Intensified training augments cardiac function, but not blood volume, in male youth elite ice hockey team players.

While it is well-established that a period of interval training performed at near maximal effort, such as speed endurance training (SET), enhances intense exercise performance in well-trained individuals, less is known about its effect on cardiac morphology and function as well as blood volume. To investigate this, we subjected 12 Under-20 Danish national team ice hockey players (age 18 ± 1 years, mean ± SD) to 4 weeks of SET, consisting of 6-10 × 20 s skating bouts at maximal effort interspersed by 2 min of recovery conducted three times weekly. This was followed by 4 weeks of regular training (follow-up). We assessed resting cardiac function and dimensions using transthoracic echocardiography and quantified total blood volume with the carbon monoxide rebreathing technique at three time points: before SET, after SET and after the follow-up period. After SET, stroke volume had increased by 10 (2-18) mL (mean (95% CI)), left atrial end-diastolic volume by 10 (3-17) mL, and circumferential strain improved by 0.9%-points (1.7-0.1) (all P < 0.05). At follow-up, circumferential strain and left atrial end-diastolic volume were reverted to baseline levels, while stroke volume remained elevated. Blood volume and morphological parameters for the left ventricle, including mass and end-diastolic volume, did not change during the study. In conclusion, our findings demonstrate that a brief period of SET elicits beneficial central cardiac adaptations in elite ice hockey players independent of changes in blood volume.

Performance and Fatigue Patterns in Elite Cyclists During 6 h of Simulated Road Racing.

Fatigue resistance is vital for success in elite road cycling, as repeated, intense efforts challenge the athletes' ability to sustain peak performance throughout prolonged races. The present study combined recurrent performance testing and physiological measures during 6 h simulated racing with laboratory testing to investigate factors influencing fatigue resistance. Twelve male national elite cyclists (25 ± 3 years; 76 ± 6 kg and VO2max of 5.2 ± 0.5 L/min) completed incremental power and maximal fat oxidation tests. Subsequently, they underwent field testing with physiological measures and fatigue responses evaluated through peak sprint power and 5 km time trial (TT) testing after 0, 2, 4, and 6 h of exercise. Peak power declined from 1362 ± 176 W in first sprint to 1271 ± 152 W after 2 h (p < 0.01) and then stabilized. In contrast, TT mean power gradually declined from 412 ± 38 W in the first TT to 384 ± 41 W in the final trial, with individual losses ranging from 2% to 14% and moderately correlated (r2 = 0.45) to accumulated exercise time above lactate threshold. High carbohydrate intake (~90 g/h) maintained blood glucose levels, but post-TT [lactate] decreased from 15.1 ± 2 mM to 7.1 ± 2.3 mM, while fat oxidation increased from 0.7 ± 0.3 g/min at 0 h to 1.1 ± 0.1 g/min after 6 h. The study identifies fatigue patterns in national elite cyclists. Peak sprint power stabilized after an initial impairment from 0 to 2 h, while TT power gradually declined over the 6 h simulated race, with increased differentiation in fatigue responses among athletes.

Burn size and environmental conditions modify thermoregulatory responses to exercise in burn survivors.

This project tested the hypothesis that burn survivors can perform mild/moderate-intensity exercise in temperate and hot environments without excessive elevations in core body temperature. Burn survivors with low (23 ± 5%TBSA; N = 11), moderate (40 ± 5%TBSA; N = 9), and high (60 ± 8%TBSA; N = 9) burn injuries performed 60 minutes of cycle ergometry exercise (72 ± 15 watts) in a 25°C and 23% relative humidity environment (ie, temperate) and in a 40°C and 21% relative humidity environment (ie, hot). Absolute gastrointestinal temperatures (TGI) and changes in TGI (ΔTGI) were obtained. Participants with an absolute TGI of >38.5°C and/or a ΔTGI of >1.5°C were categorized as being at risk for hyperthermia. For the temperate environment, exercise increased ΔTGI in all groups (low: 0.72 ± 0.21°C, moderate: 0.42 ± 0.22°C, and high: 0.77 ± 0.25°C; all P < .01 from pre-exercise baselines), resulting in similar absolute end-exercise TGI values (P = .19). Importantly, no participant was categorized as being at risk for hyperthermia, based upon the aforementioned criteria. For the hot environment, ΔTGI at the end of the exercise bout was greater for the high group when compared to the low group (P = .049). Notably, 33% of the moderate cohort and 56% of the high cohort reached or exceeded a core temperature of 38.5°C, while none in the low cohort exceeded this threshold. These data suggest that individuals with a substantial %TBSA burned can perform mild/moderate intensity exercise for 60 minutes in temperate environmental conditions without risk of excessive elevations in TGI. Conversely, the risk of excessive elevations in TGI during mild/moderate intensity exercise in a hot environment increases with the %TBSA burned.

