Interactive effects of exercise intensity and recovery posture on postexercise hypotension.

Postexercise reduction in blood pressure, termed postexercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a V̇o2max test on a cycle ergometer and five exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with 1 h of recovery in each of the three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic [standing: -33 (11) vs. -21 (8) mmHg; seated: -34 (32) vs. -17 (37) mmHg, P < 0.01], diastolic [standing: -18 (7) vs. -8 (5) mmHg; seated: -10 (10) vs. -1 (4) mmHg, P < 0.01], and mean arterial pressures [-13 (8) vs. -2 (4) mmHg, P < 0.01], whereas in the supine recovery posture, the reduction in diastolic [-9 (9) vs. -4 (3) mmHg, P = 0.08) and mean arterial pressures [-7 (5) vs. -3 (4) mmHg, P = 0.06] was not consistently affected by prior exercise intensity. PEH is more pronounced during recovery from exercise performed above CP versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.NEW & NOTEWORTHY The magnitude of postexercise hypotension is greater following the intensity above the critical power in a standing position.

Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans.

Intermittent fasting and exercise provide neuroprotection from age-related cognitive decline. A link between these two seemingly distinct stressors is their capability to steer the brain away from exclusively glucose metabolism. This cerebral substrate switch has been implicated in upregulating brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie some of these neuroprotective effects. We examined the isolated and interactive effects of (1) 20-h fasting, (2) 90-min light exercise, and (3) high-intensity exercise on peripheral venous BDNF in 12 human volunteers. A follow-up study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 h decreased glucose and increased ketones (P ≤ 0.0157) but had no effect on BDNF (P ≥ 0.4637). Light cycling at 25% of peak oxygen uptake ( V ̇ O 2 peak ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ ) increased serum BDNF by 6 ± 8% (independent of being fed or fasted) and was mediated by a 7 ± 6% increase in platelets (P < 0.0001). Plasma BDNF was increased from 336 pg l-1 [46,626] to 390 pg l-1 [127,653] by 90-min of light cycling (P = 0.0128). Six 40-s intervals at 100% of V ̇ O 2 peak ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ increased plasma and serum BDNF, as well as the BDNF-per-platelet ratio 4- to 5-fold more than light exercise did (P ≤ 0.0044). Plasma BDNF was correlated with circulating lactate during the high-intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407). Changes in cerebral shear stress - whether occurring naturally during exercise or induced experimentally with inspired CO2 - did not correspond with changes in BDNF (P ≥ 0.2730). BDNF responses to low-intensity exercise are mediated by increased circulating platelets, and increasing either exercise duration or particularly intensity is required to liberate free BDNF. KEY POINTS: Intermittent fasting and exercise both have potent neuroprotective effects and an acute upregulation of brain-derived neurotrophic factor (BDNF) appears to be a common mechanistic link. Switching the brain's fuel source from glucose to either ketone bodies or lactate, i.e. a cerebral substrate switch, has been shown to promote BDNF production in the rodent brain. Fasting for 20 h caused a 9-fold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest. Prolonged (90 min) light cycling exercise increased plasma- and serum-derived BDNF irrespective of being fed or fasted and seemed to be independent of changes in cerebral shear stress. Six minutes of high-intensity cycling intervals increased every metric of circulating BDNF by 4 to 5 times more than prolonged low-intensity cycling; the increase in plasma-derived BDNF was correlated with a 6-fold increase in circulating lactate irrespective of feeding or fasting. Compared to 1 day of fasting with or without prolonged light exercise, high-intensity exercise is a much more efficient means to increase BDNF in circulation.

The athlete's vein: venous adaptations in the lower limbs of endurance athletes.

Endurance exercise induces cardiovascular adaptations; the athletic phenotypes of the heart and arteries are well characterized, but few studies have investigated the effects of chronic exercise on the venous system. The aim of this study was to describe the anatomy and function of lower-limb deep and superficial veins in athletes compared with controls. Endurance-trained athletes and untrained controls (13 males, 7 females per group) were examined using ultrasound to measure vein diameter and flow, and air plethysmography to assess calf venous volume dynamics and muscle pump function at rest, during a single step, ambulation (10 steps) and after acute treadmill exercise (30 min ∼80% age-predicted heart rate maximum). Diameters of three of the seven deep veins assessed were larger in athletes (P ≤ 0.0167) and more medial calf perforators were detectable (5 vs. 3, P = 0.0039). Calf venous volume was 22% larger in athletes (P = 0.0057), and calf muscle pump ejection volume and ambulatory venous volume after 10 steps were both greater in athletes (20 and 46% respectively, P ≤ 0.0482). Following acute exercise, flow recovery profiles in deep and superficial veins draining the leg were not different between groups, despite athletes performing approximately four times more work. After exercise, venous volume and ejection volume were reduced by ∼20% in athletes with no change in controls (interaction, P ≤ 0.0372) and although ambulatory venous volume reduced, this remained greater in athletes. These findings highlight venous adaptations that compensate for the demands of regular endurance exercise, all of which are suited to enhance flow through the lower-limb venous system.NEW & NOTEWORTHY Although much literature exists describing adaptations to the heart and arteries in response to endurance exercise training, less is known about the effects on the venous system. Characteristics of "the athlete's vein" described here include deep and perforator vein remodeling, improved drainage, and greater calf venous volume at rest and on calf muscle pump activation. Following exercise, athletes demonstrated prompt flow recovery and appropriate volume reductions, and veins beneficially adapt to better tolerate the demands of regular physical activity.

