Neurovascular coupling during dynamic upper body resistance exercise in healthy individuals.

During unilateral static and rhythmic handgrip exercise, middle cerebral artery blood velocity (MCAv) increases in the contralateral side to the exercising limb. However, whether this neurovascular coupling-mediated increase in contralateral MCAv is apparent against a background of fluctuating perfusion pressure produced by dynamic resistance exercise (RE) is unclear. We examined the cerebral haemodynamic response to unilateral dynamic RE in 30 healthy individuals (female = 16, mean ± SD: age, 26 ± 6 years; height, 175 ± 10 cm; weight, 74 ± 15 kg; body mass index, 24 ± 5 kg m-2). Participants completed four sets of 10 paced repetitions (15 repetitions min-1) of unilateral bicep curl exercise at 60% of the predicted one-repetition maximum (7 ± 3 kg). Beat-to-beat blood pressure, bilateral MCAv and end-tidal carbon dioxide were measured throughout. One-way ANOVA was used to analyse cardiovascular variables and two-way ANOVA to analyse dependent cerebrovascular variables (side × sets, 2 × 5). A linear mixed model analysis was also performed to investigate the effects of end-tidal carbon dioxide and mean arterial blood pressure on MCAv. In comparison to baseline, within-exercise mean arterial blood pressure increased (P < 0.001) across the sets, whereas bilateral MCAv decreased (P < 0.001). However, no significant interaction effect was observed for any dependent variables (all P > 0.787). The linear mixed model revealed that end-tidal carbon dioxide had the greatest effect on MCAv (estimate = 1.019, t = 8.490, P < 0.001). No differences were seen in contralateral and ipsilateral MCAv during dynamic RE, suggesting that neurovascular coupling contributions during dynamic RE might be masked by other regulators, such as blood pressure.

The effects of habitual resistance exercise training on cerebrovascular responses to lower body dynamic resistance exercise: A cross-sectional study.

Dynamic resistance exercise (RE) produces sinusoidal fluctuations in blood pressure with simultaneous fluctuations in middle cerebral artery blood velocity (MCAv). Some evidence indicates that RE may alter cerebrovascular function. This study aimed to examine the effects of habitual RE training on the within-RE cerebrovascular responses. RE-trained (n = 15, Female = 4) and healthy untrained individuals (n = 15, Female = 12) completed four sets of 10 paced repetitions (15 repetitions per minute) of unilateral leg extension exercise at 60% of predicted 1 repetition maximum. Beat-to-beat blood pressure, MCAv and end-tidal carbon dioxide were measured throughout. Zenith, nadir and zenith-to-nadir difference in mean arterial blood pressure (MAP) and mean MCAv (MCAvmean) for each repetition were averaged across each set. Two-way ANOVA was used to analyse dependent variables (training × sets), Bonferroni corrected t-tests were used for post hoc pairwise comparisons. Group age (26 ± 7 trained vs. 25 ± 6 years untrained, P = 0.683) and weight (78 ± 15 vs. 71 ± 15 kg, P = 0.683) were not different. During exercise average MAP was greater for the RE-trained group in sets 2, 3 and 4 (e.g., set 4: 101 ± 11 vs. 92 ± 7 mmHg for RE trained and untrained, respectively, post hoc tests all P = < 0.012). Zenith MAP and zenith-to-nadir MAP difference demonstrated a training effect (P < 0.039). Average MCAvmean and MCAvmean zenith-to-nadir difference was not different between groups (interaction effect P = 0.166 and P = 0.459, respectively). Despite RE-trained individuals demonstrating greater fluctuations in MAP during RE compared to untrained, there were no differences in MCAvmean. Regular RE may lead to vascular adaptations that stabilise MCAv during RE.

Directional sensitivity of the cerebral pressure-flow relationship in young healthy individuals trained in endurance and resistance exercise.

