High-intensity Dynamic Exercise Research Articles

Non-invasive ventilatory support accelerates the oxygen uptake and heart rate kinetics and improves muscle oxygenation dynamics in COPD-HF patients

BackgroundThe aim of this study was to explore the effects of non-invasive positive pressure ventilation (NIPPV) associated with high-intensity exercise on heart rate (HR) and oxygen uptake (V̇O2) recovery kinetics in in patients with coexistence of chronic obstructive pulmonary disease (COPD) and heart failure (HF). MethodsThis is a randomized, double blinded, sham-controlled study involving 14 HF-COPD patients, who underwent a lung function test and Doppler echocardiography. On two different days, patients performed incremental cardiopulmonary exercise testing (CPET) and two constant-work rate tests (80% of CPET peak) receiving Sham or NIPPV (bilevel mode - Astral 150) in a random order until the limit of tolerance (Tlim). During exercise, oxyhemoglobin and deoxyhemoglobin were assessed using near-infrared spectroscopy (Oxymon, Artinis Medical Systems, Einsteinweg, Netherland). ResultsThe kinetic variables of both V̇O2 and HR during the high-intensity constant workload protocol were significantly faster in the NIPPV protocol compared to Sham ventilation (P < 0.05). Also, there was a marked improvement in oxygenation and lower deoxygenation of both peripheral and respiratory musculature in TLim during NIPPV when contrasted with Sham ventilation. ConclusionsNIPPV applied during high-intensity dynamic exercise can effectively improve exercise tolerance, accelerate HR and V̇O2 kinetics, improve respiratory and peripheral muscle oxygenation in COPD-HF patients. These beneficial results from the effects of NIPPV may provide evidence and a basis for high-intensity physical training for these patients in cardiopulmonary rehabilitation programs.

High-Resolution Dynamics of Hemodilution After Exercise-Related Hemoconcentration.

Hemoconcentration during acute intense exercise is intensively investigated, while the rearrangement of hematological parameters during the recovery period is less understood. The aim of our study was to understand the mechanisms of hemodilution after short-term dynamic exercise. Twelve euhydrated male kayak athletes and 6 untrained controls were examined on a spiroergometer. In addition to the continuous recording of circulatory parameters, blood samples were taken at rest, at maximum load, and during restitution with a dense sampling frequency. Hemoglobin, hematocrit, osmolality, blood components, and core temperature were measured. The hemoconcentration, independently of training status, reached its maximum (athletes Δ9.59% [4.18%] vs controls Δ11.85% [2.71%]) in the first minute of the recovery period. There was a significant increase in core temperature, reducing the viscosity of blood and promoting tissue oxygenation. High cardiac output and the increased blood flow compensate for viscosity being elevated by hemoconcentration during exercise. Hemoconcentration was maintained for 7 to 10minutes and then diluted back to baseline 30minutes after exercise. Temporarily higher viscosity during reduced cardiac output may result in a critical hemoconcentration zone, elevating the risk of circulatory overload. Elite athletes have a faster cardiac output decrease compared with that of hemodilution, making the circulation more vulnerable. We supposed that hemodilution was guided independently by plasma- and erythrocyte-related effectors. After high-intensity dynamic acute exercise, hemodilution is driven by independent factors, and a critical hemoconcentration zone may be formed during the recovery period in trained elite athletes.

Regulation of muscle potassium: exercise performance, fatigue and health implications.

This review integrates from the single muscle fibre to exercising human the current understanding of the role of skeletal muscle for whole-body potassium (K+) regulation, and specifically the regulation of skeletal muscle [K+]. We describe the K+ transport proteins in skeletal muscle and how they contribute to, or modulate, K+ disturbances during exercise. Muscle and plasma K+ balance are markedly altered during and after high-intensity dynamic exercise (including sports), static contractions and ischaemia, which have implications for skeletal and cardiac muscle contractile performance. Moderate elevations of plasma and interstitial [K+] during exercise have beneficial effects on multiple physiological systems. Severe reductions of the trans-sarcolemmal K+ gradient likely contributes to muscle and whole-body fatigue, i.e. impaired exercise performance. Chronic or acute changes of arterial plasma [K+] (hyperkalaemia or hypokalaemia) have dangerous health implications for cardiac function. The current mechanisms to explain how raised extracellular [K+] impairs cardiac and skeletal muscle function are discussed, along with the latest cell physiology research explaining how calcium, β-adrenergic agonists, insulin or glucose act as clinical treatments for hyperkalaemia to protect the heart and skeletal muscle in vivo. Finally, whether these agents can also modulate K+-induced muscle fatigue are evaluated.

