Dynamic Leg Exercise Research Articles

Effect of acute ambient temperature exposure on cardio-pulmonary and respiratory kinetics in men

Aim: The goal of the study was to compare the kinetic responses of heart rate (HR) and pulmonary (V̇O2pulm) and muscular (V̇O2musc) oxygen uptake during dynamic leg exercise across different acute ambient temperature conditions in a climatic chamber.Methods: Thirteen physically healthy, active, male volunteers demonstrated pseudorandom binary sequence (PRBS) work rate (WR) changes between 30 and 80 W at 15 °C, 25 °C and 35 °C, respectively. HR was measured beat-to-beat using an echocardiogram and V̇O2pulm by breath-by-breath gas exchange; V̇O2musc estimations were assessed by applying a circulatory model and cross-correlation functions.Results: No significant differences were observed across the various temperature conditions in each case for HR, V̇O2pulm or V̇O2musc kinetics (p > 0.05). Baroreflex regulation based on HR kinetics does not seem to be influenced between ambient temperatures of 15 °C and 35 °C during dynamic exercise.Conclusions: The results imply that ambient temperatures of 15 °C, 25 °C and 35 °C have no effect on HR, V̇O2pulm or V̇O2musc kinetics during dynamic moderate exercise. The applied approach may be of interest for assessments of the cardio-pulmonary and respiratory health statuses of individuals working or performing sports in extreme temperature environments. Furthermore, differentiation between systemic (e.g. cardio-dynamic: HR) and specific (e.g. exercising tissues: V̇O2musc) determinants of the relevant physiological systems may improve the evaluation of an individual’s health status.

Muscle Sympathetic Nerve Responses to Passive and Active One‐legged Cycling: Insight into the Contributions of Central Command

Prior studies using neuromuscular blockade to increase perception of effort during mild or moderate intensity handgrip exercise have demonstrated that activation of higher brain regions, termed central command, contribute importantly to cardiac parasympathetic withdrawal but have limited influence on muscle sympathetic activation. The purpose of the present study was to investigate the contribution of central command to the control of muscle sympathetic nerve activity (MSNA) during dynamic one‐legged cycling. Heart rate (HR), mean arterial pressure (MAP), stroke volume, and MSNA (contralateral leg microneurography) were measured in 18 healthy participants (9 men; 22±3 yr of age) at baseline and during two minutes of upright passive cycling movement and active unloaded cycling, each separated by 10 minutes of rest. The increases in HR were greater during the first (Δ3±3 vs. Δ11±7 bpm, p<0.0001) and second (Δ3±4 vs. Δ9±6 bpm, p<0.0001) minute, and MAP during the second minute (Δ4±3 vs. Δ7±5 mmHg, p<0.01), of active unloaded cycling compared to passive cycling movement. Stroke volume increased over time (p<0.001) but was not different between passive and active unloaded cycling (p>0.05). MSNA burst frequency decreased similarly during the first (Δ−4±5 vs. Δ−3±5 bursts/min, p>0.05) and second (Δ−6±4 vs. Δ−4±4 bursts/min, p>0.05) minute of passive and active unloaded cycling. In contrast, total MSNA demonstrated attenuated reductions during the first (Δ−3.2±3.0 vs. Δ−0.6±3.3 arbitrary units/min, p<0.05 [Δ−18±16% vs. Δ0±31%, p<0.05]) and second (Δ−4.5±3.3 vs. Δ−1.5±3.5 arbitrary units/min, p<0.01 [Δ−28±17% vs. Δ−11±24%, p<0.05]) minute of active unloaded cycling. These results support the concept that muscle sympathetic burst occurrence and strength can be regulated independently and suggest that during dynamic leg exercise central command primarily alters vasoconstrictor outflow through modulations in muscle sympathetic burst strength.Support or Funding InformationThis research was supported by a Natural Science and Engineering Research Council (NSERC) of Canada Discovery Grant (P.J.M), the Canada Foundation for Innovation (P.J.M.), and a Canadian Institutes of Health Research Fredrick Banting and Charles Best Canada Graduate Scholarship (A.V.I.).

Whole-Body Vibration Exercise Therapy Improves Cardiac Autonomic Function and Blood Pressure in Obese Pre- and Stage 1 Hypertensive Postmenopausal Women.

