Capillary Density of Skeletal Muscle: A Contributing Mechanism for Exercise Intolerance in Class II–III Chronic Heart Failure Independent of Other Peripheral Alterations

AbstractOBJECTIVESThe study was conducted to determine if the capillary density of skeletal muscle is a potential contributor to exercise intolerance in class II–III chronic heart failure (CHF).BACKGROUNDPrevious studies suggest that abnormalities in skeletal muscle histology, contractile protein content and enzymology contribute to exercise intolerance in CHF.METHODSThe present study examined skeletal muscle biopsies from 22 male patients with CHF compared with 10 age-matched normal male control patients. Aerobic capacities, myosin heavy chain (MHC) isoforms, enzymes, and capillary density were measured.RESULTSThe patients with CHF demonstrated a reduced peak oxygen consumption when compared to controls (15.0 ± 2.5 vs. 19.8 ± 5.0 ml·kg−1·min−1, p <0.05). Using cell-specific antibodies to directly assess vascular density, there was a reduction in capillary density in CHF measured as the number of endothelial cells/fiber (1.42 ± 0.28 vs. 1.74 ± 0.35, p = 0.02). In CHF, capillary density was inversely related to maximal oxygen consumption (r = 0.479, p = 0.02). The MHC IIx isoform was found to be higher in patients with CHF versus normal subjects (28.5 ± 13.6 vs. 19.5 ± 9.4, p <0.05).CONCLUSIONSThere was a significant reduction in microvascular density in patients with CHF compared with the control group, without major differences in other usual histologic and biochemical aerobic markers. The inverse relationship with peak oxygen consumption seen in the CHF group suggests that a reduction in microvascular density of skeletal muscle may precede other skeletal muscle alterations and play a critical role in the exercise intolerance characteristic of patients with CHF

Increases in the flux of carbon belowground stimulate nitrogen uptake and sustain the long-term enhancement of forest productivity under elevated CO2

The earth’s future climate state is highly dependent upon changes in terrestrial C storage in response to rising concentrations of atmospheric CO2. Here we show that consistently enhanced rates of net primary production (NPP) are sustained by a C-cascade through the root-microbe-soil system; increases in the flux of C belowground under elevated CO2 stimulated microbial activity, accelerated the rate of soil organic matter decomposition and stimulated tree uptake of N bound to this SOM. This process set into motion a positive feedback maintaining greater C gain under elevated CO2 as a result of increases in canopy N content and higher photosynthetic N-use efficiency. The ecosystem-level consequence of the enhanced requirement for N and the exchange of plant C for N belowground is the dominance of C storage in tree biomass but the preclusion of a large C sink in the soil

Increases in the flux of carbon belowground stimulate nitrogen uptake and sustain the long-term enhancement of forest productivity under elevated CO₂.

The earth's future climate state is highly dependent upon changes in terrestrial C storage in response to rising concentrations of atmospheric CO₂. Here we show that consistently enhanced rates of net primary production (NPP) are sustained by a C-cascade through the root-microbe-soil system; increases in the flux of C belowground under elevated CO₂ stimulated microbial activity, accelerated the rate of soil organic matter decomposition and stimulated tree uptake of N bound to this SOM. This process set into motion a positive feedback maintaining greater C gain under elevated CO₂ as a result of increases in canopy N content and higher photosynthetic N-use efficiency. The ecosystem-level consequence of the enhanced requirement for N and the exchange of plant C for N belowground is the dominance of C storage in tree biomass but the preclusion of a large C sink in the soil