Effects of High Intensity Dynamic Resistance Exercise and Whey Protein Supplements on Osteosarcopenia in Older Men with Low Bone and Muscle Mass. Final Results of the Randomized Controlled FrOST Study.

The present study aimed to evaluate the effect of high intensity dynamic resistance exercise (HIT-DRT) and whey protein supplementation (WPS) on bone mineral density (BMD) and sarcopenia parameters in osteosarcopenic men. Men ≥ 72 years with osteosarcopenia (n = 43) were randomly assigned to a HIT-RT (HIT-RT: n = 21) or a non-training control group (n = 22). Supervised HIT-RT twice/week was applied for 18 months, while the control group maintained their habitual lifestyle. Supplying WPS, total protein intake amounted to 1.5–1.6 (HIT-RT) and 1.2 g/kg/body mass/d (control). Both groups were supplied with calcium and vitamin D. Primary study outcomes were BMD and the sarcopenia Z-score. After adjusting for multiplicity, we observed significant positive effects for sarcopenia Z-score (standardized mean difference (SMD): 1.40), BMD at lumbar spine (SMD: 0.72) and total hip (SMD: 0.72). In detail, effect sizes for skeletal muscle mass changes were very pronounced (1.97, p < 0.001), while effects for functional sarcopenia parameters were moderate (0.87, p = 0.008; handgrip strength) or low (0.39, p = 0.209; gait velocity). Apart from one man who reported short periods of temporary worsening of existing joint pain, no HIT-RT/WPS-related adverse effects or injuries were reported. We consider HIT-RT supported by whey protein supplementation as a feasible, attractive, safe and highly effective option to fight osteosarcopenia in older men.

Effects of acute inspiratory loading during treadmill running on cerebral, locomotor and respiratory muscle oxygenation in women soccer players

Respiratory limitation can be a primary mechanism for exercise cessation in female athletes. This study aimed to assess the effects of inspiratory loading (IL) on intercostal muscles (IM), vastus lateralis (VL) and cerebral (Cox) muscles oxygenation in women soccer players during high-intensity dynamic exercise. Ten female soccer players were randomized to perform in order two constant-load tests on a treadmill until the exhaustion time (Tlim) (100 % of maximal oxygen uptake- V˙O2). They breathed freely or against a fixed inspiratory loading (IL) of 41 cm H2O (∼30 % of maximal inspiratory pressure). Oxygenated (Δ[OxyHb]), deoxygenated (Δ[DeoxyHb]), total hemoglobin (Δ[tHb]) and tissue saturation index (ΔTSI) were obtained by NIRs. Also, blood lactate [La—] was obtained. IL significantly reduced Tlim (224 ± 54 vs 78 ± 20; P < 0.05) and increased [La—], V˙O2, respiratory cycles and dyspnea when corrected to Tlim (P < 0.05). IL also resulted in decrease of Δ[OxyHb] of Cox and IM during exercise compared with rest condition. In addition, decrease of Δ[OxyHb] was observed on IM during exercise when contrasted with Sham (P < 0.05). Furthermore, significant higher Δ[DeoxyHb] of IM and significant lower Δ[DeoxyHb] of Cox were observed when IL was applied during exercise in contrast with Sham (P < 0.05). These results were accompanied with significant reduction of Δ[tHb] and ΔTSI of IM and VL when IL was applied (P < 0.05). High-intensity exercise with IL decreased respiratory and peripheral muscle oxygenation with negative impact on exercise performance. However, the increase in ventilatory work did not impact cerebral oxygenation in soccer players.

Transcranial Doppler-determined change in posterior cerebral artery blood flow velocity does not reflect vertebral artery blood flow during exercise.

