Prior High-intensity Exercise Research Articles

Effects of prior high-intensity endurance exercise in subsequent 4-km cycling time trial performance and fatigue development

To investigate the effects of prior high-intensity endurance exercise on time trial (TT) performance and fatigue responses. Eleven male cyclists visited the lab in two separate visits. The first visit was composed by a maximal cycling incremental test (MIT) followed by 15 min of passive rest before a 4-km cycling TT. The second visit (control, CON) was composed by moderate-intensity exercise for 5 min before the TT. Fatigue of knee extensors was assessed by isometric maximal voluntary contractions (IMVC), while the central (voluntary activation [VA]) and peripheral fatigue (peak torque of potentiated twitches [TwPt]) were evaluated using electrically-evoked contractions performed before and 1 min after the TT. Power output (PO), oxygen uptake (V̇O 2 ) and rating of perceived exertion (RPE) were recorded throughout the TT. TT performance (+2.6%) and average PO (+5.7%) improved in MIT compared to CON condition. While peripheral fatigue level was greater in MIT condition ( P < 0.05), the central fatigue was lower compared to CON condition ( P < 0.05). There were greater overall V̇O 2 values (3.9 ± 0.4 vs 3.6 ± 0.4 L·min −1 ) but similar RPE responses (15 ± 2 vs 15 ± 3 a.u.) in MIT compared to CON. These findings indicate that prior high-intensity endurance exercise has positive effects in subsequent TT performance compare to moderate-intensity warm-up, despite exacerbated peripheral fatigue development. This response might be driven by greater aerobic reliance and exertion tolerance. Étudier les effets d’un pré exercice d’endurance à haute intensité sur la performance chronométrique (PC) et la fatigue. Onze cyclistes masculins sont venus à deux reprises au laboratoire. La première session était composée d’un test triangulaire maximal (TTM) suivi de 15 min de récupération passive avant la PC de 4 km à vélo. La seconde session était d’un exercice d’intensité modérée pendant 5 mis avant la PC (la condition contrôle, CON). La fatigue des extenseurs du genou était évaluée avec des contractions volontaires maximales isométriques (CVMI), dans un même temps la fatigue centrale [activation volontaire (AC)] et périphérique [pic de force des potentiels des twitches (PfPT)] était évaluée en utilisant l’électrostimulation avant et 1 min après la PC. La consommation d’oxygène (V̇O 2 ) et évaluation de l’effort perçu (RPE) était mesurée pendant toute la durée de la PC. La PC (+2,6 %) et la PO moyenne (+5,7 %) se sont améliorées dans le MIT par rapport à la condition CON. Alors que le niveau de fatigue périphérique était plus élevé en condition MIT ( p < 0,05), la fatigue centrale était plus faible par rapport à la condition CON ( p < 0,05). Il y avait des valeurs de V̇O2 plus élevées (3,9 ± 0,4 vs 3,6 ± 0,4 L·min −1 ) mais des réponses RPE similaires (15 ± 2 vs 15 ± 3 ua) dans le TTM par rapport à CON. Ces résultats indiquent que les exercices d’endurance de haute intensité antérieure ont des effets positifs sur la PC subséquent par rapport à un échauffement d’intensité modérée, malgré un développement de fatigue périphérique exacerbé. Cette réponse pourrait être motivée par une plus grande dépendance aérobie et tolérance à l’effort.

A Prior High-Intensity Exercise Bout Attenuates the Vascular Dysfunction Resulting From a Prolonged Sedentary Bout.

