John J. Durocher

Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA (r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.

Neural and cardiovascular responses to emotional stress in humans

Sympathetic neural responses to mental stress are well documented but controversial, whereas sympathetic neural responses to emotional stress are unknown. The purpose of this study was to investigate neural and cardiovascular responses to emotional stress evoked by negative pictures and reexamine the relationship between muscle sympathetic nerve activity (MSNA) and perceived stress. Mean arterial pressure (MAP), heart rate (HR), MSNA, and perceived stress levels were recorded in 18 men during three randomized trials: 1) neutral pictures, 2) negative pictures, and 3) mental stress. MAP and HR increased during mental stress (Delta14 +/- 2 mmHg and Delta15 +/- 2 beats/min, P < 0.001) but did not change during viewing of negative or neutral pictures. MSNA did not change during viewing of neutral (Delta1 +/- 1 burst/min, n = 16) or negative (Delta0 +/- 1 burst/min, n = 16) pictures or during mental stress (Delta1 +/- 2 burst/min, n = 13). Perceived stress levels were higher during mental stress (3 +/- 0 arbitrary units) than during viewing negative pictures (2 +/- 0 arbitrary units, P < 0.001). Perceived stress levels were not correlated to changes in MSNA during negative pictures (r = 0.10, P = 0.84) or mental stress (r = 0.36, P = 0.23). In conclusion, our results demonstrate robust increases in MAP and HR during mental stress, but not during emotional stress evoked by negative pictures. Although the influence of mental stress on MSNA remains unresolved, our findings challenge the concept that perceived stress levels modulate MSNA during mental stress.

Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

Neurovascular responses to mental stress in prehypertensive humans

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120-139 and/or diastolic 80-89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans.

Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (> 0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope = -1.95 ± 0.18 bursts·(100 beats)⁻¹)·mmHg⁻¹; r = -0.86 ± 0.03] or total MSNA [slope = -438 ± 91 units·(beat)⁻¹ mmHg⁻¹; r = -0.76 ± 0.06]. During mental stress, the slope between burst incidence and DAP was significantly reduced [slope = -1.14 ± 0.12 bursts·(100 beats)⁻¹·mmHg⁻¹; r = -0.72 ± 0.03; P < 0.01], indicating attenuation of sympathetic BRS. A more detailed analysis revealed an attenuation of sympathetic BRS during the first 2 min of mental stress (P < 0.01) but no change during the final 3 min of mental stress (P = 0.25). The present study demonstrates that acute mental stress attenuates sympathetic BRS, which may partially contribute to sympathoexcitation during the mental stress-pressor response. However, this attenuation appears to be isolated to the onset of mental stress. Moreover, variable MSNA responses to mental stress do not appear to be directly related to sympathetic BRS.

The effect of squat depth on multiarticular muscle activation in collegiate cross-country runners.

Abstract Gorsuch, J, Long, J, Miller K, Primeau, K, Rutledge, S, Sossong, A, and Durocher, JJ. The effect of squat depth on multiarticular muscle activation in collegiate cross-country runners. J Strength Cond Res 27(9): 2619–2625, 2013—The squat is a closed-chain lower body exercise commonly performed by many athletes. Muscle activity has been examined during partial and parallel squats in male weightlifters, but not in male and female runners. Therefore, this study measured muscle activity with surface electromyography (EMG) during partial and parallel squats in 20 Division I collegiate cross-country runners (10 males and 10 females) in a randomized crossover design. We hypothesized the parallel squat would increase extensor muscle activitation (i.e. hamstrings and erector spinae). Furthermore, we sought to determine if changes in muscle activity were different between males and females. Participants performed 6 repetitions using their 10 repetition maximum loads for each condition during EMG testing. EMG was performed on the right rectus femoris, biceps femoris, lumbar erector spinae, and lateral head of the gastrocnemius. Rectus femoris activity (0.18 ± 0.01 vs. 0.14 ± 0.01 mV) and erector spinae activity (0.16 ± 0.01 vs. 0.13 ± 0.01 mV) were significantly higher (p < 0.05) during the parallel squat than during the partial squat condition. This increase in muscle activity may be attributed to greater ranges of motion at the hip and knee joints. Biceps femoris and gastrocnemius activity were similar between conditions. No significant differences existed between males and females (squat condition × gender; p > 0.05). During preliminary isokinetic testing, both male and female runners demonstrated deficient hamstrings-to-quadriceps ratios, which would not likely improve by performing parallel squats based on our EMG findings. Despite the reduced load of the parallel squat, rectus femoris and erector spinae activity were elevated. Thus, parallel squats may help runners to train muscles vital for uphill running and correct posture, while preventing injury by using lighter weights through a larger range of motion.

