Postexercise Hemodynamics Research Articles

Impact of mask wearing during high-intensity exercise on post-exercise hemodynamics

Impact of mask wearing during high-intensity exercise on post-exercise hemodynamics

The Impact Of Mask-wearing During High-intensity Exercise On Post-exercise Hemodynamics

The Impact Of Mask-wearing During High-intensity Exercise On Post-exercise Hemodynamics

Greater post-exercise hypotension in healthy young untrained men after exercising in a hot compared to a temperate environment

This research examined the effects of exercising in a hot compared to a temperate environment on post-exercise hemodynamics in untrained men. We hypothesized exercise in a hot compared to a temperate environment would elicit greater post-exercise hypotension, and this would be attributable to higher cutaneous vascular conductance and sweat loss, and lower heart rate variability (HRV) and cardiac baroreflex sensitivity (cBRS). In a randomized counterbalanced order, 12 untrained healthy men completed two trials involving 40-min leg-cycling exercise at either 23 °C (CON) or 35 °C (HOT). Post-exercise participants rested supine for 60 min at 23 °C whilst hemodynamic and thermoregulatory measurements were assessed. Post-exercise hypotension was greater after exercising in a hot than a temperate environment as indicated by a lower mean arterial pressure at 60 min recovery (CON 83 ± 5 mmHg, HOT 78 ± 5 mmHg, Mean difference [95% confidence interval], −5 [–8, −3] mmHg). Throughout recovery, cutaneous vascular conductance was higher, and cBRS and HRV were lower after exercising in a hot than in a temperate environment (P < 0.05). Sweat loss was greater on HOT than on CON (P < 0.001). Post-exercise hypotension after exercising in the hot environment was associated with sweat loss (r = 0.66, P = 0.02), and changes in cutaneous vascular conductance (r = 0.64, P = 0.03), and HRV (Root mean square of the successive difference in R-R interval [RMSSD]) r=0.75, P = 0.01 and and log high frequency [HF] r=0.66, P = 0.02), but not cBRS (all, r ≤ 0.2, P > 0.05). Post-exercise hypotension was greater after exercise in a hot compared to a temperate environment and may be partially explained by greater sweat loss and cutaneous vascular conductance, and lower HRV.

Investigating the roles of exercise intensity and biological sex on postexercise alterations in cardiac function.

The term exercise-induced cardiac fatigue (EICF) has typically been used to describe a transient reduction in cardiac function following prolonged-strenuous exercise. Recent evidence demonstrates that EICF can occur following only 45 min of high-intensity exercise when assessed using exercising stress echocardiography. This investigation sought to examine whether sprint intervals (SIT; 6 × 30 s Wingate tests), or 90-min moderate-cycling with sprint intervals (MIX; 90 min with 1 × 30 s Wingate test every 15 min) would cause greater EICF than 90 min (CON) or 3 h (LONG) moderate-cycling assessed using stress echocardiography, with a secondary aim to interrogate sex differences in EICF. Seventeen participants (M: 9, F: 8) underwent three cycling sessions with stress-echocardiography performed before-and-after each condition at a target heart rate (HR) of 100 beats·min-1, with the CON testing occurring at the mid-point of the 3 h LONG condition. For all conditions, measures of left ventricular (LV) systolic [stroke volume, ejection fraction (EF), peak longitudinal strain, isovolumetric contraction time, S') and diastolic (E/A, E', isovolumetric relaxation time, longitudinal strain rate) function were reduced after exercise (all P < 0.05). In the right ventricle (RV), systolic function was reduced (tricuspid annular plane systolic excursion, S', peak longitudinal strain and strain rate) following all conditions, and fractional area change was reduced to the greatest degree following SIT (condition × time, P = 0.01). Females demonstrated lesser impairments in LV EF, and elastance (ESP/ESV) compared with males (P < 0.05). Markers of EICF occurred similarly following all cycling loads, suggesting the functional changes may be due to altered loading conditions and reduced stress-echocardiography workload. However, males experienced greater cardiac alterations in some measures, likely due to greater changes in postexercise loading conditions.NEW & NOTEWORTHY This investigation sought to determine the role of exercise intensity on the magnitude of exercise-induced cardiac fatigue using stress echocardiography to maintain loading conditions, with a secondary purpose of assessing sex differences. Unexpectedly, it was found that all cycling loads elicited the same magnitude of functional alteration, which likely represents a common response to exercise and stress echocardiography, rather than intrinsic cardiac impairment. Males demonstrated greater alterations than females, likely due to sex differences in postexercise hemodynamics.

