Effects of aerobic exercise on ambulatory blood pressure responses to acute partial sleep deprivation: impact of chronotype and sleep quality.

Blood pressure (BP) follows a circadian rhythm intertwined with the sleep-wake cycle. Acute partial sleep deprivation (PSD; sleep ≤ 6 h) can increase BP, associated with increased cardiovascular risk. Acute exercise can reduce BP for up to 24 h, a phenomenon termed postexercise hypotension. The present study tested whether aerobic exercise could mitigate the augmented 24-h ambulatory BP caused by acute PSD. Twenty-four young otherwise healthy adults (22 ± 3 yr; 14 females; self-reported chronotypes: 6 early/10 intermediate/8 late; Pittsburgh sleep quality index: 17 good/7 poor sleepers) completed a randomized crossover trial in which, on different days, they slept normally (2300-0700), restricted sleep [0330-0700 (PSD)], and cycled for 50 min (70-80% predicted heart rate maximum) before PSD. Ambulatory BP was assessed every 30 min until 2100 the next day. Acute PSD increased 24-h systolic BP (control 117 ± 9 mmHg, PSD 122 ± 9 mmHg; P < 0.001) and prior exercise attenuated (exercise + PSD 120 ± 9 mmHg; P = 0.04 vs. PSD) but did not fully reverse this response (exercise + PSD, P = 0.02 vs. control). Subgroup analysis revealed that the 24-h systolic BP reduction following exercise was specific to late types (PSD 119 ± 7 vs. exercise + PSD 116 ± 6 mmHg; P < 0.05). Overall, habitual sleep quality was negatively correlated with the change in daytime systolic BP following PSD (r = -0.56, P < 0.01). These findings suggest that the ability of aerobic cycling exercise to counteract the hemodynamic effects of acute PSD in young adults may be dependent on chronotype and that habitual sleep quality can predict the daytime BP response to acute PSD.NEW & NOTEWORTHY We demonstrate that cycling exercise attenuates, but does not fully reverse, the augmented 24-h ambulatory blood pressure (BP) response caused by acute partial sleep deprivation (PSD). This response was primarily observed in late chronotypes. Furthermore, daytime BP after acute PSD is related to habitual sleep quality, with better sleepers being more prone to BP elevations. This suggests that habitual sleeping habits can influence BP responses to acute PSD and their interactions with prior cycling exercise.

Physiological and clinical responses to cycling 7850 km over 85 days in a physically active middle-aged man with idiopathic Parkinson's disease.

This case characterizes the clinical motor, perceived fatigue, gait and balance, cardiovascular, neuromuscular, and cardiopulmonary responses after cycling 7850 km over 85 days in a physically active 57-year-old male with idiopathic Parkinson's disease (PD). The participant cycled 73/85 days (86%); averaging 107.5 ± 48.9 km/day over 255.4 ± 108.8 min. Average cycling heart rate was 117 ± 11 bpm. The Unified Parkinson Disease Rating Scale (UPDRS) Part III motor score decreased from 46 to 26 (-44%), while the mean Parkinson Fatigue Scale (PFS-16) score decreased from 3.4 to 2.3 (-32%). Peak power output on a maximal aerobic exercise test increased from 326 to 357 W (+10%), while peak isotonic power of single-leg knee extension increased from 312 to 350 W (+12%). Maximal oxygen uptake following the trip was 53.1 mL/min/kg or 151% of predicted. Resting heart rate increased from 48 to 71 bpm (+48%). The systolic and diastolic blood pressure responses to a 2-min submaximal static handgrip exercise were near absent at baseline (∆2/∆2 mm Hg) but appeared normal post-trip (∆17/∆9 mm Hg). Gait and static balance measures were unchanged. This case report demonstrates the capacity for physiological and clinical adaptations to a high-volume, high-intensity cycling regiment in a physically active middle-aged male with PD.

Blood Pressure Responses to Postexercise Circulatory Occlusion Are Attenuated After Exercise-Induced Muscle Weakness.

PURPOSE: Exercise blood pressure (BP) responses are thought to be determined by relative exercise intensity (percent maximal voluntary contraction (MVC) strength). However, cross-sectional studies report that during a static contraction, higher absolute force is associated with greater BP responses to relative intensity exercise and subsequent muscle metaboreflex activation with postexercise circulatory occlusion (PECO). We hypothesized that a bout of unaccustomed eccentric exercise would reduce knee extensor MVC and subsequently attenuate BP responses to PECO. METHODS: Continuous BP, heart rate, muscle oxygenation, and knee extensor electromyography were recorded in 21 young healthy individuals (female, n = 10) during 2 min of 20% MVC static knee extension exercise and 2 min of PECO, performed before and 24 h after 300 maximal knee extensor eccentric contractions to cause exercise-induced muscle weakness. As a control, 14 participants repeated the eccentric exercise 4 wks later to test whether BP responses were altered when exercise-induced muscle weakness was attenuated via the protective effects of the repeated bout effect. RESULTS: Eccentric exercise reduced MVC in all participants (144 ± 43 vs 110 ± 34 N·m, P < 0.0001). BP responses to matched relative intensity static exercise (lower absolute force) were unchanged after eccentric exercise ( P > 0.99) but were attenuated during PECO (systolic BP: 18 ± 10 vs 12 ± 9 mm Hg, P = 0.02). Exercise-induced muscle weakness modulated the deoxygenated hemoglobin response to static exercise (64% ± 22% vs 46% ± 22%, P = 0.04). When repeated after 4 wks, exercise-induced weakness after eccentric exercise was attenuated (-21.6% ± 14.3% vs -9.3 ± 9.7, P = 0.0002) and BP responses to PECO were not different from control values (all, P > 0.96). CONCLUSIONS: BP responses to muscle metaboreflex activation, but not exercise, are attenuated by exercise-induced muscle weakness, indicating a contribution of absolute exercise intensity on muscle metaboreflex activation.