Delineating the impacts of air temperature and humidity for endurance exercise.

NEW FINDINGS: What is the central question of this study? What are the independent effects of air temperature and humidity on performance, physiological and perceptual responses during endurance exercise? What is the main finding and its importance? When examined independently, elevated air temperature increased heat strain and impaired aerobic exercise performance, but to a lesser extent than has been reported previously. These findings highlight the importance of absolute humidity relative to temperature when exercising or working under severe heat stress. ABSTRACT: Many studies have reported that ambient heat stress increases physiological and perceptual strain and impairs endurance exercise, but effects of air temperature per se remain almost unexamined. Most studies have used matched relative humidity, thereby exponentially increasing absolute humidity (water content in air) concurrently with temperature. Absolute (not relative) humidity governs evaporative rate and is more important at higher work rates and air temperatures. Therefore, we examined the independent effects of air temperature and humidity on performance, thermal, cardiovascular and perceptual measures during endurance exercise. Utilizing a crossover design, 14 trained participants (7 females) completed 45 min fixed-intensity cycling (70% V ̇ O 2 peak ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ ) followed by a 20-km time trial in each of four environments: three air temperatures at matched absolute humidity (Cool, 18°C; Moderate, 27°C; and Hot, 36°C; at 1.96 kPa, air velocity ∼4.5 m/s), and one at elevated humidity (Hot Humid, 36°C at 3.92 kPa). Warmer air caused warmer skin (0.5°C/°C; P < 0.001), higher heart rate (1 bpm/°C; P < 0.001), sweat rate (0.04 l/h/°C; P < 0.001) and thermal perceptions during fixed-intensity exercise, but minimally affected core temperature (<0.01°C/°C; P = 0.053). Time-trial performance was comparable between Cool and Moderate (95% CI: -1.4, 5.9%; P = 0.263), but 3.6-6% slower in Hot (95% CI: ±2.4%; P ≤ 0.006). Elevated humidity increased core temperature (P < 0.001), perceived temperature and discomfort but not skin temperature or heart rate, and reduced mean blood pressure (P = 0.046) during fixed-intensity exercise. Elevated humidity impaired time-trial performance by 3.4% (95% CI: ±2.2%; P = 0.006). In conclusion, these findings quantify the importance of absolute humidity alongside air temperature when exercising under severe heat stress.

Physiological relationship between cardiorespiratory fitness and fitness for surgery: a narrative review.

Epidemiological evidence has highlighted a strong relationship between cardiorespiratory fitness and surgical outcomes; specifically, fitter patients possess heightened resilience to withstand the surgical stress response. This narrative review draws on exercise and surgical physiology research to discuss and hypothesise the potential mechanisms by which higher fitness affords perioperative benefit. A higher fitness, as indicated by higher peak rate of oxygen consumption and ability to sustain metabolic homeostasis (i.e. higher anaerobic threshold) is beneficial postoperatively when metabolic demands are increased. However, the associated adaptations with higher fitness, and the related participation in regular exercise or physical activity, might also underpin the observed perioperative benefit through a process of hormesis, a protective adaptive response to the moderate and intermittent stress of exercise. Potential mediators discussed include greater antioxidant capacity, metabolic flexibility, glycaemic control, lean body mass, and improved mood.

Energetic and Cognitive Demands of Treading Water: Effects of Technique and Expertise.