NEW FINDINGS: What is the central question of this study? Does habitual exercise modality affect the directionality of the cerebral pressure-flow relationship? What is the main finding and its importance? These data suggest the hysteresis-like pattern of dynamic cerebral autoregulation appears present in long-term sedentary and endurance-trained individuals, but absent in resistance-trained individuals. This is the first study to expand knowledge on the directional sensitivity of the cerebral pressure-flow relationship to trained populations. ABSTRACT: Evidence suggests the cerebrovasculature may be more efficient at dampening cerebral blood flow (CBF) variations when mean arterial pressure (MAP) transiently increases, compared to when it decreases. Despite divergent MAP and CBF responses to acute endurance and resistance training, the long-term impact of habitual exercise modality on the directionality of dynamic cerebral autoregulation (dCA) is currently unknown. Thirty-six young healthy participants (sedentary (n = 12), endurance-trained (n = 12), and resistance-trained (n = 12)) undertook a 5-min repeated squat-stand protocol at two forced MAP oscillation frequencies (0.05 and 0.10 Hz). Middle cerebral artery mean blood velocity (MCAv) and MAP were continuously monitored. We calculated absolute (ΔMCAvT /ΔMAPT ) and relative (%MCAvT /%MAPT ) changes in MCAv and MAP with respect to the transition time intervals of both variables to compute a time-adjusted ratio in each MAP direction, averaged over the 5-min repeated squat-stand protocols. At 0.10 Hz repeated squat-stands, ΔMCAvT /ΔMAPT and %MCAvT /%MAPT were lower when MAP increased compared with when MAP decreased for sedentary (ΔMCAvT /ΔMAPT : P = 0.032; %MCAvT /%MAPT : P = 0.040) and endurance-trained individuals (ΔMCAvT /ΔMAPT : P = 0.012; %MCAvT /%MAPT P = 0.007), but not in the resistance-trained individuals (ΔMCAvT /ΔMAPT : P = 0.512; %MCAvT /%MAPT P = 0.666). At 0.05 Hz repeated squat-stands, time-adjusted ratios were similar for all groups (all P > 0.605). These findings suggest exercise training modality does influence the directionality of the cerebral pressure-flow relationship and support the presence of a hysteresis-like pattern during 0.10 Hz repeated squat-stands in sedentary and endurance-trained participants, but not in resistance-trained individuals. In future studies, assessment of elite endurance and resistance training habits may further elucidate modality-dependent discrepancies on directional dCA measurements.

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.

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.

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.

Influence of menstrual phase and arid vs. humid heat stress on autonomic and behavioural thermoregulation during exercise in trained but unacclimated women.

KEY POINTS: Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, one in two of such women believe their menstrual cycle negatively impacts training and performance. Forthcoming large international events will expose female athletes to hot environments, and studies evaluating aerobic exercise performance in such environments across the menstrual cycle are sparse, with mixed findings. We have identified that autonomic heat loss responses at rest and during fixed-intensity exercise in well-trained women are not affected by menstrual cycle phase, but differ between dry and humid heat. Furthermore, exercise performance is not different across the menstrual cycle, yet is lower in humid heat, in conjunction with reduced evaporative cooling. Menstrual cycle phase does not appear to affect exercise performance in the heat in well-trained women, but humidity impairs performance, probably due to reduced evaporative power. ABSTRACT: We studied thermoregulatory responses of ten well-trained [V̇O2 max , 57 (7) ml min-1  kg-1 ] eumenorrheic women exercising in dry and humid heat, across their menstrual cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30 min work trial), to assess behavioural regulation. Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and fixed-intensity exercise, rectal temperature was ∼0.2°C higher in ML than EF (P < 0.01) independent of environment (P = 0.66). Mean skin temperature did not differ between menstrual phases (P ≥ 0.13) but was higher in DRY than HUM (P < 0.01). Local sweat rate and/or forearm blood flow differed as a function of menstrual phase and environment (interaction: P ≤ 0.01). Exercise performance did not differ between phases [EF: 257 (37), ML: 255 (43) kJ, P = 0.62], but was 7 (9)% higher in DRY than HUM [263 (39), 248 (40) kJ; P < 0.01] in conjunction with equivalent autonomic regulation and thermal strain but higher evaporative cooling [16 (6) W m2 ; P < 0.01]. In well-trained women exercising in the heat: (1) menstrual phase did not affect performance, (2) humidity impaired performance due to reduced evaporative cooling despite matched WBGT and (3) behavioural responses nullified thermodynamic and autonomic differences associated with menstrual phase and dry vs. humid heat.

Mild dehydration modifies the cerebrovascular response to the cold pressor test.