Comparisons Between Normobaric Normoxic and Hypoxic Recovery on Post-exercise Hemodynamics After Sprint Interval Cycling in Hypoxia.

The aim of this study was to investigate the effects of either normoxic or hypoxic recovery condition on post-exercise hemodynamics after sprint interval leg cycling exercise rather than hemodynamics during exercise. The participants performed five sets of leg cycling with a maximal effort (30 s exercise for each set) with a 4-min recovery of unloaded cycling between the sets in hypoxia [fraction of inspired oxygen (FiO2) = 0.145]. The load during pedaling corresponded to 7.5% of the individual’s body weight at the first set, and it gradually reduced from 6.5 to 5.5%, 4.5, and 3.5% for the second to fifth sets. After exercise, the participants rested in a sitting position for 30 min under normoxia (room-air) or hypoxia. Mean arterial pressure decreased over time during recovery (p < 0.001) with no condition and interaction effects (p > 0.05). Compared to pre-exercise values, at 30 min after exercise, mean arterial pressure decreased by 5.6 ± 4.8 mmHg (mean ± standard deviation) during hypoxic recovery, and by 5.3 ± 4.6 mmHg during normoxic recovery. Peripheral arterial oxygen saturation (SpO2) at all time points (5, 10, 20, and 30 min) during hypoxic recovery was lower than during normoxic recovery (all p < 0.05). The area under the hyperemic curve of tissue oxygen saturation (StO2) at vastus lateralis defined as reperfusion curve above the baseline values during hypoxic recovery was lower than during normoxic recovery (p < 0.05). Collectively, post-exercise hypotension after sprint interval leg cycling exercise was not affected by either normoxic or hypoxic recovery despite marked differences in SpO2 and StO2 during recovery between the two conditions.

Skeletal Muscle Hyperemia: A Potential Bridge Between Post-exercise Hypotension and Glucose Regulation.

For both healthy individuals and patients with type 2 diabetes (T2D), the hemodynamic response to regular physical activity is important for regulating blood glucose, protecting vascular function, and reducing the risk of cardiovascular disease. In addition to these benefits of regular physical activity, evidence suggests even a single bout of dynamic exercise promotes increased insulin-mediated glucose uptake and insulin sensitivity during the acute recovery period. Importantly, post-exercise hypotension (PEH), which is defined as a sustained reduction in arterial pressure following a single bout of exercise, appears to be blunted in those with T2D compared to their non-diabetic counterparts. In this short review, we describe research that suggests the sustained post-exercise vasodilation often observed in PEH may sub-serve glycemic regulation following exercise in both healthy individuals and those with T2D. Furthermore, we discuss the interplay of enhanced perfusion, both macrovascular and microvascular, and glucose flux following exercise. Finally, we propose future research directions to enhance our understanding of the relationship between post-exercise hemodynamics and glucose regulation in healthy individuals and in those with T2D.

Central aortic hemodynamics following acute lower and upper-body exercise in a cold environment among patients with coronary artery disease

Exercise is beneficial to cardiovascular health, evidenced by reduced post-exercise central aortic blood pressure (BP) and wave reflection. We assessed if post-exercise central hemodynamics are modified due to an altered thermal state related to exercise in the cold in patients with coronary artery disease (CAD). CAD patients (n = 11) performed moderate-intensity lower-body exercise (walking at 65–70% of HRmax) and rested in neutral (+ 22 °C) and cold (− 15 °C) conditions. In another protocol, CAD patients (n = 15) performed static (five 1.5 min work cycles, 10–30% of maximal voluntary contraction) and dynamic (three 5 min workloads, 56–80% of HRmax) upper-body exercise at the same temperatures. Both datasets consisted of four 30-min exposures administered in random order. Central aortic BP and augmentation index (AI) were noninvasively assessed via pulse wave analyses prior to and 25 min after these interventions. Lower-body dynamic exercise decreased post-exercise central systolic BP (6–10 mmHg, p < 0.001) and AI (1–6%, p < 0.001) both after cold and neutral and conditions. Dynamic upper-body exercise lowered central systolic BP (2–4 mmHg, p < 0.001) after exposure to both temperatures. In contrast, static upper-body exercise increased central systolic BP after exposure to cold (7 ± 6 mmHg, p < 0.001). Acute dynamic lower and upper-body exercise mainly lowers post-exercise central BP in CAD patients irrespective of the environmental temperature. In contrast, central systolic BP was elevated after static exercise in cold. CAD patients likely benefit from year-round dynamic exercise, but hemodynamic responses following static exercise in a cold environment should be examined further.Clinical trials.gov: NCT02855905 04/08/2016.

