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

2009 ◽  
Vol 107 (6) ◽  
pp. 1743-1756 ◽  
Author(s):  
Stephen J. Bailey ◽  
Anni Vanhatalo ◽  
Daryl P. Wilkerson ◽  
Fred J. DiMenna ◽  
Andrew M. Jones
Keyword(s):  
Exercise Intensity ◽  
High Intensity ◽  
Exercise Tolerance ◽  
Slow Component ◽  
High Intensity Exercise ◽  
Step Cycle ◽  
Exercise Tests ◽  
Recovery Duration ◽  
Prior Exercise ◽  
Ergometer Exercise

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 O2 uptake (V̇o2) 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 V̇o2 (i.e., 80%Δ) after no prior exercise (control) and after six different combinations of prior exercise intensity and recovery duration: 40%Δ with 3 min (40-3-80), 9 min (40-9-80), and 20 min (40-20-80) of recovery and 70%Δ with 3 min (70-3-80), 9 min (70-9-80), and 20 min (70-20-80) of recovery. Overall V̇o2 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 V̇o2 slow component amplitude; the phase II time constant was not significantly altered with any prior exercise/recovery combination. Exercise tolerance at 80%Δ 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%Δ did not significantly influence exercise tolerance regardless of the recovery duration. These data demonstrate that prior high-intensity exercise (∼70%Δ) can enhance the tolerance to subsequent high-intensity exercise provided that it is coupled with adequate recovery duration (≥9 min). This combination presumably optimizes the balance between preserving the effects of prior exercise on V̇o2 kinetics and providing sufficient time for muscle homeostasis (e.g., muscle phosphocreatine and H+ concentrations) to be restored.

Influence of endurance training on muscle [PCr] kinetics during high-intensity exercise

2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford
Keyword(s):  
Endurance Training ◽  
High Intensity ◽  
Slow Component ◽  
Knee Extension ◽  
High Intensity Exercise ◽  
Whole Body ◽  
Time To Exhaustion ◽  
Exercise Tests ◽  
Before And After ◽  
Knee Extension Exercise

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.

Pulmonary O2 uptake kinetics as a determinant of high-intensity exercise tolerance in humans

2011 ◽  
Vol 110 (6) ◽  
pp. 1598-1606 ◽  
Author(s):  
Scott R. Murgatroyd ◽  
Carrie Ferguson ◽  
Susan A. Ward ◽  
Brian J. Whipp ◽  
Harry B. Rossiter
Keyword(s):  
Steady State ◽  
High Intensity ◽  
Exercise Tolerance ◽  
Slow Component ◽  
Progressive Increase ◽  
High Intensity Exercise ◽  
Exercise Intolerance ◽  
Exercise Onset ◽  
O2 Uptake Kinetics ◽  
Two Parameters

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W′) and power asymptote termed “critical power” (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O2 uptake (V̇o2) kinetics would relate to the P-tolerable duration (tlim) parameters. We hypothesized that 1) the fundamental time constant (τV̇o2) would relate inversely to CP; and 2) the slow-component magnitude (ΔV̇o2sc) would relate directly to W′. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine V̇o2max, CP, and W′; and 3) repeated constant-P tests (WR6) normalized to a 6 min tlim for τV̇o2 and ΔV̇o2sc estimation. The WR6 tlim averaged 365 ± 16 s, and V̇o2max (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171–294 W) was inversely correlated with τV̇o2 (18–38 s; R2 = 0.90), and W′ (12.8–29.9 kJ) was directly correlated with ΔV̇o2sc (0.42–0.96 l/min; R2 = 0.76). These findings support the notions that 1) rapid V̇o2 adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when V̇o2 kinetics are slower; and 2) exercise exceeding this limit initiates a “fatigue cascade” linking W′ to a progressive increase in the O2 cost of power production (V̇o2sc), which, if continued, results in attainment of V̇o2max and exercise intolerance. Collectively, these data implicate V̇o2 kinetics as a key determinant of high-intensity exercise tolerance in humans.

scholarly journals Influence of acute plasma volume expansion on V̇o2 kinetics, V̇o2peak, and performance during high-intensity cycle exercise

2006 ◽  
Vol 101 (3) ◽  
pp. 707-714 ◽  
Author(s):  
Nicolas J. A. Berger ◽  
Iain T. Campbell ◽  
Daryl P. Wilkerson ◽  
Andrew M. Jones
Keyword(s):  
Gas Exchange ◽  
Plasma Volume ◽  
High Intensity ◽  
Volume Expansion ◽  
Time To Exhaustion ◽  
Cycle Exercise ◽  
Step Cycle ◽  
Plasma Volume Expansion ◽  
Exercise Tests ◽  
Ergometer Exercise

