And this may include several hours, depending on how hard and how long the exercise is. You could imagine that it might be due to a lag in oxygen delivery. It takes some time for the cardiac output, for the muscle blood flow to increase, and for the oxygen to diffuse into the skeletal muscle tissue. Alternatively, oxygen delivery might increase quite quickly, and the lag might be due to sluggishness in mitochondrial respiration.
A number of experiments over the years have tried to identify, is it oxygen delivery, is it oxygen utilization? And depending on the exercise intensity and the situations of those experiments results have been obtained in support or against either mechanism. So probably both continue to contribute to some extent.
During exercise, as I said, at a given exercise intensity, there is an oxygen requirement. And during prolonged exercise, there is a general upward drift in VO2. What mechanisms might contribute to this increase in VO2? Well, most of it is due to changes within the active muscles themselves.
Some of the factors, some of the changes, in skeletal muscle that contribute to that include recruitment of lower efficiency type two fibers, changes in the efficiency of ATP production to oxygen consumption, an increase in muscle temperature, an increased reliance on free fatty acid metabolism, which tends to have a higher oxygen requirement, and elevated catecholamines, which can impact on metabolism.
Factors outside the muscle which could contribute to this increased oxygen consumption include an increased oxygen requirement of the ventilatory muscles and of the heart as they increase their activity during prolonged exercise. Have a look at the post-exercise period. There are a number of processes going on that are thought to contribute to the maintenance of a slightly higher VO2 during recovery. In the short to medium term after exercise, heart rate and ventilation will remain slightly elevated, and that will increase the oxygen requirement.
There will be an increase in temperature which is maintained for some time after exercise, and that might also contribute to a slight increase in VO2. Also, mitochondrial uncoupling, or again, a change in the ATP to VO2 ratio might contribute to a need for higher oxygen uptake. And the synthesis of key proteins that might contribute to the adaptive response to exercise. And these are energy-dependent. If we look at creatine phosphate re-synthesis, which is occurring in this early recovery period, this is a process that occurs very rapidly.
It is dependent on oxygen availability. If you occlude the circulation and prevent oxygen from being delivered to the muscles, you prevent the resynthesis of creatine phosphate.
And this is often, well, the resynthesis of creatine phosphate is often used as a marker of oxidative capacity. In this study, you can see the modeling of the rates of creatine phosphate re-synthesis. The increase in from first threshold to peak exercise, that from first threshold to second threshold, and that from second threshold to peak exercise were also calculated as the dependent variables.
We performed these correlation analyses to identify independent variables that were entered in the stepwise multiple regression analysis. Variables that significantly correlated with the increase in during exercise testing were then entered in the stepwise multiple regression analysis to identify the cardiorespiratory factors related to the increase in , while considering multicollinearity. Statistical analyses were performed using the Statistical Package for the Social Sciences software version Any p values less than 0.
A flow diagram of study participants is shown in Fig 1. Eighteen individuals with stroke participated in the study. Table 1 shows the characteristics of the participants. No significant adverse events occurred during or after the exercise test. All participants stopped the exercise test due to their inability to maintain cycling cadence more than 40 rpm.
All participants met at least one of the criteria for reaching maximal effort. One and nine participants met three and two criteria for reaching maximal effort, respectively.
Median interquartile range values of the ratings of perceived exertion for dyspnea and leg effort at the end of the test were 13 13—15 and 15 13—15 , respectively. Measurement values at rest, first threshold, second threshold, and peak exercise are shown in Table 2 and Fig 2. Therefore, we excluded the data of second threshold from statistical analyses. Relationships of work rate with A , respiratory rate B , tidal volume C , minute ventilation D , heart rate E , stroke volume F , cardiac output G , and arterial-venous oxygen difference H during the exercise test.
