Saitoh T, Ferreira LF, Barstow TJ, Poole DC, Ooue A, Kondo N, Koga S. Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise. Am J Physiol Regul Integr Comp Physiol 297: R615-R621, 2009. First published June 17, 2009 doi:10.1152/ajpregu.00048.2009.-We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O2 uptake (pV O2) kinetics during subsequent heavy exercise. Seven healthy men completed two 6-min bouts of heavy work rate cycling exercise, separated by 6 min of unloaded exercise. The changes in the concentration of deoxyhemoglobin/myoglobin (⌬de-oxy-[HbϩMb]) were assessed simultaneously at 10 different sites on the rectus femoris muscle using multichannel near-infrared spectroscopy. Prior exercise had no effect on either the time constant or the amplitude of the primary component pV O2, whereas it reduced the amplitude of the slow component (SC). ⌬Deoxy-[HbϩMb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 Ϯ 1.3 vs. 9.3 Ϯ 1.4 s; P Ͻ 0.01) and slower primary component time constant (: 9.3 Ϯ 1.3 vs. 17.8 Ϯ 1.0 s; P Ͻ 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the of ⌬deoxy- [HbϩMb] (26.6 Ϯ 11.8 vs. 13.7 Ϯ 5.6%; P Ͻ 0.01) and the point-by-point heterogeneity [root mean square error (RMSE)] during the primary component in the second bout. However, neither the change in the CV for nor RMSE of ⌬deoxy-[HbϩMb] correlated with the reduction in the SC in pV O2 kinetics during subsequent heavy exercise. In conclusion, prior exercise reduced the spatial heterogeneity of the primary component of muscle deoxygenation kinetics. This effect was not correlated with alterations in the pV O2 response during subsequent heavy exercise. near-infrared spectroscopy; spatial heterogeneity; oxygen uptake kinetics; muscle oxygen delivery THE BALANCE BETWEEN MUSCLE O 2 uptake (mV O 2 ) and muscle O 2 delivery (mQ O 2 ) by capillary blood flow, i.e., the ratio mV O 2 / mQ O 2 , is reflected by the level of muscle oxygenation (14,19,25,27,32). Thus the profile of muscle oxygenation can provide important information concerning the adequacy of the vascular response and the O 2 pressures essential for driving bloodmuscle O 2 flux.Prior heavy exercise has been used as an experimental intervention to alter mQ O 2 and elucidate the mechanisms of the mV O 2 kinetics following the onset of exercise (3, 7-11, 15, 16, 22-24, 30 -33, 39, 42, 44, 47, 51-53, 55). Collectively, previous studies reported that prior exercise in the upright position does not alter the phase II time constant of pulmonary O 2 uptake (pV O 2 ) response in the subsequent bout of heavy exercise (3, 7-11, 22, 30, 32, 44, 47, 52), with a few exceptions (16,46,53). The net amplitude of phase II is unaltered in some studies using 6-to 8-min recovery between heavy exercise bouts (7, 10, 44, 52) and incre...

The mechanism that alters the pulmonary VO2 response to heavy-intensity exercise following prior heavy exercise has been frequently ascribed to an improvement in pre-exercise blood flow (BF) or O(2) delivery. Interventions to improve O(2) delivery have rarely resulted in a similar enhancement of VO2. However, the actual limb blood flow and VO2 dynamics in the second bout of repeated exercise remain equivocal. Seven healthy female subjects (21-32 years) performed consecutive 6-min (separated by 6 min of 10 W exercise) bilateral knee extension (KE) exercise in a semisupine position at a work rate halfway between the lactate threshold (LT) and VO2peak. Femoral artery blood flow (FBF) was measured by Doppler ultrasound simultaneously with breath-by-breath VO2 each protocol being repeated at least four times for precise kinetic characterization. The effective time-constant (tau') of the VO2 response was reduced following prior exercise (bout 1: 61.0 +/-10.5 vs. bout 2: 51.6+/-9.0 s; mean +/- SD; P<0.05), which was a result of a reduced slow component (bout 1: 16.0+/-8.0 vs. bout 2: 12.5+/-6.7 %; P<0.05) and an unchanged 'primary' tau. FBF was consistently faster than VO2. However, there was no bout-effect on tau' FBF (bout 1: 28.2+/-12.0 vs. bout 2: 34.2+/-8.5 s). The relationship between the exercise-associated VO2 (i.e., deltaVO2) and Delta FBF was similar between bouts, with a tendency (N.S: P>0.05) for deltaVO2/deltaFBF to be increased during the transition to bout 2 rather than decreased, as hypothesized. The return of VO2 kinetics toward first order, therefore, was associated with an 'appropriate', not enhanced, BF to the working muscles. Whether a relative prior-hyperemia in bout 2 enables a more homogeneous intramuscular distribution of BF and/or metabolic response is unclear, however, these data are consistent with events more proximal to the exercise muscle in mediating the VO2 response during repeated heavy-intensity KE exercise.