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V̇o2) kinetics, V̇o2peak, and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed “step” cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V̇o2max on three occasions: twice as a “control” (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 ± 1.0 vs. postinfusion: 14.7 ± 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 ± 2 vs. postinfusion: 41 ± 3%; P < 0.01). Despite this reduction in arterial O2 content, APVE had no effect on V̇o2 kinetics (phase II time constant, Con: 33 ± 15 vs. APVE: 34 ± 12 s; P = 0.74), and actually resulted in an increased V̇o2peak (Con: 3.90 ± 0.56 vs. APVE: 4.12 ± 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 ± 58 vs. APVE: 424 ± 64 s; P = 0.04). The maximum O2 pulse was also enhanced by the treatment (Con: 21.3 ± 3.4 vs. APVE: 22.7 ± 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V̇o2 kinetics but enhances V̇o2peak and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

scholarly journals Complex I is bypassed during high intensity exercise

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Avlant Nilsson ◽  
Elias Björnson ◽  
Mikael Flockhart ◽  
Filip J. Larsen ◽  
Jens Nielsen
Keyword(s):  
High Intensity ◽  
Complex I ◽  
Atp Synthesis ◽  
Metabolic Model ◽  
High Intensity Exercise ◽  
Whole Body ◽  
Synthesis Rate ◽  
Proteomics Data ◽  
Exercise Tests

Abstract Human muscles are tailored towards ATP synthesis. When exercising at high work rates muscles convert glucose to lactate, which is less nutrient efficient than respiration. There is hence a trade-off between endurance and power. Metabolic models have been developed to study how limited catalytic capacity of enzymes affects ATP synthesis. Here we integrate an enzyme-constrained metabolic model with proteomics data from muscle fibers. We find that ATP synthesis is constrained by several enzymes. A metabolic bypass of mitochondrial complex I is found to increase the ATP synthesis rate per gram of protein compared to full respiration. To test if this metabolic mode occurs in vivo, we conduct a high resolved incremental exercise tests for five subjects. Their gas exchange at different work rates is accurately reproduced by a whole-body metabolic model incorporating complex I bypass. The study therefore shows how proteome allocation influences metabolism during high intensity exercise.

scholarly journals Exercise training intensity determination in cardiovascular rehabilitation: Should the guidelines be reconsidered?

2019 ◽  
Vol 26 (18) ◽  
pp. 1921-1928 ◽  
Author(s):  
Dominique Hansen ◽  
Kim Bonné ◽  
Toon Alders ◽  
Ann Hermans ◽  
Katrien Copermans ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Heart Rate ◽  
Exercise Intensity ◽  
High Intensity ◽  
Ventilatory Threshold ◽  
Cardiopulmonary Exercise Test ◽  
High Intensity Exercise ◽  
Cardiovascular Rehabilitation ◽  
Correct Determination ◽  
Low Intensity Exercise

Aims In the rehabilitation of cardiovascular disease patients a correct determination of the endurance-type exercise intensity is important to generate health benefits and preserve medical safety. It remains to be assessed whether the guideline-based exercise intensity domains are internally consistent and agree with physiological responses to exercise in cardiovascular disease patients. Methods A total of 272 cardiovascular disease patients without pacemaker executed a maximal cardiopulmonary exercise test on bike (peak respiratory gas exchange ratio >1.09), to assess peak heart rate (HRpeak), oxygen uptake (VO2peak) and cycling power output (Wpeak). The first and second ventilatory threshold (VT1 and VT2, respectively) was determined and extrapolated to %VO2peak, %HRpeak, %heart rate reserve (%HRR) and %Wpeak for comparison with guideline-based exercise intensity domains. Results VT1 was noted at 62 ± 10% VO2peak, 75 ± 10% HRpeak, 42 ± 14% HRR and 47 ± 11% Wpeak, corresponding to the high intensity exercise domain (for %VO2peak and %HRpeak) or low intensity exercise domain (for %Wpeak and %HRR). VT2 was noted at 84 ± 9% VO2peak, 88 ± 8% HRpeak, 74 ± 15% HRR and 76 ± 11% Wpeak, corresponding to the high intensity exercise domain (for %HRR and %Wpeak) or very hard exercise domain (for %HRpeak and %VO2peak). At best (when using %Wpeak) in only 63% and 72% of all patients VT1 and VT2, respectively, corresponded to the same guideline-based exercise intensity domain, but this dropped to about 48% and 52% at worst (when using %HRR and %HRpeak, respectively). In particular, the patient’s VO2peak related to differently elicited guideline-based exercise intensity domains ( P < 0.05). Conclusion The guideline-based exercise intensity domains for cardiovascular disease patients seem inconsistent, thus reiterating the need for adjustment.

Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity

1987 ◽  
Vol 63 (2) ◽  
pp. 654-658 ◽  
Author(s):  
M. S. Sothmann ◽  
A. B. Gustafson ◽  
M. Chandler
Keyword(s):  
Oxygen Consumption ◽  
Exercise Intensity ◽  
High Intensity ◽  
Maximal Oxygen Consumption ◽  
High Intensity Exercise ◽  
The Relationship ◽  
Circulating Levels

Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.