Exercise training induces thrombogenic benefits in recent but not late postmenopausal females.

Although regular physical activity is known to improve cardiovascular health in men, evidence for its beneficial effects in postmenopausal females is less convincing and it remains unclear whether initiation of exercise training soon after, rather than many years after menopause impacts the magnitude of training-induced adaptations. We evaluated exercise-induced changes in markers of thrombotic risk and conduit artery function in recent≤5yr compared with late≥10yr postmenopausal females. Fourteen recent≤5yr and 13 late≥10yr healthy postmenopausal females completed 8 wk of regular intensive exercise training, consisting of floorball and cycling. Markers of thrombotic risk and vascular health were assessed before and after the intervention, and data were analyzed using a linear mixed model. Exercise training reduced markers of thrombotic risk, including an 11% reduction (P = 0.007) in agonist-induced platelet reactivity and a reduction (P = 0.027) in incipient clot microstructure (∼40% reduction in clot mass) in the recent≤5yr but not the late≥10yr (P = 0.380; P = 0.739, respectively) postmenopausal females. There was no change in conduit artery function, as measured by brachial (recent≤5yr, P = 0.804; late≥10yr, P = 0.311) and popliteal artery (recent≤5yr, P = 0.130; late≥10yr, P = 0.434) flow-mediated dilation. Only the late≥10yr postmenopausal females exhibited an increase (by 9.6%, P = 0.022) in intracellular adhesion molecule-1 levels after training, which may have impacted the thrombogenic adaptation in this group. These findings suggest that 8 wk of high-intensity exercise training reduces thrombotic risk in recent≤5yr, but not late≥10yr postmenopausal females. Thus, regular physical activity initiated soon after, rather than many years after menopause and at a higher age, may be more efficient for reducing thrombogenic risk.NEW & NOTEWORTHY Eight weeks of high-intensity exercise training reduces platelet reactivity as well as blood clot density and strength in females ≤5 yr past menopause but not in females ≥10 yr past menopause. The divergent response in the late postmenopausal females may be explained by training-induced low-grade systemic inflammation. These findings suggest that regular physical activity initiated soon after menopause, compared with many years after menopause, may be more efficient for reducing the risk of blood clots.

Inhaled formoterol impairs aerobic exercise capacity in endurance-trained individuals: a randomised controlled trial.

Background: The 2022 Global Initiative for Asthma guidelines emphasise the inhaled long-acting ß2-agonist formoterol as part of the first treatment step, and therefore formoterol use among athletes will probably increase. However, prolonged supratherapeutic use of inhaled ß2-agonists impairs training outcomes in moderately trained men. We investigated whether inhaled formoterol, at therapeutic doses, imposes detrimental effects in endurance-trained individuals of both sexes. Methods: 51 endurance-trained participants (31 male, 20 female; mean±sd maximal oxygen consumption (V̇ O2 max) 62±6 mL·min-1·kg bw-1 and 52±5 mL·min-1·kg bw-1, respectively) inhaled formoterol (24 µg; n=26) or placebo (n=25) twice daily for 6 weeks. At baseline and follow-up, we assessed V̇ O2 max and 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. Results: Compared to placebo, formoterol increased lean body mass by 0.7 kg (95% CI 0.2-1.2 kg; treatment×trial p=0.022), but decreased V̇ O2 max by 5% (treatment×trial p=0.013) and incremental exercise performance by 3% (treatment×trial p<0.001). In addition, formoterol lowered muscle citrate synthase activity by 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 complexes 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. Conclusion: 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.

Altered cardiac ß1 responsiveness in hyperthermic older adults.

Compared with younger adults, passive heating induced increases in cardiac output are attenuated by ∼50% in older adults. This attenuated response may be associated with older individuals' inability to maintain stroke volume through ionotropic mechanisms and/or through altered chronotropic mechanisms. The purpose of this study was to identify the interactive effect of age and hyperthermia on cardiac responsiveness to dobutamine-induced cardiac stimulation. Eleven young (26 ± 4 yr) and 8 older (68 ± 5 yr) participants underwent a normothermic and a hyperthermic (baseline core temperature +1.2°C) trial on the same day. In both thermal conditions, after baseline measurements, intravenous dobutamine was administered for 12 min at 5 µg/kg/min, followed by 12 min at 15 µg/kg/min. Primary measurements included echocardiography-based assessments of cardiac function, gastrointestinal and skin temperatures, heart rate, and mean arterial pressure. Heart rate responses to dobutamine were similar between groups in both thermal conditions (P > 0.05). The peak systolic mitral annular velocity (S'), i.e., an index of left ventricular longitudinal systolic function, was similar between groups for both thermal conditions at baseline. While normothermic, the increase in S' between groups was similar with dobutamine administration. However, while hyperthermic, the increase in S' was attenuated in the older participants with dobutamine (P < 0.001). Healthy, older individuals show attenuated inotropic, but maintained chronotropic responsiveness to dobutamine administration during hyperthermia. These data suggest that older individuals have a reduced capacity to increase cardiomyocyte contractility, estimated by changes in S', via ß1-adrenergic mechanisms while hyperthermic.