We examined whether a change in posterior cerebral artery flow velocity (PCAv) reflected the posterior cerebral blood flow in healthy subjects during both static and dynamic exercise. PCAv and vertebral artery (VA) blood flow, as an index of posterior cerebral blood flow, were continuously measured during an exercise trial using transcranial Doppler (TCD) ultrasonography and Doppler ultrasound, respectively. Static handgrip exercise significantly increased both PCAv and VA blood flow. Increasing intensity of dynamic exercise further increased VA blood flow from moderate exercise, while PCAv decreased to almost resting level. During both static and dynamic exercise, the PCA cerebrovascular conductance (CVC) index significantly decreased from rest (static and high-intensity dynamic exercise, -11.5 ± 12.2% and -18.0 ± 16.8%, means ± SD, respectively) despite no change in the CVC of VA. These results indicate that vasoconstriction occurred at PCA but not VA during exercise-induced hypertension. This discrepancy in vascular response to exercise between PCA and VA may be due to different cerebral arterial characteristics. Therefore, to determine the effect of exercise on posterior cerebral circulation, at least, we need to carefully consider which cerebral artery to measure, regardless of exercise mode.NEW & NOTEWORTHY We examined whether transcranial Doppler-determined flow velocity in the posterior cerebral artery can be used as an index of cerebral blood flow during exercise. However, the changes in posterior cerebral artery flow velocity during exercise do not reflect vertebral artery blood flow.

Intelligent physical exercise training intervention at the workplace for health promotion among office workers: A randomized controlled trial

Background: Health promotion at the workplace can be effective by introducing physical exercise training for preventing lifestyle diseases such as cardiovascular, metabolic, and musculoskeletal disorders. The present aim was to assess the effects of individually tailored intelligent physical exercise programs for office workers on cardiovascular health risk indicators. Methods: The study was a randomized controlled trial among office workers allocated to either a training (N=194) or a control group (N=195). The intervention lasted one year, and the training group trained onehour high intensity dynamic exercise everyweek during working hours and were recommended 30min of moderate intensity physical activity 6 days a week during leisure time. Before and after the intervention participants completed a health check including a standardized submaximal bicycle test with heart rate monitoring for indirect estimate of maximal oxygen uptake (VO2max), body mass, BMI, blood pressure (BP), and blood profile. Data from the first health check were used to individually tailor the intelligent physical exercise training. Trial registration was in ClinicalTrials.gov, number: NCT01366950. Results: At baseline, the training group had a (mean± SD) VO2max of 3.3±0.9 l/min and a fitness level (VO2max per body mass) of 36±11 (ml/min/kg), systolic/diastolic BP 124±17/82±11mmHg, blood glucose 5.3±1mmol/l, and blood cholesterol 5.1±0.9mmol/l. An intention-to-treat analysis showed a significant 5% increase in VO2max and fitness level in the training group compared with the control group. Furthermore, within the training group a significant decrease occurred in systolic/diastolic BP of 3.4/2.8mmHg, and blood glucose of 0.2mmol/l. No intervention effect was found on BMI, blood cholesterol, and triglycerides. In a per protocol analysis among employees in the training group with an adherence ≥70% (N=102) compared to the control group showed a significant 10% increase in VO2max and fitness level. Further, within the high adherence group a decrease in systolic/diastolic BP of 4.4/3.3mmHg, and blood cholesterol of 0.2mmol/l was seen. Discussion:High intensity intelligent physical exercise training combined with recommendations of moderate intensity physical activity significantly increased VO2max and fitness level. The magnitude of increase implied a decrease in cardiovascular health risk based on findings in larger epidemiological studies. Of note is that this increase was larger among those with the highest adherence. Within the training group deceases in systolic BP and blood glucose/cholesterol additionally indicateddecreasedhealth risks. In all this study was effective in decreasing health risk indicators among office workers.

