Effect of inspiratory threshold loading on ventilatory kinetics during constant-load exercise.

Humoral factors play an important role in the control of exercise hyperpnea. The role of neuromechanical ventilatory factors, however, is still being investigated. We tested the hypothesis that the afferents of the thoracopulmonary system, and consequently of the neuromechanical ventilatory loop, have an influence on the kinetics of oxygen consumption (VO2), carbon dioxide output (VCO2), and ventilation (VE) during moderate intensity exercise. We did this by comparing the ventilatory time constants (tau) of exercise with and without an inspiratory load. Fourteen healthy, trained men (age 22.6 +/- 3.2 yr) performed a continuous incremental cycle exercise test to determine maximal oxygen uptake (VO2max = 55.2 +/- 5.8 ml x min(-1) x kg(-1)). On another day, after unloaded warm-up they performed randomized constant-load tests at 40% of their VO2max for 8 min, one with and the other without an inspiratory threshold load of 15 cmH2O. Ventilatory variables were obtained breath by breath. Phase 2 ventilatory kinetics (VO2, VCO2, and VE) could be described in all cases by a monoexponential function. The bootstrap method revealed small coefficients of variation for the model parameters, indicating an accurate determination for all parameters. Paired Student's t-tests showed that the addition of the inspiratory resistance significantly increased the tau during phase 2 of VO2 (43.1 +/- 8.6 vs. 60.9 +/- 14.1 s; P < 0.001), VCO2 (60.3 +/- 17.6 vs. 84.5 +/- 18.1 s; P < 0.001) and VE (59.4 +/- 16.1 vs. 85.9 +/- 17.1 s; P < 0.001). The average rise in tau was 41.3% for VO2, 40.1% for VCO2, and 44.6% for VE. The tau changes indicated that neuromechanical ventilatory factors play a role in the ventilatory response to moderate exercise.

Long maximal incremental tests accurately assess aerobic fitness in class II and III obese men.

This study aimed to compare two different maximal incremental tests with different time durations [a maximal incremental ramp test with a short time duration (8-12 min) (STest) and a maximal incremental test with a longer time duration (20-25 min) (LTest)] to investigate whether an LTest accurately assesses aerobic fitness in class II and III obese men. Twenty obese men (BMI≥35 kg.m-2) without secondary pathologies (mean±SE; 36.7±1.9 yr; 41.8±0.7 kg*m-2) completed an STest (warm-up: 40 W; increment: 20 W*min-1) and an LTest [warm-up: 20% of the peak power output (PPO) reached during the STest; increment: 10% PPO every 5 min until 70% PPO was reached or until the respiratory exchange ratio reached 1.0, followed by 15 W.min-1 until exhaustion] on a cycle-ergometer to assess the peak oxygen uptake [Formula: see text] and peak heart rate (HRpeak) of each test. There were no significant differences in [Formula: see text] (STest: 3.1±0.1 L*min-1; LTest: 3.0±0.1 L*min-1) and HRpeak (STest: 174±4 bpm; LTest: 173±4 bpm) between the two tests. Bland-Altman plot analyses showed good agreement and Pearson product-moment and intra-class correlation coefficients showed a strong correlation between [Formula: see text] (r=0.81 for both; p≤0.001) and HRpeak (r=0.95 for both; p≤0.001) during both tests. [Formula: see text] and HRpeak assessments were not compromised by test duration in class II and III obese men. Therefore, we suggest that the LTest is a feasible test that accurately assesses aerobic fitness and may allow for the exercise intensity prescription and individualization that will lead to improved therapeutic approaches in treating obesity and severe obesity.

Effect of a 1-hour single bout of moderate-intensity exercise on fat oxidation kinetics.