Whole-body vibration (WBV) is an unconventional exercise therapy that appears to provide the same benefits of resistance training in postmenopausal women while being more safe and gentle on the joints. This study evaluated the effect of an 8-week WBV exercise regimen on heart rate variability (HRV) and blood pressure (BP) in obese postmenopausal women. Randomized controlled study with two parallel groups. Twenty-five (age 50-65 years) obese (body-mass index >30 and <40 kg/m2) postmenopausal women. Participants were randomly assigned to a WBV training group or nonexercising control group. Participants in the WBV group completed the supervised training 3 times a week. WBV training consisted of four static and four dynamic leg exercises (normal, high, and wide-stance squats and calf-raises) with vertical vibration (25-40 Hz and low-high amplitude) progressed throughout the 8 weeks. Brachial systolic BP (SBP) and diastolic BP (DBP) and HRV: sympathovagal balance (natural logarithm of low frequency [LnLF]/natural logarithm of high frequency [LnHF]; normalized low frequency [nLF]/normalized high frequency [nHF]), parasympathetic tone (LnHF, nHF, natural logarithm of root mean square of successive differences [LnRMSSD]), sympathetic tone (LnLF, nLF), natural logarithm of total power, and heart rate (HR). There were significant group × time interactions (p < 0.05) for brachial SBP, DBP, LnLF/LnHF, and nLF/nHF that significantly decreased (p < 0.01) after WBV, compared with no changes after control. There was a significant (p < 0.05) increase in nHF and decrease in nLF in the WBV group compared with baseline, yet the changes were not different than those in the control group. No significant changes were observed in LnTP, LnLF, LnHF, LnRMSSD, or HR after 8 weeks in either group. WBV training for 8 weeks is an adequate unconventional exercise intervention for improving sympathovagal balance and BP in previously sedentary obese postmenopausal women.

Analysis of cardio-pulmonary and respiratory kinetics in different body positions: impact of venous return on pulmonary measurements.

The aim of the study was to compare the kinetics responses of heart rate (HR), pulmonary ([Formula: see text]O2pulm), and muscular ([Formula: see text]O2musc) oxygen uptake during dynamic leg exercise across different body positions (-6°, 45°, and 75°). Ten healthy individuals [six men, four women; age 23.4±2.8years; height 179.7±8.3cm; body mass 73±12kg (mean±SD)] completed pseudo-random binary sequence (PRBS) work rate (WR) changes between 30 and 80W in each posture. HR was measured beat-to-beat by echocardiogram and [Formula: see text]O2pulm by breath-by-breath gas exchange. [Formula: see text]O2musc kinetics were assessed by the procedure of Hoffmann et al. (Eur J Appl Physiol 113:1745-1754, 2013) applying a circulatory model and cross-correlation functions (CCF). For [Formula: see text]O2pulm kinetics significant differences between -6° (CCF-values: 0.292±0.040) and 45° (0.256±0.034; p<0.01; n=10) as well as between -6° and 75° (0.214±0.057; p<0.05; n=10) were detected at lag '40s' of the CCF course as interaction effects (factors: Lag×Posture). HR and [Formula: see text]O2musc kinetics yield no significant differences across the postures. The analysis of cardio-dynamic and respiratory kinetics, especially with an emphasis on muscular and cellular level, has to consider venous return and cardiac output distortions. Simplified observations of kinetics responses resulting in time constants and time delays only should be replaced by the time-series analysis for a more sophisticated evaluation. The results illustrate that isolated [Formula: see text]O2pulm measurements without cardio-dynamic influences may not represent the kinetics responses originally revealed at muscular level.