Impact of Resistance Exercise under Hypoxia on Postexercise Hemodynamics in Healthy Young Males.

We investigated the effects of resistance exercise under hypoxia on postexercise hemodynamics in eight healthy young males. The subjects belonged to a track & field club (sprinters, hurdlers, and long jumpers) and engage in regular physical training (1-2 h per day, 3-5 days per week). Each participant performed eight sets of bilateral leg squats with a one-minute interval under normoxia (room air) and hypoxia (13 % FiO2). During a 60-minute recovery, we set normoxic condition either after normoxic or hypoxic exercise. These two experimental protocols (normoxia and hypoxia) were performed in a random order with a one-week washout period. The leg squat exercise consists of 50 % 1-RM (14 repetitions) × 5 sets and 50% 1-RM (repetitions max; 7 repetitions) × 3 sets. The resting period between each set was 1 min, and a total of 91 repetitions were performed. Blood pressure, heart rate (HR), and several biomarkers were measured pre- and postexercise. The mean arterial pressure (MAP) significantly decreased after exercise compared to the pre-exercise values under both conditions (P < 0.05). The MAP at 20 and 30 min of recovery in hypoxia was significantly lower than in normoxia (P < 0.05, respectively). The antidiuretic hormone significantly increased after 60 min of recovery in both conditions; moreover, the values in hypoxia were significantly higher than those in normoxia (P < 0.05). The delta changes in MAP from baseline (pre-exercise) were significantly related to changes in HR from baseline in normoxia (r = 0.560, P < 0.001) but not in hypoxia. These results suggest that the hypoxic condition elicits greater hypotension after resistance exercise in comparison to normoxia. Moreover, the underlying mechanisms for the attenuation of hypotension after resistance exercise may differ between normoxia and hypoxia.

Greater fluid loss does not fully explain the divergent hemodynamic balance mediating postexercise hypotension in endurance-trained men.

Following exercise, mean arterial pressure (MAP) is reduced ~5-10 mmHg from preexercise baseline. In nonendurance-trained males, postexercise hypotension results from peripheral vasodilation not offset by increased cardiac output (CO). By contrast, postexercise hypotension occurs through a reduction in CO from preexercise baseline in endurance-trained males. The reason(s) explaining these divergent responses remain unknown. Exercise at fixed percentage of peak oxygen consumption (V̇o2peak) is associated with a greater rate of metabolic heat production in trained individuals and therefore elevated sweat rates, both when compared with untrained individuals. We hypothesized that greater fluid loss would explain the postexercise reduction in CO of endurance-trained males. Twelve endurance-trained males (Trained: V̇o2peak, 64 ± 5 ml O2·kg-1·min-1) cycled for 60 min at 60% V̇o2peak (Trained60%). On separate days, 12 nonendurance trained males (Untrained: V̇o2peak, 49 ± 3 ml O2·kg-1·min-1) cycled at 1) 60% V̇o2peak (Untrained60%), and 2) a rate of heat production equivalent to that achieved by the Trained group (UntrainedMatched). Fluid loss was similar between Trained60% (-1.32 ± 0.20 kg) and UntrainedMatched (-1.32 ± 0.23 kg; P = 0.99) but was greater in these conditions relative to Untrained60% (-0.95 ± 0.11 kg; both P < 0.01). During the final 30 min of postexercise supine recovery, MAP was similarly reduced by 5 ± 2 mmHg in all three conditions ( P = 0.91). The reduction in MAP was mediated by a 0.5 ± 0.3 l/min reduction in CO from baseline in Trained60% ( P = 0.01). In contrast, CO returned to baseline following exercise during UntrainedMatched and Untrained60% (both P ≥ 0.30). These data demonstrate that greater fluid loss does not fully explain the divergent postexercise hemodynamic responses observed in trained relative to untrained males. NEW & NOTEWORTHY Even when matched for exercise-induced fluid loss, cardiac output was decreased in trained males but returned to baseline following exercise in their untrained counterparts. However, as per our hypothesis, reductions in stroke volume were similar between groups. This suggests that exercise-induced fluid loss is an important determinant of the stroke volume response during recovery but factors affecting heart rate such as exercise intensity and/or heat stress are also important determinants of postexercise hemodynamics.

