Onset Of High-intensity Exercise Research Articles

High-intensity interval training improves respiratory and cardiovascular adjustments before and after initiation of exercise.

Purpose: High-intensity interval training (HIIT) may induce training-specific physiological adaptations such as improved respiratory and cardiovascular adjustments before and after the onset of high-intensity exercise, leading to improved exercise performance during high-intensity exercise. The present study investigated the effects of HIIT on time-dependent cardiorespiratory adjustment during maximal exercise and before and after initiation of high-intensity exercise, as well as on maximal exercise performance. Methods: 21 healthy male college students were randomly assigned to HIIT group (n = 11) or control group (n = 10). HIIT group performed training on a cycle ergometer once a week for 8 weeks. The training consisted of three bouts of exercise at 95% maximal work rate (WRmax) until exhaustion. Before and after the HIIT program, dynamic cardiorespiratory function was investigated by ramp and step exercise tests, and HIIT-induced cardiac morphological changes were assessed using echocardiography. Results: HIIT significantly improved not only maximal oxygen uptake and minute ventilation, but also maximal heart rate (HR), systolic blood pressure (SBP), and time to exhaustion in both exercise tests (p < 0.05). Time-dependent increases in minute ventilation (VE) and HR before and at the start of exercise were significantly enhanced after HIIT. During high-intensity exercise, there was a strong correlation between percent change (from before to after HIIT program) in time to exhaustion and percent change in HRmax (r = 0.932, p < 0.001). Furthermore, HIIT-induced cardiac morphological changes such as ventricular wall hypertrophy was observed (p < 0.001). Conclusion: We have demonstrated that HIIT at 95% WRmax induces training-specific adaptations such as improved cardiorespiratory adjustments, not only during maximal exercise but also before and after the onset of high-intensity exercise, improvement of exercise performance mainly associated with circulatory systems.

Physiological role of anticipatory cardiorespiratory responses to exercise.

This study aimed to investigate whether anticipatory cardiorespiratory responses vary depending on the intensity of the subsequent exercise bout, and whether anticipatory cardiorespiratory adjustments contribute importantly to enhancing exercise performance during high‐intensity exercise. Eleven healthy men were provided advance notice of the exercise intensity and a countdown to generate anticipation during 10 min prior to exercise at 0, 50, 80 or 95% maximal work‐rate (Experiment 1). A different group of subjects (n = 15) performed a time to exhaustion trial with or without anticipatory countdown (Experiment 2). In Experiment 1, heart rate (HR), oxygen uptake (VO2) and minute ventilation (VE) during pre‐exercise resting period increased over time and depended on the subsequent exercise intensity. Specifically, there was already a 7.4% increase in HR from more than 5 min prior to the start of exercise at 95% maximal work‐rate, followed by progressively augmented increases of 12.5% between 2 and 3 min before exercise, 24.4% between 0 and 1 min before exercise. In Experiment 2, the initial HR for the first 10 s of exercise in the task with anticipation was 11.4% larger compared to without anticipation (p < 0.01), and the difference in HR between the two conditions decreased in a time‐dependent manner. In contrast, the initial increases in VO2 and VE were significantly lower in the task with anticipation than that without anticipation. The time to exhaustion during high‐intensity exercise was 14.6% longer under anticipation condition compared to no anticipation (135 ± 26 s vs. 119 ± 26 s, p = 0.003). In addition, the enhanced exercise performance correlated positively with increased HR response just before and immediately after exercise onset (p < 0.01). These results showed that anticipatory cardiorespiratory adjustments (feedforward control) via the higher brain that operate before starting exercise may play an important role in minimizing the time delay of circulatory response and enhancing performance after onset of high‐intensity exercise in man.

