Exercise-training-induced changes in metabolic capacity with age: the role of central cardiovascular plasticity.

Although aging is typically associated with a decline in maximal oxygen consumption (VO2max), young and old subjects, of similar initial muscle metabolic capacity, increased quadriceps VO2max equally when this small muscle mass was trained in isolation. As it is unclear if this preserved exercise-induced plasticity with age is still evident with centrally challenging whole body exercise, we assessed maximal exercise responses in 13 young (24 ± 2 years) and 13 old (60 ± 3 years) males, matched for cycling VO2max (3.82 ± 0.66 and 3.69 ± 0.30 L min(-1), respectively), both before and after 8 weeks of high aerobic intensity cycle exercise training. As a consequence of the training both young and old significantly improved VO2max (13 ± 6 vs. 6 ± 7 %) and maximal power output (20 ± 6 vs. 10 ± 6 %, respectively) from baseline, however, the young exhibited a significantly larger increase than the old. Similarly, independently assessed maximal cardiac output (Q max) tended to increase more in the young (16 ± 14 %) than in the old (11 ± 12 %), with no change in a-vO2 difference in either group. Further examination of the components of Q max provided additional evidence of reduced exercise-induced plasticity in both maximal heart rate (young -3 %, old 0 %) and stroke volume (young 19 ± 15, old 11 ± 11 %) in the old. In combination, these findings imply that limited central cardiovascular plasticity may be responsible, at least in part, for the attenuated response to whole body exercise training with increasing age.

A somatosensory circuit for cooling perception in mice.

The temperature of an object provides important somatosensory information for animals performing tactile tasks. Humans can perceive skin cooling of less than one degree, but the sensory afferents and central circuits that they engage to enable the perception of surface temperature are poorly understood. To address these questions, we examined the perception of glabrous skin cooling in mice. We found that mice were also capable of perceiving small amplitude skin cooling and that primary somatosensory (S1) cortical neurons were required for cooling perception. Moreover, the absence of the menthol-gated transient receptor potential melastatin 8 ion channel in sensory afferent fibers eliminated the ability to perceive cold and the corresponding activation of S1 neurons. Our results identify parts of a neural circuit underlying cold perception in mice and provide a new model system for the analysis of thermal processing and perception and multimodal integration.