Diamonds, circles, and squares represent the mean values at rest, first threshold, and peak exercise, respectively. Vertical and horizontal bars represent standard deviation. The data of second threshold were excluded, as it was obtained from only 11 participants. From rest to first threshold, correlations between the increases in and other cardiorespiratory variables are shown in Table 3 and Fig 3.
The increase in significantly correlated with the increases in tidal volume Fig 3B , minute ventilation Fig 3C , heart rate Fig 3D , cardiac output Fig 3F , and arterial-venous oxygen difference Fig 3G.
The increases in did not significantly correlate with age, Fugl-Meyer lower extremity motor scores, and anthropometric characteristics Table 3. The increase in arterial-venous oxygen difference was a major cardiorespiratory factor related to the increase in from rest to first threshold.
Correlations of the increases in with respiratory rate A , tidal volume B , minute ventilation C , heart rate D , stroke volume E , cardiac output F , and arterial-venous oxygen difference G from rest to first threshold. From rest to peak exercise, correlations between the increases in and other cardiorespiratory variables are shown in Table 5 and Fig 4.
The increases in significantly correlated with the increases in tidal volume Fig 4B , minute ventilation Fig 4C , heart rate Fig 4D , cardiac output Fig 4F , and arterial-venous oxygen difference Fig 4G.
The increases in also significantly correlated with body mass Table 5. The increase in arterial-venous oxygen difference was a major cardiorespiratory factor related to the increase in from rest to peak exercise. Correlations of the increases in with respiratory rate A , tidal volume B , minute ventilation C , heart rate D , stroke volume E , cardiac output F , and arterial-venous oxygen difference G from rest to peak exercise. From first threshold to peak exercise, correlations between the increases in and other cardiorespiratory variables are shown in Table 7 and Fig 5.
The increases in significantly correlated with the increases in respiratory rate Fig 5A , tidal volume Fig 5B , minute ventilation Fig 5C , heart rate Fig 5D , and arterial-venous oxygen difference Fig 5G. The increases in also significantly correlated with Fugl-Meyer lower extremity motor scores and body mass Table 7. Correlations of the increases in with respiratory rate A , tidal volume B , minute ventilation C , heart rate D , stroke volume E , cardiac output F , and arterial-venous oxygen difference G from first threshold to peak exercise.
The cardiorespiratory factors related to the increase in from first threshold to second threshold and then from second threshold to peak exercise were determined in 11 participants who reached second threshold. The increase in from first threshold to second threshold was not correlated with the increases in other cardiorespiratory variables Table 9.
From second threshold to peak exercise, the increases in significantly correlated with the increases in respiratory rate, tidal volume, minute ventilation, heart rate, and arterial-venous oxygen difference Table The increases in did not significantly correlate with age, Fugl-Meyer lower extremity motor scores, and anthropometric characteristics Table This is the first study to explore cardiorespiratory factors related to the increase in during graded exercise in individuals with stroke.
This study demonstrated that the increase in arterial-venous oxygen difference was a major cardiorespiratory factor related to both the increases in from rest to first threshold and that from rest to peak exercise. Our results also demonstrated no significant confounding effects of age, functional impairment, and anthropometric characteristics on the relationships between increases in and other cardiorespiratory variables during exercise testing.
These findings suggest that the impaired ability of skeletal muscles to extract oxygen is a main cardiorespiratory factor related to the decrease in cardiorespiratory fitness in individuals with stroke. The decrease in functional muscle mass due to paralysis can limit the increases in and other cardiorespiratory variables during exercise testing. The influences of the amount of active muscle mass on cardiorespiratory responses to exercise have been investigated by comparing cardiorespiratory outcomes during one-legged and two-legged cycling exercises in healthy people [ 18 ].
Minute ventilation and arterial-venous oxygen difference responses are also lower during one-legged cycling exercises [ 45 , 46 , 51 ]. Furthermore, the level of catecholamines is lower during one-legged cycling exercises compared to that in two-legged cycling exercises [ 46 , 52 ]. As catecholamines stimulate cardiorespiratory functions, lower levels of catecholamines during one-legged cycle exercises explain the lower cardiorespiratory responses [ 18 ].