This study sought to determine the impact of an acute prior bout of high-intensity interval aerobic exercise on attenuating the vascular dysfunction associated with a prolonged sedentary bout. Ten young (24 ± 1y) healthy males completed two 3-hour sessions of prolonged sitting with (SIT-EX) and without (SIT) a high-intensity interval aerobic exercise session performed immediately prior. Prior to and 3 hours into the sitting bout, leg vascular function was assessed with the passive leg movement technique, and blood samples were obtained from the lower limb to evaluate changes in oxidative stress (malondialdehyde and superoxide dismutase) and inflammation (interleukin-6). No presitting differences in leg vascular function (assessed via passive leg movement technique-induced hyperemia) were revealed between conditions. After 3 hours of prolonged sitting, leg vascular function was significantly reduced in the SIT condition, but unchanged in the SIT-EX. Lower limb blood samples revealed no alterations in oxidative stress, antioxidant capacity, or inflammation in either condition. This study revealed that lower limb vascular dysfunction was significantly attenuated by an acute presitting bout of high-intensity interval aerobic exercise. Further analysis of lower limb blood samples revealed no changes in circulating oxidative stress or inflammation in either condition.

Physiological responses at the lactate-minimum-intensity with and without prior high-intensity exercise

ABSTRACTThis study examined the physiological responses during exercise-to-exhaustion at the lactate-minimum-intensity with and without prior high-intensity exercise. Eleven recreationally trained males performed a graded exercise test, a lactate minimum test and two constant-load tests at lactate-minimum-intensity until exhaustion, which were applied with or without prior hyperlactatemia induction (i.e., 30-s Wingate test). The physiological responses were significantly different (P < 0.05) between constant-load tests for pulmonary ventilation (), blood-lactate-concentration ([La−]), pH, bicarbonate concentration ([HCO3]) and partial pressure of carbon dioxide during the initial minutes. The comparisons within constant-load tests showed steady state behaviour for oxygen uptake and the respiratory exchange ratio, but heart rate and rating of perceived exertion increased significantly during both exercise conditions, while the increased only during constant-load effort. During effort performed after high-intensity exercise: , [La−], pH and [HCO3] differed at the start of exercise compared to another condition but were similar at the end (P > 0.05). In conclusion, the constant-load exercises performed at lactate-minimum-intensity with or without prior high-intensity exercise did not lead to the steady state of all analysed parameters; however, variables such as [La−], pH and [HCO3] – altered at the beginning of effort performed after high-intensity exercise – were reestablished after approximately 30 min of exercise.

Locomotor muscle fatigue is not critically regulated after prior upper body exercise.

This study examined the effects of prior upper body exercise on subsequent high-intensity cycling exercise tolerance and associated changes in neuromuscular function and perceptual responses. Eight men performed three fixed work-rate (85% peak power) cycling tests: 1) to the limit of tolerance (CYC); 2) to the limit of tolerance after prior high-intensity arm-cranking exercise (ARM-CYC); and 3) without prior exercise and for an equal duration as ARM-CYC (ISOTIME). Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force during supramaximal electrical femoral nerve stimulation. Voluntary activation was assessed using twitch interpolation during maximal voluntary contractions. Cycling time during ARM-CYC and ISOTIME (4.33 ± 1.10 min) was 38% shorter than during CYC (7.46 ± 2.79 min) (P < 0.001). Twitch force decreased more after CYC (-38 ± 13%) than ARM-CYC (-26 ± 10%) (P = 0.004) and ISOTIME (-24 ± 10%) (P = 0.003). Voluntary activation was 94 ± 5% at rest and decreased after CYC (89 ± 9%, P = 0.012) and ARM-CYC (91 ± 8%, P = 0.047). Rating of perceived exertion for limb discomfort increased more quickly during cycling in ARM-CYC [1.83 ± 0.46 arbitrary units (AU)/min] than CYC (1.10 ± 0.38 AU/min, P = 0.003) and ISOTIME (1.05 ± 0.43 AU/min, P = 0.002), and this was correlated with the reduced cycling time in ARM-CYC (r = -0.72, P = 0.045). In conclusion, cycling exercise tolerance after prior upper body exercise is potentially mediated by central fatigue and intolerable levels of sensory perception rather than a critical peripheral fatigue limit.