A-42 Free Communication/Poster - Non-traditional Sports

It has been proposed that III-IV muscle afferents (MA) from the working muscles are a major contributor to central fatigue (CF), i.e. exercise-induced reduction in voluntary activation (VA). However, in many studies, CF is not observed after high intensity dynamic exercise. This may be related to the relatively long time (∼2 min) between exhaustion on the exercising ergometer and the measurement of CF on the dynamometer. For this reason we developed a one leg dynamic exercise (OLDE) involving the knee extensors (active extension and passive flexion) on a dynamometer allowing a short delay (∼10 s) to assess i) the discharge of MA via post exercise muscle ischemia (PEMI, study 1) and ii) the extent of exercise-induced CF (study 2). PURPOSE: These studies aim to investigate the discharge of MA and extent of CF induced by OLDE to exhaustion. METHODS: Both studies consisted of 4 sessions performed on the right leg (1 familiarisation, 1 incremental test and 2 experimental time to exhaustion tests at 85% peak power). In study 1 (n=10), PEMI (300 mmHg) was performed on the exercising thigh and mean arterial pressure (MAP) was measured. In study 2 (n=8), VA, M-wave (M), cervicomedullary motor evoked potential (CMEP), motor evoked potential (MEP) and cortical silent period (CSP) were measured on the knee extensors. In both studies, measurements were performed pre and post exercise (at exhaustion or after 3 min). Two-way repeated ANOVAs were used for statistical analysis. Data are presented as change according to baseline ±SD. RESULTS: MAP during PEMI was higher at exhaustion (+18±17%, P<0.05) and recovered after 3 min (+7±11%). OLDE induced a decrease in VA (-11±10%, P<0.05) at exhaustion and after 3 min (-5±4%, P<0.05). CMEP/M area was lower at exhaustion (-39±11%, P<0.01) and recovered after 3 min (-6±17%). MEP/M area was higher at exhaustion (+28±27%, P<0.01) and after 3 min (+15±19%, P<0.01). CMEP/MEP area decreased at exhaustion (P<0.001) and recovered after 3 min. CSP was higher at exhaustion (+32±23%, P<0.01) and recovered after 3 min (+2±16%). CONCLUSION: These studies highlight the importance of minimising the time delay to assess exercise-induced CF. This is the first study to show increased intracortical inhibition and decreased spinal excitability associated with discharge of MA at exhaustion following dynamic contractions.

Effects of N-acetylcysteine on isolated mouse skeletal muscle: contractile properties, temperature dependence, and metabolism

The effects of the general antioxidant N-acetylcysteine (NAC) on muscle function and metabolism were examined. Isolated paired mouse extensor digitorum longus muscles were studied in the absence or presence of 20 mM NAC. Muscles were electrically stimulated to perform 100 isometric tetanic contractions (300 ms duration) at frequencies resulting in ∼85% of maximal force (70-150 Hz at 25-40 °C). NAC did not significantly affect peak force in the unfatigued state at any temperature but significantly slowed tetanic force development in a temperature-dependent fashion (e.g., time to 50% of peak tension averaged 35 ± 2 ms [control] and 37 ± 1 ms [NAC] at 25 °C vs. 21 ± 1 ms [control] and 52 ± 6 ms [NAC, P < 0.01] at 40 °C). During repeated contractions, NAC maximally enhanced peak force by the fifth tetanus at all temperatures (by ∼30%). Thereafter, the effect of NAC disappeared rapidly at high temperatures (35-40 °C) and more slowly at the lower temperatures (25-30 °C). At all temperatures, the enhancing effect of NAC on peak force was associated with a slowing of relaxation. NAC did not significantly affect myosin light chain phosphorylation at rest or after five contractions (∼50% increase vs. rest). After five tetani, lactate and inorganic phosphate increased about 20-fold and 2-fold, respectively, both in control and NAC-treated muscles. Interestingly, after five tetani, the increase in glucose 6-P was ∼2-fold greater, whereas the increase in malate was inhibited by ∼75% with NAC vs. control, illustrating the metabolic effects of NAC. NAC slightly decreased the maximum shortening velocity in early fatigue (five to seven repeated tetani). These data demonstrate that the antioxidant NAC transiently enhances muscle force generation by a mechanism that is independent of changes in myosin light chain phosphorylation and inorganic phosphate. The slowing of relaxation suggests that NAC enhances isometric force by facilitating fusion (i.e., delaying force decline between pulses). The initial slowing of tension development and subsequent slowing of relaxation suggest that NAC would result in impaired performance during a high-intensity dynamic exercise.

Blood pressure regulation II: what happens when one system must serve two masters—oxygen delivery and pressure regulation?

