Cerebral autoregulation maintains cerebral blood flow (CBF) despite marked changes in mean arterial pressure (MAP). Sodium nitroprusside (SNP) reduces blood pressure by vasodilatation but is reported to lower CBF, probably by a reduction in its perfusion pressure. We evaluated the influence of SNP on CBF and aimed for a 20% and then 40% reduction in MAP, while keeping MAP ≥ 50 mmHg, to challenge cerebral autoregulation. In 19 healthy men (age 24 ± 4 years; mean ± SD) duplex ultrasound determined right internal carotid (ICA) and vertebral artery (VA) blood flow. The SNP reduced MAP (from 83 ± 8 to 69 ± 8 and 58 ± 4 mmHg; both P < 0.0001), total peripheral resistance, and arterial CO tension (P aC O2; 41 ± 3 vs. 39 ± 3 and 37 ± 4 mmHg; both P < 0.01). Yet ICA flow increased with the moderate reduction in MAP but returned to the baseline value with the large reduction in MAP (336 ± 66 vs. 365 ± 69; P = 0.013 and 349 ± 82 ml min ; n.s.), while VA flow (114 ± 34 vs. 112 ± 38 and 110 ± 42 ml min ; both n.s.) and CBF ((ICA + VA flow) × 2; 899 ± 135 vs. 962 ± 127 and 918 ± 197 ml min ; both n.s.) were maintained with increased cerebrovascular conductance. In conclusion, CBF is maintained during SNP-induced reduction in MAP despite reduced P aC O2 and the results indicate that SNP dilates cerebral vessels and increases ICA flow.

The 2022 asthma guidelines emphasise inhaled long-acting beta2-agonist formoterol as part of first treatment step, and therefore formoterol use among athletes will likely increase. However, prolonged supratherapeutic use of inhaled beta2-agonist impairs training outcomes in moderately-trained men. Here, we investigated whether inhaled formoterol, at therapeutic doses, imposes detrimental effects in endurance-trained individuals of both sexes.Fifty-one endurance-trained participants (31/20 male/female; maximal oxygen consumption(V′O2max): (mean±sd) 62±6/52±5 mLO2/min·kg−1) inhaled formoterol (n=26, 24 µg) or placebo (n=25) twice-daily for 6 weeks. At baseline and follow-up, we assessed V′O2maxand incremental exercise performance during a bike-ergometer ramp-test, body composition by Dual-Energy-X-ray-absorptiometry, muscle oxidative capacity by high-resolution mitochondrial-respirometry, enzymatic activity assays and immunoblotting, intravascular volumes by carbon-monoxide rebreathing, and cardiac left ventricle mass and function by echocardiography.Compared to placebo, formoterol increased lean body mass by 0.7 kg (95%CI: 0.2 to 1.2, treatment×trial p=0.022), but decreased V′O2max5% (treatment×trial p=0.013) and incremental exercise performance 3% (treatment×trial p<0.001). Formoterol also lowered muscle citrate synthase activity 15% (treatment×trial, p=0.063), mitochondrial complex-II and III content (treatment×trial p=0.028 and p=0.007, respectively), and maximal mitochondrial respiration through complex-I and I+II by 14% and 16% (treatment×trial p=0.044 and p=0.017, respectively). No apparent changes were observed in cardiac parameters and intravascular blood volumes. All effects were sex-independent.Our findings demonstrate that inhaled therapeutic doses of formoterol impair aerobic exercise capacity in endurance-trained individuals, which is in part related to impaired muscle mitochondrial oxidative capacity. Thus, if low-dose formoterol fails to control respiratory symptoms in asthmatic athletes, physicians may consider alternative treatment options.

Preload to the heart may be limited during rowing because both blood pressure and central venous pressure increase when force is applied to the oar. Considering that only the recovery phase of the rowing stroke allows for unhindered venous return, rowing may induce large fluctuations in stroke volume (SV). Thus, the purpose of this study was to evaluate SV continuously during the rowing stroke. Eight nationally competitive oarsmen (mean ± standard deviation: age 21 ± 2 years, height 190 ± 9 cm, and weight 90 ± 10 kg) rowed on an ergometer at a targeted heart rate of 130 and 160 beats per minute. SV was derived from arterial pressure waveform by pulse contour analysis, while ventilation and force on the handle were measured. Mean arterial pressure was elevated during the stroke at both work rates (to 133 ± 10 [P < .001] and 145 ± 11 mm Hg [P = .024], respectively). Also, SV fluctuated markedly during the stroke with deviations being largest at the higher work rate. Thus, SV decreased by 27 ± 10% (31 ± 11 mL) at the beginning of the stroke and increased by 25 ± 9% (28 ± 10 mL) in the recovery (P = .013), while breathing was entrained with one breath during the drive of the stroke and one prior to the next stroke. These observations indicate that during rowing cardiac output depends critically on SV surges during the recovery phase of the stroke.