The cold pressor test (CPT) is widely used in clinical practice and physiological research. It is characterized by a robust autonomic response, with associated increases in heart rate (HR), mean arterial pressure (MAP) and mean middle cerebral artery blood flow velocity (MCAv(mean)). Hydration status is not commonly reported when conducting this test, yet blood viscosity alone can modulate MCAv(mean), potentially modifying the MCAv(mean) response to the CPT. We investigated the effect of mild dehydration on the physiological response to the CPT in 10 healthy men (mean ± SD: age 28 ± 5 years; body mass 83 ± 5 kg). All participants completed two CPTs, cold water (0°C) immersion of both feet for 90 s, with the order of the euhydration and dehydration trials counterbalanced. Beat-to-beat MCAv, MAP, HR and breath-by-breath partial pressure of end-tidal CO2 (P(ET,CO2)) were measured continuously. Participants' pain perception was measured 1 min into the CPT using a visual analog scale (no pain = 0; maximal pain = 10). Dehydration significantly elevated plasma osmolality and urine specific gravity and reduced body mass (all P < 0.01). The MAP and HR responses were not different between treatments (both P > 0.05). After 90 s of immersion, the change in MCAv(mean) from baseline was less in the dehydration compared with the euhydration trial (change 0 ± 5 versus 7 ± 7 cm s(-1), P = 0.01), as was P(ET,CO2) (change -3 ± 2 versus 0 ± 3 mmHg, P = 0.02). Dehydration was associated with greater relative pain sensation during the CPT (7.0 ± 1.3 vs 5.8 ± 1.8, P = 0.02). Our results demonstrate that mild dehydration can modify the cerebrovascular response to the CPT, with dehydration increasing perceived pain, lowering P ET ,CO2 and, ultimately, blunting the MCAv(mean) response.

Cerebrovascular, cardiovascular and strength responses to acute ammonia inhalation.

PURPOSE: Ammonia is used as a stimulant in strength based sports to increase arousal and offset fatigue however little is known about its physiological and performance effects. The purpose of this study was twofold (1) establish the physiological response to acute ammonia inhalation (2) determine whether the timing of the physiological response corresponds with a performance enhancement, if any. METHODS: Fifteen healthy males completed two trials. Trial one investigated the beat-to-beat middle cerebral artery blood flow velocity (MCAv), heart rate (HR) and mean arterial pressure (MAP) response to ammonia inhalation. During trial two, participants performed a maximal single mid-thigh pull (MTP) at various time points following ammonia inhalation in a randomised order: MTPs were conducted immediately, 15, 30 and 60 s following ammonia inhalation. A MTP with no ammonia inhalation served as the control. During this trial maximal MTP force, rate of force development (RFD) and electromyography (EMG) activity were recorded. RESULTS: MCAvmean increased and peaked on average by 6 cm s(-1) (P < 0.001), 9.4 ± 5.5 s following ammonia inhalation. Similarly, HR was increased by 6 ± 11 beats per minute 15 s following ammonia inhalation (P < 0.001). MAP remained unchanged following inhalation (P = 0.51). The use and timing of ammonia inhalation had no effect on maximal force, RFD or EMG (all P > 0.2) compared to control. CONCLUSIONS: MCAv was elevated despite no increase in MAP occurring; this is indicative of a cerebrovascular vasodilation. Despite the marked cerebrovascular and cardiovascular response to ammonia inhalation no ergogenic effect was observed during the MTP, irrespective of the timing of administration.

Postexercise orthostatic intolerance: influence of exercise intensity.