Erratum.

Physiological ReportsVolume 5, Issue 8 e13268 ErratumOpen Access Erratum This article corrects the following: The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal-weight individuals Kanokwan Bunsawat, Sushant M. Ranadive, Abbi D. Lane-Cordova, Huimin Yan, Rebecca M. Kappus, Bo Fernhall, Tracy Baynard, Volume 5Issue 7Physiological Reports First Published online: March 31, 2017 First published: 18 April 2017 https://doi.org/10.14814/phy2.13268Citations: 1AboutSections ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat In Bunsawat et al. (2017), the following errors were published in the article. The last line of the Abstract, “An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction” should instead read “An assessment of arterial stiffness response to acute exercise may serve as a useful detection tool for subclinical vascular dysfunction.” In the Limitations section, the line “and central arterial waveforms derived via transfer function has also been validated” should instead read “and central arterial waveforms derived via transfer function have also been validated.” In the last sentence of the Conclusion, the line “the vascular responses to vigorous exercise may serve as a means to detect tool for subclinical vascular dysfunction” should instead read “the vascular responses to vigorous exercise may serve as a detection tool for subclinical vascular dysfunction.” We apologize for the errors. Reference Bunsawat, K., S. M. Ranadive, A. D. Lane-Cordova, H. Yan, R. M. Kappus, B. Fernhall, et al. 2017. The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal-weight individuals. Physiol. Rep. 5: e13226. Citing Literature Volume5, Issue8April 2017e13268 ReferencesRelatedInformation

The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal-weight individuals.

Central arterial stiffness is associated with incident hypertension and negative cardiovascular outcomes. Obese individuals have higher central blood pressure (BP) and central arterial stiffness than their normal‐weight counterparts, but it is unclear whether obesity also affects hemodynamics and central arterial stiffness after maximal exercise. We evaluated central hemodynamics and arterial stiffness during recovery from acute maximal aerobic exercise in obese and normal‐weight individuals. Forty‐six normal‐weight and twenty‐one obese individuals underwent measurements of central BP and central arterial stiffness at rest and 15 and 30 min following acute maximal exercise. Central BP and normalized augmentation index (AIx@75) were derived from radial artery applanation tonometry, and central arterial stiffness was obtained via carotid‐femoral pulse wave velocity (cPWV) and corrected for central mean arterial pressure (cPWV/cMAP). Central arterial stiffness increased in obese individuals but decreased in normal‐weight individuals following acute maximal exercise, after adjusting for fitness. Obese individuals also exhibited an overall higher central BP (P < 0.05), with no exercise effect. The increase in heart rate was greater in obese versus normal‐weight individuals following exercise (P < 0.05), but there was no group differences or exercise effect for AIx@75. In conclusion, obese (but not normal‐weight) individuals increased central arterial stiffness following acute maximal exercise. An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction.

Postexercise Hemodynamics in Patients With Type 2 Diabetes: Effect of Exercise Intensity and Duration

Background: For individuals with type 2 diabetes (T2D), the hemodynamic response to regular exercise is critical for regulating blood glucose, protecting vascular function, and reducing cardiovascular disease risk, but the hemodynamic responses to differing doses of acute exercise in T2D are unclear. We aimed to compare postexercise (PE) hemodynamics in patients with T2D in response to 4 doses of dynamic exercise.Methods: Eight subjects with well-controlled T2D (42–64 years old.; hemoglobin A1c: 6.6% ± 0.9%) participated in 4 study days, during which they exercised on a cycle ergometer at 4 different combinations of exercise duration and intensity: 30 min at 40% V˙O2peak (30@40), 30 min at 60% V˙O2peak (30@60), 60 min at 40% V˙O2peak (60@40), and 60 min at 60% V˙O2peak (60@60). Heart rate, arterial pressure, and femoral blood flow (Doppler ultrasound) were measured pre-exercise and every 15 min through 120 min PE. Femoral vascular conductance was calculated as flow/pressure.Results: Compared with pre-exercise baseline, femoral blood flow and femoral vascular conductance were higher through at least 105 min of recovery in all conditions (all P &amp;lt; .05), except for the 30@40 trial. Compared with the pre-exercise measures, systolic blood pressure was lower through at least 75 min of recovery in all conditions (all P &amp;lt; .05), except for the 30@40 trial.Conclusion: These results suggest that exercise must be at least moderate in intensity or prolonged in duration (&amp;gt;30 min) to promote sustained PE elevations in skeletal muscle blood flow and reductions in systolic blood pressure in patients with T2D.

