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Inspiratory function is essential for alveolar ventilation and expulsive behaviors that promote airway clearance (e.g., coughing and sneezing). Current evidence demonstrates that inspiratory dysfunction occurs during healthy aging and is accentuated by chronic heart failure (CHF). This inspiratory dysfunction contributes to key aspects of CHF and aging cardiovascular and pulmonary pathophysiology including: (1) impaired airway clearance and predisposition to pneumonia; (2) inability to sustain ventilation during physical activity; (3) shallow breathing pattern that limits alveolar ventilation and gas exchange; and (4) sympathetic activation that causes cardiac arrhythmias and tissue vasoconstriction. The diaphragm is the primary inspiratory muscle; hence, its neuromuscular integrity is a main determinant of the adequacy of inspiratory function. Mechanistic work within animal and cellular models has revealed specific factors that may be responsible for diaphragm neuromuscular abnormalities in CHF and aging. These include phrenic nerve and neuromuscular junction alterations as well as intrinsic myocyte abnormalities, such as changes in the quantity and quality of contractile proteins, accelerated fiber atrophy, and shifts in fiber type distribution. CHF, aging, or CHF in the presence of aging disturbs the dynamics of circulating factors (e.g., cytokines and angiotensin II) and cell signaling involving sphingolipids, reactive oxygen species, and proteolytic pathways, thus leading to the previously listed abnormalities. Exercise-based rehabilitation combined with pharmacological therapies targeting the pathways reviewed herein hold promise to treat diaphragm abnormalities and inspiratory muscle dysfunction in CHF and aging.

The purpose of this study was to compare the effects of 3 different modalities of exercise on metabolic control, insulin resistance, inflammatory markers, adipocytokines, and tissue expression of insulin receptor substrate (IRS)-1 after 12 weeks of training among patients with type 2 diabetes mellitus. Forty-eight patients with type 2 diabetes mellitus were randomly assigned to 4 groups of training (3 times a week, 60 minutes per session): aerobic group (n = 12), resistance group (n = 12), combined (aerobic and resistance) group (n = 12), and control group (n = 12). Fasting and postprandial blood glucose, glycated hemoglobin, lipid profile, insulin resistance index (homeostasis model assessment of insulin resistance), adipocytokines (adiponectin, visfatin, and resistin), tumor necrosis factor, interleukin, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline and at the end of the study. Patients also underwent a muscle microbiopsy before and after training to quantify IRS-1 expression. All 4 groups displayed decreases in blood pressure, fasting plasma glucose, postprandial plasma glucose, lipid profile, and hs-CRP (P < .05); and there was no difference across the groups. After training, the IRS-1 expression increased by 65% in the resistance group (P < .05) and by 90% in the combined group (P < .01). Exercise training favorably affects glycemic parameters, lipid profile, blood pressure, and hs-CRP. In addition, resistance and combined training can increase IRS-1 expression., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The conventional continuous wave near-infrared spectroscopy (CW-NIRS) has enabled identification of regional differences in muscle deoxygenation following onset of exercise. However, assumptions of constant optical factors (e.g., path length) used to convert the relative changes in CW-NIRS signal intensity to values of relative concentration, bring the validity of such measurements into question. Furthermore, to justify comparisons among sites and subjects, it is essential to correct the amplitude of deoxygenated hemoglobin plus myoglobin [deoxy(Hb+Mb)] for the adipose tissue thickness (ATT). We used two time-resolved NIRS systems to measure the distribution of the optical factors directly, thereby enabling the determination of the absolute concentrations of deoxy(Hb+Mb) simultaneously at the distal and proximal sites within the vastus lateralis (VL) and the rectus femoris muscles. Eight subjects performed cycle exercise transitions from unloaded to heavy work rates (>gas exchange threshold). Following exercise onset, the ATT-corrected amplitudes (A(p)), time delay (TD(p)), and time constant (τ(p)) of the primary component kinetics in muscle deoxy(Hb + Mb) were spatially heterogeneous (intersite coefficient of variation range for the subjects: 10-50 for A(p), 16-58 for TD(p), 14-108% for τ(p)). The absolute and relative amplitudes of the deoxy(Hb+Mb) responses were highly dependent on ATT, both within subjects and between measurement sites. The present results suggest that regional heterogeneity in the magnitude and temporal profile of muscle deoxygenation is a consequence of differential matching of O(2) delivery and O(2) utilization, not an artifact caused by changes in optical properties of the tissue during exercise or variability in the overlying adipose tissue.