During high-intensity dynamic exercise, O2 delivery to active skeletal muscles is enhanced through marked increases in both cardiac output and skeletal muscle blood flow. When the musculature is vigorously engaged in exercise, the human heart lacks the pumping capacity to meet the blood flow demands of both the skeletal muscles and other organs such as the brain. Vasoconstriction must therefore be induced through activation of sympathetic nervous activity to maintain blood flow to the brain and to produce the added driving pressure needed to increase flow to the skeletal muscles. In this review, we first briefly summarize the local vascular and neural control mechanisms operating during high-intensity exercise. This is followed by a review of the major neural mechanisms regulating blood pressure during high-intensity exercise, focusing mainly on the integrated activities of the arterial baroreflex and muscle metaboreflex. In high cardiac output situations, such as during high-intensity dynamic exercise, small changes in total peripheral resistance can induce large changes in blood pressure, which means that rapid and fine regulation is necessary to avoid unacceptable drops in blood pressure. To accomplish this rapid regulation, arterial baroreflex function may be modulated in various ways through activation of the muscle metaboreflex and/or other neural mechanisms. Moreover, this modulation of the arterial baroreflex may change over the time course of an exercise bout, or to accommodate changes in exercise intensity. Within this model, integration of arterial baroreflex modulation with other neural mechanisms plays an important role in cardiovascular control during high-intensity exercise.

The brain at work

Our understanding of the cerebral blood flow (CBF) response to exercise has evolved dramatically over some 20 years in parallel with the advent of new methods to measure brain perfusion in humans. Previously, the Kety–Schmidt method was the only method available for evaluation of CBF in humans. The outflow from the brain through the internal jugular vein was taken to represent CBF and no change was found during exercise, probably because the spinal veins become more important when humans are upright as is the case for most exercise studies (Ide & Secher, 2000). As a consequence, it was often considered that exercise was the exception for which cerebral ‘activation’ (and maybe thinking?) was not required. Yet, with the introduction of methods that evaluate brain tissue flow (133Xenon-clearance) or inflow to the brain through the common or, ideally the internal carotic artery, an ∼20% increase in CBF during mild- to moderate-intensity dynamic exercise was observed. The CBF then levels out or maybe decreases when exercise becomes intense, with the decrease in the arterial carbon dioxide tension accompanying the exponential increase in ventilation. Thus CBF, and indeed cerebral oxygenation responses during incremental exercise, were hypothesised to follow an inverted U-shaped curve. The vast majority of human studies have applied a transcranial Doppler (TCD) approach to evaluate changes in CBF during exercise. Although this approach has the advantage that it can be used during high-intensity dynamic exercise of a large muscle mass, when using the TCD technique one must assume that the diameter of the isonated artery does not change. This assumption has become universally accepted although TCD was introduced by R. Aaslid (1984) to detect vasospasm after neurosurgical procedures. In support of the supposition that the diameter of the isonated artery at the base of the brain (often the middle cerebral artery (MCA)) remains constant during exercise, an inverted U-shape response to incremental exercise is detected with the TCD, and the magnitude of the increase in mean flow velocity is similar to that determined by other estimates of CBF (∼20%). In contrast, the diameter of the MCA increases in response to hypoxia (Wilson et al. 2011) and constricts in response to the administration of the α1-adrenergic receptor agonist phenylephrine (Ogoh et al. 2011), indicating that there is a need for new ambulatory methods for the evaluation of CBF. In a recent issue of The Journal of Physiology, Vogiatzis et al. (2011) introduced a new method using near-infrared spectroscopy to detect CBF (in the frontal lobe) during progressive exercise after bolus injection of idocyanine green, with and without hypoxia, in trained cyclists. It is comforting that the inverted U-shape CBF response to incremental exercise is confirmed by this initiative, and that the validity of the method is supported by an increase in CBF during hypoxia. Yet, as mentioned by the authors, the determined CBF is unreasonably low (23 ml min−1 100 g−1) compared to a normal value of ∼50 ml min−1 100 g−1 and the increase with CBF during exercise is twice as large as normally found. Near-infrared light has to pass through the skin and the scalp to reach the frontal lobe and the authors consider that the low skin (and scalp) blood flow could influence the result. Accordingly, it would be of value if this method for determination of CBF were repeated during exercise after skin blood flow is eliminated, e.g. by cooling the skin or after the administration of phenylephrine (Ogoh et al. 2011). The TCD technique has been invaluable for the development in understanding the brain at work both under normoxic and hypoxic conditions; however, it is problematic that the TCD evaluation of CBF is expressed as a velocity. Such a limitation may be surmounted by using near-infrared spectroscopy to determine CBF during exercise (Vogiatzis et al. 2011), although the extent of the influence of skin blood flow must be established. Similarly, flow in basal cerebral arteries may be evaluated by duplex ultrasound (Wilson et al. 2011) as it is established for peripheral arteries. Accordingly, we now have two additional methods available to take the evaluation of CBF during hypoxic exercise to new heights and the study by Vogiatzis et al. (2011) provides support to the notion that exercise in hypoxia is limited by cerebral oxygen supply and brain oxygenation.