17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension.

17β-Estradiol (E2) exerts protective effects on right ventricular (RV) function in pulmonary arterial hypertension (PAH). Since acute exercise-induced increases in afterload may lead to RV dysfunction in PAH, we sought to determine whether E2 allows for superior RV adaptation after an acute exercise challenge. We studied echocardiographic, hemodynamic, structural, and biochemical markers of RV function in male and female rats with sugen/hypoxia (SuHx)-induced pulmonary hypertension, as well as in ovariectomized (OVX) SuHx females, with or without concomitant E2 repletion (75 μg·kg(-1)·day(-1)) immediately after 45 min of treadmill running at 75% of individually determined maximal aerobic capacity (75% aerobic capacity reserve). Compared with males, intact female rats exhibited higher stroke volume and cardiac indexes, a strong trend for better RV compliance, and less pronounced increases in indexed total pulmonary resistance. OVX abrogated favorable RV adaptations, whereas E2 repletion after OVX markedly improved RV function. E2's effects on pulmonary vascular remodeling were complex and less robust than its RV effects. Postexercise hemodynamics in females with endogenous or exogenous E2 were similar to hemodynamics in nonexercised controls, whereas OVX rats exhibited more severely altered postexercise hemodynamics. E2 mediated inhibitory effects on RV fibrosis and attenuated increases in RV collagen I/III ratio. Proapoptotic signaling, endothelial nitric oxide synthase phosphorylation, and autophagic flux markers were affected by E2 depletion and/or repletion. Markers of impaired autophagic flux correlated with endpoints of RV structure and function. Endogenous and exogenous E2 exerts protective effects on RV function measured immediately after an acute exercise challenge. Harnessing E2's mechanisms may lead to novel RV-directed therapies.

The influence of thermal factors on postexercise haemodynamics in trained and untrained men

Previous work suggests that the cardiovascular mechanisms underlying the postexercise reduction in mean arterial pressure (MAP) differ between exercise‐trained and untrained men. However, these studies compared responses based on the same percentage of peak oxygen consumption (VO2peak) resulting in different rates of heat production during exercise. Thus, we evaluated if exercise‐induced differences in the requirement for heat loss, and therefore sweat loss, may influence postexercise haemodynamics. Twelve trained (T60) (VO2peak, 64 ± 4 mL/kg/min) and twelve untrained (UT60) (VO2peak, 49 ± 3 mL/kg/min) males, individually matched for body surface area, cycled for 60 min at 60% of VO2peak­. On a separate day the untrained group performed an additional 60 min of cycling at the same heat production as their trained match in T60 (UTMatch). Sweat loss was assessed by change in body weight (ΔBW). MAP and cardiac output (CO) were measured at baseline and every 10 min during 60 min of postexercise recovery. ΔBW was similar between T60 and UT­Match (T60: ‐1.32 ± 0.36 kg; UTMatch: ‐1.32 ± 0.32 kg) and greater in these conditions relative to UT60 (‐0.95 ± 0.13 kg; both P &lt; 0.05). Further, MAP was ~5 mmHg below baseline following 20 min of recovery in each condition (all P &lt; 0.05). Postexercise CO was ~7% below baseline in T60 (P &lt; 0.05) whereas it was elevated relative to T60 (both P &lt; 0.05) and similar to baseline (both P &gt; 0.05) in UT60 and UTMatch. We show that the differing mechanisms between trained and untrained males underlying the postexercise reduction in MAP are not the result of differences in exercise‐induced heat load and therefore fluid loss. Support: Natural Sciences and Engineering Research Council of Canada.