Muscle vascular dysfunction, a hallmark of chronic diseases such as heart failure and diabetes, impairs the matching of blood flow (Q(m)) to O(2) utilization (V(O(2m))) following exercise onset. One recently described consequence of this behavior is that arterial-venous O(2) difference [(a-v)(O(2)), the mirror image of muscle vascular oxygenation] transiently overshoots the subsequent steady-state and, in so doing, may provide important information regarding Q(m) versus V(O(2m)) dynamics. Using computer simulations, we tested the hypothesis that key parameters of the (a-v)(O(2)) overshoot - peak response, downward time constant (tau(D)), and total area - would relate quantitatively to Q(m) kinetics. Our results demonstrated significant proportionality (all p<0.01) between Q(m) mean response time and peak (r(2)=0.56), tau(D) (r(2)=72) and total area (r(2)=0.97) of (a-v)(O(2)) overshoot. These results suggest that analysis of (a-v)(O(2)) or its proxy, muscle vascular oxygenation [measured using near-infrared spectroscopy or phosphorescence quenching], provides valuable information regarding blood flow and vascular function particularly in reference to V(O(2m)) kinetics., (Copyright 2010 Elsevier B.V. All rights reserved.)

We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O(2) uptake (pVO(2)) 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 (Delta deoxy-[Hb+Mb]) 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 pVO(2), whereas it reduced the amplitude of the slow component (SC). Delta deoxy-[Hb+Mb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 +/- 1.3 vs. 9.3 +/- 1.4 s; P < 0.01) and slower primary component time constant (tau: 9.3 +/- 1.3 vs. 17.8 +/- 1.0 s; P < 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the tau of Delta deoxy-[Hb+Mb] (26.6 +/- 11.8 vs. 13.7 +/- 5.6%; P < 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 tau nor RMSE of Delta deoxy-[Hb+Mb] correlated with the reduction in the SC in pVO(2) 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 pVO(2) response during subsequent heavy exercise.

It is unclear whether measurement of limb or conduit artery blood flow during recovery from exercise provides an accurate representation of flow to the muscle capillaries where gas exchange occurs. To investigate this, we: (a) examined the kinetic responses of femoral artery blood flow (QFA), estimated muscle capillary blood flow (Qcap) and estimated muscle oxygen uptake (VO2m) following cessation of exercise; and (b) compared these responses to verify the adequacy of O2 delivery during recovery. Pulmonary VO2 (VO2p) was measured breath by breath, QFA was measured using Doppler ultrasonography, and deoxy-haemoglobin/myoglobin (deoxy-[Hb/Mb]) was estimated by near-infrared spectroscopy over the rectus femoris in nine healthy subjects during a series of transitions from moderate knee-extension exercise to rest. The time course of Qcap was estimated by rearranging the Fick equation [i.e. Qcap(t) alpha VO2m(t)/deoxy-[Hb/Mb](t)], using the primary component of Vo2p to represent VO2m and deoxy-[Hb/Mb] as a surrogate for arteriovenous O2 difference. There were no significant differences among the overall kinetics of VO2m (tau, 31.4+/-8.2 s), QFA [mean response time (MRT), 34.5+/-20.4 s] and Qcap (MRT, 31.7+/-14.7 s). The VO2m kinetics were also significantly correlated (P<0.05) with those of both QFA and Qcap. Both QFA and Qcap appear to be coupled with VO2m during recovery from moderate knee-extension exercise, such that extraction falls (thus cellular energetic state is not further compromised) throughout recovery.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.

Muscles produce oxidants, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), from a variety of intracellular sources. Oxidants are detectable in muscle at low levels during rest and at higher levels during contractions. RNS depress force production but do not appear to cause fatigue of healthy muscle. In contrast, muscle-derived ROS contribute to fatigue because loss of function can be delayed by ROS-specific antioxidants. Thiol regulation appears to be important in this biology. Fatigue causes oxidation of glutathione, a thiol antioxidant in muscle fibers, and is reversed by thiol-specific reducing agents. N-acetylcysteine (NAC), a drug that supports glutathione synthesis, has been shown to lessen oxidation of cellular constituents and delay muscle fatigue. In humans, NAC pretreatment improves performance of limb and respiratory muscles during fatigue protocols and extends time to task failure during volitional exercise. These findings highlight the importance of ROS and thiol chemistry in fatigue, show the feasibility of thiol-based countermeasures, and identify new directions for mechanistic and translational research.