Arterial thrombosis is the primary cause of death worldwide, with the most important risk factors being smoking, unhealthy diet, and physical inactivity. However, although there are clear indications in the literature of beneficial effects of physical activity in lowering the risk of cardiovascular events, exercise can be considered a double-edged sword in that physical exertion can induce an immediate pro-thrombotic environment. Epidemiological studies show an increased risk of cardiovascular events after acute exercise, a risk, which appear to be particularly apparent in individuals with lifestyle-related disease. Factors that cause the increased susceptibility to arterial thrombosis with exercise are both chemical and mechanical in nature and include circulating catecholamines and vascular shear stress. Exercise intensity plays a marked role on such parameters, and evidence in the literature accordingly points at a greater susceptibility to thrombus formation at high compared to light and moderate intensity exercise. Of importance is, however, that the susceptibility to arterial thrombosis appears to be lower in exercise-conditioned individuals compared to sedentary individuals. There is currently limited data on the role of acute and chronic exercise on the susceptibility to arterial thrombosis, and many studies include incomplete assessments of thrombogenic clotting profile. Thus, further studies on the role of exercise, involving valid biomarkers, are clearly warranted.

Hemorrhage is a leading cause of battlefield and civilian trauma deaths. Several pain medications, including fentanyl, are recommended for use in the prehospital (i.e., field setting) for a hemorrhaging solider. However, it is unknown whether fentanyl impairs arterial blood pressure (BP) regulation, which would compromise hemorrhagic tolerance. Thus, the purpose of this study was to test the hypothesis that an analgesic dose of fentanyl impairs hemorrhagic tolerance in conscious humans. Twenty-eight volunteers (13 females) participated in this double-blinded, randomized, placebo-controlled trial. We conducted a pre-syncopal limited progressive lower-body negative pressure test (LBNP; a validated model to simulate hemorrhage) following intravenous administration of fentanyl (75 µg) or placebo (saline). We quantified tolerance as a cumulative stress index (mmHg•min), which was compared between trials using a paired, two-tailed t-test. We also compared muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat BP (photoplethysmography) during the LBNP test using a mixed effects model (time [LBNP stage] x trial). LBNP tolerance was not different between trials (Fentanyl: 647 ± 386 vs. Placebo: 676 ± 295 mmHg•min, P=0.61, Cohen's d = 0.08). Increases in MSNA burst frequency (time: p<0.01, trial: p=0.29, interaction: p=0.94) and reductions in mean BP (time: p<0.01, trial: p=0.50, interaction: p=0.16) during LBNP were not different between trials. These data, the first to be obtained in conscious humans, demonstrate that administration of an analgesic dose of fentanyl does not alter MSNA or BP during profound central hypovolemia, nor does it impair tolerance to this simulated hemorrhagic insult.

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Introduction Although evaporative heat loss capacity is reduced in burn-injured individuals with extensive skin grafts, the thermoregulatory strain due to a prior burn injury during exercise-heat stress may be negligible if the burn is located underneath protective clothing with low vapor permeability. Purpose This study aimed to test the hypothesis that heat strain during exercise in a hot–dry environment while wearing protective clothing would be similar with and without a simulated torso burn injury. Methods Ten healthy individuals (8 men/2 women) underwent three trials wearing: uniform (combat uniform, tactical vest, and replica torso armor plates), uniform with a 20% total body surface area simulated torso burn (uniform + burn), or shorts (and sports bra) only (control). Exercise consisted of treadmill walking (5.3 km·h−1; 3.7% ± 0.9% grade) for 60 min at a target heat production of 6.0 W·kg−1 in 40.0°C ± 0.1°C and 20.0% ± 0.6% relative humidity conditions. Measurements included rectal temperature, heart rate, ratings of perceived exertion (RPE), and thermal sensation. Results No differences in rectal temperature (P ≥ 0.85), heart rate (P ≥ 0.99), thermal sensation (P ≥ 0.73), or RPE (P ≥ 0.13) occurred between uniform + burn and uniform trials. In the control trial, however, core temperature, heart rate, thermal sensation, and RPE were lower compared with the uniform and uniform + burn trials (P ≤ 0.04 for all). Conclusions A 20% total body surface area simulated torso burn injury does not further exacerbate heat strain when wearing a combat uniform. These findings suggest that the physiological strain associated with torso burn injuries is not different from noninjured individuals when wearing protective clothing during an acute exercise-heat stress.

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