Hypoxia Attenuates Cardiopulmonary Reflex Control Of The Sympathetic Nerve Activity During Dynamic Leg Exercise

PURPOSE: The purpose of the present study was to test the hypothesis that cardiopulmonary baroreflex control of sympathetic vasomotor outflow is modulated by a powerful sympatho-excitatory drive from exercise pressor reflex, central command, and/or arterial chemoreflex. To test this hypothesis, under hypoxic conditions, muscle sympathetic nerve activity (MSNA) was recorded during leg cycling with an increase in central blood volume by increasing pedal frequency to increase the activity of cardiopulmonary baroreceptors. METHODS: Subjects performed mild leg cycle exercise at different pedal frequencies of 60 and 80 rpm (60EX and 80EX trials) while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). The exercise workload of the 80EX trial was adjusted to get the same oxygen uptake as the 60EX trial. Stroke volume (SV) and cardiac output (CO) were measured non-invasively using impedance cardiology. MSNA was recorded via microneurography of the right median nerve at the elbow. RESULTS: Changes in thoracic impedance, SV, and CO in the 80EX trial were greater than those in the 60EX trial. MSNA burst frequency during hypoxic exercise in the 80EX trial (39±4 bursts/min) did not differ from that in the 60EX trial (39±3 bursts/min). CONCLUSIONS: These results suggest that a cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by hypoxia-induced heightened sympathetic nerve activity.

Antioxidants Attenuate the Exercise Induced Resetting of the Arterial Baroreflex in Healthy Human Subjects: Implications for Exercise Induced Hypertension

Patients with Exercise‐induced‐Hypertension (EiHT) exhibit exaggerated increases in arterial pressure at the onset of exercise which may prevent EiHT patients from participating in exercise training programs. EiHT is thought to occur due to dysregulated resetting of the arterial baroreflex (ABR). Prior studies in animal models demonstrate that reactive oxygen species (ROS) generated in the brainstem scavenge the sympathoinhibitory function of central Nitric Oxide (NO) and, thereby enable ABR resetting of the operating point (OP) pressure and hypertension. We tested the hypothesis that a centrally and peripherally active antioxidant cocktail (CT; composed of Vitamin E and C with Co‐Q10) will attenuate the exercise induced resetting of the ABR's centering point (CP) and OP pressures compared to the same exercise intensity performed with a vehicle placebo (PL). Seven healthy human subjects were recruited and performed 700 back‐supported semi‐recumbent dynamic leg exercise at moderate (HR at 120 beats per minute: e120) and heavy (HR at 150 beats per minute: e150) intensities. Mean arterial pressure (MAP) was continuously recorded using photoplethysmography at the finger, while HR was recorded via a three lead electrocardiogram (ECG). On experimental day 1, subjects were either given the CT or PL 1 hr. (time of peak plasma concentrations) prior to the start of exercise. On a separate experiment day 2, the subjects repeated the same exercise intensity protocol with the other test article (CT or PL) in a randomized repeated measures design. During exercise with the PL ingestion, the CP of the ABR was reset to higher MAPs from rest to e120 (100 ± 3 mm Hg to 121 ± 3 mm Hg, P&lt;0.02) but not e150 (113 ± 3 mm Hg, P=0.15). The absence of resetting at the higher work intensity was likely due to cardiovascular drift (decreasing MAP). Ingestion of the CT prior to the exercise protocols prevented the increase of the CP to higher MAPs from rest to e120 and e150 (rest: 97 ± 3 mm Hg, e120: 106 ± 3 mm Hg, e150: 106 ± 3 mm Hg, P &gt;0.21). Furthermore, the OP‐pressure of the ABR was attenuated with CT ingestion compared to PL at e120 (placebo e120: 116 ± 0.8 mm Hg, CT e120: 111 ± 0.8 mm Hg, P = 0.04). These data: (a) confirm that centrally derived ROS contribute to exercise induced ABR resetting; and (b) indicate that EiHT could be treated by ingestion of an anti‐oxidant cocktail prior to the start of exercise

Hypoxia attenuates cardiopulmonary reflex control of sympathetic nerve activity during mild dynamic leg exercise