NEW FINDINGS: What is the central question of this study? Following exercise, hypotension is often reported and syncope is more likely. It is unresolved whether the postexercise hypotension associated with different exercise intensities contributes to the rate at which syncope develops. What is the main finding and its importance? The physiological events that induce presyncope are the same both before and after exercise; however, more intense exercise accelerated the development of hypocapnia, hypotension and, ultimately, syncope. These data indicate that higher intensity exercise induces a postexercise hypotension that reduces cardiovascular reserve, an earlier development of hypocapnia and, ultimately, cerebral hypoperfusion. After exercise, a reduction in mean arterial pressure is often experienced and is referred to as postexercise hypotension. Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise intensity-mediated effect on postexercise hypotension. We examined the effect of exercise intensity on time to presyncope, induced via combined head-up tilt and lower body negative pressure following 1 h of cycling at 30 and 70% of heart rate range. Healthy participants (n = 8; mean ± SD, 28 ± 5 years old) completed orthostatic testing to presyncope before and after exercise. Beat-to-beat middle cerebral artery blood flow velocity (MCAv), mean arterial pressure and cerebral oxygenation (measured by near-infrared spectroscopy) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95 ± 6 and 147 ± 5 beats min(-1) for 30 and 70% heart rate range, respectively, with average power outputs of 103 ± 22 and 221 ± 45 W, respectively. Time to presyncope occurred 32% sooner after the 70% heart rate range trial (952 ± 484 versus 1418 ± 435 s; P = 0.004). Both before and after exercise, presyncope occurred at the same reduction in MCAv (grouped mean, -30 ± 11 cm s(-1) ), mean arterial pressure (-18 ± 13 mmHg), total oxygenation index (-6 ± 2%) and partial pressure of end-tidal CO2 (-16 ± 8 mmHg; all P > 0.1). At presyncope following exercise, the MCAv response was related more to the change in partial pressure of end-tidal CO2 from the baseline preceding orthostatic testing (r(2)  = 0.50, P = 0.01) than to the hypotension (r(2)  = 0.12, P = 0.17). Presyncope both before and after exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise.

Nicotine exacerbates exertional heat strain in trained men: a randomized, placebo-controlled, double-blind study.

To determine whether using nicotine exacerbates exertional heat strain through an increased metabolic heat production (Hprod) or decreased skin blood flow (SkBF), 10 nicotine-naïve trained males [37 ± 12 yr; peak oxygen consumption (V̇o2peak): 66 ± 10 mL·min-1·kg-1] completed four trials at 20°C and 30°C following overnight transdermal nicotine (7 mg·24 h-1) and placebo use in a crossover, double-blind design. They cycled for 60 min (55% V̇o2peak) followed by a time trial (∼75% V̇o2peak) during which measures of gastrointestinal (Tgi) and mean weighted skin ([Formula: see text]sk) temperatures, SkBF, Hprod, and mean arterial pressure (MAP) were made. The difference in ΔTgi between nicotine and placebo trials was greater during 30°C (0.4 ± 0.5°C) than 20°C (0.1 ± 0.7°C), with [Formula: see text]sk higher during nicotine than placebo trials (0.5 ± 0.5°C, P = 0.02). SkBF became progressively lower during nicotine than placebo trials (P = 0.01) and progressively higher during 30°C than 20°C trials (P < 0.01); MAP increased from baseline (P < 0.01) and remained elevated in all trials. The difference in Hprod between 30°C and 20°C trials was lower during nicotine than placebo (P = 0.01) and became progressively higher during 30°C than 20°C trials with exercise duration (P = 0.03). Mean power output during the time trial was lower during 30°C than 20°C trials (24 ± 25 W, P = 0.02), and although no effect of nicotine was observed (P > 0.59), two participants (20%) were unable to complete their 30°C nicotine trials as one reached the ethical limit for Tgi (40.0°C), whereas the other withdrew due to "nausea and chills" (Tgi = 39.7°C). These results demonstrate that nicotine use increases thermal strain and risk of exertional heat exhaustion by reducing SkBF.NEW & NOTEWORTHY In naïve participants, acute nicotine use exerts a hyperthermic effect that increases the risk of heat exhaustion during exertional heat strain, which is driven by a blunted skin blood flow response. This has implications for 1) populations that face exertional heat strain and demonstrate high nicotine use (e.g., athletes and military, 25%-50%) and 2) study design whereby screening and exclusion for nicotine use or standardization of prior use (e.g., overnight abstinence) is encouraged.

Human temperature regulation when given the opportunity to behave.

