Onset Of Moderate-intensity Exercise Research Articles

The algorithm used for the calculation of gas exchange affects the estimation of O2 uptake kinetics at the onset of moderate-intensity exercise.

At the start of a moderate-intensity square-wave exercise, after a short delay, breath-by-breath O2 uptake at the mouth is approximated to a mono-exponential function, whose time constant is considered matched to that of the O2 uptake of the working muscles. We compared the kinetic parameters obtained from the breath-by-breath gas exchange data yielded by the 'Independent-breath' algorithm (IND), which accounts for the changes in lung gas stores, with those obtained with the classical 'Expiration-only' algorithm (EXP). The two algorithms were applied on the same flow and gas fraction traces acquired on 10 healthy volunteers, performing 10 times the same moderate-intensity exercise transition. Repeated O2 uptake responses were stacked together and the kinetic parameters of a mono-exponential function were estimated by non-linear regression, removing the data pertaining to 1-s progressively longer initial periods (ΔTr ). Independently of ΔTr , the mean response time (time constant + time delay) obtained for the IND data was faster compared to the EXP data (∼43s vs. ∼47s, P<0.001), essentially because of shorter time delays. Between ΔTr =16s and ΔTr =29s, the time constants of the IND data decreased (30.7s vs. 28.0s, P<0.05; drop=10%), but less than those of the EXP data (32.2s vs. 26.2s, P<0.001; drop=23%); with the same ΔTr , the time constants of the two algorithms' data were not different (P>0.07). The different decrease in the time constant, together with the different mean response time, suggests that the data yielded by the two algorithms provide a different picture of the phenomena occurring at the beginning of the exercise.

Blood flow restriction accelerates aerobic training-induced adaptation of {dot{text{V}}}{text{O}}_{2} kinetics at the onset of moderate-intensity exercise

It is unclear whether blood flow restriction (BFR) accelerates the adaptation of the time constant (τ) of phase II oxygen uptake ( {dot{text{V}}}{text{O}}_{2} ) kinetics in the moderate-intensity exercise domain via moderate-intensity aerobic training. Therefore, healthy participants underwent moderate-intensity [45–60% {dot{text{V}}}{text{O}}_{2} Reserve] aerobic cycle training with or without BFR (BFR group, n = 9; CON group, n = 9) for 8 weeks to evaluate {dot{text{V}}}{text{O}}_{2} kinetics during moderate-intensity cycle exercise before (Pre) and after 4 (Mid) and 8 (Post) weeks of training. Both groups trained for 30 min, 3 days weekly. BFR was performed for 5 min every 10 min by applying cuffs to the upper thighs. The τ significantly decreased by Mid in the BFR group (23.7 ± 2.9 s [Pre], 15.3 ± 1.8 s [Mid], 15.5 ± 1.4 s [Post], P < 0.01) and by Post in the CON group (27.5 ± 2.0 s [Pre], 22.1 ± 0.7 s [Mid], 18.5 ± 1.9 s [Post], P < 0.01). Notably, the BFR group’s τ was significantly lower than that of the CON group at Mid (P < 0.01) but not at Post. In conclusion, BFR accelerates the adaptation of the {dot{text{V}}}{text{O}}_{2} kinetics of phase II by moderate-intensity aerobic training.

Influence of the fitting window on the O2 uptake kinetics at the onset of moderate intensity exercise.