High Intensity Interval Grip (HIIG) Exercise Does Not Induce Post‐Exercise Hypotension in Older Women

Handgrip has been used as an exercise stimulus to perturbate blood pressure over the long‐term (2‐16mmHg reduction) and short‐term (1‐3mmHg reduction). Majority of previous research has been completed using a commercial device (Zona) with a preset exercise protocol of 4x2min @ 30%MVC with 1min rest intervals. Acute exercise using ZONA modestly reduces SBP and increases HR shortly following exercise cessation in mixed samples of middle aged to older men and women. The purpose of this research was to compare the acute cardiovascular impact of Zona exercise to an in‐house accessible protocol of 32x5sec @ 100%MVC with 5sec rest intervals (High Intensity Interval Grip: HIIG) in older (age:57.7±5.2yrs), normotensive (109±9.4/73.1±7.8mmHg), post‐menopausal (8.4±5.6yrs) women. Nineteen women completed 5 laboratory visits; familiarization, baseline, and three randomly assigned experimental conditions: Zona, HIIG, and Control. For each experimental visit, resting SBP, DBP, and HR were made every 2min for 10mins, exercise was completed, and then post‐exercise SBP, DBP, and HR were made every 3min for 30mins. There were two calculations of post‐exercise hemodynamics; a 30min average change and a 6min rolling average change. There were no statistically significant changes from rest in the 30mins post‐exercise for all variables. As a description, based on 30min average change values Zona resulted in increased SBP (+1.6mmHg), increased DBP (+1.4mmHg), and reduced HR (‐2.1bpm) while HIIG resulted in slightly reduced SBP (‐0.2mmHg), slightly increased DBP (+0.2mmHg), and reduced HR (‐2.2bpm). The absence of BP reduction with either acute stimulus suggests cardiovascular regulation differs in this cohort of normotensive, post‐menopausal women. Canadian Institutes of Health Research, CGS Doctoral Award.

Gender Influence on Post-resistance Exercise Hypotension and Hemodynamics

Post-resistance exercise hypotension has been extensively described in men and women. However, gender influence on this response has not yet been clear. Gender might change post-exercise hemodynamics, since men and women respond differently during exercise. Thus, the purpose was to compare post-resistance exercise hypotension and its hemodynamic determinants in men and women. Normotensive subjects (22-male, 22-female) underwent 2 sessions: control (40 min of rest) and exercise (6 resistance exercises, 3 sets, 20 repetitions, at 40-50% of 1RM). Blood pressure, heart rate, and cardiac output were measured prior to and following interventions. Blood pressure decrease after exercise was similar between the genders. However, hemodynamic determinants responded differently in men and women. Systemic vascular resistance reduced in women (-4.6±1.9U, P<0.05), while cardiac output decreased in men (-0.6±0.2 L/min, P<0.05). This response was accompanied by a decrease in stroke volume in men (-21.6±5.1 ml, P<0.05) and a more pronounced increase in heart rate in men than in women (+11.3±1.3 vs. +6.5±1.7 bpm, P<0.05, respectively). In conclusion, post-resistance exercise hypotension was similar in men and women. However, its hemodynamic determinants differ between the genders, depending on cardiac output decrease in men and on systemic vascular resistance decrease in women.

Free Radical-Mediated Lipid Peroxidation and Systemic Nitric Oxide Bioavailability: Implications for Postexercise Hemodynamics

The metabolic vasodilator mediating postexercise hypotension (PEH) is poorly understood. Recent evidence suggests an exercise-induced reliance on pro-oxidant-stimulated vasodilation in normotensive young human subjects, but the role in the prehypertensive state is not known. Nine prehypertensives (mean arterial pressure (MAP), 106 ± 5 mm Hg; 50 ± 10 years old) performed 30 minutes of cycle exercise and a nonexercise trial. Arterial distensibility was characterized by simultaneously recording upper- and lower-limb pulse wave velocity (PWV) via oscillometry. Systemic vascular resistance and conductance were determined by MAP/Q and Q/MAP, respectively. Venous blood was assayed for indirect markers of oxidative stress (lipid hydroperoxides (LOOH); spectrophotometry), plasma nitric oxide (NO) and S-nitrosothiols (fluorometry), atrial natriuretic peptide (ANP), and angiotensin II (ANG-II) (radioimmunoassay). Exercise reduced MAP (6mm Hg) and vascular resistance (15%) at 60 minutes after exercise, whereas conductance was elevated (20%) (P < 0.05). The hypotension resulted in a lower MAP at 60 and 120 minutes after exercise compared with nonexercise (P < 0.05). Upper-limb PWV was also 18% lower after exercise compared with baseline (P < 0.05). Exercise increased LOOH coincident with the nadir in hypotension and vascular resistance but failed to affect plasma NO or S-nitrosothiols. Exercise-induced increases in LOOH were related to ANG-II (r = 0.97; P < 0.01) and complemented by elevated ANP concentrations. These data indicate attenuated vascular resistance after exercise with increased oxidative stress and unchanged NO. Whether free radicals are obligatory for PEH requires further investigation, although it seems that oxidative stress occurs during the hyperemia underlying PEH.