Although we did not assess the amount of functional muscle mass during exercise, the above studies suggest that the decrease in functional muscle mass due to paralysis can explain the relationships between increases in and other cardiorespiratory variables during exercise testing observed in this study. The increase in arterial-venous oxygen difference was a major independent variable for the increases in from rest to first threshold and that from rest to peak exercise.
From first threshold to peak exercise, the increase in arterial-venous oxygen difference was also an independent variable for the increases in , while cardiac output was not. These results support the findings of Jakovljevic et al. Skeletal muscle changes after stroke, such as muscle atrophy and shift of muscle fiber type from type I slow-twitch muscle fibers to type II fast-twitch muscle fibers particularly in the paretic lower extremity, are observed in individuals with stroke [ 53 ].
The impaired vasodilatory function and reduction in blood flow in the paretic lower extremity have also been reported [ 54 , 55 ]. In addition to the decrease in functional muscle mass during exercise, these changes in skeletal muscles after stroke can reduce their ability to extract oxygen.
This may further increase the dependence on anaerobic glycolysis for energy output, thus increasing the output of lactate [ 56 , 57 ]. However, from our respiratory exchange ratio data, we expected blood lactate concentration to remain low in this study. These findings support the relationships between the increases in and arterial-venous oxygen difference during exercise testing observed in this study.
Furthermore, this study demonstrated that the increase in cardiac output was related to the increases in from rest to first threshold and that from rest to peak exercise irrespective of the increase in arterial-venous oxygen difference.
From first threshold to peak exercise, we observed the significant increases in heart rate and cardiac output, but not in stroke volume. These results suggest that the increase in heart rate contributed to the increase in cardiac output in this phase. In addition, our correlational analysis indicated that the increase in during exercise testing was related with the increase in heart rate, but not the increase in stroke volume.
These results of our study support the findings of Tomczak et al. As mentioned above, the increases in heart rate and cardiac output during exercise testing may be limited by lower levels of catecholamines due to the decrease in functional muscle mass after stroke [ 18 ].
In addition, the decreased functional muscle mass in individuals with stroke can reduce the increases in heart rate and cardiac output, just matching the needs of the lower muscle mass [ 18 ]. These findings can explain the relationship between the increases in and cardiac output during exercise testing observed in this study. Sisante et al. Therefore, the decrease in tidal volume is believed to limit minute ventilation and at peak exercise in individuals with stroke [ 19 , 21 ].
The paralysis of expiratory muscles on the affected side, decreased motion of the diaphragm, and reduced chest wall excursion may limit the increases in tidal volume during exercise [ 13 , 58 ].
These findings support the relationship between increases in and the increases in tidal volume and minute ventilation during exercise testing. Both from rest to first threshold and from rest to peak exercise, there was no significant correlation between the increases in and respiratory rate. Therefore, the tidal volume response may be related to response irrespective of respiratory rate response during exercise testing. The increase in minute ventilation was a major independent variable for the increase in from first threshold to peak exercise, and then from second threshold to peak exercise, but not from rest to peak exercise.
There was no occurrence of cardiorespiratory factors related to the increase in from first threshold to second threshold, which may be attributed to low increment of in this phase.
This may explain why the increases in arterial-venous oxygen difference and cardiac output rather than the increase in minute ventilation were selected as the independent variables for the increases in from rest to peak exercise. These results suggest that the ability of skeletal muscles to extract oxygen and cardiac function rather than respiratory function are related to cardiorespiratory fitness in individuals with stroke.
Considering the influences of the amount of active muscle mass on cardiorespiratory responses to exercise [ 18 ], it is important to increase the amount of functional muscle mass during exercise for enhancing the cardiorespiratory responses in individuals with stroke.