Being able to tread water effectively can improve the likelihood of survival following accidental immersion. People tread water in various ways, ranging from rudimentary 'doggy-paddle' to more elaborate techniques like the eggbeater, but little is known about the energetic and cognitive requirements of treading water. We therefore aimed to measure the demands of treading water techniques for people of different experience levels. Three cohorts, comprising 21 adult water treading experts (water polo players), 15 intermediate swimmers and 16 inexperienced swimmers, treaded water for 3 min each using four different techniques while cognitive and energetic economy measures were taken. For inexperienced swimmers, the flutter kick and breaststroke patterns produced the lowest self-reported physical and task load (rating of perceived exertion, NASA task load index), while cognitive (probe reaction time), cardiac (heart rate) and metabolic (oxygen consumption) load did not differ between techniques. In contrast, for expert water treaders, both breaststroke and eggbeater patterns produced lower cognitive, cardiac and metabolic loads. For intermediate swimmers, breaststroke resulted in the lowest cardiac and metabolic loads, as well as self-reported task load. Probe reaction time was highest while performing the eggbeater technique, indicating that this technique was challenging to coordinate and cognitively demanding. While the energetic demands of antiphase kicking patterns (such as eggbeater in experts or flutter kick in beginners) may be similarly low, the symmetric coordination of upright breaststroke may explain why this pattern's cognitive economy was favourable for all groups. As the eggbeater can be challenging to perform for many people, an upright breaststroke technique is an adequate alternative to adopt in survival situations.

Contribution of the carotid body to thermally mediated hyperventilation in humans.

Humans hyperventilate under heat and cold strain. This hyperventilatory response has detrimental consequences including acid-base dysregulation, dyspnoea, decreased cerebral blood flow and accelerated brain heating. The ventilatory response to hypoxia is exaggerated under whole-body heating and cooling, indicating that altered carotid body function might contribute to thermally mediated hyperventilation. To address whether the carotid body might contribute to heat- and cold-induced hyperventilation, we indirectly measured carotid body tonic activity via hyperoxia, and carotid body sensitivity via hypoxia, under graded heat and cold strain in 13 healthy participants in a repeated-measures design. We hypothesised that carotid body tonic activity and sensitivity would be elevated in a dose-dependent manner under graded heat and cold strain, thereby supporting its role in driving thermally mediated hyperventilation. Carotid body tonic activity was increased in a dose-dependent manner with heating, reaching 175% above baseline (P < 0.0005), and carotid body suppression with hyperoxia removed all of the heat-induced increase in ventilation (P = 0.9297). Core cooling increased carotid body activity by up to 250% (P < 0.0001), but maximal values were reached with mild cooling and thereafter plateaued. Carotid body sensitivity to hypoxia was profoundly increased by up to 180% with heat stress (P = 0.0097), whereas cooling had no detectable effect on hypoxic sensitivity. In summary, cold stress increased carotid body tonic activity and this effect was saturated with mild cooling, whereas heating had clear dose-dependent effects on carotid body tonic activity and sensitivity. These dose-dependent effects with heat strain indicate that the carotid body probably plays a primary role in driving heat-induced hyperventilation. KEY POINTS: Humans over-breathe (hyperventilate) when under heat and cold stress, and though this has detrimental physiological repercussions, the mechanisms underlying this response are unknown. The carotid body, a small organ that is responsible for driving hyperventilation in hypoxia, was assessed under incremental heat and cold strain. The carotid body drive to breathe, as indirectly assessed by transient hyperoxia, increased in a dose-dependent manner with heating, reaching 175% above baseline; cold stress similarly increased the carotid body drive to breathe, but did not show dose-dependency. Carotid body sensitivity, as indirectly assessed by hypoxic ventilatory responses, was profoundly increased by 70-180% with mild and severe heat strain, whereas cooling had no detectable effect. Carotid body hyperactivity and hypersensitivity are two interrelated mechanisms that probably underlie the increased drive to breathe with heat strain, whereas carotid body hyperactivity during mild cooling may play a subsidiary role in cold-induced hyperventilation.

Pulsatile flow in venous perforators of the lower limb.

Teaching traditionally asserts that the arterial pressure pulse is dampened across the capillary bed to the extent that pulsatility is nonexistent in the venous circulation of the lower limbs. Herein, we present evidence of transmission of arterial pulsations across the capillary network into perforator veins in the lower limbs of healthy, heat-stressed humans. Perforator veins are connections from the superficial veins that drain into the deep veins. When assessed using ultrasound at rest, they infrequently demonstrate flow, and a pulsatile flow waveform is not described. We investigated perforator vein pulsatility in 10 young, healthy volunteers who underwent passive heating by +2°C core body temperature via a hot-water-perfused suit, and 5 who also underwent active heating by +2°C via low-intensity cycling while wearing the hot-water-perfused suit. At +0.5°C increments in temperature, blood velocity in an ankle perforator vein was measured using duplex ultrasound. In all perforators with heating, sustained flow was demonstrated, with a pulsatile waveform that was synchronous with the cardiac cycle. The maximum velocity was 30 ± 13 cm/s with passive heating and approximately half with active heating (P = 0.04). The small veins of the skin at the ankle also demonstrated increased perfusion with pulsatility, seen with low-velocity microvascular imaging technology. We consider explanations for this pulsatility and conclude that it is propagated from the arterial inflow through the skin microcirculation as a result of increased dilatation and flow volume and that this is a normal response to increased skin blood flow.