This study aimed to test the primary hypotheses that human thermoregulatory behavior is: (1) initiated before changes in rectal or esophageal temperatures; and (2) accompanied by indiscernible differences in sweating or shivering. This was achieved by placing nine, healthy, males in a situation where they were free to move between a cold (~8 °C) and a hot (~46 °C) environment. Upon behaving [i.e., move from cold to hot (C→H) or from hot to cold (H→C)], skin, rectal, and esophageal temperatures, indices of cutaneous vasomotor tone, metabolism and evaporation, and local and whole-body thermal discomfort were recorded. Rectal temperatures were similar at H→C (37.1 ± 0.2 °C) and C→H (37.1 ± 0.2 °C); yet esophageal temperatures were higher at C→H (36.9 ± 0.2 vs. 36.8 ± 0.2 °C). Skin temperature (C→H, 28.4 ± 0.9 vs. H→C, 35.0 ± 0.6 °C) and vasomotor tone were drastically different upon the decision to behave. Metabolic heat production was lower at H→C (79 ± 10 W/m(2)) than at C→H (101 ± 20 W/m(2)), yet there were no statistical differences in evaporative heat loss (C→H, 23 ± 33 W/m(2) vs. H→C, 52 ± 36 W/m(2)). Whole-body thermal discomfort was similar at C→H and H→C, yet there were inter-segmental differences. These findings indicate that skin temperature, not core temperature, plays a signaling role in the decision to behaviorally thermoregulate. However, this behavior does not occur in the complete absence of autonomic thermoregulatory responses.

Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.

BACKGROUND: During hyperthermia, the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM-induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear. METHODS: Healthy participants (n = 12, 1 female, mean ± SD: age 24 ± 3 years) completed a 30 mmHg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post-VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAvmean ) also calculated. RESULTS: Passive heating significantly raised core temperature from baseline (37.9 ± 0.2 vs. 37.1 ± 0.1°C at rest, p < 0.01). MAP during phases I through III of the VM was lower during hyperthermia (interaction effect p < 0.01). Although an interaction effect was observed for MCAvmean (p = 0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55 ± 12 vs. 49.3 ± 8 cm s- 1 for normothermia and hyperthermia, respectively, p = 0.03). Pulsatility index was increased 1-min post-VM in both conditions (0.71 ± 0.11 vs. 0.76 ± 0.11 for pre- and post-VM during normothermia, respectively, p = 0.02, and 0.86 ± 0.11 vs. 0.99 ± 0.09 for hyperthermia p < 0.01), although for pulse time only main effects of time (p < 0.01), and condition (p < 0.01) were apparent. CONCLUSION: These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia.

The effects of vibration therapy on muscle force loss following eccentrically induced muscle damage.

The purpose of this study was to investigate the effects of acute vibration therapy (VT) on performance recovery after a bout of strenuous eccentric exercise. Eight healthy males completed 300 maximal eccentric contractions of the quadriceps of one leg on an isokinetic dynamometer. Immediately after exercise and 12 and 24 h post-exercise, the subjects underwent either VT or a control treatment of no VT. Five sets of 1 min VT was performed at 26 Hz, with 6 mm peak-to-peak displacement, on a commercially available vibration machine. At least 2 weeks after the initial trial, the subjects completed the second trial using the contralateral leg and other treatment. Peak and average peak isometric tension and isokinetic concentric and eccentric torque were measured prior to exercise and 24 and 48 h post-exercise. Treatment with VT resulted in significantly (all P < 0.05) greater decrements in peak (-38%) and average peak eccentric (-39%) torque 24 h after eccentric exercise as compared to a control treatment (-24 and -29%, respectively). These results suggest that the use of 26 Hz VT in the first 24 h after damaging exercise may be detrimental to the magnitude of force loss and/or recovery over this period.

Cerebral autoregulation across the menstrual cycle in eumenorrheic women.