The present study aimed to examine the effects of a prior 1-hour continuous exercise bout (CONT) at an intensity (Fat(max)) that elicits the maximal fat oxidation (MFO) on the fat oxidation kinetics during a subsequent submaximal incremental test (IncrC). Twenty moderately trained subjects (9 men and 11 women) performed a graded test on a treadmill (Incr), with 3-minute stages and 1-km.h(-1) increments. Fat oxidation was measured using indirect calorimetry and plotted as a function of exercise intensity. A mathematical model (SIN) including 3 independent variables (dilatation, symmetry, and translation) was used to characterize the shape of fat oxidation kinetics and to determine Fat(max) and MFO. On a second visit, the subjects performed CONT at Fat(max) followed by IncrC. After CONT performed at 57% +/- 3% (means +/- SE) maximal oxygen uptake (Vo(2max)), the respiratory exchange ratio during IncrC was lower at every stage compared with Incr (P < .05). Fat(max) (56.4% +/- 2.3% vs 51.5% +/- 2.4% Vo(2max), P = .013), MFO (0.50 +/- 0.03 vs 0.40 +/- 0.03 g.min(-1), P < .001), and fat oxidation rates from 35% to 70% Vo(2max) (P < .05) were significantly greater during IncrC compared with Incr. However, dilatation and translation were not significantly different (P > .05), whereas symmetry tended to be greater in IncrC (P = .096). This study showed that the prior 1-hour continuous moderate-intensity exercise bout increased Fat(max), MFO, and fat oxidation rates over a wide range of intensities during the postexercise incremental test. Moreover, the shape of the postexercise fat oxidation kinetics tended to have a rightward asymmetry.

Effects of 2 different prior endurance exercises on whole-body fat oxidation kinetics: light vs. heavy exercise.

This study aimed to compare the effects of 2 different prior endurance exercises on subsequent whole-body fat oxidation kinetics. Fifteen men performed 2 identical submaximal incremental tests (Incr2) on a cycle ergometer after (i) a ∼40-min submaximal incremental test (Incr1) followed by a 90-min continuous exercise performed at 50% of maximal aerobic power-output and a 1-h rest period (Heavy); and (ii) Incr1 followed by a 2.5-h rest period (Light). Fat oxidation was measured using indirect calorimetry and plotted as a function of exercise intensity during Incr1 and Incr2. A sinusoidal equation, including 3 independent variables (dilatation, symmetry and translation), was used to characterize the fat oxidation kinetics and to determine the intensity (Fat(max)) that elicited the maximal fat oxidation (MFO) during Incr. After the Heavy and Light trials, Fat(max), MFO, and fat oxidation rates were significantly greater during Incr2 than Incr1 (p < 0.001). However, Δ (i.e., Incr2-Incr1) Fat(max), MFO, and fat oxidation rates were greater in the Heavy compared with the Light trial (p < 0.05). The fat oxidation kinetics during Incr2(Heavy) showed a greater dilatation and rightward asymmetry than Incr1(Heavy), whereas only a greater dilatation was observed in Incr2(Light) (p < 0.05). This study showed that although to a lesser extent in the Light trial, both prior exercise sessions led to an increase in Fat(max), MFO, and absolute fat oxidation rates during Incr2, inducing significant changes in the shape of the fat oxidation kinetics.

The decreased oxygen uptake during progressive exercise in ischemia-induced heart failure is due to reduced cardiac output rate

We tested the hypothesis that the inability to increase cardiac output during exercise would explain the decreased rate of oxygen uptake (VO2) in recent onset, ischemia-induced heart failure rats. Nine normal control rats and 6 rats with ischemic heart failure were studied. Myocardial infarction was induced by coronary ligation. VO2 was measured during a ramp protocol test on a treadmill using a metabolic mask. Cardiac output was measured with a flow probe placed around the ascending aorta. Left ventricular end-diastolic pressure was higher in ischemic heart failure rats compared with normal control rats (17 ± 0.4 vs 8 ± 0.8 mmHg, P = 0.0001). Resting cardiac index (CI) tended to be lower in ischemic heart failure rats (P = 0.07). Resting heart rate (HR) and stroke volume index (SVI) did not differ significantly between ischemic heart failure rats and normal control rats. Peak VO2 was lower in ischemic heart failure rats (73.72 ± 7.37 vs 109.02 ± 27.87 mL min-1 kg-1, P = 0.005). The VO2 and CI responses during exercise were significantly lower in ischemic heart failure rats than in normal control rats. The temporal response of SVI, but not of HR, was significantly lower in ischemic heart failure rats than in normal control rats. Peak CI, HR, and SVI were lower in ischemic heart failure rats. The reduction in VO2 response during incremental exercise in an ischemic model of heart failure is due to the decreased cardiac output response, largely caused by depressed stroke volume kinetics.

