Onset Of Constant-load Exercise Research Articles

Comparison of oxygen uptake at the onset of decrement-load and constant-load exercise.

The purpose of the present study was to examine whether the level of oxygen uptake (V(.)(O2) at the onset of decrement-load exercise (DLE) is lower than that at the onset of constant-load exercise (CLE), since power output, which is the target of V(.)(O2) response, is decreased in DLE. CLE and DLE were performed under the conditions of moderate and heavy exercise intensities. Before and after these main exercises, previous exercise and post exercise were performed at 20 watts. DEL was started at the same power output as that for CLE and power output was decreased at a rate of 15 watts per min. V(.)(O2) in moderate CLE increased at a fast rate and showed a steady state, while V(.)(O2) in moderate DLE increased and decreased linearly. V(.)(O2) at the increasing phase in DLE was at the same level as that in moderate CLE. V(.)(O2) immediately after moderate DLE was higher than that in the previous exercise by 98+/-77.5 ml/min. V(.)(O2) in heavy CLE increased rapidly at first and then slowly increased, while V(.)(O2) in heavy DLE increased rapidly, showing a temporal convexity change, and decreased linearly. V(.)(O2) at the increasing phase of heavy DLE was the same level as that in heavy CLE. V(.)(O2) immediately after heavy DLE was significantly higher than that in the previous exercise by 156+/-131.8 ml/min. Thus, despite the different modes of exercise, V(.)(O2) at the increasing phase in DLE was at the same level as that in CLE due to the effect of the oxygen debt expressed by the higher level of V(.)(O2) at the end of DLE than that in the previous exercise.

The V̇O2 Slow Component: Relationship between Plasma Ammonia and EMG Activity

An increased recruitment of type II muscle fibers has been suggested as a major cause of the slow component of O(2) uptake (VO(2)) kinetics. Furthermore, the rise in plasma ammonia (NH(3)) during high-intensity exercise, where a slow component is observed, has been associated with the activation of type II muscle fibers. Therefore, the purpose of this study was to examine the relationship between the VO(2) slow component, plasma NH3 concentration, and electromyography (EMG) responses during constant-load cycling. Eight healthy adults (mean age +/- SEM: 21.4 +/- 1.0 yr) performed 7 min of heavy constant-load exercise. The breath-by-breath VO(2) response was characterized using a two-term exponential model. Plasma NH(3) concentration was measured at rest, following 3 min of unloaded cycling and at 3 and 7 min of constant-load exercise. Surface EMG activity of the right vastus lateralis muscle was measured during the final 10 s of every minute of exercise. The amplitude of the slow component was 561 +/- 52 mL.min(-1), and occurred 132 +/- 11 s following the onset of constant-load exercise. Plasma NH(3) concentration increased significantly from 3 to 7 min of constant-load exercise by 32.2 +/- 2.9 micromol.L(-1). The rise in plasma NH(3) concentration correlated significantly with the amplitude of the slow component (r = 0.79, P < 0.05). The mean power frequency of the EMG increased significantly while the integrated EMG/VO(2) ratio remained constant over the duration of the slow component. The rise in NH(3) concentration and the amplitude and spectral components of the EMG are consistent with a progressive increase in the recruitment of type II muscle fibers during the slow component phase of exercise.

Determinants of Oxidative Phosphorylation Onset Kinetics in Isolated Myocytes

At the onset of constant-load exercise, pulmonary oxygen uptake (VO(2)) exhibits a monoexponential increase, following a brief time delay, to a new steady state. To date, the specific factors controlling VO(2) onset kinetics during the transition to higher rates of work remain largely unknown. To study the control of respiration in the absence of confounding factors such as blood flow heterogeneity and fiber type recruitment patterns, the onset kinetics of mitochondrial respiration were studied at the start of contractions in isolated single myocytes. Individual myocytes were microinjected with a porphyrin compound to allow phosphorescent measurement of intracellular PO(2) (P(i)O(2), an analog of VO(2)). Peak tension and P(i)O(2) were continuously monitored under a variety of conditions designed to test the role of work intensity, extracellular PO(2), cellular metabolites, and enzyme activation on the regulation of VO(2) onset kinetics.

Intra-breath profiles of alveolar gas exchange and the initial limb-to-lung transit delay during exercise in humans: relevance for modeling the exercise hyperpnea.