Resistance Exercise Training Does Not Affect Post-exercise Hypotension And Wave Reflection In Women With Fibromyalgia

It has been suggested that women with Fibromyalgia (FM) have altered hemodynamic responses to acute resistance exercise. Currently there are no data on wave reflection in response to resistance exercise in women with FM. In addition, the effects of resistance exercise training (RET) on hemodynamics and wave reflection in response to acute resistance exercise are unknown in women with FM. PURPOSE: The purpose of this study was to assess the effects of RET on aortic wave reflection and hemodynamics during recovery from acute resistance exercise in women with Fibromyalgia and healthy women (HW). METHODS: Nine women with FM (42 ± 5 yrs; mean ± SD) and 14 HW (45 ± 5 yrs) completed testing at baseline and after 12 weeks of whole-body RET that consisted of 3 sets of 5 exercises. Heart rate (HR), digital blood pressure (BP, plethysmography), aortic BP and wave reflection (radial tonometry) were assessed before and 20 minutes after acute leg resistance exercise. RESULTS: Aortic (FM and HW: -11.1 ± 2.1% and -10.1 ± 2.4%) and digital diastolic BP (DBP) (FM and HW: -12.5 ± 2.6% and -11.5 ± 2.1%) were significantly decreased (p<0.05) and aortic (FM and HW: 46.2 ± 7.5% and 25.0 ± 6.6%) and digital pulse pressures (PP) (FM and HW: 38.2 ± 6.0% and 27.7 ± 2.8%) were significantly increased (p<0.05) after acute exercise before RET. There was no effect of acute resistance exercise on HR, wave reflection (augmentation index and reflection time), digital or aortic systolic BP. RET improved muscle strength without affecting acute DBP and PP responses. CONCLUSIONS: Acute resistance exercise produces post-exercise diastolic hypotension without affecting SBP, HR, and wave reflection responses in women with and without FM. RET does not alter resting and post-exercise hemodynamics and aortic wave reflection in premenopausal women. Supported by ACSM Foundation Research Grant (FRG).

Acute Hyperoxic Exercise &amp; Redox Regulation of Blood Coagulation

Hyperoxia negatively impacts on post exercise hemodynamic status in the human whereas the effect on coagulation is not clear. 9 males (50 ±10 years) were studied for 2-hours following 30-minutes of cycle exercise at 70% maximal oxygen consumption in hyperoxia (50% O2) and normoxia (21% O2). Subjects were followed post-exercise for 2-hours. Echocardiography assessed cardiac output (Q̇) determined systemic vascular resistance (SVR) [MAP/Q̇] and vascular conductance (SVC) [Q̇/MAP]. Blood was sampled from an antecubital vein pre-, immediately post-, 1-hour (P1) and 2-hours post- (P2) exercise and corrected for hemoconcentration/dilution. Plasma was assayed for fibrinogen, international normalized ratio (INR), activated partial thromboplastin time (aPTT), activated partial thromboplastin time ratio (aPTTr), and prothrombin time (PT) by coagulometry. Lipid hydroperoxides (LOOH) were determined spectrophotometrically whilst blood was also assayed for selective antioxidants (HPLC & fluorimetry). Hyperoxic exercise blunted post-exercise hemodynamics by significantly attenuating the reductions in SVR and MAP (P<0.05). Ascorbic acid was elevated across the hyperoxic exercise trial in comparison to the normoxic condition (P<0.05) with a selective increase by P2 (P<0.05). Hyperoxic exercise has a deleterious effect on post-exercise hemodynamics but not hemostasis when corrected for plasma volume change.

Redox Regulation of Post-exercise Hemodynamics Following Hyperoxia in Man

Redox Regulation of Post-exercise Hemodynamics Following Hyperoxia in Man