What is the central question of this study? The cardiopulmonary baroreflex inhibits adjustment of sympathetic vasomotor outflow during mild-intensity dynamic exercise. However, it is unclear how suppression of sympathetic vasomotor outflow by the cardiopulmonary baroreflex is modulated by a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or the arterial chemoreflex. What is the main finding and its importance? Hypoxia-induced heightened sympathetic nerve activity during dynamic exercise attenuated cardiopulmonary baroreflex control of sympathetic vasomotor outflow. This could facilitate the redistribution of blood flow to the active muscles by sympathetically mediated vasoconstriction of inactive muscles. Muscle sympathetic nerve activity (MSNA) does not increase during mild-intensity dynamic leg exercise in normoxic conditions, despite activation of central command and the exercise pressor reflex. Suppression of MSNA could be caused by muscle pump-induced loading of cardiopulmonary baroreceptors. In contrast, MSNA increases during mild dynamic leg exercise in hypoxic conditions. We hypothesized that hypoxic exercise, which induces a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or arterial chemoreflex, attenuates cardiopulmonary reflex control of sympathetic vasomotor outflow. To test this hypothesis, MSNA was recorded during leg cycling in hypoxic conditions and with increased central blood volume by increasing the pedalling frequency to change the cardiopulmonary baroreflex. Subjects performed two leg cycle exercises at different pedal cadences of 60 and 80 r.p.m. (60EX and 80EX trials, respectively) in two (haemodynamic and MSNA) measurement conditions while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). Thoracic impedance, stroke volume and cardiac output were measured non-invasively using impedance cardiography. During the MSNA test, MSNA was recorded via microneurography at the right median nerve at the elbow. Changes in thoracic impedance, stroke volume and cardiac output during the 80EX trial were greater than those during the 60EX trial. The MSNA burst frequency during hypoxic exercise in the 80EX trial (39 ± 4 bursts min(-1)) did not differ from that during the 60EX trial (39 ± 3 bursts min(-1)). These results suggest that the cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by heightened hypoxia-induced sympathetic nerve activity.

Expiratory Resistive Loading Increases in Sympathetic Vasomotor Outflow and BP During Dynamic Leg Exercise

High intensity voluntary contraction of the inspiratory muscles against resistive loads augments an increase in muscle sympathetic nerve activity (MSNA) with a corresponding increase in arterial blood pressure (BP) through an inspiratory muscle fatigue-induced metaboreflex. We hypothesized that expiratory muscle fatigue would also elicit increases in MSNA and BP during dynamic leg exercise. PURPOSE: The purpose of this study was to clarify the influence of an enhancement of expiratory muscle activity on sympathetic vasoconstrictor outflow and BP during submaximal exercise. METHODS: The subjects performed two 10-min exercise bouts at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without expiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each constant at 0.5 s)]. MSNA was recorded via microneurography of the right median nerve at the elbow. RESULTS: A large increase in MSNA burst frequency (BF) occurred during exercise with expiratory resistance, accompanied by an augmentation of mean BP (MBP) (with resistance: MSNA BF +39.0%, MBP +42.5%, without resistance: MSNA BF: +12.8%, MBP: +22.9%, from resting values). CONCLUSIONS: These results suggest that an enhancement of expiratory muscle activity leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

The role of muscle sympathetic nerve activity in limiting exercise capacity in heart failure.

The role of muscle sympathetic nerve activity in limiting exercise capacity in heart failure.

Sympathetic vasomotor outflow and blood pressure increase during exercise with expiratory resistance.

The purpose of the present study was to elucidate the effect of increasing expiratory muscle work on sympathetic vasoconstrictor outflow and arterial blood pressure (BP) during dynamic exercise. We hypothesized that expiratory muscle fatigue would elicit increases in sympathetic vasomotor outflow and BP during submaximal exercise. The subjects performed four submaximal exercise tests; two were maximal expiratory pressure (PEmax) tests and two were muscle sympathetic nerve activity (MSNA) tests. In each test, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and voluntary hyperpnoea with and without expiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 sec)]. PEmax was estimated before and immediately after exercises. MSNA was recorded via microneurography of the right median nerve at the elbow. PEmax decreased following exercise with expiratory resistive breathing, while no change was found without resistance. A progressive increase in MSNA burst frequency (BF) appeared during exercise with expiratory resistance (MSNA BF, without resistance: +22 ± 5%, with resistance: +44 ± 8%, P < 0.05), accompanied by an augmentation of BP (mean BP, without resistance: +5 ± 2%, with resistance: +29 ± 5%, P < 0.05). These results suggest that an enhancement of expiratory muscle activity leads to increases in sympathetic vasomotor outflow and BP during dynamic leg exercise.

Divergent muscle sympathetic responses to dynamic leg exercise in heart failure and age-matched healthy subjects.