Prior heavy-intensity exercise's enhancement of oxygen-uptake kinetics and short-term high-intensity exercise performance independent of aerobic-training status.

Prior high-intensity exercise can improve exercise performance during severe-intensity exercise. These positive alterations have been attributed, at least in part, to enhancement of overall oxygen-uptake (VO2) kinetics. To determine the effects of prior heavy-intensity exercise on VO2 kinetics and short-term high-intensity exercise performance in individuals with different aerobic-training statuses. Fifteen active subjects (UT; VO2max = 43.8 ± 6.3 mL · kg-1 · min-1) and 10 well-trained endurance cyclists (T; VO2max = 66.7 ± 6.7 mL · kg-1 · min-1) performed the following protocols: an incremental test to determine lactate threshold and VO2max, 4 maximal constant-load tests to estimate critical power, and two 3-min bouts of cycle exercise, involving 2 min of constant-work-rate exercise at severe intensity followed by a 1-min all-out sprint test. This trial was performed without prior intervention and 10 min after prior heavy-intensity exercise (ie, 6 min at 90% critical power). The mean response time of VO2 was shortened after prior exercise for both UT (30.7 ± 9.2 vs 24.1 ± 7.2 s) and T (31.8 ± 5.2 vs 25.4 ± 4.3 s), but no group-by-condition interaction was detected. The end-sprint performance (ie, mean power output) was improved in both groups (UT ~4.7%, T ~2.0%; P < .05) by prior exercise. The effect of prior heavy-intensity exercise on overall VO2 kinetics and short-term high-intensity exercise performance is independent of aerobic-training status.

Improvement of 800-m Running Performance With Prior High-Intensity Exercise

Prior high-intensity exercise increases the oxidative energy contribution to subsequent exercise and may enhance exercise tolerance. The potential impact of a high-intensity warm-up on competitive performance, however, has not been investigated. To test the hypothesis that a high-intensity warm-up would speed VO2 kinetics and enhance 800-m running performance in well-trained athletes. Eleven highly trained middle-distance runners completed two 800-m time trials on separate days on an indoor track, preceded by 2 different warm-up procedures. The 800-m time trials were preceded by a 10-min self-paced jog and standardized mobility drills, followed by either 6 × 50-m strides (control [CON]) or 2 × 50-m strides and a continuous high-intensity 200-m run (HWU) at race pace. Blood [La] was measured before the time trials, and VO2 was measured breath by breath throughout exercise. 800-m time-trial performance was significantly faster after HWU (124.5 ± 8.3 vs CON, 125.7 ± 8.7 s, P < .05). Blood [La] was greater after HWU (3.6 ± 1.9 vs CON, 1.7 ± 0.8 mM; P < .01). The mean response time for VO2 was not different between conditions (HWU, 27 ± 6 vs CON, 28 ± 7 s), but total O2 consumed (HWU, 119 ± 18 vs CON, 109 ± 28 ml/kg, P = .05) and peak VO2 attained (HWU, 4.21 ± 0.85 vs CON, 3.91 ± 0.63 L/min; P = .08) tended to be greater after HWU. These data indicate that a sustained high-intensity warm-up enhances 800-m time-trial performance in trained athletes.

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.

Prior intense exercise reduces arterial carbon dioxide pressure in extreme obesity