Acute physiological and psychophysical responses to different modes of heat stress.

NEW FINDINGS: What is the central question of this study? What are the profiles of acute physiological and psychophysical strain during and in recovery from different modes of heating, and to what extent do these diminish after repeated exposure? What is the main finding and its importance? Mode of heating affects the strain profiles during heat stress and recovery. Exercise in the heat incurred the greatest cardiovascular strain during heating and recovery. Humid heat was poorly tolerated despite heat strain being no greater than in other heating modes, and tolerance did not improve with multiple exposures. ABSTRACT: Heat stress is common and arises endogenously and exogenously. It can be acutely hazardous while also increasingly advocated to drive health and performance-related adaptations. Yet, the nature of strain (deviation in regulated variables) imposed by different heating modes is not well established, despite the potential for important differences. We, therefore, compared three modes of heat stress for thermal, cardiovascular and perceptual strain profiles during exposure and recovery when experienced as a novel stimulus and an accustomed stimulus. In a crossover design, 13 physically active participants (five females) underwent 5 days of 60-min exposures to hot water immersion (40°C), sauna (55°C, 54% relative humidity) and exercise in the heat (40°C, 52% relative humidity), and a thermoneutral water immersion control (36.5°C), each separated by ≥4 weeks. Physiological (thermal, cardiovascular, haemodynamic) and psychophysical strain responses were assessed on days 1 and 5. Sauna evoked the warmest skin (40°C; P < 0.001) but exercise in the heat caused the largest increase in core temperature, sweat rate, heart rate (post hoc comparisons all P < 0.001) and systolic blood pressure (P ≤ 0.002), and possibly decrease in diastolic blood pressures (P ≤ 0.130), regardless of day. Thermal sensation and feeling state were more favourable on day 5 than on day 1 (P ≤ 0.021), with all modes of heat being equivalently uncomfortable (P ≥ 0.215). Plasma volume expanded the largest extent during immersions (P < 0.001). The current data highlight that exercising in the heat generates a more complex strain profile, while passive heat stress in humid heat has lower tolerance and more cardiovascular strain than hot water immersion.

A crossover control study of three methods of heat acclimation on the magnitude and kinetics of adaptation.

NEW FINDINGS: What is the central question to the study? Are primary indices of heat adaptation (e.g., expansion of plasma volume and reduction in resting core temperature) differentially affected by the three major modes of short-term heat acclimation, that is, exercise in the heat, hot water immersion and sauna? What it the main finding and its importance? The three modes elicited typical adaptations expected with short-term heat acclimation, but these were not significantly different between modes. This comparison has not previously been made and highlights that individuals can expect similar adaptation to heat regardless of the mode used. ABSTRACT: Heat acclimation (HA) can improve heat tolerance and cardiovascular health. The mode of HA potentially impacts the magnitude and time course of adaptations, but almost no comparative data exist. We therefore investigated adaptive responses to three common modes of HA, particularly with respect to plasma volume. Within a crossover repeated-measures design, 13 physically active participants (five female) undertook four, 5-day HA regimes (60 min/day) in randomised order, separated by ≥4 weeks. Rectal temperature (Tre ) was clamped at neutrality via 36.6°C (thermoneutral) water immersion (TWI; i.e., control condition), or raised by 1.5°C via heat stress in 40°C water, sauna (55°C, 52% relative humidity), or exercise in humid heat (40°C, 52% relative humidity; ExH). Adaptation magnitude was assessed as the pooled response across days 4-6, while kinetics was assessed via the 6-day time series. Plasma volume expansion was similar in all heated conditions but only higher than TWI in exercise in the heat (ExH) (by 4%, P = 0.036). Approximately two-thirds of the expansion was attained within the initial 24 h and was moderately related to that present on day 6, regardless of HA mode (r = 0.560-0.887). Expansion was mediated by conservation of both sodium and albumin content, with little evidence for these having differential roles between modes (P = 0.706 and 0.320, respectively). Resting Tre decreased by 0.1-0.3°C in all heated conditions, and systolic blood pressure decreased by 4 mmHg, but not differentially between conditions (P ≥ 0.137). In conclusion, HA mode did not substantially affect the magnitude or rate of adaptation in key resting markers of short-term HA.

Ultrasound Measurements of Subcutaneous Fat Thickness Are Robust Against Hydration Changes.

