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.

Short-term training alters the control of mitochondrial respiration rate before maximal oxidative ATP synthesis.

AIM: Short-term exercise training may induce metabolic and performance adaptations before any changes in mitochondrial enzyme potential. However, there has not been a study that has directly assessed changes in mitochondrial oxidative capacity or metabolic control as a consequence of such training in vivo. Therefore, we used (31) P-magnetic resonance spectroscopy ((31) P-MRS) to examine the effect of short-term plantar flexion exercise training on phosphocreatine (PCr) recovery kinetics and the control of respiration rate. METHOD: To this aim, we investigated 12 healthy men, experienced with this exercise modality (TRA), and 7 time-control subjects (TC). RESULTS: After 5 days of training, maximum work rate during incremental plantar flexion exercise was significantly improved (P < 0.01). During the recovery period, the maximal rate of oxidative adenosine triphosphate synthesis (PRE: 28 ± 13 mm min(-1) ; POST: 26 ± 15 mm min(-1) ) and the PCr recovery time constant (PRE: 31 ± 19 s; POST: 29 ± 16) were not significantly altered. In contrast, the Hill coefficient (nH ) describing the co-operativity between respiration rate and ADP was significantly increased in TRA (PRE: nH = 2.7 ± 1.4; POST: nH = 3.4 ± 1.9, P < 0.05). Meanwhile, there were no systematic variations in any of these variables in TC. CONCLUSION: This study reveals that 5 days of training induces rapid adaptation in the allosteric control of respiration rate by ADP before any substantial improvement in muscle oxidative capacity occurs.