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HIGHLIGHTED TOPICS
Skeletal and Cardiac Muscle Blood Flow
School of Physical and Health Education, Queen's University, Kingston, Ontario, Canada K7L 3N6
Submitted 1 December 2003 ; accepted in final form 19 May 2004
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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exercise hyperemia; muscle pump; muscle blood flow; vascular conductance
5–7 s of exercise (23, 26, 28, 30, 32, 33). Because blood flow through a muscle vascular bed is thought to be proportional to 1) the arteriovenous pressure difference across that bed and 2) the vascular conductance of that bed, a number of studies have tried to determine whether the muscle pump, rapid vasodilation, or both contribute to the immediate increase in exercising muscle blood flow (7, 11, 12, 21, 23, 25–27, 33, 36).
Studies that indicate that the muscle pump is the sole contributor to immediate exercise hyperemia provide three lines of evidence. First, they demonstrate that the magnitude of the initial muscle blood flow increase in a rest-to-mild or moderate locomotion transition in dog or rat treadmill exercise is sensitive to speed (contraction frequency) but not grade (contraction intensity) (24–26). Second, they demonstrate an 5-s delay in the onset of vasodilation following topical application of vasodilators directly onto isolated arterioles (41). Finally, during the writing of this paper, Sheriff and Zidon (27) employed an exercise-to-exercise transition approach and observed a delay of 5 s in exercise hyperemia with increases in contraction intensity (treadmill grade) during rat treadmill locomotion.
In contrast, evidence from studies that support a rapid vasodilatory contribution comes from 1) human forearm exercise models demonstrating that the initial rise (first 2–5 s) in calculated forearm vascular conductance (FVC) at exercise onset is related to work intensity, not contraction frequency (33), and 2) immediate and continued increases in muscle blood flow over four to five cardiac cycles following a single forearm contraction in humans (5, 35, 36) and a stimulated tetanic contraction in dog hindlimbs (21).
The continued controversy surrounding which mechanisms contribute to the immediate exercise hyperemia is, in part, due to previous experimental approaches that have exclusively focused on this issue in the context of rest-to-exercise transitions. A critical limitation of such an approach is that both the muscle pump effect and vasodilatory mechanisms may be initiated at exercise onset. To overcome this, the present study examined the immediate forearm blood flow (FBF) response to an increase in work rate imposed by increasing contraction intensity during rhythmic dynamic forearm exercise with the forearm above heart level to minimize gains in the arteriovenous pressure gradient with muscle contraction-induced venous emptying. Muscle pump effectiveness does not appear to be enhanced across all contraction intensities (25, 26, 35). Thus identification of a contraction intensity above which no further increases in forearm venous emptying occur (threshold intensity) could afford an approach to examine vasodilatory onset in isolation of the muscle pump. Specifically, transitions between contraction intensities above this threshold intensity could be examined. This could then be compared with a similar increase in exercise intensity from rest to exercise. We also assessed the forearm hemodynamic response to these transitions with the forearm below heart to evaluate whether local arterial pressure influenced the vasodilatory response. With this approach, we tested the hypothesis that vasodilatory onset in exercising human skeletal muscle occurs immediately following the first contraction of a change in exercise intensity.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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Eleven healthy young subjects (6 women, 5 men) volunteered for this study. The mean age of the subjects was 24.6 ± 1.6 yr, height was 176.3 ± 3.1 cm, and weight was 79.9 ± 4.2 kg. After receiving a complete verbal and written description of the experimental protocol and potential risks, each subject provided signed consent to the testing procedures on a form approved by Health Sciences Human Research Ethics Board at Queen's University.
Experimental Design
Exercise protocol.