Utilization of near-infrared spectroscopy (NIRS) in clinical exercise testing to detect microvascular abnormalities requires characterization of the responses in healthy individuals and theoretical foundation for data interpretation. We examined the profile of the deoxygenated hemoglobin signal from NIRS {deoxygenated hemoglobin + myoglobin [deoxy-(Hb+Mb)] approximately O(2) extraction} during ramp exercise to test the hypothesis that the increase in estimated O(2) extraction would be close to hyperbolic, reflecting a linear relationship between muscle blood flow (Q(m)) and muscle oxygen uptake (Vo(2)(m)) with a positive Q(m) intercept. Fifteen subjects (age 24 +/- 5 yr) performed incremental ramp exercise to fatigue (15-35 W/min). The deoxy-(Hb+Mb) response, measured by NIRS, was fitted by a hyperbolic function [f(x) = ax/(b + x), where a is the asymptotic value and b is the x value that yields 50% of the total amplitude] and sigmoidal function {f(x) = f(0) + A/[1 + e(-(-c+dx))], where f(0) is baseline, A is total amplitude, and c is a constant dependent on d, the slope of the sigmoid}, and the goodness of fit was determined by F test. Only one subject demonstrated a hyperbolic increase in deoxy-(Hb+Mb) (a = 170%, b = 193 W), whereas 14 subjects displayed a sigmoidal increase in deoxy-(Hb+Mb) (f(0) = -7 +/- 7%, A = 118 +/- 16%, c = 3.25 +/- 1.14, and d = 0.03 +/- 0.01). Computer simulations revealed that sigmoidal increases in deoxy-(Hb+Mb) reflect a nonlinear relationship between microvascular Q(m) and Vo(2)(m) during incremental ramp exercise. The mechanistic implications of our findings are that, in most healthy subjects, Q(m) increased at a faster rate than Vo(2)(m) early in the exercise test and slowed progressively as maximal work rate was approached.

To test the hypothesis that, during exercise, substantial heterogeneity of muscle hemoglobin and myoglobin deoxygenation [deoxy(Hb + Mb)] dynamics exists and to determine whether such heterogeneity is associated with the speed of pulmonary O(2) uptake (pVo(2)) kinetics, we adapted multi-optical fibers near-infrared spectroscopy (NIRS) to characterize the spatial distribution of muscle deoxygenation kinetics at exercise onset. Seven subjects performed cycle exercise transitions from unloaded to moderate [GET) work rates and the relative changes in deoxy(Hb + Mb), at 10 sites in the quadriceps, were sampled by NIRS. At exercise onset, the time delays in muscle deoxy(Hb + Mb) were spatially inhomogeneous [intersite coefficient of variation (CV), 3~56% for GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O(2) extraction were also spatially inhomogeneous (intersite CV, 6~48% for GET) and faster (P < 0.05) than those of phase 2 pVo(2). However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pVo(2) kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of Vo(2) and O(2) delivery increase across the regions sampled.

In humans at exercise onset, intramuscular phosphocreatine decreases immediately, whereas muscle oxygen (O2) uptake seems to rise after a delay of up to 15 s which is inconsistent with models of metabolic control. Novel microcirculatory investigations reveal that elevated capillary-to-myocyte O2 flux in rat muscle is, in fact, initiated simultaneously with contractions.

The aim of this study was to examine the effects of assuming constant reduced scattering coefficient (mu'(s)) on the muscle oxygenation response to incremental exercise and its recovery kinetics. Fifteen subjects (age: 24 +/- 5 yr) underwent incremental cycling exercise. Frequency domain near-infrared spectroscopy (NIRS) was used to estimate deoxyhemoglobin concentration {[deoxy(Hb+Mb)]} (where Mb is myoglobin), oxyhemoglobin concentration {[oxy(Hb+Mb)]}, total Hb concentration (Total[Hb+Mb]), and tissue O(2) saturation (Sti(O(2))), incorporating both continuous measurements of mu'(s) and assuming constant mu'(s). When measuring mu'(s), we observed significant changes in NIRS variables at peak work rate Delta[deoxy(Hb+Mb)] (15.0 +/- 7.8 microM), Delta[oxy(Hb+Mb)] (-4.8 +/- 5.8 microM), DeltaTotal[Hb+Mb] (10.9 +/- 8.4 microM), and DeltaSti(O(2))(-11.8 +/- 4.1%). Assuming constant mu'(s) resulted in greater (P < 0.01 vs. measured mu'(s)) changes in the NIRS variables at peak work rate, where Delta[deoxy(Hb+Mb)] = 24.5 +/- 15.6 microM, Delta[oxy(Hb+Mb)] = -9.7 +/- 8.2 microM, DeltaTotal[Hb+Mb] = 14.8 +/- 8.7 microM, and DeltaSti(O(2))= -18.7 +/- 8.4%. Regarding the recovery kinetics, the large 95% confidence intervals (CI) for the difference between those determine measuring mu'(s) and assuming constant mu'(s) suggested poor agreement between methods. For the mean response time (MRT), which describes the overall kinetics, the 95% confidence intervals were MRT - [deoxy(Hb+Mb)] = 26.7 s; MRT - [oxy(Hb+Mb)] = 11.8 s, and MRT - Sti(O(2))= 11.8 s. In conclusion, mu'(s) changed from light to peak exercise. Furthermore, assuming a constant mu'(s) led to an overestimation of the changes in NIRS variables during exercise and distortion of the recovery kinetics.