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.

Dynamic arterial baroreflex function during high intensity exercise in humans: insights into sympathetic control

Dynamic arterial baroreflex function during high intensity exercise in humans: insights into sympathetic control

Effects of nitric oxide synthase inhibition on vascular conductance during high speed treadmill exercise in rats.

To determine the functional role of nitric oxide (NO) in regulating vascular conductance during high intensity dynamic exercise in skeletal muscles composed of all major fibre types, female Wistar rats (277 +/- 4 g; n = 7) were run on a motor-driven treadmill at a speed and gradient (60 m min(-1), 10 % gradient) established to yield maximal oxygen uptake (V(O2,max)). Vascular conductance (ml min(-1) (100 g)(-1) mmHg(-1)), defined as blood flow normalised to mean arterial pressure (MAP), was determined using radiolabelled microspheres during exercise before and after NO synthase (NOS) inhibition with N (G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1), I.A.). The administration of L-NAME increased MAP from pre-L-NAME baseline values, demonstrating that NOS activity is reduced. The administration of L-NAME also reduced vascular conductance in 20 of the 28 individual hindlimb muscles or muscle parts examined during high speed treadmill exercise. These reductions in vascular conductance correlated linearly with the estimated sum of the percentage of slow twitch oxidative (SO) and fast twitch oxidative glycolytic (FOG) types of fibres in each muscle (Deltaconductance = -0.0082(%SO + %FOG) - 0.0105; r = 0.66; P < 0.001). However, if the reduction in vascular conductance found in the individual hindquarter muscles or muscle parts was expressed as a percentage decrease from the pre-L-NAME value (%Delta = (pre-L-NAME conductance - post-L-NAME conductance)/ pre-L-NAME conductance x 100), then the reduction in vascular conductance was similar in all muscles examined (average %Delta = -23 +/- 2 %). These results suggest that NO contributes substantially to the regulation of vascular conductance within and among muscles of the rat hindquarter during high intensity exercise. When expressed in absolute terms, the results suggest that the contribution of NO to the regulation of vascular conductance during high intensity exercise is greater in muscles that possess a high oxidative capacity. In contrast, if results are expressed in relative terms, then the contribution of NO to the regulation of vascular conductance during high intensity exercise is similar across the different locomotor muscles located in the rat hindlimb and independent of the fibre type composition.

RELIABILITY OF HEART RATE VARIABILITY DURING DYNAMIC HANDGRIP EXERCISE

This study examined test-retest reliability of heart rate variability (HRV) during low (H20:20%MVC) and high (H60: 60%MVC) intensity dynamic handgrip exercise. 6 women and 3 men (age:22 ± 2yrs) participated in three tests with no more than two weeks between sessions. During each session, MVC was measured and handgrip exercise (0.50 hz) performed using a Biodex handgrip dynamometer. Visits land 3 (V1 and V3) consisted of 5 minutes of both H20 and H60 exercise, each preceded by 5 min spontaneous breathing (SB) in the supine position (SB1 and SB2, respectively). Visit 2 (V2) involved 5 min of SB1 and 5 minutes of H60 exercise. ECG (Biopac MP100) were continuously collected during each session. Data were analyzed in 2.2 min segments using MATLAB and Acqknowledge (3.0) software to obtain mean R-R interval, standard deviation (SDNN), low frequency (LF: 0–0.15 hz) and high frequency (HF:0.15–0.40hz) power, and normalized frequency units (power/sum of LF and HF). A repeated measure ANOVA with Tukey's post hoc analysis was used to test for significance across day and condition. Reliability was tested using Hoyt's reliability analysis. Mean R-R (V3: SB1:943.3 ± 129.2ms, H20: 883.8 ± 140.7ms, SB2:943.0 ± 147.9ms, H60:756.5 ± 112.6ms) and HFnu (V3:SB1:44.7 ± 24.8%, H20:47.6 ± 26.0%, SB2:29.8 ± 17.9%, H60:29.1 ± 19.7%) decreased and LFnu (V3:SB1:55.3 ± 24.8%, H20:52.4 ± 26.0%, SB2:70.2 ± 17.9%, H60:70.9 ± 19.7%) increased in an intensity dependent manner during exercise (p < 0.05). SDNN decreased during exercise (V3: SB1:56.2 ± 30.2ms, H20:40.7 ± 16.0ms, SB2:92.6 ± 33.6ms, H60:39.6 ± 17.4ms; p < 0.05 from SB), but was not intensity dependent. The reliability coefficients for R-R and HRV are in the table. These data indicate time and frequency domain during dynamic exercise are reliable over a one month period.Table