Subjects assumed a supine posture with their right arm extended laterally for 30 min before beginning any dynamic handgrip exercise. Handgrip exercises involved raising and lowering a weight of 10% (mild exercise) or 20% (moderate exercise) of the subject's predetermined maximal voluntary contraction (MVC) through a vertical distance of 5 cm by squeezing a handgripping device connected to a pulley system. In our laboratory, these forearm exercise work rates result in steady-state FBF that is approximately fivefold (rest to 10% MVC) and approximately eightfold (rest to 20% MVC) above rest, respectively. Exercise took place at a contraction rate of 1:2 s work-rest schedule, with concentric and eccentric contractions each contributing to 50% of the work phase, and a metronome provided the timing. The exercise was carried out with the right arm supported and positioned either 21 cm above or below heart level, as measured from the midforearm. These different arm positions altered the hydrostatic contribution to local arterial pressure (pressure in arm below was 30 mmHg greater than in arm above) and, therefore, allowed assessment of vasodilatory onset with exercise transitions under different conditions of local arterial transmural pressure. Subjects completed two trials in each arm position in a counterbalanced design. In each exercise trial, data were collected for 1 min of rest followed by a step increase in workload to mild exercise for 3 min and followed again by a further increase in workload to moderate exercise for 30 s. Each trial was separated by at least 15 min of rest to allow blood flow to return to baseline.
Data collection and analysis. In each trial, beat-by-beat heart rate (HR) (ECG), mean arterial blood pressure (MAP) (arterial tonometry; Colin 7000, Trudell Medical, London, ON), and brachial artery mean blood velocity (MBV) (pulsed Doppler velocimetry, Multigon 500B, Transcranial Doppler, Multigon Industries, Yonkers, NY) were collected continuously on a computer-based system at 200 Hz. Forearm effective perfusion pressure (EPP) (the local arterial pressure of the forearm) was estimated by adding or subtracting the hydrostatic distance from the MAP being measured continuously at the level of the heart. Brachial arterial MBV was measured from the spectra of a pulsed Doppler ultrasound signal. A flat probe with an operating frequency of 4 MHz was fixed to the skin over the brachial artery in the antecubital fossa region of the right elbow. The angle of the transducer crystal relative to the skin was 45°. The ultrasound gate was set to insonate the total width of the artery lumen. With this setup, a clear Doppler signal was maintained both at rest and during the handgrip exercise. Beat-by-beat MBV was calculated as the average of the instantaneous MBV values over each cardiac cycle defined by the R-wave-to-R-wave interval. Baseline MBV was taken as the mean of 10 contraction-free full cardiac cycles before the addition of weight. During exercise, the onset of vasodilation was assessed by evaluating the MBV for a complete cardiac cycle during relaxation (Fig. 1). Using this section of the MBV profile allowed for assessment of the FVC, unaffected by muscle contraction impedance of arterial blood flow. With the use of echo Doppler (Vingmed System 5 GE Medical Systems) sited over the brachial artery immediately proximal to the pulsed Doppler probe, arterial cross-sectional area was measured at rest and during steady state (3rd min of exercise) with a linear 10-MHz probe. Vessel diameter was estimated as the average of three online measurements from frozen screen images during diastole. All measures were made by the same operator.
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FVC was calculated as:
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Assessment of Muscle Pump Effectiveness
In separate experiments, contraction-induced venous emptying in the transition from rest-to-mild and mild-to-moderate exercise intensity was evaluated in 5 of the 11 subjects. With the use of the aforementioned exercise protocol, forearm venous volume changes (strain gauge plethysmography; model EC-6, D. E. Hokanson) with increased contraction intensity were measured during the rest-to-exercise and exercise-to-exercise transition. Briefly, a mercury-in-Silastic rubber strain gauge was placed just distal to the elbow around the largest circumference of the forearm. Peak venous emptying was assessed by using the smallest forearm circumference occurring immediately on relaxation of forearm contractions (Fig. 2). Baseline venous volume during relaxation in steady-state mild exercise was calculated as the mean of 10 contraction-induced peak venous emptyings during steady-state exercise.
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Initial comparison of the main effects of arm position and workload were analyzed by repeated-measures two-way ANOVA (SigmaStat 2.03, SPSS, Chicago, IL) with arm position and contraction intensity forming the independent variables. Comparisons of the effects of arm position and workload over time were analyzed by repeated-measures three-way ANOVA, with arm position, contraction intensity, and time forming the independent variables. The level of significance was set at P < 0.05, and any differences were further assessed with Tukey's post hoc test. Paired t-tests were used to compare venous emptying between the rest-to-mild and mild-to-moderate exercise conditions for both the arm-above and arm-below positions. Data are presented as means ± SE.