Therefore, exercises that recruit more muscle mass, such as combined arm and leg exercises could be beneficial to improve cardiorespiratory fitness in these individuals. Studies reported that functional impairment is related to cardiorespiratory responses during exercise testing in individuals with stroke [ 25 , 37 , 59 ].
However, we found no significant confounding effects of functional impairment on the relationships between the increases in and other cardiorespiratory variables during exercise testing, which may be attributed to the fact that our study participants presented with relatively mild functional impairment. Although all participants stopped the exercise test due to their inability to maintain cycling cadence, seven participants did not reach the second threshold during exercise testing.
In addition, 14 participants did not achieve a respiratory exchange ratio value greater than 1. Although a respiratory exchange ratio greater than 1. In individuals with stroke, impairments in strength, coordination, muscle endurance, and sensorimotor control contribute to difficulties in pedaling at a high work rate [ 60 ].
The reserve and heart rate reserve percentages were recommended for prescribing aerobic exercise intensity for individuals with stroke [ 61 ]. Therefore, it is probably difficult for individuals with stroke to achieve sufficient intensity of exercise prescription during exercise testing using a recumbent cycle ergometer.
An exercise test, using the combined arm and leg modality such as the total-body recumbent stepper, may be useful for guiding exercise prescription in these individuals [ 42 ]. This study had several limitations. First, all participants were in the subacute stages of recovery from stroke. Therefore, generalization of the findings to individuals with chronic stroke should be made with caution.
Second, the sample size was relatively small, although that was determined based on power analysis. Therefore, we could not perform subgroup analyses to determine whether cardiorespiratory variables related to the increase in during exercise testing would be different between participants who reached and those who failed to reach the second threshold or participants who reached and those who failed to reach a respiratory exchange ratio value greater than 1.
Third, we used a recumbent cycle ergometer. A treadmill [ 6 ], a total-body recumbent stepper [ 42 ], a robotics-assisted tilt table [ 36 ], and an arm crank ergometer [ 37 ] are also used to assess cardiorespiratory fitness in individuals with stroke.
Differences in the amount of active muscle mass among exercise devices may affect the relationships observed between the increases in and other cardiorespiratory variables during exercise testing. Further studies are warranted to examine whether the major cardiorespiratory factors related to the increase in during exercise differ among different exercise devices.
Finally, as this study used a cross-sectional observational design, the factors related to the temporal changes in at first threshold and at peak exercise could not be examined. Further longitudinal studies are needed to examine whether impairments in arterial-venous oxygen difference and cardiac output affect the temporal changes in for the development of appropriate therapies to improve cardiorespiratory fitness in individuals with stroke.
Our results suggest that the ability of skeletal muscles to extract oxygen is a major cardiorespiratory factor related to the increase in during exercise testing in individuals with stroke. Our findings could potentially contribute to the development of appropriate therapies to improve cardiorespiratory fitness in individuals with stroke.
The lungs take in oxygen from the air we breathe where it gets perfused into the blood stream; the heart and blood vessels deliver it into the working muscles; and the skeletal muscles utilize that oxygen to execute muscular contractions and produce work. A cardiovascular assessment is a good tool to measure the efficiency of the aforementioned physiological functions.
Normative data correlates time on the treadmill with aerobic fitness. There are many factors that can influence VO 2 max, e. Nevertheless, the trend is that a higher VO 2 max allows one to produce more energy, thereby performing more work.
With this in mind, VO 2 max is the "gold standard" measure of overall fitness. Aerobic fitness is assessed by having the subject perform exercise at increased loads, for 12 to 15 minutes, while breathing into a mouthpiece which collects information on inspired and expired air.
A treadmill, personal bike on a Computrainer, or a stationary bicycle are typically used. The test starts with an easy-moderate work load which is maintained for a minutes.
VO2 max values cannot be used in every day training, but follow-up VO2 tests can be used as a measure of progress.
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