Multi-sensor integration systems for the tactical combat pilot.
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Biomedical subjects
Publications and source records attributed to David G Newman.
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BACKGROUND: The cardiovascular system is highly adaptable to sustained +Gz acceleration. Little is known as to whether the cardiovascular system can adapt to acute, repetitive +Gz exposures. This study tested the hypothesis that the cardiovascular system would adapt to repeated orthostatic challenges in a single session. METHODS: Over a 70-min period, 14 subjects were exposed to 10 +75 degrees head-up tilts (HUT). Each tilt involved a 5-min supine period followed by a 2-min HUT. Heart rate (HR), systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), total peripheral resistance (TPR), stroke volume (SV), and cardiac output (CO) were determined non-invasively. Cardiovascular responses to HUT10 for the final 30 s of the supine period and the first 30 s of the tilt period were compared with those of HUT1. Integrated cardiac baroreflex sensitivity (BRS) was assessed using the Valsalva maneuver. RESULTS: MAP and DBP increased in both supine (MAP p = 0.009, DBP p = 0.002) and tilt periods (MAP p = 0.003, DBP p = 0.009) for HUT10 compared with HUT1. TPR increased during the tilt period only (p = 0.001) during HUT10 compared with HUT1. CO and SV were decreased during the supine period at HUT10 relative to HUT1; however, there were no differences in the tilt period at HUT10 for either CO or SV. There was no change in the response of BRS, HR, or SBP from HUT1 to HUT10. CONCLUSIONS: This study indicates that 10 repetitive HUTs can elicit changes in the cardiovascular responses to orthostasis, reflected by an increased vascular resistance.
INTRODUCTION: The cardiovascular system is adaptable to multiple exposures to gravity over several days, and to repeated exposures in a single day. This study aimed to investigate if the cardiovascular adaptation observed following 10 +75 degrees head-up tilts (HUT) would improve the responses to the squat-stand test (SST). METHODS: There were 16 subjects who were randomly allocated into either a tilting group that underwent 10 +75 degrees HUTs in 70 min (Tilting) or a control group that underwent 70 min of rest (Control). Before and after HUT or rest, subjects performed a SST (SST1 and SST2, respectively). Heart rate (HR), BP [systolic (SBP), diastolic (DBP), mean (MAP)], total peripheral resistance (TPR), stroke volume (SV), and cardiac output (CO) were determined during both SSTs. The final 30 s of squat and the first 30 s of stand (divided into three 10-s blocks termed Stand10, Stand20, and Stand30) were compared between SST1 and SST2. RESULTS: In the Tilting condition, during the squat phase of SST2, the following were significantly elevated: SBP (131 +/- 9 to 140 +/- 7.2 mmHg) and MAP (94 +/- 8.7 to 105 +/- 10.2 mmHg); DBP (76 +/- 9.4 to 87 +/- 11.9 mmHg); TPR (1197 +/- 524.6 to 229 +/- 610.5 dyn x s(-1) x cm(-5)) and HR were significantly decreased (78 +/- 6.9 to 73 +/- 7.5 bpm) compared with SST1. At Stand10, DBP and MAP were significantly increased (59 +/- 9.5 to 69 +/- 15.7 mmHg and 74 +/- 8.9 to 84 +/- 14.7 mmHg, respectively); at Stand20, SBP was increased (121 +/- 17 to 128 +/- 22 mmHg); and at Stand30 the following were increased: DBP (64 +/- 8.8 to 75 +/- 16.1 mmHg); SBP (127 +/- 9.2 to 139 +/- 15.8 mmHg); and MAP (79 +/- 8 to 90 +/- 14.9 mmHg). There were no differences observed between SST1 and SST2 in the Control group. DISCUSSION: Cardiovascular responses to the SST can be improved with 10 consecutive +75 degrees HUTs. This is predominantly due to an increase in DBP, indicative of a change in vascular resistance.
INTRODUCTION: Only one previous study has assessed almost loss of consciousness (A-LOC) in operational fighter pilots, reporting an incidence rate of 14%. Research also indicates that 8-13% of pilots have experienced G-induced loss of consciousness (G-LOC). A-LOC can be as insidious as G-LOC due to the associated altered state of awareness and relative incapacitation time, making it a significant risk factor in the high +Gz environment. Royal Australian Air Force (RAAF) pilots currently fly the F/A-18 and Hawk 127, producing +Gz accelerations up to +7.5 Gz, which places these pilots at risk of both A-LOC and G-LOC. METHODS: A survey was administered to 100 active RAAF fighter pilots requesting information on G-induced visual and cognitive disturbances, A-LOC symptoms, and G-LOC. Details regarding type of aircraft, flying maneuvers performed and mission outcome were also sought. RESULTS: There were 65 RAAF fighter pilots who completed the survey (age 20-53 yr, height 168-193 cm, weight 64-110 kg, jet hours 30-5700 h). Of these pilots, 98% indicated they had experienced at least one visual or cognitive disturbance in the high G environment: gray-out 98%; black-out 29%; and A-LOC symptoms 52%, including abnormal sensation in limbs, disorientation, and confusion. There were 9% who indicated they had experienced G-LOC (50% were the pilot flying the aircraft). DISCUSSION: These findings indicate that RAAF fighter pilots are experiencing a similar rate of visual disturbances and G-LOC when compared with other air forces. However, RAAF pilots reported a much higher incidence of A-LOC compared with the only other study of operational fighter pilots.