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RESULTS |
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Table 1 summarizes the absolute FBF, calculated FVC, EPP, and HR responses during rest-to-mild and mild-to-moderate-intensity exercise trials for the first relaxation following contraction in arm above and arm below heart level. FBF and FVC increased immediately (0–1 s after the first contraction) in both transitions for both arm positions (both P < 0.05). The increase in FVC with the arm above heart level was significantly greater than with the arm below heart level for both exercise transitions (both P < 0.05). EPP increased slightly but significantly in the first full cardiac cycle, unaffected by contraction in the rest-to-mild exercise transition with the arm above heart level (P < 0.05). In the arm-below heart level condition, estimated EPP increased 20 mmHg in the rest-to-mild exercise transition (this estimate assumes that muscle contraction-induced venous emptying eliminated the forearm venous hydrostatic column; see METHODS). The hydrostatic effects of placing the arm above and below heart level resulted in a difference of 30 mmHg in the EPP between arm positions during contractions; i.e., local forearm arterial pressure was 30 mmHg greater with the arm below vs. above heart level. HR increased significantly in all transitions and arm positions (P < 0.05).
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FBF.
Figure 3, A(i) and B(i), shows the absolute changes in relaxation-phase FBF over the first nine contractions (30 s) for the rest-to-mild and mild-to-moderate exercise transitions within arm-above and arm-below heart level conditions, respectively. For the above-heart level condition, the rate and magnitude of increase in FBF during both transitions were not different (P = 0.271). FBF increased immediately (0–1 s after first contraction ended) and reached an initial plateau by the second relaxation (3–4 s after first contraction ended). For the arm-below heart condition, the initial (first relaxation) increase in flow was the same for the rest-to-mild exercise and mild-to-moderate exercise transitions. Thereafter, the increase in FBF was greater in the rest-to-mild exercise transition (P < 0.05).
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30 s), calculated during the relaxation phase of each duty cycle for the rest-to-mild and mild-to-moderate exercise transitions within arm-above and arm-below heart level conditions, respectively. Systemic MAP was slightly elevated (3%) with the onset of each transition. In the below-heart level condition, we assumed muscle contraction-induced elimination of the hydrostatic column on the venous side at the onset of the rest-to-mild exercise transition. Hence, the calculated EPP in the forearm increased by 22%, despite only small increases in the systemic response.
FVC.
Figure 4 summarizes the calculated FVC responses in the rest-to-mild and mild-to-moderate exercise transitions for both above- and below-heart level conditions. In both the arm above- and arm-below heart conditions, FVC was substantially elevated following release of the first contraction, and this increase was not different in rest-to-mild vs. mild-to-moderate exercise transitions within each arm position. However, there was an effect of arm position such that this immediate increase was blunted in the arm-below heart position, where local arterial pressure was 30 mmHg greater. The continued increase in FVC over the next eight contractions was identical for all work rate transitions, except for mild-to-moderate exercise with the arm below heart, which demonstrated a blunted response.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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Isolation of Vasodilatory Contribution to Immediate Exercise Hyperemia
As stated by Sheriff and Zidon (27), a limitation that has hampered previous experimental attempts to determine the separate contributions of the muscle pump vs. vasodilation at the onset of exercise stems from the fact that both mechanisms may be initiated in a rest-to-exercise transition. Thus experimental designs that eliminate the contribution of either the muscle pump or vasodilation are required to isolate the impact of either at exercise onset.
Work from Sheriff's laboratory (24, 25, 27) has repeatedly applied the rationale that contraction intensity is of minimal importance for the muscle pump effect to examine the role of vasodilation vs. the muscle pump in immediate exercise hyperemia. Recently, Sheriff and Zidon (27) applied this rationale in an attempt to isolate vasodilatory onset in an exercise-exercise transition, where exercise intensity was increased by increasing contraction intensity rather than frequency. That study employed a rat treadmill locomotion model and observed an 5-s delay in the onset of increases in muscle blood flow when treadmill grade was increased. This indicated that there could not have been a contraction intensity-dependent effect of the muscle pump and that vasodilation in this particular exercise model was delayed.