Breathing pattern and thoracoabdominal motion during exercise in chronic obstructive pulmonary disease

Subjects with chronic obstructive pulmonary disease (COPD) present breathing pattern and thoracoabdominal motion abnormalities that may contribute to exercise limitation. Twenty-two men with stable COPD (FEV1 = 42.6 ± 13.5% predicted; age 68 ± 8 years; mean ± SD) on usual medication and with at least 5 years of diagnosis were evaluated at rest and during an incremental cycle exercise test (10 watts/2 min). Changes in respiratory frequency, tidal volume, rib cage and abdominal motion contribution to tidal volume and the phase angle that measures the asynchrony were analyzed by inductive respiratory plethysmography at rest and during three levels of exercise (30-50, 70-80, and 100% maximal work load). Repeated measures ANOVA followed by pre-planned contrasts and Bonferroni corrections were used for analyses. As expected, the greater the exercise intensity the higher the tidal volume and respiratory frequency. Abdominal motion contributed to the tidal volume increase (rest: 49.82 ± 11.19% vs exercise: 64.15 ± 9.7%, 63.41 ± 10%, and 65.56 ± 10.2%, respectively, P < 0.001) as well as the asynchrony [phase angle: 11.95 ± 7.24° at rest vs 22.2 ± 15° (P = 0.002), 22.6 ± 9° (P < 0.001), and 22.7 ± 8° (P < 0.001), respectively, at the three levels of exercise]. In conclusion, the increase in ventilation during exercise in COPD patients was associated with the major motion of the abdominal compartment and with an increase in the asynchrony independent of exercise intensity. It suggests that cycling exercise is an effective way of enhancing ventilation in COPD patients.

Effect of L-carnitine on exercise performance in patients with mitochondrial myopathy

Exercise intolerance due to impaired oxidative metabolism is a prominent symptom in patients with mitochondrial myopathy (MM), but it is still uncertain whether L-carnitine supplementation is beneficial for patients with MM. The aim of our study was to investigate the effects of L-carnitine on exercise performance in MM. Twelve MM subjects (mean age±SD=35.4±10.8 years) with chronic progressive external ophthalmoplegia (CPEO) were first compared to 10 healthy controls (mean age±SD=29±7.8 years) before they were randomly assigned to receive L-carnitine supplementation (3 g/daily) or placebo in a double-blind crossover design. Clinical status, body composition, respiratory function tests, peripheral muscle strength (isokinetic and isometric torque) and cardiopulmonary exercise tests (incremental to peak exercise and at 70% of maximal), constant work rate (CWR) exercise test, to the limit of tolerance [Tlim]) were assessed after 2 months of L-carnitine/placebo administration. Patients with MM presented with lower mean height, total body weight, fat-free mass, and peripheral muscle strength compared to controls in the pre-test evaluation. After L-carnitine supplementation, the patients with MM significantly improved their Tlim (14±1.9 vs 11±1.4 min) and oxygen consumption ( V ˙ O 2 ) at CWR exercise, both at isotime (1151±115 vs 1049±104 mL/min) and at Tlim (1223±114 vs 1060±108 mL/min). These results indicate that L-carnitine supplementation may improve aerobic capacity and exercise tolerance during high-intensity CWRs in MM patients with CPEO.