Unlike normal weight individuals, individuals with extreme obesity do not show a decrease in arterial carbon dioxide pressure (PaCO₂) from rest to peak exercise. This indicates that breathing is compromised. The objective of this study was to determine if prior high intensity exercise lowers PaCO₂ in comparison with a first bout, normalized for the same metabolic rate. Oxygen consumption during incremental, ramped exercise was matched to constant workload exercise (75% of peak power). Both protocols were to volitional exhaustion 39 ± 8 min apart. Eleven obese subjects (BMI = 47 ± 8 kg/m², aerobic capacity = 2.3 ± 0.6 L/min) were evaluated. Forty paired samples were obtained at the same metabolic rate between the two protocols. The mean absolute difference and 95% CI were large for arterial oxygen pressure (PaO₂) = 9 (6, 11) mmHg and alveolar to arterial oxygen pressure difference (AaDO2) = 7 (5, 8) mmHg. The mean absolute difference for arterial oxyhemoglobin saturation (%SaO₂) = 0.5 (0.4, 0.7) %; PaCO2 = 4 (3, 4) mmHg; physiological dead space to tidal volume ratio (VD/VT) = 0.04 (0.03, 0.05); and alveolar ventilation (VA) = 3 (2, 4) L/min. The recovery period after the first bout of exercise reduced the PaCO₂ by 3 mmHg when matched for similar metabolic rates. Constant workload exercise predicted VA, %SaO2, V(D)/V(T), and PaCO₂, but not PaO₂ or AaDO₂ during incremental exercise at similar metabolic rates. Given a sufficient chemical stimulus, obese subjects will attempt to breathe more, although this does not mean more VA, which removes CO₂.

Optimizing the “priming” effect: influence of prior exercise intensity and recovery duration on O2 uptake kinetics and severe-intensity exercise tolerance

It has been suggested that a prior bout of high-intensity exercise has the potential to enhance performance during subsequent high-intensity exercise by accelerating the O(2) uptake (Vo(2)) on-response. However, the optimal combination of prior exercise intensity and subsequent recovery duration required to elicit this effect is presently unclear. Eight male participants, aged 18-24 yr, completed step cycle ergometer exercise tests to 80% of the difference between the preestablished gas exchange threshold and maximal Vo(2) (i.e., 80%Delta) after no prior exercise (control) and after six different combinations of prior exercise intensity and recovery duration: 40%Delta with 3 min (40-3-80), 9 min (40-9-80), and 20 min (40-20-80) of recovery and 70%Delta with 3 min (70-3-80), 9 min (70-9-80), and 20 min (70-20-80) of recovery. Overall Vo(2) kinetics were accelerated relative to control in all conditions except for 40-9-80 and 40-20-80 conditions as a consequence of a reduction in the Vo(2) slow component amplitude; the phase II time constant was not significantly altered with any prior exercise/recovery combination. Exercise tolerance at 80%Delta was improved by 15% and 30% above control in the 70-9-80 and 70-20-80 conditions, respectively, but was impaired by 16% in the 70-3-80 condition. Prior exercise at 40%Delta did not significantly influence exercise tolerance regardless of the recovery duration. These data demonstrate that prior high-intensity exercise ( approximately 70%Delta) can enhance the tolerance to subsequent high-intensity exercise provided that it is coupled with adequate recovery duration (>or=9 min). This combination presumably optimizes the balance between preserving the effects of prior exercise on Vo(2) kinetics and providing sufficient time for muscle homeostasis (e.g., muscle phosphocreatine and H(+) concentrations) to be restored.

Influence of priming exercise on pulmonary O2uptake kinetics during transitions to high-intensity exercise at extreme pedal rates

We investigated the pedal rate dependency of the effect of priming exercise on pulmonary oxygen uptake (Vo(2)) kinetics. Seven healthy men completed two, 6-min bouts of high-intensity cycle exercise (separated by 6 min of rest) using different combinations of extreme pedal rates for the priming and criterion exercise bouts (i.e., 35-->35, 35-->115, 115-->35, and 115-->115 rev/min). Pulmonary gas exchange and heart rate were measured breath-by-breath, and muscle oxygenation was assessed using near-infrared spectroscopy. When the priming bout was performed at 35 rev/min (35-->35 and 35-->115 conditions), the phase II Vo(2) time constant (tau) was not significantly altered (bout 1: 31 +/- 7 vs. bout 2: 30 +/- 5 s and bout 1: 48 +/- 16 vs. bout 2: 46 +/- 21 s, respectively). However, when the priming bout was performed at 115 rev/min (115-->35 and 115-->115 conditions), the phase II tau was significantly reduced (bout 1: 31 +/- 7 vs. bout 2: 26 +/- 5 s and bout 1: 48 +/- 16 vs. bout 2: 39 +/- 9 s, respectively, P < 0.05). Muscle oxygenation was significantly higher after priming exercise in all four conditions, but significant effects on Vo(2) kinetics were only evident when muscle O(2) extraction (measured as Delta[deoxyhemoglobin]/DeltaVo(2)) was elevated in the fundamental response phase. These data indicate that prior high-intensity exercise at a high pedal rate can speed Vo(2) kinetics during subsequent high-intensity exercise, presumably through specific priming effects on type II muscle fibers.