People with diminished ventricular contraction who develop heart failure have higher sympathetic nerve firing rates at rest compared with healthy individuals of a similar age and this is associated with less exercise capacity. During handgrip exercise, sympathetic nerve activity to muscle is higher in patients with heart failure but the response to leg exercise is unknown because its recording requires stillness. We measured sympathetic activity from one leg while the other leg cycled at a moderate level and observed a decrease in nerve firing rate in healthy subjects but an increase in subjects with heart failure. Because these nerves release noradrenaline, which can restrict muscle blood flow, this observation helps explain the limited exercise capacity of patients with heart failure. Lower nerve traffic during exercise was associated with greater peak oxygen uptake, suggesting that if exercise training attenuated sympathetic outflow functional capacity in heart failure would improve. The reflex fibular muscle sympathetic nerve (MSNA) response to dynamic handgrip exercise is elicited at a lower threshold in heart failure with reduced ejection fraction (HFrEF). The present aim was to test the hypothesis that the contralateral MSNA response to mild to moderate dynamic one-legged exercise is augmented in HFrEF relative to age- and sex-matched controls. Heart rate (HR), blood pressure and MSNA were recorded in 16 patients with HFrEF (left ventricular ejection fraction = 31 ± 2%; age 62 ± 3 years, mean ± SE) and 13 healthy control subjects (56 ± 2 years) before and during 2 min of upright one-legged unloaded cycling followed by 2 min at 50% of peak oxygen uptake (V̇O2,peak). Resting HR and blood pressure were similar between groups whereas MSNA burst frequency was higher (50.0 ± 2.0 vs. 42.3 ± 2.7 bursts min(-1), P = 0.03) and V̇O2,peak lower (18.0 ± 2.0 vs. 32.6 ± 2.8 ml kg(-1) min(-1), P < 0.001) in HFrEF. Exercise increased HR (P < 0.001) with no group difference (P = 0.1). MSNA burst frequency decreased during mild to moderate dynamic exercise in the healthy controls but increased in HFrEF (-5.5 ± 2.0 vs. 6.9 ± 1.8 bursts min(-1), P < 0.001). Exercise capacity correlated inversely with MSNA burst frequency at 50% V̇O2,peak (n = 29; r = -0.64; P < 0.001). At the same relative workload, one-legged dynamic exercise elicited a fall in MSNA burst frequency in healthy subjects but sympathoexcitation in HFrEF, a divergence probably reflecting between-group differences in reflexes engaged by cycling. This finding, coupled with an inverse relationship between MSNA burst frequency during loaded cycling and subjects' V̇O2,peak, is consistent with a neurogenic determinant of exercise capacity in HFrEF.

Enhanced muscle pump during mild dynamic leg exercise inhibits sympathetic vasomotor outflow.

Muscle sympathetic nerve activity (MSNA) is not increased during leg cycling at light and mild intensities, despite activation of central command and the exercise pressor reflex. We determined whether increasing central blood volume and loading the cardiopulmonary baroreceptors modulate sympathetic vasomotor outflow during leg cycling. To this end, we changed the pedaling frequency to enhance skeletal muscle pump. Subjects performed two leg cycle exercises at differential pedal rates of 60 and 80 rpm (60EX and 80EX trials) for two conditions (with and without MSNA measurement). In each trial, subjects completed leg cycling with a differential workload to maintain constant oxygen consumption (VO2). MSNA was recorded via microneurography at the right median nerve of the elbow. Without MSNA measurement, thoracic impedance, stroke volume (SV), and cardiac output (CO) were measured non‐invasively using impedance cardiography. Heart rate and VO2 during exercise did not differ between the 60EX and 80EX trials. Changes in thoracic impedance, SV, and CO during the 80EX trial were greater than during the 60EX trial. MSNA during the 60EX trial was unchanged compared with that at rest (25.8 ± 3.1 [rest] to 28.3 ± 3.4 [exercise] bursts/min), whereas a significant decrease in MSNA was observed during the 80EX trial (25.8 ± 2.8 [rest] to 19.7 ± 2.0 [exercise] bursts/min). These results suggest that a muscle pump‐induced increase in central blood volume, and thereby loading of cardiopulmonary baroreceptors, could inhibit sympathetic vasomotor outflow during mild dynamic leg exercise, despite activation of central command and the exercise pressor reflex.