Low-dose fentanyl does not alter muscle sympathetic nerve activity, blood pressure, or tolerance during progressive central hypovolemia.

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 presyncopal 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) × 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.

Results for World Rowing Federation and Olympic events 1893-2019.

Results in rowing have improved and here we estimate results for Olympic and World rowing championships based on the winning results from 1893 to 2019 obtained in the current seven Olympic events for men (n = 556) and women (n = 239). Data were collected from the official World Rowing Federation online records and from published results and the development analysed by linear regression analysis for the year of competition. Results improved by about 0.7 s per year (15 ± 9.4%) (mean ± SD). Depending on the event, 2020 predicted mean time for the winning boat for men is 363 s (range 326-397) vs. 404 s (362-439) for women (10.3 ± 1.1% slower). The ten-year coefficient of variance for the original boats in Olympic and World Rowing Federation regatta remaining within the Olympic programme, single scull and eight, decreased from 9 ± 2% (1893-1903) to 2 ± 0.4% (2009-2019). Reduced variability in winning times illustrates the standardization of the rowing course and boats, and the improvement in performance point to that body size becomes ever more important for success in competitive rowing.

Thermoregulatory Responses with Size-matched Simulated Torso or Limb Skin Grafts.

PURPOSE: This study aimed to test the hypothesis that a simulated burn injury on the torso will be no more or less detrimental to core temperature control than on the limbs during uncompensable exercise-heat stress. METHODS: Nine nonburned individuals (7 men, 2 women) completed the protocol. On separate occasions, burn injuries of identical surface area (0.45 ± 0.08 m2 or 24.4% ± 4.4% of total body surface area) were simulated on the torso or the arms/legs using an absorbent, vapor-impermeable material that impedes sweat evaporation in those regions. Participants performed 60 min of treadmill walking at 5.3 km·h-1 and a 4.1% ± 0.8% grade, targeting 6 W·kg-1 of metabolic heat production in 40.1°C ± 0.2°C and 19.6% ± 0.6% relative humidity conditions. Rectal temperature, heart rate, and perceptual responses were measured. RESULTS: Rectal temperature increased to a similar extent with simulated injuries on the torso and limbs (condition-by-time interaction, P = 0.86), with a final rectal temperature 0.9°C ± 0.3°C above baseline in both conditions. No differences in heart rate, perceived exertion, or thermal sensation were observed between conditions (condition-by-time interactions, P ≥ 0.50). CONCLUSIONS: During uncompensable exercise-heat stress, sized-matched simulated burn injuries on the torso or limbs evoke comparable core temperature, heart rate, and perceptual responses, suggesting that the risk of exertional heat illness in such environmental conditions is independent of injury location.

Does Exercise Influence the Susceptibility to Arterial Thrombosis? An Integrative Perspective.

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.

Fluctuations in cardiac stroke volume during rowing.

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.

Burn Injury Does Not Exacerbate Heat Strain during Exercise while Wearing Body Armor.

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; 3.7% ± 0.9% grade) for 60 min at a target heat production of 6.0 W·kg 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.

Sodium nitroprusside dilates cerebral vessels and enhances internal carotid artery flow in young men.

KEY POINTS: Sodium nitroprusside lowers blood pressure by vasodilatation but is reported to reduce cerebral blood flow. In healthy young men sodium nitroprusside reduced blood pressure, total peripheral resistance, and arterial CO2 tension and yet cerebral blood flow was maintained, with an increase in internal carotid artery blood flow and cerebrovascular conductance. Sodium nitroprusside induces both systemic and cerebral vasodilatation affecting internal carotid artery more than vertebral artery flow. ABSTRACT: 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 CO2 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-1 ; n.s.), while VA flow (114 ± 34 vs. 112 ± 38 and 110 ± 42 ml min-1 ; both n.s.) and CBF ((ICA + VA flow) × 2; 899 ± 135 vs. 962 ± 127 and 918 ± 197 ml min-1 ; 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.