Influence of prior exercise on muscle [phosphorylcreatine] and deoxygenation kinetics during high‐intensity exercise in men

(31)Phosphate-magnetic resonance spectroscopy and near infrared spectroscopy (NIRS) were used for the simultaneous assessment of changes in quadriceps muscle metabolism and oxygenation during consecutive bouts of high-intensity exercise. Six male subjects completed two 6 min bouts of single-legged knee-extension exercise at 80% of the peak work rate separated by 6 min of rest while positioned inside the bore of a 1.5 T superconducting magnet. The total haemoglobin and oxyhaemoglobin concentrations in the area of the quadriceps muscle interrogated with NIRS were significantly higher in the baseline period prior to the second compared with the first exercise bout, consistent with an enhanced muscle oxygenation. Intramuscular phosphorylcreatine concentration ([PCr]) dynamics were not different over the fundamental region of the response (time constant for bout 1, 51 +/- 15 s versus bout 2, 52 +/- 17 s). However, the [PCr] dynamics over the entire response were faster in the second bout (mean response time for bout 1, 72 +/- 16 s versus bout 2, 57 +/- 8 s; P < 0.05), as a consequence of a greater fall in [PCr] in the fundamental phase and a reduction in the magnitude of the 'slow component' in [PCr] beyond 3 min of exercise (bout 1, 10 +/- 6% versus bout 2, 5 +/- 3%; P < 0.05). These data suggest that the increased muscle O(2) availability afforded by the performance of a prior bout of high-intensity exercise does not significantly alter the kinetics of [PCr] hydrolysis at the onset of a subsequent bout of high-intensity exercise. The greater fall in [PCr] over the fundamental phase of the response following prior high-intensity exercise indicates that residual fatigue acutely reduces muscle efficiency.

Central circulatory and peripheral O2 extraction changes as interactive facilitators of pulmonary O2 uptake during a repeated high-intensity exercise protocol in humans

It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake [Formula: see text] response at the onset of subsequent identical exercise. To clarify the roles of central O(2) delivery and/or peripheral O(2) extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O(2) content difference [Formula: see text] to the [Formula: see text] transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II [Formula: see text] response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the [Formula: see text] speeding at 10 and 30 s, respectively. After this, the contribution of [Formula: see text] became increasingly more predominant: being responsible to an estimated 64% of the [Formula: see text] speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and [Formula: see text] clearly interact to determine the [Formula: see text] response, the speeding of [Formula: see text] kinetics by prior high-intensity KE exercise is predominantly attributable to increases in [Formula: see text].

Determination of muscle pH and glycolytic flux by magnetic resonance spectroscopy in contracting human skeletal muscle may have systematic errors

To the Editor : 31P magnetic resonance spectroscopy (MRS) is a powerful noninvasive technique to quantitatively assess phosphate metabolites and intracellular pH in vivo and has proven useful in describing the metabolic changes occurring in intact muscle. However, there are limitations and pitfalls

Prior Arm Exercise Speeds the &amp;OV0312;O2 Kinetics during Arm Exercise above the Heart Level