Effect of posture on heart rate control prior to and following dynamic leg exercise (881.8)

Reflex control of cardiovascular function is paramount in maintaining homeostasis both before and after exercise. We investigated the influence of posture on arterial baroreflex function both before and after prolonged moderate to high intensity exercise.9 healthy subjects (1 female) aged 24.4 years (±1.16) volunteered for protocol 1 of the study and 13 healthy subjects (3 female) aged 25.5 years (±0.88) volunteered for protocol 2. Each subject underwent graded exercise test either upright (UR) (protocol 1) or semi‐recumbent (SR) (protocol 2). During both protocols 1 and 2 neck pressure/neck suction protocols were performed at rest, exercising HRs of 120 and 150 bpm, and recovery. Reflex data for HR and MAP were analyzed and baroreflex curves were calculated. Repeated measure ANOVAs was performed and Neuman‐Keuls post hoc analysis was used when differences were detected. Significance was set at P&lt;0.05.Significant differences were identified in operating point values of HR between SR and UR at rest (P&lt;0.001), and between rest and recovery in both SR and UR (p&lt;0.001). Differences were also identified in Carotid‐cardiac baroreflex response range and maximum gain between and within all conditions (p&lt;0.05).Differences in the neural reflexive control of HR at rest and during recovery are related to postural changes in cardiopulmonary loading.Grant Funding Source: Supported by TACSM SRDA

Effects of antioxidants on cerebrovascular hemodynamics during moderate and high intensity exercise (1183.6)

It has been identified that central reactive oxygen species (ROS) scavenge nitric oxide (NO) and increase central sympathetic nerve activity (SNA) outflow. During dynamic exercise increases in ROS have been measured across the brain. We tested the hypothesis that during dynamic leg cycling exercise, antioxidants would increase middle cerebral artery blood velocity (MCAv) and cerebrovascular conductance (CVCi). Five healthy subjects performed back supported semi‐recumbent dynamic leg cycling with antioxidant cocktail (AxT) and without AxT (placebo ‐ Pl). Arterial pressures (AP) and MCAv were measured continuously during moderate intensity dynamic leg exercise at heart rates (HR) of 120 bpm (e120) and heavy intensity at HR of 150 bpm (e150). No differences in AP were observed between Pl and Axt at e120 and e150 (P蠅0.50). MCAv during AxT at e120 and e150 was increased above Pl (P=0.06). However, the calculated CVCi was significantly greater at e120 and e150 between CT and Pl (P=0.05). From these data we conclude that Axt scavenged exercise induced central ROS resulting in increased central NO induced cerebrovascular vasodilation during exercise.

Time courses of central hemodynamics during rapid changes in posture

Changes in posture cause blood volume redistribution, affecting cardiac filling and stroke volume (SV). We hypothesized that the time courses of ventricular filling would differ between the right and left ventricle during a rapid (2 s) tilt and that changes in right ventricular filling pressure would be more swift because of the direct coupling to the systemic circulation. We further hypothesized that the transient imbalance between right and left ventricular filling pressure would influence left ventricular SV changes. Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), left ventricular stroke volume, heart rate, and arterial pressure were recorded beat-by-beat during rapid tilts from supine to upright positions and back again, during rest and dynamic 100-W leg exercise. RAP changes had a faster time course than PCWP during down-tilts, both during rest and exercise (1 ± 1 vs. 6 ± 2 s and 2 ± 2 vs. 6 ± 2 s, respectively; P < 0.05). This discrepancy caused a transient decrease in the end-diastolic pressure difference between the right and left ventricle. The decreased pressure difference in diastole impeded left ventricular filling because of ventricular interdependence, causing SV to fall transiently. The mechanisms of ventricular interdependence were also involved in reverse during up-tilt, where SV was maintained for 2-3 s despite falling PCWP. Furthermore, the decrease in RAP during up-tilt in the resting condition was biphasic with an initial fast and a second slower component, which might suggest the effect of venous valves. This was not seen during dynamic leg exercise where blood pooling is prevented by the venous muscle pump.