Ultrasound is an appealing tool to assess body composition, combining the portability of a field method with the accuracy of a laboratory method. However, unlike other body composition methods, the effect of hydration status on validity is unknown. This study evaluated the impact of acute hydration changes on ultrasound measurements of subcutaneous fat thickness and estimates of body fat percentage. In a crossover design, 11 adults (27.1 ± 10.5 years) completed dehydration and hyperhydration trials to alter body mass by approximately ±2%. Dehydration was achieved via humid heat (40 °C, 60% relative humidity) with exercise, whereas hyperhydration was via ingestion of lightly salted water. Ultrasound measurements were taken at 11 body sites before and after each treatment. Participants lost 1.56 ± 0.58 kg (-2.0 ± 0.6%) during the dehydration trial and gained 0.90 ± 0.21 kg (1.2 ± 0.2%) during the hyperhydration trial even after urination. The sum of fat thicknesses as measured by ultrasound differed by <0.90 mm across trials (p = .588), and ultrasound estimates of body fat percentage differed by <0.5% body fat. Ultrasound measures of subcutaneous adipose tissue were unaffected by acute changes in hydration status by extents beyond which are rare and overtly self-correcting, suggesting that this method provides reliable and robust body composition results even when subjects are not euhydrated.

HIITing the brain with exercise: mechanisms, consequences and practical recommendations.

The increasing number of older adults has seen a corresponding growth in those affected by neurovascular diseases, including stroke and dementia. Since cures are currently unavailable, major efforts in improving brain health need to focus on prevention, with emphasis on modifiable risk factors such as promoting physical activity. Moderate-intensity continuous training (MICT) paradigms have been shown to confer vascular benefits translating into improved musculoskeletal, cardiopulmonary and cerebrovascular function. However, the time commitment associated with MICT is a potential barrier to participation, and high-intensity interval training (HIIT) has since emerged as a more time-efficient mode of exercise that can promote similar if not indeed superior improvements in cardiorespiratory fitness for a given training volume and further promote vascular adaptation. However, randomised controlled trials (RCTs) investigating the impact of HIIT on the brain are surprisingly limited. The present review outlines how the HIIT paradigm has evolved from a historical perspective and describes the established physiological changes including its mechanistic bases. Given the dearth of RCTs, the vascular benefits of MICT are discussed with a focus on the translational neuroprotective benefits including their mechanistic bases that could be further potentiated through HIIT. Safety implications are highlighted and components of an optimal HIIT intervention are discussed including practical recommendations. Finally, statistical effect sizes have been calculated to allow prospective research to be appropriately powered and optimise the potential for detecting treatment effects. Future RCTs that focus on the potential clinical benefits of HIIT are encouraged given the prevalence of cognitive decline in an ever-ageing population.

The acute effect of resistance exercise on limb blood flow.

NEW FINDINGS: What is the central question of this study? How does resistance exercise affect peripheral haemodynamics in the active and inactive limb? What is the main finding and its importance? Preliminary data indicate that resistance exercise increases flow and shear rate in the active limb transiently. The same exercise has minimal, short-lasting influence on peripheral haemodynamics in the inactive limb, but further research is required to elaborate on resistance exercise-mediated changes in vascular function in active and inactive limbs. ABSTRACT: Current evidence indicates that to achieve maximum health benefits, regular resistance exercise should be a key component of structured physical activity. Several studies have revealed that regular resistance exercise may be associated with impaired vascular function, although this finding is inconsistent. Proposed explanations for impairment include substantial increases in blood pressure and increased retrograde blood flow in active limbs promoted by resistance exercise. However, few studies have examined the acute haemodynamics of resistance exercise in active - and even fewer in inactive - limbs. The purpose of this study was to characterise the haemodynamic responses in peripheral arteries in active and inactive limbs in response to resistance exercise using upper and lower limbs. Ten participants (five male, five female) familiar with resistance training performed three sets of 10 isotonic repetitions of right-sided bicep curls or knee extensions on separate days. Blood flow, shear rate and muscle oxygenation in the active and inactive limb, and blood pressure were measured before and for 3 min after each set. Blood flow increased in response to resistance exercise in the active limb (∼8-fold and ∼6-fold for the upper and lower limb respectively), with concurrent significant increases in mean and antegrade shear rate. In the inactive limb, blood flow more than doubled for both upper and lower limb exercise, transiently, with no significant change in retrograde shear rate. These acute blood flow profiles following resistance exercise are not indicative of long-term vessel impairment based on current understanding of blood flow and shear stress patterns.

Acute exercise-related cognitive effects are not attributable to changes in end-tidal CO2 or cerebral blood velocity.