To test the hypothesis that the initial O2 uptake kinetics during exercise where the rise in blood flow (and, by implication, O2 delivery) to the working muscles during an abrupt increase in exercise intensity is reduced (i.e., arm exercise performed above the level of the heart) would be faster when preceded by a bout of high-intensity exercise. Eleven physically active males completed two protocols, each consisting of two consecutive bouts of 6 min of high-intensity arm crank exercise separated by 6 min of recovery. In one protocol, the arm crank exercise was performed with the arms below the level of the heart (<HL); in the other, the arms were above the level of the heart (>HL). In the <HL protocol, the VO2 fast component time constant was not significantly affected by prior exercise (35.9+/-8.7 and 35.5+/-8.9 s in bouts 1 and 2, respectively). The amplitudes of the VO2 fast and slow component were respectively significantly higher and significantly lower in the second bout. In the >HL protocol, the amplitudes of the VO2 fast and slow component were unaffected by prior exercise, whereas the VO2 fast component time constant was significantly reduced in the second bout (49.8+/-22.1 vs 40.7+/-13.2 s; P<0.05). The results of this study demonstrate that prior high-intensity exercise caused a significant speeding of the VO2 fast component response during subsequent high-intensity arm crank exercise performed above, and not below, the level of the heart.

High-energy phosphate metabolism during two bouts of progressive calf exercise in humans measured by phosphorus-31 magnetic resonance spectroscopy

According to the literature the steady-state level of phosphocreatine (PCr) has a linear relationship to the workload during muscle exercise intensities below the lactate threshold, whereas this linearity is impaired during exercise intensities above the lactate threshold. The purpose of this study was to investigate the linearity between PCr kinetics and workload during two bouts of isotonic incremental calf exercise with transitions from moderate- to high-intensity as well as from high- to moderate-intensity work rates. Using a whole-body 1.5 T MR scanner and a self-built exercise bench, we performed serial phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS) with a time resolution of 30 s in nine healthy male volunteers. Changes in PCr, inorganic phosphate (Pi) and pH were statistically evaluated in comparison to the baseline. The exercise protocol started with a 4.5 W interval of 6 min followed by two bouts of 1.5 W increments. The workload was increased in 2-min intervals up to 9 W during the first bout and up to 7.5 W during the second bout. The second bout was preceded by a 4.5 W interval of 2 min and followed by a 4.5 W interval of 4 min. PCr hydrolysis achieved a steady state during each increment and was highly linear to the work rate (r (2), -0.796; P <0.001). Pi accumulated during each bout, whereas the pH decreased continuously during the first bout and did not exhibit any substantial decrease during the second bout. The metabolite levels and pH were expressed as the median value and the range. Our study confirms that steady-state PCr levels also have a linear relationship to work intensities above the lactate threshold, while pH changes do not have any impact on PCr degradation. The lack of substantial changes in pH during the second exercise bout indicates that prior high-intensity exercise leads to an activation of oxidative phosphorylation.

Intensity-dependent tolerance to exercise after attaining V̇o2 max in humans

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W') with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W' can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1). a ramp-incremental and 2). three high-intensity constant-load bouts at different work rates, to estimate lactate (theta(L)) and CP thresholds, W', and maximum oxygen uptake (Vo2 max). Subsequently, subjects cycled to the limit of tolerance (for approximately 360 s) on three occasions, each followed by a work rate reduction to 1). 110% CP, 2). 90% CP, and 3). 80% theta(L) for a 20-min target. W' averaged 20.9 +/- 2.35 kJ or 246 +/- 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 +/- 12 s. Each subject completed 20 min at 80% theta(L), but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 +/- 306 s, with oxygen consumption at 89 +/- 8% Vo2 max. The results support the suggestion that replenishing W' after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.

Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses.

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

The effect of prior high-intensity cycling exercise on the VO2 kinetics during high-intensity cycling exercise is situated at the additional slow component.