This study evaluates the validity and reliability of the Baecke questionnaire on habitual physical activity when applied to a population of HIV/AIDS subjects. Validity was determined by comparing measurements for 30 subjects of peak oxygen uptake, peak workload, and energy expenditure with scores for occupational physical activity (OPA), physical exercise in leisure (PEL), leisure and locomotion activities (LLA), and total score (TS). Reliability was determined by testing and retesting 29 subjects at intervals of 15-30 days. Validity was evaluated with the Pearson correlation and reliability analyses were done using the intraclass correlation, paired Student t-test, and Bland-Altman methods. Peak VO2 and peak workload had significant correlation with PEL (r = 0.41; r = 0.43; respectively). Energy expenditure had a significant correlation with OPA (r = 0.64). The intraclass coefficients were 0.70 or more for OPA, PEL and TS. There was no difference in OPA, PEL, LLA and TS between the two evaluations. The Bland-Altman methods showed that there was good agreement between the measurements for all habitual physical activities scores. Results show that the Baecke questionnaire is valid for the evaluation of habitual physical activity among people living with HIV/AIDS.

We examined the validity and usefulness of a low-pass filter (LPFILTER) to reduce point-to-point variability and enhance parameter estimation of the kinetics of blood flow (BF). Computer simulations were used to determine the power spectrum of simulated responses. Moreover, we studied the leg BF response to a single transition in four subjects during supine knee-extension exercise using three methods of data processing [beat-by-beat, average of 3 cardiac cycles (AVG3 BEATS), and LPFILTER]. The power spectrum of BF containing the kinetics information (0.05; n=4). However, LPFILTER (cutoff=0.2 Hz) resulted in a significantly lower standard error of the estimate for all parameters (P<0.05). The means+/-SD for the standard error of the estimate for Beat-by-Beat, AVG3 BEATS, and LPFILTER were, respectively, time constant-phase 1=5.0+/-1.1 s, 4.5+/-2.1 s, and 0.3+/-0.2 s; time delay-phase 2=17.8+/-7.9 s, 12.8+/-7.5 s, and 1.4+/-1.4 s; time constant-phase 2=15.8+/-4.6 s, 9.9+/-2.9 s, and 1.1+/-0.5 s. In conclusion, LPFILTER appeared to be a valid procedure providing a high signal-to-noise ratio and data density and thus LPFILTER resulted in the smallest confidence interval for parameter estimates of BF kinetics.

Aims and Background: We attempted to determine the best method of performing the exercises in rehabilitation after breast cancer surgery and their influence on postoperative complications. Currently, there are no guidelines for these exercises. The scope of this study was to evaluate the effect of two schemes of physiotherapy exercises (directed or free) on shoulder function and lymphatic disturbance in postoperative rehabilitation., Subjects: Sixty women who underwent a modified radical mastectomy or quadrantectomy with axillary dissection were randomized into two groups., Methods: The physiotherapy technique used was kinesiotherapy. The directed group performed physiotherapy following a regimen of 19 exercises. The free group performed the exercises following the biomechanical physiological movements of the shoulder without a previously defined sequence or number of repetitions., Results: The averages of the flexion, abduction and external rotational movements of the shoulder showed better recovery with statistical significance in the directed group compared to the free group. There was no significant difference between the groups in lymphatic disturbance., Conclusion: At the end of 42 days of follow-up, the movements of flexion, extension, abduction and external rotation of the shoulder were better rehabilitated in the directed group. The two schemes of exercises were not different with regard to lymphatic disturbance.