In the present study, we applied the exercise-exercise transition approach of Sheriff and Zidon (27) to isolate vasodilatory onset in the human forearm exercise model. In addition, to further eliminate the muscle pump effect, we performed exercise with the arm above heart level. In this position, the lack of a hydrostatic column results in an unstressed venous volume. Others have drawn attention to the importance of a venous hydrostatic column for the function of the muscle pump (17). Consistent with this, Tschakovsky et al. (36) previously demonstrated that mechanical emptying of unstressed volume does not enhance FBF. Finally, we used strain gauge plethysmography to measure changes in forearm volume to confirm the lack of effect of an increase in contraction intensity on forearm venous volume. Our laboratory has previously used the same approach to demonstrate that, with the arm below heart level, forearm venous emptying was not enhanced with contraction intensities >10% MVC intensity (35). Figures 2 and 5 support the contention that the muscle pump effect is not enhanced with changes in dynamic forearm handgrip contraction intensity with the arm positioned above heart level, where venous volume is unstressed. The above rationale provides the basis for the following interpretation of these data.
Evidence for Contribution of Vasodilation to Immediate Exercise Hyperemia
The strongest evidence supporting a role for rapid vasodilation at the onset of an increase in exercise intensity in this study comes from the responses observed with the arm above heart level. In the mild-to-moderate exercise transition in this arm position, we believe that we have successfully isolated vasodilatory contributions as described above. Therefore, the immediate increase in FBF and calculated vascular conductance observed in this transition are interpreted to represent rapid vasodilation rather than the effect of the muscle pump.
An additional important consideration is as follows. Examination of the changes in FBF [Fig. 3A(i)] and calculated FVC (Fig. 4) profile in the mild-to-moderate exercise transition illustrates a rapid increase plateauing by the second relaxation phase (4 s following transition). That plateau is maintained through the sixth to seventh relaxation phases (16–19 s into the transition). Such a plateau indicates that initial mechanisms responsible for exercise hyperemia exert an immediate effect complete by 5 s of exercise, and additional mechanisms do not contribute until after 15–20 s of exercise (23, 26, 28, 30, 32, 33). Studies examining the FBF response to a single contraction observe a continued FBF increase for four to five cardiac cycles following contraction release (5, 12, 35, 36). This can only be explained by a vasodilation in the first few seconds of exercise, as the arteriovenous pressure gradient would actually be decreasing over time following contraction. Thus the observation of a plateau in FBF by 4 s of the mild-to-moderate exercise transition is inconsistent with a delay in vasodilatory contribution to early exercise hyperemia.
Rest-to-mild exercise transition FBF and calculated vascular conductance responses with the arm above heart level were identical in time course and magnitude to the mild-to-moderate exercise transition response. We interpret this to indicate that vasodilatory onset was as rapid in the rest-to-mild as in the mild-to-moderate exercise transition. It must be acknowledged that, in this in vivo experiment, it is not possible to definitively determine that the vasodilatory stimulus evoked by the rest-to-mild contraction intensity transition was the same as in the mild-to-moderate transition. Additionally, the response of vessels with different tone to a given vasodilator stimulus may be different (9). Thus identical magnitude of change between transitions cannot conclusively demonstrate the lack of a muscle pump contribution at the onset of the rest-to-mild exercise transition. However, given the lack of change in forearm volume at the onset of contractions with the arm above heart level (Figs. 2 and 5) and previous demonstration that mechanical emptying of unstressed venous volume does not enhance FBF (36), a muscle pump contribution seems unlikely. Furthermore, the identical rest-to-mild and mild-to moderate hyperemia time course is inconsistent with vasodilatory time course being different in the rest-to-mild vs. mild-to-moderate exercise transition. This is consistent with previous findings in our laboratory (35, 36). Therefore, we would suggest that, in this exercise model, rapid vasodilation is clearly contributing at the onset of the rest-to-mild exercise transition and may, in fact, be the exclusive contributor to the observed hyperemia.
