Blake G. Perry

Cerebral hemodynamics during graded Valsalva maneuvers

The Valsalva maneuver (VM) produces large and abrupt changes in mean arterial pressure (MAP) that challenge cerebral blood flow and oxygenation. We examined the effect of VM intensity on middle cerebral artery blood velocity (MCAv) and cortical oxygenation responses during (phases I–III) and following (phase IV) a VM. Healthy participants (n = 20 mean ± SD: 27 ± 7 years) completed 30 and 90% of their maximal VM mouth pressure for 10 s (order randomized) whilst standing. Beat-to-beat MCAv, cerebral oxygenation (NIRS) and MAP across the different phases of the VM are reported as the difference from standing baseline. There were significant interaction (phase * intensity) effects for MCAv, total oxygenation index (TOI) and MAP (all P < 0.01). MCAv decreased during phases II and III (P < 0.01), with the greatest decrease during phase III (−5 ± 8 and −19 ± 15 cm·s−1 for 30 and 90% VM, respectively). This pattern was also evident in TOI (phase III: −1 ± 1 and −5 ± 4%, both P < 0.05). Phase IV increased MCAv (22 ± 15 and 34 ± 23 cm·s−1), MAP (15 ± 14 and 24 ± 17 mm Hg) and TOI (5 ± 6 and 7 ± 5%) relative to baseline (all P < 0.05). Cerebral autoregulation, indexed, as the %MCAv/%MAP ratio, showed a phase effect only (P < 0.001), with the least regulation during phase IV (2.4 ± 3.0 and 3.2 ± 2.9). These data illustrate that an intense VM profoundly affects cerebral hemodynamics, with a reactive hyperemia occurring during phase IV following modest ischemia during phases II and III.

The cerebrovascular response to graded Valsalva maneuvers while standing

The Valsalva maneuver (VM) produces large and abrupt increases in mean arterial pressure (MAP) at the onset of strain (Phase I), however, hypotension, sufficient to induce syncope, occurs upon VM release (phase III). We examined the effect of VM intensity and duration on middle cerebral artery blood velocity (MCAv) responses. Healthy men (n = 10; mean ± SD: 26 ± 4 years) completed 30%, 60%, and 90% of their maximal VM mouth pressure, for 5 and 10 sec (order randomized) while standing. Beat‐to‐beat MCAv and MAP during phase I (peak), at nadir (phase III), and recovery are reported as the change from standing baseline. During phase I, MCAv rose 15 ± 6 cm·s−1 (P < 0.001), which was not reliably different between intensities (P = 0.11), despite graded increases in MAP (P < 0.001; e.g., +12 ± 9 mmHg vs. +35 ± 14 for 5 sec 30% and 90% VM, respectively). During Phase III, the MCAv response was duration‐ (P = 0.045) and intensity dependent (P < 0.001), with the largest decrease observed following the 90% VM (e.g., −19 ± 13 and −15 ± 11 cm·s−1 for 5 and 10 sec VM, respectively) with a concomitant decrease in MAP (P < 0.001, −23 ± 11 and −23 ± 9 mmHg). This asymmetric response may be attributable to the differential modulators of MCAv throughout the VM. The mechanical effects of the elevated intrathoracic pressure during phase I may restrain increases in cerebral perfusion via related increases in intracranial pressure; however, during phase III the decrease in MCAv arises from an abrupt hypotension, the extent of which is dependent upon both the duration and intensity of the VM.

Middle cerebral artery blood flow velocity in response to lower body positive pressure

Lower body positive pressure (LBPP) has been used in the treatment of haemorrhagic shock and in offsetting g‐force induced fluid shifts. However, the middle cerebral artery blood flow velocity (MCAv) response to supine LBPP is unknown. Fifteen healthy volunteers (mean ± SD: age, 26 ± 5 year; body mass, 79 ± 10 kg; height, 174 ± 9 cm) completed 5 minutes of 20 and 40 mm Hg LBPP, in a randomized order, separated by 5 minutes rest (baseline). Beat‐to‐beat MCAv and blood pressure, partial pressure of end‐tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. All measures were similar between baseline periods (all P>0·30). Mean arterial pressure (MAP) increased by 7 ± 6 (8 ± 7%) and 13 ± 7 mm Hg (19 ± 11%) from baseline during 20 and 40 mm Hg (P<0·01), respectively. The greater MAP increase at 40 mm Hg (P<0·01 versus 20 mm Hg) was mediated via a greater increase in total peripheral resistance (P<0·01), with heart rate, cardiac output (Model flow) and PETCO2 remaining unchanged (all P>0·05) throughout. MCAv increased from baseline by 3 ± 4 cm s−1 (5 ± 5%) during 20 mm Hg (P = 0·003), whilst no change (P = 0·18) was observed during 40 mm Hg. Our results indicate a divergent response, in that 20 mm Hg LBPP‐induced modest increases in both MCAv and MAP, yet no change in MCAv was observed at the higher LBPP of 40 mm Hg despite a further increase in MAP.