Comparison of outcome of cardiac rehabilitation in black women and white women

Coronary artery disease is the leading cause of death among black women in the United States. Black women also demonstrate a greater prevalence of coronary risk factors and a higher mortality after myocardial infarction than white women. To evaluate the clinical profile and outcome of black women in an urban-based cardiac rehabilitation program, 35 black women (aged 54 +/- 13 years) and 47 white women (aged 57 +/- 10 years) were prospectively studied. Black women had similar admitting diagnoses as white women, with recent myocardial infarction being the most common (37%). Coronary risk factors were more prevalent in black women than white women in the program: hypertension (71% vs 53%; p = 0.09) diabetes mellitus (46% vs 26%; p = 0.06), obesity (74% vs 49%; p < 0.05). Cholesterol and high-density lipoprotein levels were similarly elevated in black (251 +/- 53 mg/dl) and in white (248 +/- 52 mg/dl) women, whereas 34% of black and 21% of white women were active smokers. There was no significant difference in initial exercise capacity at program entry. Fewer black women (51%) completed the 12-week program than white women (64%), p = NS. Comparison of initial and follow-up exercise tests after 12 weeks of moderate to high-intensity dynamic exercise demonstrated significant and similar improvements in functional capacity in both black (4.2 +/- 1.6 vs 5.6 +/- 1.7 METs; p < 0.001) and white (4.8 +/- 2.2 vs 5.7 +/- 2.2 METs; p < 0.01) women. Among obese patients, only the white women lost weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympatho‐adrenal secretion in humans: factors governing catecholamine and storage vesicle peptide co‐release *

1. In postganglionic sympathetic neurones and adrenal chromaffin cells, catecholamines are co-stored in vesicles with soluble peptides, including chromogranin A (CgA) and neuropeptide Y (NPY), which are subject to exocytotic co-release with catecholamines. 2. Plasma catecholamine, CgA and NPY responses to stimulators and inhibitors of sympatho-adrenal catecholamine storage and release were measured in humans. Short-term, high-intensity dynamic exercise, prolonged low-intensity dynamic exercise, and assumption of the upright posture, in decreasing order of potency, predominantly stimulated noradrenaline (NA) release from sympathetic nerve endings. Only high-intensity exercise elevated CgA and NPY, which did not peak until 2 min after exercise cessation. Stimulated NA correlated with plasma CgA 2 min after exercise, and with NPY 5 min after exercise. 3. Insulin-evoked hypoglycaemia and caffeine ingestion, in decreasing order of potency, predominantly stimulated adrenaline (AD) release from the adrenal medulla. During insulin hypoglycaemia AD and CgA rose, but NPY was unchanged. Neither NPY nor CgA were altered by caffeine. The rise in CgA after intense adrenal medullary stimulation was greater than its rise after intense sympathetic neuronal stimulation (1.4-versus 1.2-fold, respectively). 4. Infusion of tyramine, which disrupts sympathetic neuronal vesicular NA storage, elevated systolic blood pressure and NA, while NPY and CgA were unchanged. After reserpine, another disruptor of neuronal NA storage, NA transiently rose and then fell; NPY and CgA were unaltered. After the non-exocytotic adrenal medullary secretory stimulus glucagon. AD rose while NA, CgA and NPY did not change. After amantadine, an inhibitor of protein endocytosis, both CgA and fibrinogen rose, while NA and NPY remained unaltered. Neither CgA, NPY, nor catecholamines were altered by the catecholamine uptake and catabolism inhibitors desipramine, cortisol, and pargyline. 5. Human sympathetic nerve contained a far higher ratio of NPY to catecholamines than human adrenal medulla, while adrenal medulla contained far more CgA than sympathetic nerve. 6. It is concluded that peptides are differentially co-stored with catecholamines, with greater abundance of CgA in the adrenal medulla and NPY in sympathetic nerve. Activation of catecholamine release from either the adrenal medulla or sympathetic nerves, therefore, results in quite different changes in plasma concentrations of the catecholamine storage vesicle peptides CgA and NPY. Only profound, intense stimulation of chromaffin cells or sympathetic axons measurably perturbs plasma CgA or NPY concentration; lesser degrees of stimulation perturb plasma catecholamines only. Neither CgA nor NPY are released during non-exocytotic catecholamine secretion.