Our findings are in contrast to the 5-s delayed onset of vasodilation observed by Sheriff and Zidon (27) in rat treadmill locomotion exercise-exercise transitions. One consideration regarding elevation in contraction intensity is whether it is achieved by increased force output from motor units already active vs. increasing the number of active motor units. It is theoretically possible that increases in the number of active motor units might increase the areas in the muscle where veins are emptied, thus enhancing the muscle pump effect. In contrast, increases in force production from already active motor units might not be expected to change regional venous compression. Thus it could be suggested that, in rat locomotion, contraction intensity increases were achieved with increased force production from active motor units, whereas, in our forearm model, additional motor units were recruited. However, if this had been the case for the forearm model, increased venous emptying should have been observed with increased contraction intensity.
It has also been proposed that muscle activation in the 1-s forearm contraction model is the equivalent of accumulated muscle activation in the rodent or dog over a period of 5 s of treadmill locomotion (11). However, both magnitude and duration must be considered when assessing differences in vasodilatory delay between the present study and mild treadmill locomotion in rats (10, 11, 14). Species size and gait differences, as well as exercise modality, have the potential for influencing muscle activation magnitude and duration. For example, activities such as stair climbing, rowing, or downhill skiing can involve contractions of intensity and duration similar to the forearm contractions in this study. In contrast, it may be argued that the magnitude of increase in exercise intensity in the Sheriff and Zidon (27) study is extremely small (low-intensity work was only 50% greater than rest to begin with, and the increase in flow with higher intensity was only 25% of the rest-to-low-intensity change) and responsible for the delay in vasodilatory onset. The dependency of time to onset of vasodilation on contraction intensity has been demonstrated previously (19).
Effect of Increased Local Transmural Pressure on Rapid Vasodilation
In comparing the immediate (0–2 s) vasodilatory response between arm positions, we found that the response was blunted in both the rest-to-mild and mild-to-moderate transitions when the arm was below heart level. In a dependent position, myogenic tone may be elevated, consequent of an increase in transmural pressure. Thus the potentially augmented vasoconstrictor influence may result in an attenuation of the immediate vasodilatory response.
The continued vasodilation (4–30 s) in the arm-below position following exercise onset was not different from that of arm above; however, the blunting of this initial vasodilation in the exercise-to-exercise transition persisted for the remainder of the exercise bout (Fig. 4). To account for the divergence in the dilatory response pattern with the arm below heart level, we propose that an imbalance in vasodilator and vasoconstrictor influence between exercise transitions exists. Immediately on contraction and on transition to a higher work intensity, we assume that the same changes in magnitude of vasodilator stimulus occur, a supposition substantiated by the same magnitude of immediate increase in conductance between transitions. However, removal of candidate vasoconstrictor influences must be different. In both transitions, myogenic vasoconstriction may be present and equal. On going from rest to exercise, venoarteriolar reflex constrictor influence may be removed as the veins are emptied (34). This is thought to occur after 5 s of exercise, and the dynamics of our observed response in this transition correspond with this. In an exercise-to-exercise transition, veins are already emptied, and thus the venoarteriolar reflex does not exist as a candidate source of increased vasodilation.
Valic et al. (37) recently demonstrated that elevation in resting blood flow in dog hindlimbs attenuates exercise hyperemia. It is also possible that the fundamental differences in the observed dynamics of the vasodilatory responses may be explained by a possible sensitivity to hyperperfusion of the baseline state in the exercise-to-exercise transition (see Table 1). Disparity between arm-above and arm-below mild-to-moderate exercise transitions again can be explained by differences in underlying myogenic tone.
Assumptions for Assessing FVC (Vasodilation)
The main observation supporting a role for rapid vasodilation at the onset of an increase in exercise intensity in this study was the identical, immediate increase in FVC in the rest-to-mild and mild-to-moderate exercise transitions with the arm above heart level. In this condition, we used local arterial pressure to calculate FVC, assuming that venous pressure was negligible at rest as the veins were virtually empty. Whether local forearm arterial pressure or heart level arterial pressure was used would not have affected the nature of the FVC profile and, therefore, would not impact on the interpretation of these data.