The O2 uptake (V̇o2) data at the onset of an exercise are usually fitted with a mono-exponential function, after removal of the data pertaining to a conventional initial time period (ΔTr) lasting ∼20 s. We performed a thorough quantitative analysis on the effects of removing data pertaining to different ΔTr, aiming at identifying an objective method to establish the appropriate ΔTr. Breath-by-breath O2 uptake responses, acquired from 25 healthy adults performing a step moderate-intensity exercise, and 104 simulated biexponential responses, were analyzed. For all the responses, the kinetic parameters of a mono-exponential function and the corresponding asymptotic standard errors (ASEs) were estimated by nonlinear regression, removing the data pertaining to progressively longer initial periods (1 s each) up to 60 s. Four methods to establish objectively ΔTr were compared. The minimum estimated τ was obtained for ΔTr ≅ 35 s in both the V̇o2 and simulated data, that was about 30% lower compared with that obtained for ΔTr ≅ 0s. The average ASE values remained quite constant up to ΔTr ≅ 35 s, thereafter they increased remarkably. The τ used to generate the simulated response fell within the confidence intervals of the estimated τ in ∼85% of cases for ΔTr = 20 s ("20 s-w" method); this percentage increased to ∼92% of cases when ΔTr was established according to both the minimum τ and its narrowest confidence interval ("Mixed" method). In conclusion, the effects of removing V̇o2 data pertaining to different ΔTr are remarkable. The "Mixed" method provided estimated parameters close to those used to generate the simulated responses and is thus endorsed.NEW & NOTEWORTHY We propose a method to objectively establish the initial time period to be removed from the fitting window when, using a mono-exponential model, the kinetics of the fundamental component is determined on breath-by-breath O2 uptake data collected at the onset of a moderate-intensity exercise. Innovative statistical parameters ("Coverage" and "Concordance5%," applicable on simulated responses) were used to compare its performance with that of other three methods. The proposed method yielded the best "Coverage" and "Concordance5%."

Association between pulmonary oxygen uptake on-kinetics and acute cardiovascular responses to resistance exercise in patients with coronary artery disease: a preliminary study.

[Purpose] This study aimed to examine whether pulmonary oxygen uptake on-kinetics at the onset of moderate-intensity exercise can predict acute cardiovascular responses to resistance exercise. [Participants and Methods] The association between pulmonary oxygen uptake on-kinetics and acute cardiovascular responses to a single resistance exercise session was investigated in seven patients with low-risk coronary artery disease who underwent revascularization through percutaneous coronary intervention. The participants performed a cardiopulmonary exercise test on a cycle ergometer and a single resistance exercise session at 30% of maximum voluntary contraction on a bilateral leg-extension machine 1 week after surgery. We measured the ventilatory anaerobic threshold and pulmonary oxygen uptake on-kinetics during the cardiopulmonary exercise test; left ventricular ejection fraction at rest; and heart rate, systolic blood pressure, and rate pressure product during the single resistance exercise session. [Results] Pulmonary oxygen uptake on-kinetics showed a positive association with the amount of increase in systolic blood pressure and rate pressure product during the single resistance exercise session, but had no association with the amount of increase in heart rate. Ventilatory anaerobic threshold and left ventricular ejection fraction were not associated with these parameters. [Conclusion] These data suggested that pulmonary oxygen uptake on-kinetics can be a useful evaluation index for predicting acute systolic blood pressure and rate pressure product responses to low-intensity resistance exercise 1 week after percutaneous coronary intervention in patients with low-risk coronary artery disease.

Pulmonary oxygen uptake on-kinetics can predict acute physiological responses to resistance exercise training in healthy young men.

To clarify whether pulmonary oxygen uptake kinetics ( ) at the onset of moderate-intensity exercise can predict acute physiological responses to resistance exercise training (RET). We investigated the relationship between and acute metabolic and hemodynamic responses to a single RET session in 27 healthy young adult men. Cardiopulmonary exercise was on a cycle ergometer, and a single RET at 30% or 60% of one-repetition maximum was on a bilateral leg-extension machine. We measured the anaerobic threshold, peak and while cardiopulmonary exercising, and the rates of increase in blood lactate (Bla), heart rate (HR), systolic blood pressure (SBP) and rate pressure product (RPP) for a single RET. There were significant positive associations between and the rates of increase in Bla, HR, SBP and RPP during a single RET session (P<0·05). However, the anaerobic threshold and peak did not significantly affect these parameters. The is a useful evaluation index for predicting acute physiological responses to RET.