Effects of Weekly Interval Training at High Intensity interval training on Dynamic Cardiorespiratory Responses to Exercise

Purpose Previously we reported that high-intensity interval training (HIIT) at 80% maximal work-rate (WRmax), even when performed at a low frequency of once a week, markedly improves maximal cardiorespiratory function and maximal performance time (Med Sci Sports Exerc. 2015). However, it has not been determined whether more intense interval exercise training will have the similar effect on maximal oxygen uptake (VO2max) or alter the dynamics of the cardiorespiratory response during maximal exercise. The purpose of this study was to examine whether or not the same effect can be obtained, even with HIIT at 95%WRmax for 8 weeks which further increased exercise intensity than the previous study. Methods Seventeen healthy male college students were randomly assigned to one of the two following groups; high-intensity interval training group (HIT; n = 9) and control group (n = 8). HIT group performed the training on a cycle ergometer once a week for 8 weeks. The training was consisted of three bouts until volitional fatigue at 95%WRmax. Cardiorespiratory function during maximal ramp and step (high-intensity) exercise test was investigated before and after the intervention period. Results The training resulted in increased VO2max (+9%, p = 0.037), maximal heart rate (+4%, p = 0.023) and maximal minute ventilation (+19%, p = 0.007) during maximal ramp test, respectively. Significant changes in the dynamic response of heart rate and blood pressure at the onset of high-intensity exercise were observed after the training program compared with baseline, and improvement in exhaustion time was also observed (+ 93%, P < 0.001). In addition, increased left ventricular posterior wall thickness at rest was also observed after training (+12%, p = 0.004). Conclusion The present results indicate that more intense HIIT performed at a low frequency once a week not only increased maximal cardiorespiratory function and exercise performance, but also induced cardiovascular adaptation in the enhancement of heart rate and blood pressure response during step exercise, as well as induces cardiac morphological adaptations involving left ventricular hypertrophy, as we have already found in previous studies.

Haemodynamic effects of proportional assist ventilation during high‐intensity exercise in patients with chronic obstructive pulmonary disease

Proportional assist ventilation (PAV) has been proposed as a more physiological modality of non-invasive ventilation, thereby reducing the potential for deleterious cardio-circulatory effects during exercise, in patients with COPD. We therefore evaluated whether PAV modulates the kinetic and 'steady-state' haemodynamic responses to exercise in patients with moderate-to-severe COPD. Twenty patients underwent constant-load (75-80% peak work rate) cycle ergometer exercise testing to the limit of tolerance (T(lim)), while receiving PAV or breathing spontaneously. Stroke volume (SV), heart rate (HR) and cardiac output (CO) were monitored by impedance cardiography. Compared with unassisted breathing, PAV increased T(lim) in 8/20 patients (median improvement 113% (range 8 to 212) vs -20% (range -40 to -9)). PAV had no significant effects on 'steady-state' haemodynamic responses either in patients with or those without increased T(lim) (P > 0.05). However, at the onset of exercise, SV kinetics were slowed with PAV, in 13/15 patients with analysable data. HR dynamics remained unaltered or failed to accelerate sufficiently in nine of these patients, thereby slowing CO kinetics (T(1/2) 61 s (range 81-30) vs 89 s (range 100-47)). These deleterious effects were not, however, associated with PAV-induced changes in T(lim) (P > 0.05). PAV slowed the SV and CO kinetics at the onset of high-intensity exercise in selected patients with moderate-to-severe COPD. However, these adverse effects of PAV disappeared during the stable phase of exercise, and were not related to the ergogenic potential of PAV in this patient population.

Age‐ and sex‐related differences in muscle phosphocreatine and oxygenation kinetics during high‐intensity exercise in adolescents and adults

The aim of this investigation was to examine the adaptation of the muscle phosphates (e.g. phosphocreatine (PCr) and ADP) implicated in regulating oxidative phosphorylation, and oxygenation at the onset of high intensity exercise in children and adults. The hypotheses were threefold: primary PCr kinetics would be faster in children than adults; the amplitude of the PCr slow component would be attenuated in children; and the amplitude of the deoxyhaemoglobin/myoglobin (HHb) slow component would be reduced in children. Eleven children (5 girls, 6 boys, 13 +/- 1 years) and 11 adults (5 women, 6 men, 24 +/- 4 years) completed two to four constant work rate exercise tests within a 1.5 T MR scanner. Quadriceps muscle energetics during high intensity exercise were monitored using (31)P-MRS. Muscle oxygenation was monitored using near-infrared spectroscopy. The time constant for the PCr response was not significantly different in boys (31 +/- 10 s), girls (31 +/- 10 s), men (44 +/- 20 s) or women (29 +/- 14 s, main effects: age, p = 0.37, sex, p = 0.25). The amplitude of the PCr slow component relative to end-exercise PCr was not significantly different between children (23 +/- 23%) and adults (17 +/- 13%, p = 0.47). End-exercise [PCr] was significantly lower, and [ADP] higher, in females (18 +/- 4 mM and 53 +/- 16 microM) than males (23 +/- 4 mM, p = 0.02 and 37 +/- 11 microM, p = 0.02), but did not differ with age ([PCr]: p = 0.96, [ADP]: p = 0.72). The mean response time for muscle tissue deoxygenation was significantly faster in children (22 +/- 4 s) than adults (27 +/- 7 s, p = 0.01). The results of this study show that the control of oxidative metabolism at the onset of high intensity exercise is adult-like in 13-year-old children, but that matching of oxygen delivery to extraction is more precise in adults.