The kinetic characteristics of muscle capillary blood flow (Qcap) during recovery from exercise are controversial (e.g. one versus two phases). Furthermore, it is not clear how the overall Qcap kinetics are temporally associated with muscle oxygen uptake (VO2m) kinetics. To address these issues, we examined the kinetics of Qcap estimated from the rearrangement of the Fick equation (Qcap=VO2m/C(a-v)O2) using the kinetics of pulmonary VO2 (VO2p, primary component) and deoxy-haemoglobin concentration ([HHb]) as indices of VO2m and C(a - v)O2 (arterio-venous oxygen difference) kinetics, respectively. VO2p (l min-1) was measured breath by breath and [HHb] (microm) was measured by near infrared spectroscopy during moderate (M; below lactate threshold, LT) and heavy exercise (H, above LT) in nine subjects. The kinetics of Qcap were biphasic, with an initial fast phase (tauI; M=9.3+/-4.9 s and H=6.0+/-3.8 s) followed by a slower phase 2 (tauP; M=29.9+/-8.6 s and H=47.7+/-26.0 s). For moderate exercise, the overall kinetics of Qcap (mean response time [MRT], 36.1+/-8.6 s) were significantly slower than the kinetics of VO2p (tauP; 27.8+/-5.3 s) and [HHb] (MRT for [HHb]; 16.2+/-6.3 s). However, for heavy exercise, there was no significant difference between MRT-[HHb] (34.7+/-10.4 s) and tauP for VO2p (32.3+/-6.7 s), while MRT for Qcap (48.7+/-21.8 s) was significantly slower than MRT for [HHb] and tauP for VO2p. In conclusion, during recovery from exercise the estimated Qcap kinetics were biphasic, showing an early rapid decrease in blood flow. In addition, the overall kinetics of Qcap were slower than the estimated VO2m kinetics.

A computer model was developed to provide a theoretical framework for interpreting the dynamics of muscle capillary O(2) exchange in health and disease. We examined the effects of different muscle oxygen uptake (V O(2m)) and CvO(2) profiles on muscle blood flow (Q (m)) kinetics (Q (m)=V O(2m)/[CaO(2)-CvO(2)]). Further, we simulated V O(2m) and Q (m) responses to predict the CvO(2) profile and the underlying dynamics of capillary O(2) exchange (CvO(2)=CaO(2)-V O(2m)/Q (m)). Exponential equations describing V O(2m), CvO(2) and Q (m) responses in vivo were used in the simulations. The results indicated that Q (m) kinetics were relatively insensitive to CvO(2) parameters, but directly associated with V O(2m) kinetics. The biphasic Q (m) response produced a substantial fall in CvO(2) within the first 15-20s of the exercise transition (phase 1 of Q (m)). These results revealed that the main determinant of CvO(2) (or O(2) extraction) kinetics was the dynamic interaction of Q (m) and V O(2m) kinetics during phase 1 of Q (m).

The near-infrared spectroscopy (NIRS) signal (deoxyhemoglobin concentration; [HHb]) reflects the dynamic balance between muscle capillary blood flow (Q(cap)) and muscle O(2) uptake (Vo(2)(m)) in the microcirculation. The purposes of the present study were to estimate the time course of Q(cap) from the kinetics of the primary component of pulmonary O(2) uptake (Vo(2)(p)) and [HHb] throughout exercise, and compare the Q(cap) kinetics with the Vo(2)(p) kinetics. Nine subjects performed moderate- (M; below lactate threshold) and heavy-intensity (H, above lactate threshold) constant-work-rate tests. Vo(2)(p) (l/min) was measured breath by breath, and [HHb] (muM) was measured by NIRS during the tests. The time course of Q(cap) was estimated from the rearrangement of the Fick equation [Q(cap) = Vo(2)(m)/(a-v)O(2), where (a-v)O(2) is arteriovenous O(2) difference] using Vo(2)(p) (primary component) and [HHb] as proxies of Vo(2)(m) and (a-v)O(2), respectively. The kinetics of [HHb] [time constant (tau) + time delay [HHb]; M = 17.8 +/- 2.3 s and H = 13.7 +/- 1.4 s] were significantly (P < 0.001) faster than the kinetics of Vo(2) [tau of primary component (tau(P)); M = 25.5 +/- 8.8 s and H = 25.6 +/- 7.2 s] and Q(cap) [mean response time (MRT); M = 25.4 +/- 9.1 s and H = 25.7 +/- 7.7 s]. However, there was no significant difference between MRT of Q(cap) and tau(P)-Vo(2) for both intensities (P = 0.99), and these parameters were significantly correlated (M and H; r = 0.99; P < 0.001). In conclusion, we have proposed a new method to noninvasively approximate Q(cap) kinetics in humans during exercise. The resulting overall Q(cap) kinetics appeared to be tightly coupled to the temporal profile of Vo(2)(m).