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

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.

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

What is the central question of this study? The cold pressor test (CPT) is commonly used to investigate cerebrovascular regulation. Despite blood viscosity per se being able to modulate cerebral blood flow, it is unknown whether hydration status alters this response, nor is it commonly reported. We investigated the effects of mild dehydration on the cerebrovascular response to the CPT. What is the main finding and its importance? The main finding from this study is that when compared with euhydration, mild dehydration reduced cerebral blood flow via a decrease in the partial pressure of end‐tidal CO2. This demonstrates that hydration status is an important modulator of the cerebrovascular response to the CPT and should be reported and controlled for.

Postexercise orthostatic intolerance: influence of exercise intensity

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.

Hemodynamic response to upright resistance exercise: effect of load and repetition.

INTRODUCTION/PURPOSE Upright resistance exercise causes large transient fluctuations in blood pressure during and immediately after the performance. We examined the effect of resistance load and the number of repetitions on the middle cerebral artery blood flow velocity (MCAv) response during and after upright squatting exercise. METHODS Healthy males (n = 12; mean ± SD: 26 ± 5 yr) completed 30%, 60%, and 90% of their six-repetition maximum load, completing two and six repetitions of these loads during two visits (order randomized). Beat-to-beat MCAv, blood pressure, and continuous end-tidal PCO2 during exercise, at nadir, and during recovery are reported as the change from preexercise standing baseline. RESULTS During exercise, MCAvmean increased 31% ± 16% (P < 0.001) across all loads (P = 0.74) and repetitions (P = 0.89), whereas mean arterial pressure (MAP) increased (all P < 0.05) as load and repetitions increased (e.g., 122 ± 9 (two repetitions) vs 135 ± 11 mm Hg (six repetitions) and 128 ± 13 vs 143 ± 14 mm Hg, at 30% and 60%, respectively). Within the six-repetition sets, peak MCAvmean remained unchanged across the set (P = 0.61), whereas MAP increased (P = 0.003). The 90% load produced the lowest MCAvmean nadir (pooled means, -18 ± 6 vs -10 ± 7 cm·s, P < 0.001 vs 30%) and MAP nadir (-34 ± 7 and -43 ± 5 mm Hg, for two and six repetitions, respectively; P < 0.001) after exercise. Postexercise MCAvmean reductions occurred via a selective, load-dependent (P < 0.001) decrease in diastolic MCAv. MCAvmean remained below baseline for the longest period after the 90% six-repetition set (10 s postexercise, P < 0.01) and took the longest to recover (14.8 ± 6.9 s, P = 0.002). CONCLUSION These data indicate that higher relative loads produce a greater postexercise hypotension and result in a proportionate reduction in MCAvmean.

The effect of hypercapnia on static cerebral autoregulation

Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure (BP); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ± SD: age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady‐state elevations in mean arterial BP (MAP), induced via lower body positive pressure (LBPP). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity (MCAv), BP, partial pressure of end‐tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCAv was apparent between eupcapnic baseline and LBPPs (grouped mean 65 ± 11 cm·s−1, all P > 0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P < 0.001 vs. baseline). Conversely, MCAv during the hypercapnic +40 mm Hg stage (Δ31 ± 13 cm·s−1) was greater than hypercapnia alone (Δ25 ± 11 cm·s−1, P = 0.026), due to an increased MAP (Δ14 ± 7 mm Hg, P < 0.001 vs. hypercapnia alone and P = 0.026 vs. hypercapnia +20 mm Hg). As cardiac output and PETCO2 were similar across all hypercapnic stages (all P > 0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation.

Validity of a device designed to measure braking power in bicycle disc brakes.

Abstract Real-world cycling performance depends not only on exercise capacities, but also on efficiently traversing the bicycle through the terrain. The aim of this study was to determine if it was possible to quantify the braking done by a cyclist in the field. One cyclist performed 408 braking trials (348 on a flat road; 60 on a flat dirt path) over 5 days on a bicycle fitted with brake torque and angular velocity sensors to measure brake power. Based on Newtonian physics, the sum of brake work, aerodynamic drag and rolling resistance was compared with the change in kinetic energy in each braking event. Strong linear relationships between the total energy removed from the bicycle-rider system through braking and the change in kinetic energy were observed on the tar-sealed road (r2 = 0.989; p < 0.0001) and the dirt path (r2 = 0.952; p < 0.0001). T-tests revealed no difference between the total energy removed and the change in kinetic energy on the road (p = 0.715) or dirt (p = 0.128). This study highlights that brake torque and angular velocity sensors are valid for calculating brake power on the disc brakes of a bicycle in field conditions. Such a device may be useful for investigating cyclists’ ability to traverse through various terrains.

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

ABSTRACT 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.