The physiological differences between active and passive changes in posture have been previously established. This study determined the extent of the differences in the initial cardiovascular responses to the passive head-up tilt (HUT) and the active squat-stand test (SST). Eleven females and 13 males underwent one +75 degrees HUT and one SST. Beat-to-beat diastolic blood pressure (DBP), systolic blood pressure (SBP), mean arterial pressure (MAP) and heart rate (HR) were determined non-invasively. Data were recorded 10 s prior to (control) and 30 s after tilt or stand (event). Blood pressure and HR responses were analysed by calculating the deviation from control at 10 s (T10), 20 s (T20) and 30 s (T30) after the onset of each test. The DBP response (reflecting changes in systemic vascular resistance) at T10 was -10 (2) mmHg [mean (SEM)] for the HUT and -25 (2) mmHg for the SST ( P<0.01). DBP returned to control levels by T30 for the HUT, but remained depressed for the SST. MAP responses directly reflected these changes in DBP. HR significantly increased from control values ( P<0.001) for the HUT [+14 (1) bpm] and the SST [+16 (1) bpm], and remained elevated for the entire 30-s period for both tests. This study demonstrates that although the magnitude of the initial blood pressure decrease is greater for the active SST compared with the passive HUT, the reflex compensatory response is no different, making the SST a greater challenge for the cardiovascular reflexes.
We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TG(m)) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O(2) uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TG(m) were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P < 0.05) than in OLD, YOUNG, and TRAINED. TG(m) was elevated in TYPE 2 compared with all other groups (P < 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P < 0.01), whereas beta-hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P < 0.001; beta-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P < 0.05). In conclusion, despite markedly elevated skeletal muscle TG(m) in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TG(m) concentration or long-chain fatty acyl CoA content.
BACKGROUND: Both caffeine and orthostasis have known cardiovascular effects. The possible interaction between these factors remains unknown. This study aimed to determine the effect of caffeine consumption on cardiovascular responses to head-up tilt. METHODS: Sixteen subjects underwent three +75 degree head-up tilts: i) control, ii) acute, after a dose of 5 mg x kg(-1) body mass of caffeine or placebo, and iii) chronic, following 7 d of caffeine or placebo consumption at a daily dose of 5 mg x kg(-1) body mass. Heart rate (HR), systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) were measured using a Portapres BP monitor. RESULTS: The overall pattern of heart rate (HR) response in both caffeine and placebo groups showed a significant increase in HR after tilting for each tilt. Acute caffeine consumption significantly decreased resting HR (p < 0.05). After chronic consumption, resting HR was no longer significantly different. In the control condition, the overall pattern of response to tilt for SBP, DBP, and MAP showed no significant differences in either group. An acute dose of caffeine caused a significant fall (p < 0.05) in all BP variables in response to tilt. This effect was also seen after chronic caffeine consumption in SBP and MAP, but not in DBP. CONCLUSIONS: The results of this study indicate that both acute and chronic consumption of caffeine can lead to impaired cardiovascular function after exposure to an orthostatic challenge. This impaired function, reflected in a decreased resting HR and an inability to maintain MAP, is potentially due to impaired baroreflex function.
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BACKGROUND: Altitude-induced hypoxia is believed to decrease tolerance to orthostasis. This preliminary investigation assesses the interaction between low-level normobaric hypoxia and the cardiovascular responses to orthostasis. HYPOTHESIS: We hypothesize that low-level hypoxia at simulated altitudes up to 3350 m adversely affects cardiovascular responses to orthostasis. METHODS: Six women and eight men underwent + 75 degrees head-up tilt (HUT) at 3 simulated altitudes (115 m (377 ft), 1680 m (5500 ft) and 3350 m (11,000 ft)). Minute ventilation (VE), tidal volume (VT), breathing frequency (f), heart rate (HR), and arterial blood pressure (BP) were measured non-invasively. Ventilatory parameters (VE, VT, and f) were measured during the control period to assess the respiratory response to hypoxia. Cardiovascular variables (HR and BP) during HUT were compared and analyzed by calculating the deviation from control (pre-tilt) values. RESULTS: Respiratory data showed no significant hypoxic ventilatory response. The average HR deviation significantly decreased (p < 0.05) with HUT from 13 +/- 2 bpm (115 m) to 9 +/- 2 bpm (3350 m). The pattern of mean arterial BP deviation with HUT was similar across the three altitudes (-6.6 +/- 2.9 mm Hg at 115 m to -6.8 +/- 2.4 mm Hg at 3350 m), with no significant differences. CONCLUSIONS: Changes in HR and arterial BP are fundamental aspects of the cardiovascular response to orthostatic stress. Although there were no significant changes in the BP response to orthostasis with hypoxia, the HR changes seen in this study suggest that the ability to modulate HR under orthostatic stress is reduced with exposure to low-level normobaric hypoxia.
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This report describes a case of central serous retinopathy (CSR) in the right eye of a commercial air transport pilot which resulted in a permanent reduction in visual acuity and the loss of his license. The previously fit and well pilot developed sudden loss of central vision, which resolved spontaneously. He then went on to experience recurrent episodes of fluctuating visual acuity (down to 6/60) and visual dysfunction in the right eye. His left eye remained unaffected. Eventually his condition stabilized, and he was left with a permanent reduction in right visual acuity (6/36) with intact peripheral visual fields and a completely normal left eye. After a period of grounding of 12 mo, he sought to have his license reinstated. He was considered to be a functionally monocular pilot, and as such was granted a conditional Class 1 medical category. The aeromedical disposition of this pilot and the issues involved in determining the fitness to fly of pilots with permanent visual defects arising from CSR are discussed.