Pseudoephedrine Ingestion and Cycling Time-Trial Performance

The aim of the current study was to investigate the effect of 180 mg of pseudoephedrine (PSE) on cycling time-trial (TT) performance. Six well-trained male cyclists and triathletes (age 33 +/- 2 yr, mass 81 +/- 8 kg, height 182.0 +/- 6.7 cm, VO2max 56.8 +/- 6.8 ml x kg(-1) x min(-1); M +/- SD) underwent 2 performance trials in which they completed a 25-min variable-intensity (50-90% maximal aerobic power) warm-up, followed by a cycling TT in which they completed a fixed amount of work (7 kJ/kg body mass) in the shortest possible time. Sixty minutes before the start of exercise, they orally ingested 180 mg of PSE or a cornstarch placebo (PLA) in a randomized, crossover, double-blind manner. Venous blood was sampled immediately pre- and postexercise for the analysis of pH plus lactate, glucose, and norepinephrine (NE). PSE improved cycling TT performance by 5.1% (95% CI 0-10%) compared with PLA (28:58.9 +/- 4:26.5 and 30:31.7 +/- 4:36.7 min, respectively). There was a significant Treatment x Time interaction (p = .04) for NE, with NE increasing during the PSE trial only. Similarly, blood glucose also showed a trend (p = .06) for increased levels postexercise in the PSE trial. The ingestion of 180 mg of PSE 60 min before the onset of high-intensity exercise improved cycling TT performance in well-trained athletes. It is possible that changes in metabolism or an increase in central nervous system stimulation is responsible for the observed ergogenic effect of PSE.

Kinetics of Phosphocreatine and Deoxyhemoglobin in Children and Adults During High-Intensity Exercise

PURPOSE: To compare the kinetic response of PCr and deoxyhemoglobin (HHb) during high-intensity exercise in boys and men. METHODS: Seven men (25 ± 5 y) and six boys (13 ± 1 y) exercised using the right leg on a quadriceps ergometer within a 1.5 T MR scanner. Following habituation sessions each participant completed an incremental test to exhaustion. After a minimum 48 hours recovery, participants completed two to four constant work rate bouts on separate days. Exercise bouts consisted of 2 min rest and 7 min exercise, at an intensity equivalent to 20% of the difference between the workload at the intracellular Pi/PCr threshold and the maximal workload. Changes in HHb were determined every 1 s using a NIRS probe which was secured over the vastus lateralis muscle. 31P spectra were collected every 6 s using a 6 cm surface coil positioned beneath the right quadriceps muscle. The breakdown of PCr at the onset of exercise was modelled using a single-exponential function until the onset of the PCr slow component (SC). This point was identified using an iterative fitting window - where the time constant diverged from a plateau, a PCr SC was deemed to emerge. HHb profiles for participants were modelled as above, although a delay term was included in the model to account for the transient decrease in HHb at the onset of exercise. Data are reported as mean ± standard deviation and 95 % confidence intervals (CI) are presented. PCr and HHb data from two boys and HHb data from one adult were excluded from the analysis. RESULTS: The fundamental time constant (boys: 31 ± 11 s, CI 5 s; men: 45 ± 19 s, CI 6 s; P = 0.23), fundamental amplitude (boys: 43 ± 10%; men: 36 ± 8%, P = 0.24), and the SC amplitude (boys: 6 ± 1%; men: 12 ± 12%, P = 0.33) for PCr were similar in both groups. The net change in PCr was similar (men: 52 ± 16%; boys: 51 ± 9%, P = 0.93), as was the time constant for HHb increase in boys and men (19 ± 2 s and 22 ± 2 s, P = 0.55) respectively, with a delay of 5 ± 2 s. Responses over the last three minutes of exercise for HHB showed considerable inter-individual variation. CONCLUSIONS: Results from this study showed no differences in the breakdown of PCr or in the balance between the delivery and utilisation of O2 at the onset of highintensity exercise between boys and men. However, a trend of an age-related slowing of the breakdown of PCr at the onset of exercise warrants further investigation.

