Passive leg movement-induced hyperaemia with a spinal cord lesion: evidence of preserved vascular function.

UNLABELLED: A spinal cord injury (SCI) clearly results in greater cardiovascular risk; however, accompanying changes in peripheral vascular structure below the lesion mean that the real impact of a SCI on vascular function is unclear. AIM: Therefore, utilizing passive leg movement-induced (PLM) hyperaemia, an index of nitric oxide (NO)-dependent vascular function and the central hemodynamic response to this intervention, we studied eight individuals with a SCI and eight age-matched controls (CTRL). METHODS: Specifically, we assessed heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), leg blood flow (LBF) and thigh composition. RESULTS: In CTRL, passive movement transiently decreased MAP and increased HR and CO from baseline by 2.5 ± 1 mmHg, 7 ± 2 bpm and 0.5 ± 0.1 L min(-1) respectively. In SCI, HR and CO responses were unidentifiable. LBF increased to a greater extent in CTRL (515 ± 41 ∆mL min(-1)) compared with SCI, (126 ± 25 ∆mL min(-1)) (P < 0.05). There was a strong relationship between ∆LBF and thigh muscle volume (r = 0.95). After normalizing ∆LBF for this strong relationship (∆LBF/muscle volume), there was evidence of preserved vascular function in SCI (CTRL: 120 ± 9; SCI 104 ± 11 mL min(-1) L(-1)). A comparison of ∆LBF in the passively moved and stationary leg, to partition the contribution of the blood flow response, implied that 35% of the hyperaemia resulted from cardioacceleration in the CTRL, whereas all the hyperaemia appeared peripheral in origin in the SCI. CONCLUSION: Thus, utilizing PLM-induced hyperaemia as marker of vascular function, it is evident that peripheral vascular impairment is not an obligatory accompaniment to a SCI.

Attenuated relationship between cardiac output and oxygen uptake during high-intensity exercise.

AIM: Recent findings have challenged the belief that the cardiac output (CO) and oxygen consumption (VO(2) ) relationship is linear from rest to maximal exercise. The purpose of this study was to determine the CO and stroke volume (SV) response to a range of exercise intensities, 40-100% of VO(2max), during cycling. METHODS: Ten well-trained cyclists performed a series of discontinuous exercise bouts to determine the CO and SV vs. VO(2) responses. RESULTS: The rate of increase in CO, relative to VO(2) , during exercise from 40 to 70% of VO(2max) was 4.4 ± 1.4 L L(-1). During exercise at 70-100% of VO(2max) , the rate of increase in CO was reduced to 2.1 ± 0.9 L L(-1) (P = 0.01). Stroke volume during exercise at 80-100% of VO(2max) was reduced by 7% when compared to exercise at 50-70% of VO(2max) (134 ± 5 vs. 143 ± 5 mL per beat, P = 0.02). Whole body arterial-venous O(2) difference increased significantly as intensity increased. CONCLUSION: The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO(2) is reached.

Central and peripheral hemodynamic responses to passive limb movement: the role of arousal.

The exact role of arousal in central and peripheral hemodynamic responses to passive limb movement in humans is unclear but has been proposed as a potential contributor. Thus, we used a human model with no lower limb afferent feedback to determine the role of arousal on the hemodynamic response to passive leg movement. In nine people with a spinal cord injury, we compared central and peripheral hemodynamic and ventilatory responses to one-leg passive knee extension with and without visual feedback (M+VF and M-VF, respectively) as well as in a third trial with no movement or visual feedback but the perception of movement (F). Ventilation (Ve), heart rate, stroke volume, cardiac output, mean arterial pressure, and leg blood flow (LBF) were evaluated during the three protocols. Ve increased rapidly from baseline in M+VF (55 ± 11%), M-VF (63 ± 13%), and F (48 ± 12%) trials. Central hemodynamics (heart rate, stroke volume, cardiac output, and mean arterial pressure) were unchanged in all trials. LBF increased from baseline by 126 ± 18 ml/min in the M+VF protocol and 109 ± 23 ml/min in the M-VF protocol but was unchanged in the F protocol. Therefore, with the use of model that is devoid of afferent feedback from the legs, the results of this study reveal that, although arousal is invoked by passive movement or the thought of passive movement, as evidenced by the increase in Ve, there is no central or peripheral hemodynamic impact of this increased neural activity. Additionally, this study revealed that a central hemodynamic response is not an obligatory component of movement-induced LBF.

Maximal power and performance during a swim taper.

This study examined how altering training intensity during a taper impacts maximal mechanical power (Pmax), torque at power maximum (T), velocity at power maximum (V), and swim performance (m . sec (-1)). Using an arm ergometer with inertial loading, measurements of Pmax, T, and V were made for 7 consecutive weeks prior to the taper and during the taper in 7 female competitive collegiate swimmers. Subjects were tested over two consecutive years. Swim performance was obtained from 3 competitive meets; a conference meet (CM), the conference championship meet (CONF) and the national championship meet (NAT). A 50 to 60 % increase in the amount of "high-intensity training" during the taper of 2005 (High-Intensity Taper - HIT) resulted in Pmax values that were 8 to 14 % higher (40 to 60 Watts) at all but one time point when compared to the 2004 taper (Low-Intensity Taper - LIT). Swim performance was significantly worsened at the NAT following LIT. However, with the HIT, swim performance, Pmax, and T were maintained prior to and at NAT. A large reduction in high-intensity training during a taper reduces the length of time that Pmax, T, and swim performance can be maintained at peak levels.