Effect of healthy aging and sex on middle cerebral artery blood velocity dynamics during moderate-intensity exercise.

Blood velocity measured in the middle cerebral artery (MCAV) increases with finite kinetics during moderate-intensity exercise, and the amplitude and dynamics of the response provide invaluable insights into the controlling mechanisms. The MCAV response after exercise onset is well fit to an exponential model in young individuals but remains to be characterized in their older counterparts. The responsiveness of vasomotor control degrades with advancing age, especially in skeletal muscle. We tested the hypothesis that older subjects would evince a slower and reduced MCAV response to exercise. Twenty-nine healthy young (25 ± 1 yr old) and older (69 ± 1 yr old) adults each performed a rapid transition from rest to moderate-intensity exercise on a recumbent stepper. Resting MCAV was lower in older than young subjects (47 ± 2 vs. 64 ± 3 cm/s, P < 0.001), and amplitude from rest to steady-state exercise was lower in older than young subjects (12 ± 2 vs. 18 ± 3 cm/s, P = 0.04), even after subjects were matched for work rate. As hypothesized, the time constant was significantly longer (slower) in the older than young subjects (51 ± 10 vs. 31 ± 4 s, P = 0.03), driven primarily by older women. Neither age-related differences in fitness, end-tidal CO2, nor blood pressure could account for this effect. Thus, MCAV kinetic analyses revealed a marked impairment in the cerebrovascular response to exercise in older individuals. Kinetic analysis offers a novel approach to evaluate the efficacy of therapeutic interventions for improving cerebrovascular function in elderly and patient populations. NEW & NOTEWORTHY Understanding the dynamic cerebrovascular response to exercise has provided insights into sex-related cerebrovascular control mechanisms throughout the aging process. We report novel differences in the kinetics response of cerebrovascular blood velocity after the onset of moderate-intensity exercise. The exponential increase in brain blood flow from rest to exercise revealed that 1) the kinetics profile of the older group was blunted compared with their young counterparts and 2) the older women demonstrated a slowed response.

Dynamics of middle cerebral artery blood flow velocity during moderate-intensity exercise.

The dynamic response to a stimulus such as exercise can reveal valuable insights into systems control in health and disease that are not evident from the steady-state perturbation. However, the dynamic response profile and kinetics of cerebrovascular function have not been determined to date. We tested the hypotheses that bilateral middle cerebral artery blood flow mean velocity (MCAV) increases exponentially following the onset of moderate-intensity exercise in 10 healthy young subjects. The MCAV response profiles were well fit to a delay (TD) + exponential (time constant, τ) model with substantial agreement for baseline [left (L): 69, right (R): 64 cm/s, coefficient of variation (CV) 11%], response amplitude (L: 16, R: 13 cm/s, CV 23%), TD (L: 54, R: 52 s, CV 9%), τ (L: 30, R: 30 s, CV 22%), and mean response time (MRT) (L: 83, R: 82 s, CV 8%) between left and right MCAV as supported by the high correlations (e.g., MRT r = 0.82, P < 0.05) and low CVs. Test-retest reliability was high with CVs for the baseline, amplitude, and MRT of 3, 14, and 12%, respectively. These responses contrasted markedly with those of three healthy older subjects in whom the MCAV baseline and exercise response amplitude were far lower and the kinetics slowed. A single older stroke patient showed baseline ipsilateral MCAV that was lower still and devoid of any exercise response whatsoever. We conclude that kinetics analysis of MCAV during exercise has significant potential to unveil novel aspects of cerebrovascular function in health and disease.NEW & NOTEWORTHY Resolution of the dynamic stimulus-response profile provides a greater understanding of the underlying the physiological control processes than steady-state measurements alone. We report a novel method of measuring cerebrovascular blood velocity (MCAv) kinetics under ecologically valid conditions from rest to moderate-intensity exercise. This technique reveals that brain blood flow increases exponentially following the onset of exercise with 1) a strong bilateral coherence in young healthy individuals, and 2) a potential for unique age- and disease-specific profiles.