The effect of a perceptual cognitive task on exercise performance: the dual-task condition after brain injury

Objective: To examine the effect of additional cognitive demand on cycling performance in individuals with acquired brain injury (ABI). Design: Prospective observational study. Setting: Rivermead Rehabilitation Centre. Participants: Ten individuals with ABI ( 7 men, 3 women) ( traumatic brain injury 7, tumour 1, stroke 2) and 10 healthy controls ( 6 men, 4 women). Intervention: Individuals were asked to maintain a set cadence during a three-stage incremental cycling test in both single-task ( no additional task) and dual-task ( whilst performing an additional cognitive task) conditions. Results: The ABI group showed a slight slowing in cadence in stages 1 and 3 of the graded exercise test from the single-to the dual-task condition, although this was not significant ( p less than or equal to 0.05). The control group showed no slowing of cadence at any incremental stage. When directly comparing the ABI with the control group, the change in cadence observed in dual-task conditions was only significantly different in stage 3 ( p less than or equal to 0.05). Conclusions: Clinicians should be aware of the possibility that giving additional cognitive tasks ( such as monitoring exercise intensity) while individuals with acquired brain injury are performing exercises may detrimentally affect performance. The effect may be more marked when the individuals are performing exercise at higher intensities.

Effect of a previous high intensity running exercise on isokinetic muscular strength in individuals with different training backgrounds

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Maximal lactate steady state in running mice: Effect of exercise training

1. Maximal lactate steady state (MLSS) corresponds to the highest blood lactate concentration (MLSSc) and workload (MLSSw) that can be maintained over time without continual blood lactate accumulation and is considered an important marker of endurance exercise capacity. The present study was undertaken to determine MLSSw and MLSSc in running mice. In addition, we provide an exercise training protocol for mice based on MLSSw.2. Maximal lactate steady state was determined by blood sampling during multiple sessions of constant-load exercise varying from 9 to 21 m/min in adult male C57BL/6J mice. The constant-load test lasted at least 21 min. The blood lactate concentration was analysed at rest and then at 7 min intervals during exercise.3. The MLSSw was found to be 15.1 +/- 0.7 m/min and corresponded to 60 +/- 2% of maximal speed achieved during the incremental exercise testing. Intra- and interobserver variability of MLSSc showed reproducible findings. Exercise training was performed at MLSSw over a period of 8 weeks for 1 h/day and 5 days/week. Exercise training led to resting bradycardia (21%) and increased running performance (28%). of interest, the MLSSw of trained mice was significantly higher than that in sedentary littermates (19.0 +/- 0.5 vs 14.2 +/- 0.5 m/min; P = 0.05), whereas MLSSc remained unchanged (3.0 mmol/L).4. Altogether, we provide a valid and reliable protocol to improve endurance exercise capacity in mice performed at highest workload with predominant aerobic metabolism based on MLSS assessment.

Efeito da cadência de pedalada sobre as respostas metabólica e cardiovascular durante o exercício incremental e de carga constante em indivíduos ativos

The main purpose of this study was to analyze the effect of the pedaling cadence (500 × 100 rpm) on the heart rate (HR) and the blood lactate response during incremental and constant workload exercises in active individuals. Nine active male individuals (20.9 ± 2.9 years old; 73.9 ± 6.5 kg; 1.79 ± 0.9 m) were submitted to two incremental tests, and to 6-8 constant workload tests to determine the intensity corresponding to the maximal steady state lactate (MLSSintens) in both cadences. The maximal power (Pmax) attained during the incremental test, and the MLSSintens were significantly lower at 100 rpm (240.9 ± 12.6 W; 148.1 ± 154.W) compared to 50 rpm (263.9 ± 18.6 W; 186.1 ± 21.2 W), respectively. The HRmax did not change between cadences (50 rpm = 191.1 ± 8.8 bpm; 100 rpm = 192.6 ± 9.9 bpm). Regardless the cadence, the HRmax percentage (70, 80, 90, and 100%) determined the same lactate concentrations during the incremental test. However, when the intensity was expressed in Pmax percentage or in absolute power, the lactate and the HR values were always higher at highest cadences. The HR corresponding to MLSSintens was similar between cadences (50 rpm = 162.5 ± 9.1 bpm; 100 rpm = 160.4 ± 9.2 bpm). Based on these results, it can be conclude that regardless the cadence employed (50 × 100 rpm), the use of the HR to individualize the exercise intensity indicates similar blood lactate responses, and this relationship is also kept in the exercise of constant intensity performed at MLSSintens. On the other hand, the use of the Pmax percentages depend on the cadence used, indicating different physiological responses to a same percentage.