Following the onset of constant load exercise, pulmonary ventilation (VE), 02 uptake (VO2) and CO2 output (VCO2) all increase exponentially as a function of time, subsequent to the limb-to-lung transit time which is termed phase I (ΦI). The onset of the exponential phase (ΦII) for Vol and VCO2 is “consequent” to the arrival of altered mixed venous gas tensions at the pulmonary capillary bed resulting from increased muscle metabolic rate1. It is not known, however, whether the onset of the ΦII V E coincides with that of VO2 and VCO2, suggestive of a ‘pulmonary’ mechanism of mediation, or whether its onset is delayed i.e. consistent with a transit delay to downstream sites of chemoreception (e.g. carotid bodies) - evidence that is crucial for assembling a mechanistic control model of the transient.

Phosphocreatine hydrolysis by 31P-NMR at the onset of constant-load exercise in humans.

The kinetics of phosphocreatine (PC) breakdown in human plantar flexors at the onset of constant-load aerobic exercise was determined by high-resolution 31P-nuclear magnetic resonance spectroscopy (NMRS). The half time of the process (t1/2PC) was obtained by fitting curves (n = 13) from five subjects at various aerobic work loads for which muscle pH was not different from that at rest. Steady-state PC concentration ([PC]) was not < 70% of the resting value and was linearly related to the work load (w) ([PC] = -3.01 +/- 0.08 w + 1 (r = 0.48, 2P < 0.1)). The average t1/2PC was 16.2 s and was independent of work load. Because the half time of the muscle PC kinetics reflects the half time of the O2 uptake (MO2) kinetics (t1/2MO2), the latter is equal to that found earlier in the isolated perfused dog gastrocnemius. Whereas in the dog the above t1/2MO2 compares well with the homologous half time of the O2 uptake at the alveolar level, in humans such equivalence is found only at extremely low work loads, when the transient contribution by anaerobic glycolysis is negligible.

Effects of blood gas, pH, lactate, potassium on the oxygen uptake time courses during constant-load bicycle exercise.

Changes in the time courses of VO2 during constant-load exercise were examined in connection with other cardiorespiratory and blood chemical parameters. Eleven healthy male subjects performed a ramp exercise and three to six constant-load exercises at varying degrees of load using an electro-braked bicycle ergometer. Heart rate, ventilation, and gas exchange were measured during both types of exercise, and chemical parameters of the subject's blood (blood gas, pH, lactate, and electrolytes) were determined during two intensities of constant-load exercise. The time courses of cardiorespiratory and blood chemical data 3 min after the onset of constant-load exercise were fitted by linear regressions to see whether these parameters had reached the steady state or not. Heart rate increased significantly at a lower intensity of constant-load exercise than VE, VO2, and VCO2. While the increase in VCO2 was slower than that of VO2, a definite difference in time courses was not found between VE and VO2. The time courses of changes in blood gas, pH, bicarbonate, and lactate were not correlated with those of VO2. However, changes in blood potassium concentration were closely correlated with those of VO2 in terms of time courses and magnitude. This suggests the possibility that blood potassium may play an important role in the control of VO2 time course during constant-load exercise.

Simulation of pulmonary O2 uptake during exercise transients in humans.

Computer simulation of blood flow and O2 consumption (QO2) of leg muscles and of blood flow through other vascular compartments was made to estimate the potential effects of circulatory adjustments to moderate leg exercise on pulmonary O2 uptake (VO2) kinetics in humans. The model revealed a biphasic rise in pulmonary VO2 after the onset of constant-load exercise. The length of the first phase represented a circulatory transit time from the contracting muscles to the lung. The duration and magnitude of rise in VO2 during phase 1 were determined solely by the rate of rise in venous return and by the venous volume separating the muscle from the lung gas exchange sites. The second phase of VO2 represented increased muscle metabolism (QO2) of exercise. With the use of a single-exponential model for muscle QO2 and physiological estimates of other model parameters, phase 2 VO2 could be well described as a first-order exponential whose time constant was within 2 s of that for muscle QO2. The use of unphysiological estimates for certain parameters led to responses for VO2 during phase 2 that were qualitatively different from QO2. It is concluded that 1) the normal response of VO2 in humans to step increases in muscle work contains two components or phases, the first determined by cardiovascular phenomena and the second primarily reflecting muscle metabolism and 2) the kinetics of VO2 during phase 2 can be used to estimate the kinetics of muscle QO2. The simulation results are consistent with previously published profiles of VO2 kinetics for square-wave transients.