No Acute Effect Of Phosphodiesterase-5 Inhibition On Pulmonary Oxygen Uptake Kinetics At The Onset Of Moderate-Intensity Exercise In Trained And Untrained Adults

The nitric oxide (NO)-3′5′cyclic guanosine monophosphate (cGMP) signaling pathway has been implicated in the regulation of muscle vasodilatation as well as oxidative metabolism during exercise. Inhibition of Phosphodiesterase-5 reduces cGMP hydrolysis and might, to some extent, influence muscle hemodynamic and oxidative processes, and arguably, affect pulmonary oxygen uptake kinetics during exercise. PURPOSE: To test the hypothesis that acute administration of Tadalafil, a phosphodiesterase-5 inhibitor commonly used for therapeutic purposes, speeds pulmonary oxygen uptake kinetics at the onset of moderate-intensity exercise in trained and untrained adults. METHODS: Six untrained (mean age 23.3 ± 3.2 yr, VO2 peak 2996 ± 239 mL.min-1) and six trained (mean age 22.3 ± 1.0 yr, VO2 peak 3279 ± 353 mL.min-1) males were assigned in a randomized, double-blind, crossover design to receive either one tablet of placebo or Tadalafil (20mg), with a 7 d washout period in between. Subjects completed square-wave transitions to power outputs requiring 80% of gas exchange threshold (GET) from a baseline of unloaded cycling. Pulmonary oxygen uptake was measured breath-by-breath and individual responses were modeled using nonlinear regression techniques. Data were analyzed using repeated measures ANOVA and unpaired t tests (P < 0.05). RESULTS: The VO2 time constant was slower (P < 0.05) in the untrained compared with the trained subjects in both placebo (42 ± 14 s vs 29 ± 5 s) and Tadalafil (42 ± 15 s vs 29 ± 14 s) conditions, respectively, but unaffected by the drug ingestion. The time delay was similar in untrained and trained subjects for placebo (24 ± 7 s and 20 ± 5 s), but not for Tadalafil (28 ± 7 s and 11 ± 5 s; P < 0.05) condition, respectively; however, the time delay was also unaffected by the drug ingestion. The VO2 amplitude was smaller (P < 0.05) in the untrained compared with the trained subjects in both placebo (1285 ± 230 s vs 1755 ± 305 s) and Tadalafil (1238 ± 187 s vs 1674 ± 232 s) conditions, respectively, but unaffected by the drug ingestion. The heart rate (HR) time constant was similar in trained and untrained subjects for both placebo (42 ± 8 s and 38 ± 12 s) and Tadalafil (30 ± 12 s and 36 ± 8 s) conditions, respectively, and did not differ between the two conditions. CONCLUSION: Inhibition of Phospodiesterase-5 did not alter pulmonary oxygen uptake kinetics at the onset of moderate-intensity exercise in healthy adults, regardless of training status.

Intra-dialytic training accelerates oxygen uptake kinetics in hemodialysis patients.

End-stage renal disease is associated with several hemodynamic and peripheral muscle abnormalities that could slow the rate of change in oxygen uptake ([Formula: see text]O2) at the onset and at the end of exercise. This study was performed to determine whether an intra-dialytic aerobic training program would speed [Formula: see text]O2 kinetics at the transition to and from moderate and high-intensity exercise. This study was a randomized controlled trial. Twenty-four patients with end-stage renal disease (14 females; 47.0 ± 11.9 years) were randomly assigned to either 12-week cycle ergometer-based training at moderate exertion or a similar control period. At initial and final evaluations, patients underwent 6 min moderate and high-intensity tests to exercise intolerance (Tlim). Training improved Tlim by ∼90% (median (inter-quartile range) = 232 (59) s to 445 (451) s, p < 0.05); in contrast, Tlim decreased by ∼30% in controls (291 (134) s to 202 (131) s). [Formula: see text]O2 kinetics at the onset of moderate-intensity exercise were significantly accelerated with training leading to lower oxygen (O2) deficit (mean ± standard deviation (SD) = 3.2 ± 1.3 l vs 2.3 ± 1.2 l). Similar positive effects were found at the high-intensity test either at the onset of, or recovery from, exercise (p < 0.05). "Excess" [Formula: see text]O2 at the high-intensity test was also lessened with training. Changes in Tlim correlated with faster [Formula: see text]O2 kinetics and lower "excess" [Formula: see text]O2 (Spearman's ρ = -0.56 and -0.75, respectively; p < 0.01). A symptom-targeted intra-dialytic training program improved sub-maximal aerobic metabolism and endurance exercise capacity. [Formula: see text]O2 kinetics are valuable in providing relatively effort-independent information on the efficacy of exercise interventions in this patient population.

Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate‐intensity exercise

Pulmonary O2 uptake (V(O₂p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO₂)) ~40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P(ET, CO₂) ~20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P(ET, CO₂) ~40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (~5%). The V(O₂p) was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 V(O₂p) kinetics (τV(O₂p)) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower V(O₂p) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P(CO₂) (NORMO) restored LBF kinetics, but not V(O₂p) kinetics, which remained 'slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower V(O₂p) kinetics observed during HYPO.

The Effect of Sodium Acetate Ingestion on the Metabolic Response to Prolonged Moderate-Intensity Exercise in Humans

At rest, administration of the short-chain fatty acid acetate suppresses fat oxidation without affecting carbohydrate utilization. The combined effect of increased acetate availability and exercise on substrate utilization is, however, unclear. With local ethics approval, we studied the effect of ingesting either sodium acetate (NaAc) or sodium bicarbonate (NaHCO3) at a dose of 4 mmol·kg-1 body mass 90 min before completing 120 min of exercise at 50% VO2peak. Six healthy young men completed the trials after an overnight fast and ingested the sodium salts in randomized order. As expected NaAc ingestion decreased resting fat oxidation (mean ± SD; 0.09 ± 0.02 vs. 0.07 ± 0.02 g·min-1 pre- and post-ingestion respectively, p < .05) with no effect upon carbohydrate utilization. In contrast, NaHCO3 ingestion had no effect on substrate utilization at rest. In response to exercise, fat and CHO oxidation increased in both trials, but fat oxidation was lower (0.16 ± 0.10 vs. 0.29 ± 0.11 g·min-1, p < .05) and carbohydrate oxidation higher (1.67 ± 0.35 vs. 1.44 ± 0.22 g·min-1, p < .05) in the NaAc trial compared with the NaHCO3 trial during the first 15 min of exercise. Over the final 75 min of exercise an increase in fat oxidation and decrease in carbohydrate oxidation was observed only in the NaAc trial. These results demonstrate that increasing plasma acetate concentration suppresses fat oxidation both at rest and at the onset of moderate-intensity exercise.

Low blood flow at onset of moderate-intensity exercise does not limit muscle oxygen uptake

The effect of low blood flow at onset of moderate-intensity exercise on the rate of rise in muscle oxygen uptake was examined. Seven male subjects performed a 3.5-min one-legged knee-extensor exercise bout (24 +/- 1 W, mean +/- SD) without (Con) and with (double blockade; DB) arterial infusion of inhibitors of nitric oxide synthase (N(G)-monomethyl-l-arginine) and cyclooxygenase (indomethacin) to inhibit the synthesis of nitric oxide and prostanoids, respectively. Leg blood flow and leg oxygen delivery throughout exercise was 25-50% lower (P < 0.05) in DB compared with Con. Leg oxygen extraction (arteriovenous O(2) difference) was higher (P < 0.05) in DB than in Con (5 s: 127 +/- 3 vs. 56 +/- 4 ml/l), and leg oxygen uptake was not different between Con and DB during exercise. The difference between leg oxygen delivery and leg oxygen uptake was smaller (P < 0.05) during exercise in DB than in Con (5 s: 59 +/- 12 vs. 262 +/- 39 ml/min). The present data demonstrate that muscle blood flow and oxygen delivery can be markedly reduced without affecting muscle oxygen uptake in the initial phase of moderate-intensity exercise, suggesting that blood flow does not limit muscle oxygen uptake at the onset of exercise. Additionally, prostanoids and/or nitric oxide appear to play important roles in elevating skeletal muscle blood flow in the initial phase of exercise.