The purposes of this study were (1) to evaluate changes in blood flow in the brachial artery and basilic vein of the upper arm with a rise in internal temperature during passive heating; and (2) to investigate the contributions of blood velocity and anteroposterior vessel diameter to these blood flow changes. Ten subjects rested in the supine position between a pair of tube-lined sheets. Thermoneutral water was circulated through the tubes to keep a mean skin temperature (Tsk) of 34-35 degrees C, and then hot water was circulated to maintain Tsk of 37-38 degrees C. The blood velocity and diameter in the brachial artery and basilic vein were continuously monitored by Doppler ultrasound technique and used to calculate blood flow. Blood flow in the brachial artery and basilic vein increased linearly as the oral temperature (T(or)) rose by < or =0.6 degrees C. The magnitude of the change in blood flow did not differ significantly between the two vessels. In addition, plots of DeltaT(or) versus blood flow yielded slopes that did not differ significantly between the brachial artery and the basilic vein. As T (or) increased, blood velocity, but not diameter, also increased. In conclusion, blood flow in the brachial artery and the basilic vein increased linearly as the internal temperature variable T (or) increased < or =0.6 degrees C. In both vessels, the passive heating-induced increases in blood flow resulted primarily from a change in blood velocity, rather than from a change in diameter.

This study investigated changes in blood flow in the conduit artery, superficial vein, and deep vein of the upper arm during increase in internal temperature due to leg cycling. Additionally, we sought to demonstrate the contributions of blood velocity and vessel diameter on blood flow responses. Fourteen subjects performed supine cycling exercise at 60-69% maximal oxygen uptake for 30 min at an ambient temperature of 28 degrees C and relative humidity of 50%. Blood velocity and diameter in the brachial artery, basilic vein (superficial vein), and brachial vein (deep vein) were measured using ultrasound Doppler, and blood flow was calculated. Blood flow in the artery and superficial vein increased linearly with rising oesophageal temperature (DeltaT (oes)) after DeltaT (oes) was about 0.3 degrees C (within threshold), as well as cutaneous vascular conductance on the forearm. Changes in blood velocity in these vessels were similar to those in blood flow. Conversely, the brachial artery and superficial vein diameter did not affect the blood flow response. Blood flow variables in the deep vein did not change remarkably with rising DeltaT (oes). These results suggest that blood flow response, by an increase in velocity, in the conduit artery with rising DeltaT (oes) during exercise is similar to that in the superficial vein, but not deep vein. Also, it is indicated that these increases in blood flow relate to the increase in skin blood flow on the forearm with the rise in body temperature during exercise.

Superficial venous vascular response to exercise is mediated sympathetically, although the mechanism is not fully understood. We examined whether sympathetic activation via muscle metaboreflex plays a role in the control of a superficial vein in the contralateral resting limb during exercise. The experimental condition involved selective stimulation of muscle metaboreceptors: 12 subjects performed static handgrip exercises at 45% maximal voluntary contraction for 1.5 min followed by a recovery period with arterial occlusion of the exercise arm (OCCL). For the control condition (CONT), the same exercise protocol was performed except that the recovery period occurred without arterial occlusion. Heart rate (HR) and mean arterial blood pressure (MAP) were measured. The cross-sectional area of the basilic superficial vein (CSAvein) and blood velocity (Vvein) in the resting upper arm were measured by ultrasound while the cuff on resting upper arm was inflated constantly to a subdiastolic pressure of 50 mm Hg. Basilic vein blood flow (BFvein) was calculated as CSAvein × Vvein. During exercise under both OCCL and CONT, HR and MAP increased (p < 0.05), while CSAvein decreased (p < 0.05). During recovery under OCCL, HR returned to baseline, but the exercise-induced increase in MAP and decrease in CSAvein were maintained (p < 0.05). During recovery under CONT, HR, MAP, and CSAvein returned to baseline. BFvein did not change during exercise or recovery under either condition. These results suggest that sympathoexcitation via muscle metaboreflex may be one of the factors responsible for exercise-induced constriction of the superficial veins per se in the resting limb.