PURPOSE: Cognition, cerebral blood flow (CBF) and its major regulator (i.e., arterial CO2), increase with submaximal exercise and decline with severe exercise. These responses may depend on fitness. We investigated whether exercise-related changes in cognition are mediated in part by concomitant changes in CBF and CO2, in ten active (26 ± 3 years) and ten inactive (24 ± 6 years) healthy adults. METHODS: Participants completed two randomised sessions; exercise and a resting CO2-control-wherein end-tidal CO2 (PETCO2) was matched between sessions and clamped across conditions at exercise-associated increases (+ 3 mmHg) and hypercapnia (+ 10 mmHg). Exercise comprised inclined walking at submaximal and severe intensities. CBF was indexed using right middle cerebral artery blood velocity (MCAv). Cognition (visuomotor, switching and inhibitory response time) was measured before, during, and after exercise. RESULTS: MCAv and its inverted-U response to exercise were comparable between groups, whereas visuomotor performance improved during submaximal exercise in the active group only (p = 0.046). Submaximal, but not severe (p = 0.33), exercise increased MCAv (p ≤ 0.03). Hypercapnia increased MCAv during the CO2-control (27 ± 12%) and during submaximal exercise (39 ± 17%; p < 0.01). Despite the acute increases in MCAv, cognition was impaired during both levels of increased PETCO2 (3-6%; p ≤ 0.04), regardless of session. Overall, resting or exercise-related changes in PETCO2 and MCAv did not associate with changes in cognition (r ≤ 0.29 ± 0.34). Fitness ([Formula: see text]O2MAX) was associated with baseline cognition (r ≥ 0.50). CONCLUSION: Acute increases in PETCO2 and MCAv were not associated with improved cognition. In fact, cognitive performance was impaired at both levels of increased PETCO2, regardless of session. Finally, fitter people were found to have better cognition.

Cerebrovascular haemodynamics during isometric resistance exercise with and without the Valsalva manoeuvre.

PURPOSE: To examine the interactive effects of VM and isometric resistance exercise on cerebral haemodynamics. METHODS: Eleven healthy participants (mean ± SD 28 ± 9 years; 2 females) completed 20-s bilateral isometric leg extension at 50% of maximal voluntary contraction with continued ventilation (RE), a 20-s VM at mouth pressure of 40 mmHg (VM), and a combination (RE + VM), in randomised order. Mean beat-to-beat blood velocity in the posterior (PCAvmean) and middle cerebral arteries (MCAvmean), vertebral artery blood flow, end-tidal partial pressure of CO2 and mean arterial pressure (MAP) were measured. RE data were time aligned to RE + VM and analysed according to standard VM phases. RESULTS: Interaction effects (VM phase × condition) were observed for MCAvmean, PCAvmean, vertebral artery blood flow and MAP (all ≤ 0.010). Phase I MCAvmean was greatest for RE [88 ± 19, vs. 71 ± 11 and 78 ± 12 cm s-1 for VM (P = 0.008) and RE + VM (P = 0.021), respectively]. Greater increases in MCAvmean than PCAvmean occurred in phase I of RE only (24 ± 15% vs. 16 ± 16%, post hoc P = 0.044). In phase IIb, MAP was lower in RE than RE + VM (115 ± 15 vs. 138 ± 21 mmHg, P = 0.004), but did not reduce MCAvmean (78 ± 8 vs. 79 ± 9 cm s-1, P = 0.579) or PCAvmean (45 ± 11 vs .46 ± 11 cm s-1, P = 0.617). Phase IIb MCAvmean and PCAvmean was lowest in VM (66 ± 6 and 39 ± 8 cm s-1, respectively, all P < 0.001), whereas in Phase IV, MCAvmean, PCAvmean and MAP were greater in VM than in RE and RE + VM (all P < 0.020). CONCLUSION: RE and RE + VM produce similar cerebrovascular responses despite different MAP profiles. However, the VM produced the greatest cerebrovascular challenge afterward.

Differences in dry-bulb temperature do not influence moderate-duration exercise performance in warm environments when vapor pressure is equivalent.

PURPOSE: Recent studies have determined that ambient humidity plays a more important role in aerobic performance than dry-bulb temperature does in warm environments; however, no studies have kept humidity constant and independently manipulated temperature. Therefore, the purpose of this study was to determine the contribution of dry-bulb temperature, when vapor pressure was matched, on the thermoregulatory, perceptual and performance responses to a 30-min cycling work trial. METHODS: Fourteen trained male cyclists (age: 32 ± 12 year; height: 178 ± 6 cm; mass: 76 ± 9 kg; [Formula: see text]: 59 ± 9 mL kg-1 min-1; body surface area: 1.93 ± 0.12 m2; peak power output: 393 ± 53 W) volunteered, and underwent 1 exercise bout in moderate heat (MOD: 34.9 ± 0.2 °C, 50.1 ± 1.1% relative humidity) and 1 in mild heat (MILD: 29.2 ± 0.2 °C, 69.4 ± 0.9% relative humidity) matched for vapor pressure (2.8 ± 0.1 kPa), with trials counterbalanced. RESULTS: Despite a higher weighted mean skin temperature during MOD (36.3 ± 0.5 vs. 34.5 ± 0.6 °C, p < 0.01), none of rectal temperature (38.0 ± 0.3 vs. 37.9 ± 0.4 °C, p = 0.30), local sweat rate (1.0 ± 0.3 vs. 0.9 ± 0.4 mg cm-2 min-1, p = 0.28), cutaneous blood flow (283 ± 116 vs. 287 ± 105 PU, p = 0.90), mean power output (206 ± 37 vs. 205 ± 41 W, p = 0.87) or total work completed (371 ± 64 vs. 369 ± 70 kJ, p = 0.77) showed any difference between environments during the work trial. However, all perceptual measures (perceived exertion, thermal discomfort, thermal sensation, skin wettedness, pleasantness, all p < 0.05) were affected detrimentally during MOD compared to MILD. CONCLUSION: In a warm and compensable environment, dry-bulb temperature did not influence high-intensity cycling performance when vapor pressure was maintained, whilst the perceptual responses were affected.