Dietary Arginine Supplementation Speeds Pulmonary V˙O2 Kinetics during Cycle Exercise

To test the hypothesis that L-arginine (the substrate for nitric oxide synthase [NOS]) administration slows the VO2 kinetics at the onset of moderate-intensity exercise in humans. Seven physically active males were randomly assigned to receive either placebo (lactose) or L-arginine hydrochloride capsules (7.2 g x d(-1)) for 14 d in a double-blind crossover design, with a 7-d washout period between the two conditions. On day 11 and day 14 of each condition, the subjects completed two consecutive 6-min bouts of cycle exercise at 80% of the ventilatory threshold with a 12-min rest interval. VO2 was measured on a breath-by-breath basis, and VO2 kinetics were determined with a single exponential model from the averaged data derived from four repetitions. Capillary and venous blood samples were taken to determine plasma [La] and serum [arginine], respectively. There were no differences in circulating lactate either before or during exercise. However, serum [arginine] was higher (P < 0.05) in the arginine condition at rest (119.0 +/- 12.6 vs 103.6 +/- 15.7 micromol x L(-1) in the control condition) and after exercise (113.3 +/- 26.0 vs 103.8 +/- 12.6 micromol x L(-1) in the control condition). With regard to the pulmonary VO2 kinetics, no significant difference was observed in the time at which the phase II response emerged or in the phase II amplitude between the two conditions. However, contrary to our hypothesis, the time constant was significantly reduced after arginine administration (i.e., 13.9 +/- 3.1 vs 15.8 +/- 2.6 s in the control condition, P < or = 0.014). Exogenous L-arginine administration speeds the phase II pulmonary VO2 response by 12% at the onset of moderate-intensity exercise in humans.

Quadriceps Muscle Phosphocreatine and Deoxygenation Kinetics in Children and Adults at the Onset of Moderate Intensity Exercise

Quadriceps Muscle Phosphocreatine and Deoxygenation Kinetics in Children and Adults at the Onset of Moderate Intensity Exercise

The acute effects of differential dietary fatty acids on human skeletal muscle pyruvate dehydrogenase activity

Pyruvate dehydrogenase (PDH) is an important regulator of carbohydrate oxidation during exercise, and its activity can be downregulated by an increase in dietary fat. The purpose of this study was to determine the acute metabolic effects of differential dietary fatty acids on the activation of the PDH complex (PDHa activity) at rest and at the onset of moderate-intensity exercise. University-aged male subjects (n = 7) underwent two fat-loading trials spaced at least 2 wk apart. Subjects consumed approximately 300 g saturated (SFA) or n-6 polyunsaturated fatty acid (PUFA) fat over the course of 5 h. Following this, participants cycled at 65% of their maximum oxygen uptake for 15 min. Muscle biopsies were taken before and following fat loading and at 1 min exercise. Plasma free fatty acids increased from 0.15 +/- 0.07 to 0.54 +/- 0.19 mM over 5 h with SFA and from 0.11 +/- 0.04 to 0.35 +/- 0.13 mM with n-6 PUFA and were significantly lower throughout the n-6 PUFA trial. PDHa activity was unchanged following fat loading but increased at the onset of exercise in the SFA trial, from 1.18 +/- 0.27 to 2.16 +/- 0.37 mmol x min(-1) x kg wet wt(-1). This effect was negated in the n-6 PUFA trial (1.04 +/- 0.20 to 1.28 +/- 0.36 mmol x min(-1) x kg wet wt(-1)). PDH kinase was unchanged in both trials, suggesting that the attenuation of PDHa activity with n-6 PUFA was a result of changes in the concentrations of intramitochondrial effectors, potentially intramitochondrial NADH or Ca(2+). Our findings suggest that attenuated PDHa activity contributes to the preferential oxidation of n-6 PUFA during moderate-intensity exercise.