Retrograde blood flow in the inactive limb is enhanced during constant-load leg cycling in hypoxia

This study aimed to elucidate the effects of hypoxia on the pattern of oscillatory blood flow in the inactive limb during constant-load dynamic exercise. We hypothesised that retrograde blood flow in the brachial artery of the inactive limb would increase during constant-load leg cycling under hypoxic conditions. Three maximal exercise tests were conducted in eight healthy males on a semi-recumbent cycle ergometer while the subjects breathed a normoxic [inspired oxygen fraction (FIO2)=0.209] or two hypoxic gas mixtures (FIO2=0.155 and 0.120). Subjects then performed submaximal exercise at the same relative exercise intensity of 60% peak oxygen uptake under normoxic or the two hypoxic conditions for 30min. Brachial artery blood velocity and diameter were recorded simultaneously during submaximal exercise using Doppler ultrasonography. Antegrade blood flow gradually increased during exercise, with no significant differences among the three trials. Retrograde blood flow showed a biphasic response, with an initial increase followed by a gradual decrease during normoxic exercise. In contrast, retrograde blood flow significantly increased during moderate and severe hypoxic exercise, and remained elevated above normoxic conditions during exercise. At 30min of exercise, the magnitude of the change in retrograde blood flow during exercise was greater as the level of hypoxia increased (normoxia: -18.7±23.5mlmin(-1); moderate hypoxia: -39.3±21.4mlmin(-1); severe hypoxia: -64.0±36.3mlmin(-1)). These results indicate that moderate and severe hypoxia augment retrograde blood flow in the inactive limb during constant-load dynamic leg exercise.

Long-Term Impact of Strength Training on Muscle Strength Characteristics in Older Adults

ObjectiveTo evaluate the long-term preventive impact of strength training on muscle performance in older adults. DesignA 7-year follow-up on a 1-year randomized controlled trial comparing the effects of combined resistance training and aerobic training and whole-body vibration training on muscle performance. SettingUniversity training center. ParticipantsMen and women (N=83; control [CON] group, n=27; strength-training intervention [INT] group, n=56) between 60 and 80 years of age. InterventionsThe INT group exercised 3 times weekly during 1 year, performing a combined resistance training and aerobic training program or a whole-body vibration training program. The former training program was designed according to American College of Sports Medicine guidelines. The whole-body vibration training program included unloaded static and dynamic leg exercises on a vibration platform. The CON group did not participate in any training program. Main Outcome MeasuresStatic strength (STAT), dynamic strength at 60°/s (DYN60) and at 240°/s (DYN240), speed of movement at 20% (S20). ResultsFrom baseline to postintervention, muscle performance did not change in the CON group, except for S20 (+6.55%±2.88%, P<.001). One year of strength training increased (P≤.001) STAT (+11.46%±1.86%), DYN60 (+6.96%±1.65%), DYN240 (+9.25%±1.68%), and S20 (+7.73%±2.19%) in the INT group. Between baseline and follow-up, muscle performance decreased (P<.001) in both groups. However, STAT and DYN60 showed a significantly lower loss in the INT group (−8.65%±2.35% and −7.10%±2.38%, respectively) compared with the CON group (−16.47%±2.69% and −15.08%±2.27%, respectively). This positive impact might be due to the preservation of the training-induced gains, given the similar annual decline rates in both groups from postintervention to follow-up. Additionally, in trained participants, aging seems to impact velocity-dependent strength and power more compared with basic strength, as the total losses in DYN240 (CON, −15.93%±2.64%; INT, −11.39%±1.95%) and S20 (CON, −14.39%±2.10%; INT, −13.16%±1.72%) did not differ significantly between the groups. ConclusionsA 1-year strength-training intervention results in an improved muscle performance in older adults 7 years after their enrollment in the intervention. However, an extensive exercise program cannot attenuate the age-related decline once the intervention stops.

