Spinal cord-injured (SCI) individuals, having a sympathetic nervous system lesion, experience hypotension during sitting and standing. Surprisingly, they experience few syncopal events. This suggests adaptations in cerebrovascular regulation. Therefore, changes in systemic circulation, cerebral blood flow, and oxygenation in eight SCI individuals were compared with eight able-bodied (AB) individuals. Systemic circulation was manipulated by lower body negative pressure at several levels down to -60 mmHg. At each level, we measured steady-state blood pressure, changes in cerebral blood velocity with transcranial Doppler, and cerebral oxygenation using near-infrared spectroscopy. We found that mean arterial pressure decreased significantly in SCI but not in AB individuals, in accordance with the sympathetic impairment in the SCI group. Cerebral blood flow velocity decreased during orthostatic stress in both groups, but this decrease was significantly greater in SCI individuals. Cerebral oxygenation decreased in both groups, with a tendency to a greater decrease in SCI individuals. Thus present data do not support an advantageous mechanism during orthostatic stress in the cerebrovascular regulation of SCI individuals.

Summary Plasma volume (PV) decreased by 13 per cent following the completion of 1,000 m of maximal exercise in the horse. This study demonstrated that the critical reduction in PV following maximal exercise occurred within 10 mins of completion of exercise, as previously reported in man. Total plasma protein (TPP) increased by 23 per cent at 2 and 5 mins, and by 21 per cent at 10 mins post exercise. Therefore, it does not appear to be an accurate measurement to assess the degree of PV contraction in the horse. Protein was apparently added to the intravascular space either during or following exercise. The changes in osmolality correlated strongly with those in sodium, which is the primary determinant of alterations in plasma tonicity. The increase in osmolality (12 per cent) was similar to the reduction in PV (13 per cent) concluding that a transient hypotonic fluid loss had occurred. The increase in plasma renin activity (PRA) following maximal exercise was followed by an increase in aldosterone (ALD) concentration in both magnitude and time course. Alterations in PV should be considered when interpreting electrolyte and serum enzyme activity data collected following maximal exercise.

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PURPOSESympathetic nervous system responses to voluntary apnea are increased by hypoxia and attenuated by hyperoxia. However, whether neural firing and recruitment strategies in response to apnea can be modified by hypoxia and/or hyperoxia were previously unknown. We examined the influence of chemoreceptor stimuli on sympathetic neural firing and recruitment strategies during voluntary end‐expiratory apnea. We hypothesized increases in the firing frequency and probability of low‐threshold axons during apnea would be exaggerated during hypoxia and attenuated during hyperoxia.METHODSMulti‐unit muscle sympathetic nerve activity (MSNA, microneurography) was measured in 10 young, healthy men (31±2 yrs, 25±1 kg/m2). Data were collected at baseline and during maximal voluntary end‐expiratory apnea under normoxic (SpO2: 98±1%), hypoxic (FiO2: 0.17±0.01; SpO2: 82±1%), and hyperoxic (FiO2: 0.92±0.03; SpO2: 100±0%) conditions. Condition order was randomized and trials were separated by a minimum of 15‐min quiet normoxic rest. Action potential (AP) patterns were studied from the filtered raw signal using wavelet‐based methodology. Data are reported from the last 2‐min of baseline and during the second half of apnea, reflecting the time of highest MSNA.RESULTSThere was an increase in multi‐unit MSNA (24±3 to 35±3 bursts/min, p=0.04) during normoxic apnea, which was due to an increase in the frequency and incidence of AP spikes (243±75 to 519±134 AP/min, p=0.048; 412±133 to 773±185 AP/100 heart beats, p=0.04). An increase in the probability of AP firing more than once per burst was also observed (p=0.01). There was an increase in multi‐unit MSNA (20±4 to 46±7 bursts/min, p<0.01) during hypoxic apnea that was due to an increase in the frequency and incidence of AP spikes (192±59 to 952±266 AP/min, p<0.01; 326±89 to 1212±327 AP/100 heart beats, p<0.01). Hypoxic apnea also resulted in an increase in the probability of AP firing more than once per burst (p<0.01). Hyperoxia attenuated any increase in MSNA with apnea, such that no changes in multi‐unit MSNA (24±4 to 28±5 bursts/min, p=0.14) nor frequency or incidence of AP spikes (155±35 to 253±71 AP/min, p=0.12; 249±61 to 502±188 AP/100 heart beats, p=0.28) were observed. Hyperoxia also attenuated any increase in the probability of AP firing more than once per burst (p=0.47).CONCLUSIONThese data are the first to show neural firing and recruitment strategies in response to voluntary end‐expiratory apnea are modified by hypoxia and hyperoxia. Our results demonstrate that hypoxic apnea increases the frequency and incidence of action potential spikes, as well as the probability of multiple within‐burst firing; whereas this response was suppressed when individuals were hyperoxic. These data may have important implications for neural control of the circulation in recreational activities (i.e. diving) and/or clinical conditions prone to apnea (i.e. sleep apnea).Support or Funding Information FUNDING:AHA #15SDG25080095, NIH HL130339, Natural Sciences and Engineering Research Council of Canada Discovery Grant program.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.