On exercise thermoregulation in females: interaction of endogenous and exogenous ovarian hormones.

KEY POINTS: One in two female athletes chronically take a combined, monophasic oral contraceptive pill (OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the menstrual cycle still occurs with OCP usage. Forthcoming large international sporting events will expose female athletes to hot environments differing in their thermal profile, yet few data exist on how trained women will respond from both a thermoregulatory and performance stand-point. In the present study, we have demonstrated that a small endogenous rhythm of the menstrual cycle still affects Tcore and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation is maintained. Furthermore, humid heat affects both performance and thermoregulatory responses to a greater extent than OCP usage and the menstrual cycle does. ABSTRACT: We studied thermoregulatory responses of ten well-trained ( V̇O2max , 57 ± 7 mL min-1  kg-1 ) women taking a combined, monophasic oral contraceptive pill (OCP) (≥12 months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), aiming to assess autonomic regulation, and then a self-paced intensity (30-min work trial) to assess behavioural regulation. Trials were conducted in quasi-follicular (qF) and quasi-luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C). During rest and exercise at 125 W, rectal temperature was 0.15°C higher in qL than qF (P = 0.05) independent of environment (P = 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both P > 0.30). Exercise performance did not differ between quasi-phases (qF: 268 ± 31 kJ, qL: 263 ± 26 kJ, P = 0.31) but was 5 ± 7% higher during DRY than during HUM (273 ± 29 kJ, 258 ± 28 kJ; P = 0.03). Compared to matched eumenorrhoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P < 0.01). In well-trained, OCP-using women exercising in the heat: (i) a performance-thermoregulatory trade-off occurred that required behavioural adjustment; (ii) humidity impaired performance as a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.

Heat therapy vs. supervised exercise therapy for peripheral arterial disease: a 12-wk randomized, controlled trial.

Peripheral arterial disease (PAD) is characterized by lower limb atherosclerosis impairing blood supply and causing walking-induced leg pain or claudication. Adherence to traditional exercise training programs is poor due to these symptoms despite exercise being a mainstay of conservative treatment. Heat therapy improves many cardiovascular health outcomes, so this study tested if this was a viable alternative cardiovascular therapy for PAD patients. Volunteers with PAD were randomized to 12 wk of heat (n = 11; mean age 76 ± 8 yr, BMI 28.7 ± 3.5 kg/m2, 4 females) or exercise (n = 11; 74 ± 10 yr, 28.5 ± 6.8 kg/m2, 3 females). Heat involved spa bathing at ∼39°C, 3-5 days/wk for ≤30 min, followed by ≤30 min of callisthenics. Exercise involved ≤90 min of supervised walking and gym-based exercise, 1-2 days/wk. Following the interventions, total walking distance during a 6-min walk test increased (from ∼350 m) by 41 m (95% CI: [13, 69], P = 0.006) regardless of group, and pain-free walking distance increased (from ∼170 m) by 43 m ([22, 63], P < 0.001). Systolic blood pressure was reduced more following heat (-7 mmHg, [-4, -10], P < 0.001) than following exercise (-3 mmHg, [0, -6], P = 0.078), and diastolic and mean arterial pressure decreased by 4 mmHg in both groups (P = 0.002). There were no significant changes in blood volume, ankle-brachial index, or measures of vascular health. There were no differences in the improvement in functional or blood pressure outcomes between heat and exercise in individuals with PAD. NEW & NOTEWORTHY Heat therapy via hot-water immersion and supervised exercise both improved walking distance and resting blood pressure in peripheral arterial disease (PAD) patients over 12 wk. Adherence to heat therapy was excellent, and the heat intervention was well tolerated. The results of the current study indicate that heat therapy can improve functional ability and has potential as an effective cardiovascular conditioning tool for individuals with PAD.

Cerebrovascular regulation is not blunted during mental stress.