However, in comparing the response between arm positions, differences in local venous pressure due to a venous hydrostatic column in the below-heart position, combined with the inability to measure venular pressure, necessitated that assumptions be made regarding changes in local venous pressure from rest to exercise. In this study, we assumed that dynamic forearm contractions would empty forearm veins to the extent that venule pressure would be close enough to zero to be considered negligible on release of contraction. With this assumption, local EPP used to calculate FVC demonstrated a sudden 22% increase in the rest-to-mild exercise transition below heart level. Thus the interpretation of a blunted immediate increase in FVC in the rest-to-mild exercise transition must acknowledge this assumption. However, given that there was no EPP increase originating from changes in venous hydrostatic column in the mild-to-moderate exercise transition, and this transition demonstrated an identical blunting, we believe our assumption regarding effective local forearm perfusion pressure change in the rest-to-mild exercise transition to be reasonable and interpret the data accordingly.
Potential Mechanisms of Rapid Vasodilation
Steady-state vasodilation increases in proportion to tension developed by a given number of active motor units and in proportion to the number of active motor units at a given tension (38). It is possible that both factors may also contribute to the contraction intensity-dependent immediate vasodilatory response observed in human forearm studies. This is supported by recent in vivo evidence from Hamann et al. (10) in which the peak blood flow response to a single forearm contraction increased with both the strength and duration of muscle contraction. It, therefore, appears reasonable to hypothesize that the rapid vasodilatory mechanism(s) responsible for immediate vasodilation is related to muscle activation. Two candidates consistent with this are K+ (20) and acetylcholine (39), which increase immediately and in proportion to muscle activation.
Current evidence regarding K+ is mixed. Whereas Bunger et al. (4) observed an 20% dilation already present by 4 s (the first measurement taken) in coronary vasculature exposed to K+, Wunsch et al. (41) observed a 4- to 6-s delay in vasodilation onset following direct application to 2° resistance vessels. With regard to acetylcholine, whereas it has been observed that a motor nerve source of acetylcholine evokes vasodilation in hamster cremaster muscle (39), in dog (21) and human skeletal muscle (8) acetylcholine spillover from motor nerves does not appear to reach muscarinic receptors, as no vasodilation is observed during motor nerve stimulation of paralyzed skeletal muscle.
Our laboratory (35) and others (10) have recently proposed that mechanical compression and distortion of resistance vessels may evoke a rapid reduction in resistance vessel tone. The contraction intensity-dependent magnitude of rapid vasodilation (14, 35, 40) would suggest a graded response to mechanical compression and distortion. In this regard, smooth muscle cross bridges are known to require very little energy for the maintenance of tension (6, 13), consistent with many cross bridges being in a state of attachment without rapid cycling ("latched" state). Thus it is possible that contraction-induced disruption of latched cross bridges results in immediate reductions in vascular tone; a mechanism for vasodilation that is independent of the release and action of vasodilator substances. In this regard, simple external mechanical muscle compression models that have not observed a vasodilatory effect (1, 36) may not represent the true mechanical distortion of muscle contraction.
Finally, others have recently proposed mechanical compression and distortion effects on the vascular endothelium (10), similar to the impact of pressure and shear stress (15, 16), or direct effects on vascular smooth muscle (35). Candidate vasodilators released by the endothelium in response to mechanical distortion include nitric oxide, vasodilatory prostaglandins, and endothelial-derived hyperpolarizing factor (2, 22). Whereas isolated blockade of these factors has not revealed a contribution to early exercise hyperemia in human exercise models (3, 28, 31), multiple blockade approaches may reveal a synergistic effect of these endothelium-derived vasodilators.
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CONCLUSIONS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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GRANTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSGRANTSACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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FBF) (i) and effective perfusion pressure (EPP) (ii) resulting from the onset of mild rhythmic dynamic handgrip exercise (
, solid line) and from the transition from mild-to-moderate rhythmic dynamic handgrip exercise (
, solid line) with the arm above (A) and arm below (B) heart level. The 
Significantly different from rest-to-mild exercise transition, P < 0.05.
, arm below) and from mild-to-moderate exercise (
, arm below). The 