kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the Vo(2) total phase II and slow component amplitudes may be O(2) delivery sensitive.

The Effects of Prior Priming Exercise on the Incidence of Plateau at VO2max

The Effects of Prior Priming Exercise on the Incidence of Plateau at VO2max