There is emerging evidence that ovarian hormones play a significant role in the lower stroke incidence observed in pre-menopausal women compared with men. However, the role of ovarian hormones in cerebrovascular regulation remains to be elucidated. We examined the blood pressure-cerebral blood flow relationship (cerebral autoregulation) across the menstrual cycle in eumenorrheic women (n = 12; mean ± SD: age, 31 ± 7 years). Participants completed sit-to-stand and Valsalva maneuvers (VM, mouth pressure of 40 mmHg for 15 s) during the early follicular (EF), late follicular (LF), and mid-luteal (ML) menstrual cycle phases, confirmed by serum measurement of progesterone and 17ß-estradiol. Middle cerebral artery blood velocity (MCAv), arterial blood pressure and partial pressure of end-tidal carbon dioxide were measured. Cerebral autoregulation was assessed by transfer function analysis during spontaneous blood pressure oscillations, rate of regulation (RoR) during sit-to-stand maneuvers, and Tieck's autoregulatory index during VM phases II and IV (AI-II and AI-IV, respectively). Resting mean MCAv (MCAvmean ), blood pressure, and cerebral autoregulation were unchanged across the menstrual cycle (all p > 0.12). RoR tended to be different (EF, 0.25 ± 0.06; LF; 0.19 ± 0.04; ML, 0.18 ± 0.12 sec-1 ; p = 0.07) and demonstrated a negative relationship with 17ß-estradiol (R2  = 0.26, p = 0.02). No changes in AI-II (EF, 1.95 ± 1.20; LF, 1.67 ± 0.77 and ML, 1.20 ± 0.55) or AI-IV (EF, 1.35 ± 0.21; LF, 1.27 ± 0.26 and ML, 1.20 ± 0.2) were observed (p = 0.25 and 0.37, respectively). Although, a significant interaction effect (p = 0.02) was observed for the VM MCAvmean response. These data indicate that the menstrual cycle has limited impact on cerebrovascular autoregulation, but individual differences should be considered.

Lower body positive pressure affects systemic but not cerebral haemodynamics during incremental hyperthermia.

Hyperthermia produces profound redistribution of blood and circulatory reflex function. We investigated the potential for lower body positive pressure (LBPP) to maintain or restore haemodynamics during graded hyperthermia. Eight healthy adults rested supine in a custom-made LBPP box, sealed distal to the iliac crest. Following 5 min of normothermic rest, 20 mmHg of LBPP was applied and repeated when core temperature (Tcore ) had increased passively by +0.5 and +1°C. Primary dependent variables included mean middle cerebral artery blood velocity (MCAvmean , transcranial Doppler), mean arterial blood pressure (MAP, finger photoplethysmography), heart rate (HR) and partial pressure of end-tidal carbon dioxide (PET CO2 ). The absolute increase in MAP during LBPP was lower at Tcore +1°C (2 ± 3 mmHg), compared with normothermia (7 ± 3 p = .01). The modest increase in MCAvmean was unchanged by Tcore (normothermia, 2 ± 3 cm/s; +0.5°C, 3 ± 3 cm/s and +1°C, 3 ± 4 cm/s, p = .74). By design, PET CO2 was unchanged in all conditions from normothermic baseline (42 ± 1, p = .81). LBPP-induced changes in HR were greater at +0.5°C (-13 ± 4 b/min) and +1°C (-12 ± 6 b/min) compared with normothermia (-3 ± 3 b/min, p = .01 and p = .01, respectively). These data indicate that despite a significant attenuation in MAP to LBPP with moderate hyperthermia, MCAvmean dynamics were unchanged among the thermal manipulations.

The Acute Cardiorespiratory and Cerebrovascular Response to Resistance Exercise.

Resistance exercise (RE) is a popular modality for the general population and athletes alike, due to the numerous benefits of regular participation. The acute response to dynamic RE is characterised by temporary and bidirectional physiological extremes, not typically seen in continuous aerobic exercise (e.g. cycling) and headlined by phasic perturbations in blood pressure that challenge cerebral blood flow (CBF) regulation. Cerebral autoregulation has been heavily scrutinised over the last decade with new data challenging the effectiveness of this intrinsic flow regulating mechanism, particularly to abrupt changes in blood pressure over the course of seconds (i.e. dynamic cerebral autoregulation), like those observed during RE. Acutely, RE can challenge CBF regulation, resulting in adverse responses (e.g. syncope). Compared with aerobic exercise, RE is relatively understudied, particularly high-intensity dynamic RE with a concurrent Valsalva manoeuvre (VM). However, the VM alone challenges CBF regulation and generates additional complexity when trying to dissociate the mechanisms underpinning the circulatory response to RE. Given the disparate circulatory response between aerobic and RE, primarily the blood pressure profiles, regulation of CBF is ostensibly different. In this review, we summarise current literature and highlight the acute physiological responses to RE, with a focus on the cerebral circulation.

Anthocyanin-Rich New Zealand Blackcurrant Extract Supports the Maintenance of Forearm Blood-Flow During Prolonged Sedentary Sitting.

