Differences in vascular function between trained and untrained limbs assessed by near-infrared spectroscopy.

PURPOSE: The aim of this study was to examine whether differences in vascular responsiveness associated with training status would be more prominent in the trained limb (leg) than in the untrained limb (arm) microvasculature. METHODS: Thirteen untrained (26 ± 5 year) and twelve trained (29 ± 4 year) healthy men were submitted to a vascular occlusion test (VOT) (2 min baseline, 5 min occlusion, and 8 min re-oxygenation). The oxygen saturation signal (StO2) was assessed using near-infrared spectroscopy (NIRS) throughout the VOT. Vascular responsiveness within the microvasculature was evaluated by the re-oxygenation Slope 2 (Slope 2 StO2) and the area under the curve (StO2AUC) of (StO2) signal during re-oxygenation in the leg and arm. RESULTS: There was a significant interaction between training status and limb for the slope 2 StO2 (P < 0.01). The leg of the trained group showed a steeper slope 2 StO2 (1.35 ± 0.12% s-1) when compared to the slope 2 StO2 of the leg in their untrained counterparts (0.86 ± 0.09% s-1) (P < 0.05). There was a medium effect size of 0.58 for slope 2 StO2 on the arm and a large effect size of 1.21 for slope 2 StO2 on the leg. In addition, there was a small effect size of 0.24 for StO2AUC on the arm and a medium effect size of 0.64 for StO2AUC on the leg. CONCLUSION: The present study suggests that the vascular adaptations induced by lower limb endurance exercise training are more prominent in the trained limb than in the untrained limb microvasculature.

Fitness Level and Not Aging per se, Determines the Oxygen Uptake Kinetics Response.

Although aging has been associated to slower [Formula: see text]O2 kinetics, some evidence indicates that fitness status and not aging per se might modulate this response. The main goal of this study was to examine the [Formula: see text]O2, deoxygenated hemoglobin+myoglobin (deoxy-[Hb+Mb]) kinetics, and the NIRS-derived vascular reperfusion responses in older compared to young men of different training levels (i.e., inactive, recreationally active, and endurance trained). Ten young inactive [YI; 26 ± 5 yrs.; peak [Formula: see text]O2 ([Formula: see text]O2peak), 2.96 ± 0.55 L·min-1], 10 young recreationally active (YR; 26 ± 6 yrs.; 3.92 ± 0.33 L·min-1), 10 young endurance trained (YT; 30 ± 4 yrs.; 4.42 ± 0.32 L·min-1), 7 older inactive (OI; 69 ± 4 yrs.; 2.50 ± 0.31 L·min-1), 10 older recreationally active (OR; 69 ± 5 yrs.; 2.71 ± 0.42 L·min-1), and 10 older endurance trained (OT; 66 ± 3 yrs.; 3.20 ± 0.35 L·min-1) men completed transitions of moderate intensity cycling exercise (MODS) to determine [Formula: see text]O2 and deoxy-[Hb+Mb] kinetics, and the deoxy-[Hb+Mb]/[Formula: see text]O2 ratio. The time constant of [Formula: see text]O2 (τ[Formula: see text]O2) was greater in YI (38.8 ± 10.4 s) and OI (44.1 ± 10.8 s) compared with YR (26.8 ± 7.5 s) and OR (26.6 ± 6.5 s), as well as compared to YT (14.8 ± 3.4 s), and OT (17.7 ± 2.7 s) (p < 0.05). τ[Formula: see text]O2 was greater in YR and OR compared with YT and OT (p < 0.05). The deoxy-[Hb+Mb]/[Formula: see text]O2 ratio was greater in YI (1.23 ± 0.05) and OI (1.29 ± 0.08) compared with YR (1.11 ± 0.03) and OR (1.13 ± 0.06), as well as compared to YT (1.01 ± 0.03), and OT (1.06 ± 0.03) (p < 0.05). Similarly, the deoxy-[Hb+Mb]/ [Formula: see text]O2 ratio was greater in YR and OR compared with YT and OT (p < 0.05). There was a main effect of training (p = 0.033), whereby inactive (p = 0.018) and recreationally active men (p = 0.031) had significantly poorer vascular reperfusion than endurance trained men regardless of age. This study demonstrated not only that age-related slowing of [Formula: see text]O2 kinetics can be eliminated in endurance trained individuals, but also that inactive lifestyle negatively impacts the [Formula: see text]O2 kinetics response of young healthy individuals.

Lactate is oxidized outside of the mitochondrial matrix in rodent brain.

The nature and existence of mitochondrial lactate oxidation is debated in the literature. Obscuring the issue are disparate findings in isolated mitochondria, as well as relatively low rates of lactate oxidation observed in permeabilized muscle fibres. However, respiration with lactate has yet to be directly assessed in brain tissue with the mitochondrial reticulum intact. To determine if lactate is oxidized in the matrix of brain mitochondria, oxygen consumption was measured in saponin-permeabilized mouse brain cortex samples, and rat prefrontal cortex and hippocampus (dorsal) subregions. While respiration in the presence of ADP and malate increased with the addition of lactate, respiration was maximized following the addition of exogenous NAD+, suggesting maximal lactate metabolism involves extra-matrix lactate dehydrogenase. This was further supported when NAD+-dependent lactate oxidation was significantly decreased with the addition of either low-concentration α-cyano-4-hydroxycinnamate or UK-5099, inhibitors of mitochondrial pyruvate transport. Mitochondrial respiration was comparable between glutamate, pyruvate, and NAD+-dependent lactate oxidation. Results from the current study demonstrate that permeabilized brain is a feasible model for assessing lactate oxidation, and support the interpretation that lactate oxidation occurs outside the mitochondrial matrix in rodent brain.

Differences in oxidative metabolism modulation induced by ischemia/reperfusion between trained and untrained individuals assessed by NIRS.

Endurance training is associated with skeletal muscle adaptations that regulate the oxidative metabolism during ischemia/reperfusion. The aim of this study was to noninvasively assess in vivo differences in the oxidative metabolism activity during ischemia/reperfusion between trained and untrained individuals, using near infrared spectroscopy (NIRS) combined with a vascular occlusion test (VOT) technique (NIRS-VOT). Sixteen untrained (26.3 ± 5.1 year) and seventeen trained (29.4 ± 4.9 year) healthy young adult men were submitted to a VOT (2 min baseline, 5 min occlusion, and 8 min reperfusion). Oxygen utilization was estimated from the area under the curve of the NIRS-derived deoxyhemoglobin [HHb] signal during occlusion (AUCocc). Muscle reperfusion was derived from the area above the curve (AACrep) of the [HHb] signal after cuff release. The AUCocc of the untrained participants (21010 ± 9553 % · s) was significantly larger than the AUCocc of their trained counterparts (12320 ± 3283 % · s); P = 0.001). The AACrep of the untrained participants (5928 ± 3769 % · s) was significantly larger than the AACrep of the trained participants (3745 ± 1900 % · s; P = 0.042). There was a significant correlation between AUCocc and AACrep (r = 0.840; P = 0.001). NIRS assessment of oxidative metabolism showed that trained individuals are more efficient in shifting between oxidative and anaerobic metabolism in response to ischemia and reperfusion.