Comparison of on-ice and off-ice graded exercise testing in collegiate hockey players.

The purpose of this study was to compare lactate thresholds (LT) and maximal aerobic capacities (VO(2 max) during sport-specific skating (on ice) and cycle ergometry (off ice) in collegiate hockey players. We hypothesized that VO(2 max) and LT would be higher on ice. We also sought to determine if on-ice and off-ice VO(2 max) values were correlated. Twelve collegiate hockey players performed both graded exercise protocols in randomized order to fatigue. Both protocols included 80 s of work during each stage, followed by 40 s of rest to allow for blood lactate sampling. VO(2 max) was significantly higher on ice (46.9 +/- 1.0 mL*kg(-1)*min(-1)) than off ice (43.6 +/- 0.9 mL*kg(-1)*min(-1); p < 0.05). Maximal heart rate (HR(max)) was also higher on ice (192.2 +/- 1.8 beats*min(-1)) than off ice (186.0 +/- 1.5 beats*min(-1); p < 0.01). LT was drastically higher on ice than off ice as a percentage of VO(2 max) (85.9% +/- 1.9% vs. 69.7% +/- 1.3%; p < 0.01) and HR(max) (90.1% +/- 1.3% vs. 79.4% +/- 1.6%; p < 0.01). Finally, no correlation existed between VO(2 max) values off ice and on ice (r = -0.002; p = 0.99). Our results indicate that off-ice VO(2 max) and LT are not adequate predictors of on-ice VO(2 max) and LT in collegiate hockey players. These findings challenge the use of cycle ergometry to assess aerobic capacity at events such as the National Hockey League Entry Draft combine. We suggest that hockey players be tested in a sport-specific manner, regardless of whether those tests are performed on ice or off ice.

Sport-specific assessment of lactate threshold and aerobic capacity throughout a collegiate hockey season

The purpose of this study was to examine lactate threshold (LT) and maximal aerobic capacity with a sport-specific skating protocol throughout a competitive season in collegiate hockey players. We hypothesized that maximal aerobic capacity and skating velocity at LT would increase as the season progressed. Sixteen Division I college hockey players performed a graded exercise skating protocol to fatigue at 3 different times (pre-, mid-, and postseason). Subjects skated for 80 s during each stage, followed by 40 s of rest to allow for blood lactate sampling. Velocity at LT was similar during preseason (4.44 +/- 0.08 m.s-1) and postseason (4.52 +/- 0.05 m.s-1) testing, but was significantly elevated at midseason (4.70 +/- 0.08 m.s-1; p < 0.01), compared with preseason. In contrast, LT as a percentage of maximal heart rate (HRmax) was unchanged throughout the season. HRmax remained constant throughout the season, at approximately 190 beats.min-1. Preseason maximal aerobic capacity (48.7 +/- 0.8 mL.kg-1.min-1) was significantly higher than that at postseason (45.0 +/- 1.1 mL.kg-1.min-1; p < 0.01). In conclusion, skating velocity at LT improved from pre- to midseason, but this adaptation was not maintained at postseason. Additionally, maximal aerobic capacity was reduced from pre- to postseason. These findings suggest a need for aerobic training throughout the college hockey season.

Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans

Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo (n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.

Sympathetic neural responses to mental stress during acute simulated microgravity

Neural and cardiovascular responses to mental stress and acute 6 degrees head-down tilt (HDT) were examined separately and combined. We hypothesized sympathoexcitation during mental stress, sympathoinhibition during HDT, and an additive neural interaction during combined mental stress and HDT. Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded in 16 healthy subjects (8 men, 8 women) in the supine position during three randomized trials: 1) mental stress (via mental arithmetic), 2) HDT, and 3) combined mental stress and HDT. Mental stress significantly increased MSNA (7+/-1 to 12+/-2 bursts/min; P<0.01), MAP (91+/-2 to 103+/-2 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). HDT did not change MSNA or HR, but MAP was reduced (91+/-2 to 89+/-3 mmHg; P<0.05). Combined mental stress and HDT significantly increased MSNA (7+/-1 to 10+/-1 bursts/min; P<0.01), MAP (88+/-3 to 99+/-3 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). Increases in MSNA and HR during the combination trial were not different from the sum of the individual trials. However, the increase in MAP during the combination trial was significantly greater than the sum of the individual trials (change of 11+/-1 vs. 9+/-1 mmHg; P<0.05). We conclude that the interaction for MSNA and HR are additive during combined mental stress and HDT but that MAP responses are slightly augmented during the combined trial. These findings demonstrate that sympathetic neural responses to mental stress are unaltered by simulated microgravity.