Aging blunts hyperventilation-induced hypocapnia and reduction in cerebral blood flow velocity during maximal exercise

Cerebral blood flow (CBF) increases from rest to ∼60% of peak oxygen uptake (VO(2peak)) and thereafter decreases towards baseline due to hyperventilation-induced hypocapnia and subsequent cerebral vasoconstriction. It is unknown what happens to CBF in older adults (OA), who experience a decline in CBF at rest coupled with a blunted ventilatory response during VO(2peak). In 14 OA (71 ± 10 year) and 21 young controls (YA; 23 ± 4 years), we hypothesized that OA would experience less hyperventilation-induced cerebral vasoconstriction and therefore an attenuated reduction in CBF at VO(2peak). Incremental exercise was performed on a cycle ergometer, whilst bilateral middle cerebral artery blood flow velocity (MCA V(mean); transcranial Doppler ultrasound), heart rate (HR; ECG) and end-tidal PCO(2) (P(ET)CO(2)) were monitored continuously. Blood pressure (BP) was monitored intermittently. From rest to 50% of VO(2peak), despite greater elevations in BP in OA, the change in MCA V(mean) was greater in YA compared to OA (28% vs. 15%, respectively; P < 0.0005). In the YA, at intensities >70% of VO(2peak), the hyperventilation-induced declines in both P(ET)CO(2) (14 mmHg (YA) vs. 4 mmHg (OA); P < 0.05) and MCA V(mean) (−21% (YA) vs. −7% (OA); P < 0.0005) were greater in YA compared to OA. Our findings show (1), from rest-to-mild intensity exercise (50% VO(2peak)), elevations in CBF are reduced in OA and (2) age-related declines in hyperventilation during maximal exercise result in less hypocapnic-induced cerebral vasoconstriction

Integrative human cardiovascular responses to hyperthermia

Progressive whole-body hyperthermia with passive heat stress is associated with a host of physiological adjustments. These include large increases in peripheral blood flow and cardiac output and a smaller selective redistribution of blood flow from the cerebral and visceral tissues to the limbs, head, and torso, with perfusion pressure being only slightly reduced. Aerobic metabolism also increases in these conditions, but the magnitude is small in absolute terms, suggesting a predominant role of thermosensitive mechanisms in passive hyperthermia-induced cardiovascular adjustments. Although exercise heat stress requires substantially greater blood flow requirements compared to passive heat stress alone, the magnitude of this hyperemic response is less than would be expected given the extent to which both conditions independently increase blood flow in isolation. As a result, submaximal exercise limb blood flow is only slightly higher during small muscle-mass exercise in the heat, and is similar to control conditions during whole-body exercise. When exercise intensity is increased further towards maximal levels, the superimposition of heat stress leads to earlier reductions in regional and systemic blood perfusion, compromised locomotor limb aerobic metabolism, and ultimately results in impaired endurance capacity. This chapter provides an integrative overview of the human cardiovascular response to passive heat stress and exercise heat stress, with emphasis on its consequences on exercise performance in the heat