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women.

Seventeen fit women ran to exhaustion (14 +/- 4 min) at a constant speed and grade, reaching 95 +/- 3% of maximal O(2) consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O(2) saturation decreased from 97.6 +/- 0.5% at rest to 95.1 +/- 1.9% at 1 min and to 92.5 +/- 2.6% at exhaustion. Alveolar-arterial O(2) difference (A-aDO(2)) widened to 27 +/- 7 Torr after 1 min and was maintained at this level until exhaustion. Arterial PO(2) (Pa(O(2))) fell to 80 +/- 8 Torr at 1 min and then increased to 86 +/- 9 Torr at exhaustion. This increase in Pa(O(2)) over the exercise duration occurred due to a hyperventilation-induced increase in alveolar PO(2) in the presence of a constant A-aDO(2). Arterial O(2) saturation fell with time because of increasing temperature (+2.6 +/- 0.5 degrees C) and progressive metabolic acidosis (arterial pH: 7.39 +/- 0.04 at 1 min to 7.26 +/- 0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in Pa(O(2)) at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDO(2) or Pa(O(2)). Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDO(2), and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.

Velocity of Oxygen Uptake Response at the Onset of Exercise: A Comparison Between Children After Cardiac Surgery and Healthy Boys

A comparison was carried out concerning maximal oxygen uptake, oxygen uptake adjustment at the onset of high-intensity exercise, and maximal blood lactate between 10 healthy prepubertal boys and 35 children after repair of cardiac malformations or after Fontan operation. Mean maximal oxygen uptake (VO2) was moderately reduced in children after repair of tetralogy of Fallot or after Mustard or Senning operations and severely reduced after Fontan operations. Conversely, mean half-time of VO2 response was moderately prolonged in children after repair of tetralogy of Fallot or after Senning and Mustard operations and considerably prolonged after Fontan operations. According to our results unfavorable kinetics of VO2 response to physical exercise are present in addition to reduced aerobic power in many of the operated children. Besides being less qualified for endurance performance, these children are also less prepared for short, high-intensity exercise.

Effect of a warm-up on energy supply during high intensity exercise in horses.

The VO2(max) in racehorses is approximately double that of elite human athletes and the rate of increase in VO2 at the onset of high intensity exercise is much greater than in man. The kinetics of gas exchange are affected by a warm-up prior to exercise in humans, there being a greater aerobic contribution to high intensity exercise after warm-up. Our hypothesis was that a warm-up would increase aerobic energy delivery in racehorses during high intensity exercise. Thirteen fit Standardbred racehorses ran to fatigue at 115% of VO2(max) on a treadmill at 10% slope. Prior to acceleration, horses were exercised either for 5 min at 50% VO2(max) followed by 5 min walk, or walked for 2 min. Samples of expired gas were collected every 10 s during the run for determination of VO2 and VCO2 and measurement of maximal accumulated oxygen deficit (MAOD). Blood lactate concentration was measured 5 min post exercise. We found that with a warm-up, horses had faster kinetics of gas exchange and a greater proportion of their total energy requirement was supplied by aerobic sources. The aerobic contribution to total energy requirement with and without warm-up was, respectively, 79.3 +/- 1.0% and 72.4 +/- 1.7% (P < 0.01). There was also a higher MAOD (P < 0.01) in horses that had not been given a warm-up (mean +/- s.e.m. 34.7 +/- 2.6 and 47.3 +/- 2.6 mLO2eq/kg bwt with and without a warm-up respectively). However, there were no significant differences in total run time or estimated total energy expenditure between the 2 protocols. We concluded that during high intensity exercise to fatigue lasting 1 to 2 min, more than 70% of energy supply is from aerobic energy sources and that this contribution is even greater when the horses have received a warm-up.