O2 uptake and muscle deoxygenation kinetics during the transition to moderate-intensity exercise in different phases of the menstrual cycle in young adult females

O(2) uptake (VO2) kinetics were examined during the follicular (F) and luteal (L) phases of the menstrual cycle to determine if there was an effect of altered sex hormones on the (VO2) response to moderate-intensity exercise. Seven healthy women (age 21 +/- 2 years; mean +/- SD) performed six transitions from 20 W to moderate-intensity exercise (approximately 90% theta L) during the F and L phase. VO2 was measured breath-by-breath and deoxyhemoglobin/myoglobin (Delta HHb) was determined by near infrared spectroscopy. Progesterone and estrogen were significantly (P < 0.05) elevated during the L compared to F phase. VO2 kinetics (tau VO2) were not different in the two phases of the menstrual cycle (F, 22 +/- 5 s; L, 22 +/- 6 s; 95% confidence intervals +/-4 s) nor was the time course of the Delta HHb response (F, TD 11 +/- 2 s, tau 11 +/- 3 s; L, TD 12 +/- 2 s, tau 12 +/- 11 s; tau HHb 95% confidence intervals +/-3 s). Respiratory exchange ratio (RER) was not different between phases for baseline or steady-state exercise and the blood lactate response to exercise was not different. In conclusion, VO2 kinetics at the onset of moderate-intensity exercise are not affected by the phase of the menstrual cycle in young females suggesting either no change in, or no effect of metabolic activation on the on-transient kinetics of moderate-intensity exercise. Additionally, the similar adaptation of Delta HHb in combination with unchanged VO2 suggests that there were no differences in the adaptation of local muscle O(2) delivery.

Influence of DCA on pulmonary (.-)V(O2) kinetics during moderate-intensity cycle exercise.

To test the hypothesis that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) with dichloroacetate (DCA) would speed phase II pulmonary oxygen uptake ((.-)V(O2)) kinetics after the onset of subsequent moderate-intensity (40-45% ((.-)V(O2)) peak) cycle exercise. Seven healthy males (mean +/- SD age 25 +/- 4 yr, body mass 75.3 +/- 9.4 kg) performed four "square-wave" transitions from unloaded cycling to a work rate requiring 90% of the predetermined gas exchange threshold either with or without prior infusion of DCA (50 mg x kg body mass in 50 mL saline). Pulmonary ((.-)V(O2)) was measured breath-by-breath in all tests and ((.-)V(O2)) kinetics were determined from the averaged individual response to each condition using nonlinear regression techniques. The blood [lactate] measured immediately before the onset of exercise was significantly reduced in the DCA condition (C: 1.1 +/- 0.3 vs DCA: 0.6 +/- 0.3 mM; P < 0.01) consistent with successful activation of the PDC. However, DCA had no discernible effect on the rate at which ((.-)V(O2)) increased toward the steady state after the onset of exercise as reflected in the phase II time constant (C: 28.5 +/- 11.8 vs DCA: 29.4 +/- 14.9 s). The results suggest that PDC activation does not represent a principal intramuscular limitation to ((.-)V(O2)) kinetics after the onset of moderate-intensity exercise.