Influência da aptidão aeróbia no running anaerobic sprint test (RAST)

The aim of this study was to investigate the possible influence of different levels of aerobic fitness (VO2MAX) on the parameters of the running anaerobic sprint test (RAST). Thirty-eight subjects (Age = 18.1 ± 2.5 years, Height = 173 ± 1 cm and Body mass = 65.1 ± 6.5 kg) were classified into two groups, low and high aerobic fitness (LAF: n = 22 and HAF: n = 16). The VO2MAX was determined by an incremental exercise performed until exhaustion. The RAST was composed of six maximal efforts of 35m separated by 10s passive recovery. The VO2MAX was significantly different between groups (LAF = 51.7 ± 1.9 mL.kg -1.min-1; HAF = 58.6 ± 3.1 mL.kg -1.min-1). The mean power (MP) was significantly higher in the LAF (552.7 ± 132.1 W) in relation to the HAF group (463.6 ± 132.8 W). The impulse (ImP) was significantly correlated with the VO 2MAX in HAF. It can be concluded that there is an indication that the aerobic metabolism exerts an influence on the completion of RAST.

The effect of prior exercise intensity on oxygen uptake kinetics during high-intensity running exercise in trained subjects

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Effect of an acute β-adrenergic blockade on the blood glucose response during lactate minimum test

The aim of this study was to determine the relationship between blood lactate and glucose during an incremental test after exercise induced lactic acidosis, under normal and acute β-adrenergic blockade. Eight fit males (cyclists or triathletes) performed a protocol to determine the intensity corresponding to the individual equilibrium point between lactate entry and removal from the blood (incremental test after exercise induced lactic acidosis), determined from the blood lactate (Lacmin) and glucose (Glucmin) response. This protocol was performed twice in a double-blind randomized order by ingesting either propranolol (80 mg) or a placebo (dextrose), 120 min prior to the test. The blood lactate and glucose concentration obtained 7 minutes after anaerobic exercise (Wingate test) was significantly lower (p<0.01) with the acute β-adrenergic blockade (9.1±1.5 mM; 3.9±0.1 mM), respectively than in the placebo condition (12.4±1.8 mM; 5.0±0.1 mM). There was no difference (p>0.05) between the exercise intensity determined by Lacmin (212.1±17.4 W) and Glucmin (218.2±22.1 W) during exercise performed without acute β-adrenergic blockade. The exercise intensity at Lacmin was lowered (p<0.05) from 212.1±17.4 to 181.0±15.6 W and heart rate at Lacmin was reduced (p<0.01) from 161.2±8.4 to 129.3±6.2 beats min-1 as a result of the blockade. It was not possible to determine the exercise intensity corresponding to Glucmin with β-adrenergic blockade, since the blood glucose concentration presented a continuous decrease during the incremental test. We concluded that the similar pattern response of blood lactate and glucose during an incremental test after exercise induced lactic acidosis, is not present during β-adrenergic blockade suggesting that, at least in part, this behavior depends upon adrenergic stimulation.

Effect of community-based physical exercise interventions carried out in primary helath care on plasma inflammatory biomarkers and cardiorespiratory fitness

Pós-graduação em Ciências da Motricidade - IBRC