Differing sympathetic response during dynamic leg exercise in heart failure and age‐matched healthy subjects

In human heart failure (HF), we showed that muscle sympathetic nerve activity (MSNA) increased during dynamic handgrip exercise at a lower threshold than age‐matched healthy controls. The aim of the present study was to compare the MSNA response during contra lateral leg cycling in HF and control subjects, hypothesizing that, in contrast to the drop in MSNA reported in controls, MSNA would increase in HF. We measured heart rate (HR), blood pressure (BP) and MSNA in the fibular nerve (microneurography) in 11 HF patients (left ventricular ejection fraction= 32±2%; age 61±3 years, (mean±SE)) and 8 healthy control subjects (55±2 years), during 2 minutes of upright one‐legged unloaded cycling followed by 2 minutes at 50% of peak oxygen uptake (VO2peak). Resting HR and BP were similar between groups but MSNA was significantly greater (84.3±3.7 vs 68.8±5.5 bursts/100 heart beats, P=0.02), and VO2peak lower (18.7±2.4 vs 32.7±4.3 ml•kg/min, P=0.008) in HF. HR was increased during exercise (P=0.002) with no group difference (P=0.25). As expected, MSNA burst frequency decreased during exercise in the healthy controls yet was increased in HF (−4.8±3.3 vs +5.1±2.8 bursts/min, P=0.028). The normal reduction in MSNA is offset in HF by one or more sympathoexcitatory responses that may represent greater activation of muscle mechanoreceptor, metaboreceptor or cardiac sympathetic reflexes. (Heart and Stroke Foundation of Ontario)

Hypoxic effects on sympathetic vasomotor outflow and blood pressure during exercise with inspiratory resistance

The purpose of the present study was to clarify the influence of inspiratory resistive breathing during exercise under hypoxic conditions on muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Six healthy males completed this study. The subjects performed a submaximal exercise test using a cycle ergometer in a semirecumbent position under normoxic [inspired oxygen fraction (FiO2) = 0.21] and hypoxic (FiO2 = 0.12-0.13) conditions. The subjects carried out two 10-min exercises at 40% peak oxygen uptake [spontaneous breathing for 5 min and voluntary breathing with inspiratory resistance for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 s each)]. MSNA was recorded via microneurography of the right median nerve at the elbow. A progressive increase in MSNA burst frequency (BF) during leg-cycling exercise with inspiratory resistance in normoxia and hypoxia were accompanied by an augmentation of BP. The increased MSNA BF and mean arterial BP (MBP) during exercise with inspiratory resistive breathing in hypoxia (MSNA BF, 55.7 ± 1.4 bursts/min, MBP, 134.3 ± 6.6 mmHg) were higher than those in normoxia (MSNA BF, 39.2 ± 1.8 bursts/min, MBP, 123.6 ± 4.5 mmHg). These results suggest that an enhancement of inspiratory muscle activity under hypoxic condition leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

Carotid baroreflex responsiveness in normotensive African Americans is attenuated at rest and during dynamic leg exercise

Evidence suggests differences between African Americans (AAs) and Caucasian Americans (CAs) in cardiovascular responsiveness to physiological stressors. This study tested the hypothesis that carotid baroreflex (CBR) control of heart rate (HR) and blood pressure is reduced in AAs compared to CAs during exercise. Mean arterial pressure (MAP) and HR were continuously recorded at rest and during leg cycling in 23 non-hypertensive male subjects (12 AA; 11 CA; age 19–26 years). CBR control of HR and MAP was assessed with 5-s pulses of neck pressure (NP, simulated hypotension) and neck suction (NS, simulated hypertension) ranging from +45 to −80 Torr. Across all NS stimuli (−20, −40, −60, −80 Torr) at rest, the AA group demonstrated attenuated CBR-mediated reductions in HR (AA, −8.9 ± 1.9 vs. CA, −14.1 ± 2.3 bpm; P < 0.001) and MAP (AA, −6.4 ± 1 vs. CA, −7.8 ± 0.8 mmHg; P < 0.05). Despite similar gain and magnitude of resetting observed in the modeled stimulus response curves, an attenuation among AAs persisted in HR (AA, −8.2 ± 1.6 vs. CA, −11.8 ± 3 bpm; P < 0.05) and MAP (AA, −6.8 ± 0.9 vs. CA, −8.2 ± 1.1 mmHg; P < 0.05) responses to NS during exercise. No differences in CBR-mediated HR and MAP responses to NP were detected between groups at rest or during exercise. These data suggest impairment in the ability to defend against a hypertensive challenge among AAs during steady-state exercise compared to their CA counterparts.