Adapatation of VO2 and Muscle Deoxygenation at the Onset of Moderate-Intensity Exercise with Respiratory Alkalosis

0437 Following a period of hyperventilation-induced respiratory alkalosis (R-ALK), pulmonary O2 uptake (VO2) kinetics are either not changed (Ward et al., J. Appl. Physiol. 55:742, 1983) or slowed (Hayashi et al., Am. J. Physiol. 277:R1274, 1999) compared to control conditions, while local muscle oxygenation changes have not been examined. PURPOSE: To examine the effect of R-ALK on VO2 kinetics and muscle deoxygenation at the onset of moderate-intensity exercise. METHODS: Young male adults (n = 8) completed 5 repetitions of a step transition in work rate from 20 W cycling to a work rate corresponding to 90% of the estimated lactate threshold during control (CON; PETCO2 ∼ 40 mmHg) and following 20 min hyperventilation (R-ALK; PETCO2 ∼20 mmHg). VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively. Changes in muscle deoxy-(HHb), oxy-(HbO2) and total hemoglobin (HbTOT) were measured continuously using near-infrared spectroscopy (NIRS; Hamamatsu, NIRO 300). The adaptation of VO2, HR, and HHb were modelled with a mono-exponential equation using non-linear least-squares regression. RESULTS: During R-ALK, PETCO2 was maintained < 25 mmHg throughout the accommodation and exercise. The phase II VO2 time constant (ô VO2) was longer (P < 0.05) in R-ALK (34 ± 7 s) than CON (27 ± 8 s), while ôHR was similar between conditions (R-ALK, 47 ± 8 s; CON, 38 ± 17 s). Following a delay, the ôHHb was similar between conditions (R-Alk, 7 ± 3 s; Con, 7 ± 4 s), while the HbTOT was lower in R-ALK than CON throughout the accommodation and exercise (end-exercise HbTOT: R-Alk, 1 ± 6 μM; Con, 5 ± 5 μM). CONCLUSION: The slower adaptation of VO2 during R-ALK may be related to a reduction in local muscle perfusion (as seen by a similar HHb and lower HbTOT), although slowed metabolic processes cannot be excluded. Supported by NSERC, Canada.

Adapatation of VO2 and Muscle Deoxygenation at the Onset of Moderate-Intensity Exercise with Respiratory Alkalosis

Adapatation of VO2 and Muscle Deoxygenation at the Onset of Moderate-Intensity Exercise with Respiratory Alkalosis

VO2 OVERSHOOTS THE STEADY-STATE VALUE IN THE TRANSITION TO MODERATE EXERCISE IN TRAINED CYCLISTS

We have previously observed that some trained subjects evidence an “overshoot” in VO2 at the onset of moderate-intensity exercise. PURPOSE To systematically examine this phenomenon by comparing the VO2 responses to two moderate-intensity work rates in trained and untrained subjects. METHODS Seven trained cyclists (mean ± SD; age 20 ± 2 years, body mass 66.7 ± 6.4 kg, VO2 peak 66.6 ± 2.5 ml·kg−1 min−1) and eight sedentary subjects (age 21 ± 2 years, body mass 73.6 ± 6.7 kg, VO2 peak 42.9 ± 5.1 ml·kg−1·min−1) gave written informed consent to participate in this ethically approved study. Following a ramp exercise test to volitional exhaustion for the determination of the ventilatory threshold (VT) and VO2 peak, subjects completed 6 square-wave transitions from unloaded cycling to work rates requiring 60% of the subjects' VT (60%VT) and 80% of the subjects' VT (80%VT), and 3 square-wave transitions to 50% of the difference between VT and VO2 peak (50%Δ). VO2 was measured breath-by-breath and modelled using standard techniques. RESULTS The sedentary subjects did not overshoot the steady-state VO2 at any intensity. At 60% VT, 6 of the 7 cyclists “overshot” the steady-state VO2 (by 164 ± 44 ml between ∼45 and 125 s). At 80% VT, 4 of the 7 cyclists “overshot” the steady-state VO2 (by 185 ± 92 ml between ∼55 and 140 s). At 50%Δ, none of the cyclists evidenced an overshoot. Overshoots in VO2 were generally associated with overshoots in heart rate. CONCLUSION These results indicate that trained cyclists evidence an overshoot in VO2 before steady-state is reached in the transition to moderate-intensity exercise. The mechanism responsible for this effect is unclear but differences in motor unit recruitment or circulatory adjustment in trained compared to untrained subjects may be responsible.