Objectives: We examined the acute effects of anthocyanin-rich New Zealand blackcurrant extract and a placebo on hemodynamics during 120 min of sedentary sitting in healthy males. Additionally, we investigated whether changes in resting hemodynamics altered repeated isometric hand-grip exercise performance and post exercise forearm blood flow (FBF). Methods: Ten healthy males completed two trials during which they ingested either blackcurrant extract (1.87 mg total anthocyanins/kg bodyweight) or placebo powder. Heart rate, blood pressure and forearm blood flow were measured, and venous blood was sampled, prior to and 30, 60, 90 and 120 min-post ingestion. Participants remained seated for the duration of each trial. At 120 min post-ingestion participants completed as many repetitions of isometric hand-grip contractions as possible. Results: Heart rate, blood pressure and mean arterial pressure changed over time (all p < 0.001) but did not differ between treatments. A treatment x time interaction for FBF (p = 0.025) and forearm vascular resistance (FVR) (p = 0.002) was found. No difference in the number of isometric hand-grip contractions was observed between treatments (p = 0.68) nor was there any treatment x time interaction in post-exercise FBF (p = 0.997). Plasma endothelin-1 (p = 0.023) and nitrate (p = 0.047) changed over time but did not differ between treatments (both p > 0.1). Plasma nitrite did not change over time (p = 0.732) or differ between treatments (p = 0.373). Conclusion: This study demonstrated that acute ingestion of a single dose of blackcurrant extract maintained FBF and FVR during an extended period of sitting; however, this did not influence exercise performance during hand-grip exercise.

The Effects of Anticipation and Visual and Sensory Performance on Concussion Risk in Sport: A Review.

Sports-related concussions pose a significant public health concern, and preventative measures are needed to help reduce risk in sport. Vision training could be a suitable prevention strategy for sports-related concussion to help improve athletes' abilities to scan the visual field for oncoming objects or opponents and thus anticipate head impacts. By accurately anticipating impacts, athletes can prepare for impact or attempt to avoid the collision altogether. The purpose of this review is to explore the relationships between anticipation, visual and sensorimotor performance and head accelerations, as well as to examine the efficacy of vision training programmes in reducing concussion risk in sport. Anticipation of head impacts has been shown to help reduce linear and rotational head accelerations, particularly for mild-to-moderate severity head impacts, but less so for severe head impacts. There is conflicting evidence regarding the influences visual and sensorimotor performance and oculomotor behaviour have on concussion risk. However, preliminary research indicates vision training may help reduce concussion rates in collegiate American Football players. Therefore, this promising area of research warrants further investigation, particularly the role of anticipation and visual and sensory performance on reducing concussion risk in non-helmeted contact sports.

Is Postexercise Blood Flow Restriction a Viable Alternative to Other Resistance Exercise Protocols?

PURPOSE: The purpose of this study was to identify whether post-resistance exercise (REx) blood flow restriction (BFR) can elicit a similar acute training stimulus to that offered by either heavy REx or traditional low-load BFR REx. METHOD: Ten men completed trials with 30% one-repetition maximum (1RM) for 5 sets of 15 repetitions without BFR (30%), with BFR during exercise (30% RD), and with postexercise BFR (30% RP) and at 75% 1RM for 3 sets of 10 repetitions. Lactate and cortisol were measured before and up to 60 min after exercise. Thigh circumference, ratings of perceived exertion (RPE), and pain were measured before and after exercise. Surface electromyography was measured during exercise. RESULTS: All conditions had a large effect (effect size [ES] > 0.8) on lactate, with the largest effects observed with the 75% condition; no differences were observed between the 30% conditions. All conditions had a moderate effect (ES > 0.25 ≤ 0.4) on increasing thigh circumference. This effect was maintained (ES = 0.35) with the application of BFR after REx (30% RP). Change in RPE, from the first to last set, was significantly greater with 30% RD compared with other conditions (all p < .05). Electromyography amplitude was higher and percentage change was greater for the 75% condition compared with the other conditions (both p < .05). CONCLUSIONS: The application of BFR immediately post-REx altered several of the responses associated with REx that is aimed at inducing muscular hypertrophy. Additionally, these changes occurred with less pain and perceived exertion suggesting that this form of REx may offer an alternative, tolerable method of REx.