In previous studies conclusions about the effect of prior exercise on VO2 kinetics of subsequent high-intensity exercise are generally based on observed changes in the overall VO2 response without considering the effects on the VO2 fast and slow component. The aim of the present study was to examine the effect on the VO2 fast and slow component separately. Therefore 10 subjects performed an exercise protocol consisting of an initial 3 min period of unloaded cycling followed by two constant-load work bouts at a work rate corresponding to 90% VO2peak, separated by 3 min of rest and 3 min of unloaded cycling. VO2 was measured on a breath-by-breath basis, and the response curves were analysed by a biexponential model. To increase signal-to-noise ratio, subjects performed four repetitions of the exercise protocol, each separated by at least one day. There was no significant alteration in VO2 kinetic parameters of the primary, fast component after high-intensity exercise. However, there was a significant effect of prior high-intensity exercise on the VO2 kinetic parameters of the slow component. The time constant and the amplitude of the slow component were reduced by respectively 44% (from 231.0 +/- 111.7 s to 130.1 +/- 50.4 s) and 49% (from 824 +/- 270 ml x min(-1) to 417 +/- 134 ml x min(-1)). The results of this study indicate that the effect of high-intensity exercise on the VO2 kinetics of a subsequent high-intensity exercise is probably limited to an effect on the slow component.

Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans.

For moderate work rates (i.e. below the lactate threshold, theta), oxygen uptake (Vo2) approaches the steady state mono-exponentially. At higher work rates, the Vo2 kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra theta L cycling (with a 6 min recovery) does not significantly affect the V02 time course for a subsequent sub-theta L bout, it significantly speeds the V02 response to a subsequent supra-theta L bout (Gausche, Harmon, Lamarra & Whipp, 1989; Gerbino, Ward & Whipp, 1996). These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the V02 kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE) at a work rate equivalent to 50% of lambda le' (the difference between maximum V02,LE and theta L,LE). On one occasion this was preceded by a 6 min period of cycling at 50% lambda LE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% lambda LE in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of PH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V02 between minute 6 and 3 of each work bout (lambda V02 ¿6-3] and the 'partial' O2 deficit (O2 Def) provided indices of the slow phase of V02 kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr¿ and [NAdr]. The subsequent LE bouts were associated with reductions in both lambda V02[6-3] and O2 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: lambda V02[6-3] averaging 32 and 56% of control, respectively, and O2 Def 71 and 81%. Consequently, the increase in [lactate] and decrease in PH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V02 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.

Failure of prior low-intensity exercise to potentiate the thermic effect of glucose

We have previously shown that following recovery from 45 min exercise at 67% maximum oxygen consumption (VO2max) the thermic effect of a glucose load is increased by 65% over that observed on a non-exercise day (Young et al. 1986). The purpose of this study was to determine if potentiation of the thermic effect of glucose by prior exercise is dependent on exercise intensity. The thermic response to a 1674 kJ glucose load was measured in five subjects in the absence of exercise (control) and following recovery from 45 min cycling exercise at each of three intensities: low (34% VO2max), moderate (54% VO2max), and high (75% VO2max). The average percentage increase in oxygen consumption over baseline due to glucose ingestion was similar for the control (9.9%, SE 2.0%), and the low- (10.2%, SE 0.9%) and moderate- (12.6%, SE 1.2%) intensity exercise conditions, while a significant increase in average VO2 was observed after the high-intensity condition (18.0%, SE 2.3%, P less than 0.05). The total energy expenditure (kJ) over baseline for 3 h was also similar for the control (84.5, SE 11.7), and the low-(100.0, SE 9.2) and moderate- (118.8, SE 5.0) intensity exercise conditions. The thermic response following high-intensity exercise (146.4 kJ, SE 13.4) was significantly greater than that observed in the control (P less than 0.01) or low-intensity (P less than 0.05) exercise conditions. These findings demonstrate that unlike prior high-intensity exercise (75% VO2max), low- or moderate-intensity exercise (i.e., 34% or 54% VO2max) fails to potentiate the thermic effect of a glucose load.(ABSTRACT TRUNCATED AT 250 WORDS)