Noninvasive and in vivo assessment of upper and lower limb skeletal muscle oxidative metabolism activity and microvascular responses to glucose ingestion in humans.

This study investigated changes in muscle oxidative metabolism and microvascular responsiveness induced by glucose ingestion in the upper and lower limbs using near-infrared spectroscopy (NIRS). Fourteen individuals (aged 27 ± 1.4 years) underwent 5 vascular occlusion tests (VOT) (pre-intervention (Pre), 30 min, 60 min, 90 min, and 120 min after glucose challenge). NIRS-derived oxygen saturation (StO2) was measured on the forearm and leg muscle at each VOT. Muscle oxidative metabolism was determined by the StO2 downslope during cuff inflation (deoxygenation slope); microvascular responsiveness was estimated by the StO2 upslope (reperfusion slope) following cuff deflation. There was a significant increase in arm (p < 0.05; 1-ß = 0.860) and leg (p < 0.05; 1-ß = 1.000) oxidative metabolism activity as represented by the faster deoxygenation slope at 60, 90, and 120 min (0.08 ± 0.03, 0.08 ± 0.03, 0.08 ± 0.02%·s-1, respectively) (leg) and at 90 min (0.16 ± 0.08%·s-1) (arm) observed after glucose ingestion when compared with their respective Pre values (leg = 0.06 ± 0.02; arm = 0.11 ± 0.04%·s-1). There was a significant increase in arm (p < 0.05; 1-ß = 0.880) and leg (p < 0.05; 1-ß = 0.983) reperfusion slope at 60 min (arm = 3.63 ± 2.1%·s-1; leg = 1.56 ± 0.6%·s-1), 90 min (arm = 3.91 ± 2.1%·s-1; leg = 1.60 ± 0.6%·s-1), and 120 min (arm = 3.91 ± 1.6%·s-1; leg = 1.54 ± 0.6%·s-1) when compared with their Pre values (arm = 2.79 ± 1.7%·s-1; leg = 1.26 ± 0.5%·s-1). Our findings showed that NIRS-VOT technique is capable of detecting postprandial changes in muscle oxidative metabolism activity and microvascular reactivity in the upper and lower limb. Novelty NIRS-VOT is a promising noninvasive clinical approach that may help in the early, limb-specific detection of impairments in glucose oxidation and microvascular function.

Heart Rate-Index Estimates Oxygen Uptake, Energy Expenditure and Aerobic Fitness in Rugby Players.

The purpose of the study was to verify the suitability of heart rate-index (HRindex) in predicting submaximal oxygen consumption (VO2), energy expenditure (EE) and maximal oxygen consumption (VO2max) during treadmill running in rugby players. Fifteen professional rugby players (99.8 ± 12.7 kg, 1.85 ± 0.09 m) performed a running incremental test while VO2 (breath-by-breath) and heart rate (HR) were measured. HRindex was calculated (actual HR/resting HR) to predict submaximal and maximal VO2 ({[(HRindex x 6)-5.0] x (3.5 body weight)}) and EE. Measured and predicted VO2 and EE were compared by two-way RM-ANOVA (method, speed), correlation and Bland-Altman analysis. Measured and predicted VO2max were compared by paired t-test, correlation and Bland-Altman analysis. Submaximal VO2 and EE significantly increased (baseline VO2: 8.1 ± 1.6 ml·kg-1·min-1VO2max: 46.8 ± 4.3 ml·kg-1·min-1, baseline EE: 0.03 ± 0.01 kcal·kg-1·min-1, peak EE: 0.23 ± 0.03 kcal·kg-1·min-1) as a function of speed (p < 0.001 and p < 0.001 for VO2 and EE respectively) yet measured and predicted values at equal treadmill speeds were not significantly different (p = 0.17; p = 0.16) and highly correlated (r = 0.95; r = 0.94). The Bland-Altman analysis confirmed a non-significant bias between measured and estimated VO2 (measured: 40.3 ± 10.7, estimated: 40.7 ± 10.1 ml·kg-1·min-1, bias = 1.35 ml·kg-1·min-1, z = 1.12, precision = 3.39 ml·kg-1·min-1) and EE (measured: 20.0 ± 0.05 kcal·kg-1·min-1, estimated: 20.0 ± 0.05 kcal·kg-1·min-1, bias = 0.00 kcal·kg-1·min-1, z = 0.04, precision = 0.02 kcal·kg-1·min-1). Estimated and predicted VO2max were not statistically different (p = 0.91), highly correlated (r = 0.96), and showed a non-significant bias (bias = 0.17, z = 0.22, precision = 1.29 ml·kg-1·min-1). HRindex is a valid field method to track VO2, EE and VO2max during running in rugby players.

Serial assessment of peak VO2 and VO2 kinetics early after heart transplantation.

PURPOSE: Serial evaluation of aerobic metabolism and exercise tolerance early after heart transplantation (HT). METHODS: Fifteen heart transplant recipients (HTR), aged 52.0 +/- 9.9 yr (mean +/- SD), not undergoing structured rehabilitation programs, were tested two to four times during the first 2 yr post-HT. As a reference, a group of 11 healthy untrained controls (C) was utilized. Peak heart rate (peak HR), peak O2 uptake (peak VO2), and ventilatory threshold (VT) were determined during incremental bicycle exercise to voluntary exhaustion. VO2 kinetics were evaluated during constant-load exercise below VT, with determination of the duration of the "cardiodynamic" component (TDp) and of the time constant of the "primary" component (taup). RESULTS: Peak VO2 (L.min-1) was positively related to months post-HT (y=1.17 + 0.02x, P=0.003), and it increased by approximately 30% during the investigated period, although values in HTR were lower than in C (2.19 +/- 0.24). Peak HR was lower in HTR (136 +/- 15 beats.min-1) than in C (168 +/- 5), and it was not related to time post-HT. TDp was longer in HTR (31.4 +/- 6.3 s) than in C (23.2 +/- 6.1), and it was not related to time post-HT. A subgroup of HTR with markedly longer taup during the first months post-HT showed a significant decrease of this parameter as a function of time post-HT. CONCLUSIONS: Aerobic metabolism is impaired in HTR. Both central (cardiovascular) and peripheral (skeletal muscle) factors contribute to the reduced exercise tolerance. HTR showed, during the first 2 yr post-HT, a significant increase in peak VO2 and (in the patients with the slowest VO2 kinetics during the first months after HT) a significant improvement of the VO2 kinetics. The main gains seem to occur at the peripheral level.