Ischemic Preconditioning Acutely Improves Functional Sympatholysis during Handgrip Exercise in Healthy Males but not Females.

PURPOSE: Ischemic preconditioning (IPC), a procedure that involves the cyclic induction of limb ischemia and reperfusion via tourniquet inflation, has been reported to improve exercise capacity and performance, but the underlying mechanisms remain unclear. During exercise, sympathetically mediated vasoconstriction is dampened in active skeletal muscle. This phenomenon, termed functional sympatholysis, plays a critical role in maintaining oxygen delivery to working skeletal muscle and may contribute to determining exercise capacity. Herein, we investigate the effects of IPC on functional sympatholysis in humans. METHODS: In 20 (10M/10F) healthy young adults, forearm blood flow (Doppler ultrasound) and beat-to-beat arterial pressure (finger photoplethysmography) were measured during lower body negative pressure (LBNP; -20 mm Hg) applied at rest and simultaneously during rhythmic handgrip exercise (30% maximum contraction) before and after local IPC (4 × 5-min 220 mm Hg) or sham (4 × 5-min 20 mm Hg). Forearm vascular conductance (FVC) was calculated as forearm blood flow/mean arterial pressure and the magnitude of sympatholysis as the difference of LBNP-induced changes in FVC between handgrip and rest. RESULTS: At baseline, LBNP decreased FVC (females [F] = ∆-41% ± 19%; males [M] = ∆-44% ± 10%), and these responses were attenuated during handgrip (F = ∆-8% ± 9%; M = ∆-8% ± 7%). After IPC, LBNP induced similar decreases in resting FVC (F = ∆-37% ± 19%; M = ∆-44% ± 13%). However, during handgrip, this response was further attenuated in males (∆-3% ± 9%, P = 0.02 vs pre) but not females (∆-5% ± 10%, P = 0.13 vs pre), which aligned with an IPC-mediated increase in sympatholysis (M-pre = 36% ± 10% vs post = 40% ± 9%, P = 0.01; F-pre = 32% ± 15% vs post = 32% ± 14%, P = 0.82). Sham IPC had no effect on any variables. CONCLUSIONS: These findings highlight a sex-specific effect of IPC on functional sympatholysis and provide evidence of a potential mechanism underlying the beneficial effects of IPC on human exercise performance.

Sympathetic transduction of blood pressure during graded lower body negative pressure in young healthy adults.

Sympathetic transduction of blood pressure (BP) is correlated negatively with resting muscle sympathetic nerve activity (MSNA) in cross-sectional data, but the acute effects of increasing MSNA are unclear. Sixteen (4 female) healthy adults (26 ± 3 years) underwent continuous measurement of heart rate, BP, and MSNA at rest and during graded lower body negative pressure (LBNP) at -10, -20, and -30 mmHg. Sympathetic transduction of BP was quantified in the time (signal averaging) and frequency (MSNA-BP gain) domains. The proportions of MSNA bursts firing within each tertile of BP were calculated. As expected, LBNP increased MSNA burst frequency (P < 0.01) and burst amplitude (P < 0.02), although the proportions of MSNA bursts firing across each BP tertile remained stable (all P > 0.44). The MSNA-diastolic BP low-frequency transfer function gain (P = 0.25) was unchanged during LBNP; the spectral coherence was increased (P = 0.03). Signal-averaged sympathetic transduction of diastolic BP was unchanged (from 2.1 ± 1.0 at rest to 2.4 ± 1.5, 2.2 ± 1.3, and 2.3 ± 1.4 mmHg; P = 0.43) during LBNP, but diastolic BP responses following nonburst cardiac cycles progressively decreased (from -0.8 ± 0.4 at rest to -1.0 ± 0.6, -1.2 ± 0.6, and -1.6 ± 0.9 mmHg; P < 0.01). As a result, the difference between MSNA burst and nonburst diastolic BP responses was increased (from 2.9 ± 1.4 at rest to 3.4 ± 1.9, 3.4 ± 1.9, and 3.9 ± 2.1 mmHg; P < 0.01). In conclusion, acute increases in MSNA using LBNP did not alter traditional signal-averaged or frequency-domain measures of sympathetic transduction of BP or the proportion of MSNA bursts firing at different BP levels. The factors that determine changes in the firing of MSNA bursts relative to oscillations in BP require further investigation.