Effect of Exercise Intensity on Exogenous Glucose Requirements to Maintain Stable Glycemia At High Insulin Levels in Type 1 Diabetes

2020 ◽  
Vol 106 (1) ◽  
pp. e83-e93
Author(s):  
Vinutha B Shetty ◽  
Paul A Fournier ◽  
Nirubasini Paramalingam ◽  
Wayne Soon ◽  
Heather C Roby ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Exercise Intensity ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Moderate Intensity ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Exogenous Glucose ◽  
High Insulin

Abstract Context Under basal insulin levels, there is an inverted U relationship between exercise intensity and exogenous glucose requirements to maintain stable blood glucose levels in type 1 diabetes (T1D), with no glucose required for intense exercise (80% V̇O2 peak), implying that high-intensity exercise is not conducive to hypoglycemia. Objective This work aimed to test the hypothesis that a similar inverted U relationship exists under hyperinsulinemic conditions, with high-intensity aerobic exercise not being conducive to hypoglycemia. Methods Nine young adults with T1D (mean ± SD age, 22.6 ± 4.7 years; glycated hemoglobin, 61 ± 14 mmol/mol; body mass index, 24.0 ± 3.3 kg/m2, V̇O2 peak, 36.6 ± 8.0 mL·kg–1 min–1) underwent a hyperinsulinemic-euglycemic clamp to maintain stable glycemia (5-6 mmol·L−1), and exercised for 40 minutes at 4 intensities (35%, 50%, 65%, and 80% V̇O2peak) on separate days following a randomized counterbalanced study design. Main Outcome Measures Glucose infusion rates (GIR) and glucoregulatory hormones levels were measured. Results The GIR (± SEM) to maintain euglycemia was 4.4 ± 0.4 mg·kg–1 min–1 prior to exercise, and increased significantly by 1.8 ± 0.4, 3.0 ± 0.4, 4.2 ± 0.7, and 3.5 ± 0.7 mg·kg–1 min–1 during exercise at 35%, 50%, 65%, and 80% V̇O2 peak, respectively, with no significant differences between the 2 highest exercise intensities (P &gt; .05), despite differences in catecholamine levels (P &lt; .05). During the 2-hour period after exercise at 65% and 80% V̇O2 peak, GIRs did not differ from those during exercise (P &gt; .05). Conclusions Under hyperinsulinemic conditions, the exogenous glucose requirements to maintain stable glycemia during and after exercise increase with exercise intensity then plateau with exercise performed at above moderate intensity ( &gt; 65% V̇O2 peak). High-intensity exercise confers no protection against hypoglycemia.

Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1α mRNA: a role of β2-adrenergic receptor activation

2011 ◽  
Vol 300 (2) ◽  
pp. E341-E349 ◽  
Author(s):  
Miki Tadaishi ◽  
Shinji Miura ◽  
Yuko Kai ◽  
Emi Kawasaki ◽  
Keiichi Koshinaka ◽  
...  
Keyword(s):  
Exercise Intensity ◽  
High Intensity ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Receptor Activation ◽  
High Intensity Exercise ◽  
Treadmill Running ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Exercise Induced

There are three isoforms of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA, which promotes mitochondrial biogenesis in skeletal muscles. Compared with PGC-1α-a mRNA, PGC-1α-b or PGC-1α-c mRNA is transcribed by a different exon 1 of the PGC-1α gene. In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were investigated. All isoforms were increased in proportion to exercise intensity of treadmill running (10–30 m/min for 30 min). Preinjection of β2-adrenergic receptor (AR) antagonist (ICI 118551) inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs, but not the increase in PGC-1α-a mRNA, in response to high-intensity exercise. Although high-intensity exercise activated α2-AMP-activated protein kinase (α2-AMPK) in skeletal muscles, inactivation of α2-AMPK activity did not affect high-intensity exercise-induced mRNA expression of all PGC-1α isoforms, suggesting that activation of α2-AMPK is not mandatory for an increase in PGC-1α mRNA by high-intensity exercise. A single injection in mice of AICAR, an AMPK activator, increased mRNAs of all PGC-1α isoforms. AICAR increased blood catecholamine concentrations, and preinjection of β2-AR antagonist inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs but not the increase in PGC-1α-a mRNA. Direct exposure of epitrochlearis muscle to AICAR increased PGC-1α-a but not the -b isoform. These data indicate that exercise-induced PGC-1α expression was dependent on the intensity of exercise. Exercise or AICAR injection increased PGC-1α-b and PGC-1α-c mRNAs via β2-AR activation, whereas high-intensity exercise increased PGC-1α-a expression by a multiple mechanism in which α2-AMPK is one of the signaling pathways.

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