NEW FINDINGS: What is the central question of the study? What are the effects of acute mental stress on the mechanisms regulating cerebral blood flow? What is the main finding and its importance? The major new findings are as follows: (i) high mental stress and hypercapnia had an interactive effect on mean middle cerebral artery blood velocity; (ii) high mental stress altered the regulation of cerebral blood flow; (iii) the increased cerebrovascular hypercapnic reactivity was not driven by changes in mean arterial pressure alone; and (iv) this increased perfusion with mental stress appeared not to be justified functionally by an increase in oxygen demand (as determined by near-infrared spectroscopy-derived measures). ABSTRACT: In this study, we examined the effects of acute mental stress on cerebrovascular function. Sixteen participants (aged 23 ± 4 years; five female) were exposed to low and high mental stress using simple arithmetic (counting backwards from 1000) and more complex arithmetic (serial subtraction of 13 from a rapidly changing four-digit number), respectively. During consecutive conditions of baseline, low stress and high stress, end-tidal partial pressure of CO2 ( PET,CO2 ) was recorded at normocapnia (37 ± 3 mmHg) and clamped at two elevated levels (P < 0.01): 41 ± 1 and 46 ± 1 mmHg. Mean right middle cerebral artery blood velocity (MCAvmean ; transcranial Doppler ultrasound), right prefrontal cortex haemodynamics (near-infrared spectroscopy) and mean arterial blood pressure (MAP; finger photoplethysmography) were measured continuously. Cerebrovascular hypercapnic reactivity (ΔMCAvmean /Δ PET,CO2 ), cerebrovascular conductance (CVC; MCAvmean /MAP), CVC CO2 reactivity (ΔCVC/Δ PET,CO2 ) and total peripheral resistance (MAP/cardiac output) were calculated. Acute high mental stress increased MCAvmean by 7 ± 7%, and more so at higher PET,CO2 (32 ± 10%; interaction, P = 0.03), illustrating increased sensitivity to CO2 (i.e. its major regulator). High mental stress also increased MAP (17 ± 9%; P ≤ 0.01), coinciding with increased near-infrared spectroscopy-derived prefrontal haemoglobin volume and saturation measures. High mental stress elevated both cerebrovascular hypercapnic and conductance reactivities (main effect of stress, P ≤ 0.04). These findings indicate that the cerebrovascular response to acute high mental stress results in a coordinated regulation between multiple processes.

Implications of habitual endurance and resistance exercise for dynamic cerebral autoregulation.

NEW FINDINGS: What is the central question of this study? Does habitual resistance and endurance exercise modify dynamic cerebral autoregulation? What is the main finding and its importance? To the authors' knowledge, this is the first study to directly assess dynamic cerebral autoregulation in resistance-trained individuals, and potential differences between exercise training modalities. Forced oscillations in blood pressure were induced by repeated squat-stands, from which dynamic cerebral autoregulation was assessed using transfer function analysis. These data indicate that dynamic cerebral autoregulatory function is largely unaffected by habitual exercise type, and further document the systemic circulatory effects of regular exercise. ABSTRACT: Regular endurance and resistance exercise produce differential but desirable physiological adaptations in both healthy and clinical populations. The chronic effect of these different exercise modalities on cerebral vessels' ability to respond to rapid changes in blood pressure (BP) had not been examined. We examined dynamic cerebral autoregulation (dCA) in 12 resistance-trained (mean ± SD, 25 ± 6 years), 12 endurance-trained (28 ± 9 years) and 12 sedentary (26 ± 6 years) volunteers. The dCA was assessed using transfer function analysis of forced oscillations in BP vs. middle cerebral artery blood velocity (MCAv), induced via repeated squat-stands at 0.05 and 0.10 Hz. Resting BP and MCAv were similar between groups (interaction: both P ≥ 0.544). The partial pressure of end-tidal carbon dioxide ( PETCO2 ) was unchanged (P = 0.561) across squat-stand manoeuvres (grouped mean for absolute change +0.6 ± 2.3 mmHg). Gain and normalized gain were similar between groups across all frequencies (both P ≥ 0.261). Phase showed a frequency-specific effect between groups (P = 0.043), tending to be lower in resistance-trained (0.63 ± 0.21 radians) than in endurance-trained (0.90 ± 0.41, P = 0.052) and -untrained (0.85 ± 0.38, P = 0.081) groups at slower frequency (0.05 Hz) oscillations. Squat-stands induced mean arterial pressure perturbations differed between groups (interaction: P = 0.031), with greater changes in the resistance (P < 0.001) and endurance (P = 0.001) groups compared with the sedentary group at 0.05 Hz (56 ± 13 and 49 ± 11 vs. 35 ± 11 mmHg, respectively). The differences persisted at 0.1 Hz between resistance and sedentary groups (49 ± 12 vs. 33 ± 7 mmHg, P < 0.001). These results indicate that dCA remains largely unaltered by habitual endurance and resistance exercise with a trend for phase to be lower in the resistance exercise group at lower fequencies.