Abatement of exertional perceptions following dynamic exercise

Perceptual and physiological congruity was examined during recovery from high-intensity dynamic exercise. Nine males (24.8 +/- 0.6 yr; VO2max; 52.3 +/- 1.5 ml.kg-1.min-1) undertook in random order four maximal treadmill protocols. Treadmill speed was held constant (5.3 km.h-1) while grade was incremented by 2, 4, 6, or 8% every 3 min for protocols A, B, C, and D, respectively. Ratings of perceived exertion (RPErec; Borg 15-point scale), ventilation (VE), respiratory rate (RR), oxygen uptake (VO2), and heart rate (HR) were measured preexercise and during each min of a 12-min supine postexercise period that immediately followed treadmill testing. Ratings were obtained for the peripheral perceptual signal arising from the legs (RPErec-L), the respiratory-metabolic signal from the chest (RPErec-C), and the overall body signal (RPErec-O). Blood pH was measured preexercise and during min 1, 6, and 12 of recovery. RPErec-L and RPErec-O were lower (P less than 0.05) and blood pH higher (p less than 0.05) following protocol A than D at all recovery time points. RPErec-C, VE, and RR were lower (P less than 0.05) for protocol A than D at all recovery time points. Differences among protocols were not noted for VO2 or HR at any recovery time point. The decay in signal strength for both RPErec-L and RPErec-O following high-intensity exercise reflected the abatement of metabolic acidosis. RPErec-O was influenced by the abatement of pulmonary ventilation during the postexercise period.

Voluntary activation of human quadriceps during and after isokinetic exercise

The extent of voluntary activation in fresh and fatigued quadriceps muscles was investigated during isometric and isokinetic voluntary contractions at 20 and 150 degrees/s in 23 normal human subjects. The muscles were fatigued by a total of 4 min of maximal knee extension at an angular velocity of 85 degrees/s. Voluntary activation was determined by the superimposition of tetanic electrical stimulation at 100 Hz for 250 ms, initiated at a constant knee angle. The relationship between voluntary and stimulated force was similar to that found with the established twitch superimposition technique used on isometric contractions. In fresh muscle all the subjects showed full voluntary activation during isometric contractions. Some activation failure was seen in five subjects at 20 degrees/s [2.0 +/- 0.9 degrees (SE)] and in two subjects at 150 degrees/s (0.7 +/- 0.5). After fatigue all subjects showed some activation failure at 0 and 20 degrees/s (36.4 +/- 3.1 and 28.8 +/- 4.1 degrees, respectively), but only two showed any at 150 degrees/s (1.4 +/- 5.7). We conclude that brief high-intensity dynamic exercise can cause a considerable failure of voluntary activation. This failure was most marked during isometric and the lower-velocity isokinetic contractions. Thus a failure of voluntary activation may have greater functional significance than previous studies of isometric contractions have indicated.

Effect of increased central blood volume with water immersion on plasma catecholamines during exercise

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on the sympathoadrenal response to graded dynamic exercise, nine healthy men underwent upright leg cycle exercise on land and with WI. Plasma norepinephrine and epinephrine concentrations were used as indexes of overall sympathoadrenal activity. Oxygen consumption (VO2), heart rate, systolic blood pressure, and plasma concentrations of norepinephrine, epinephrine, and lactate were determined at work loads corresponding to approximately 40, 60, 80, and 100% peak VO2. Peak VO2 did not differ on land and with WI. Plasma norepinephrine concentration was reduced (P less than 0.05) at 80 and 100% peak VO2 with WI and on land, respectively. Plasma epinephrine and lactate concentrations were similar on land and with WI at the three submaximal work stages, but both were reduced (P less than 0.05) at peak exertion with WI. Heart rate was lower (P less than 0.05) at the three highest work intensities with WI. These results suggest that the central shift in blood volume with WI reduces the sympathoadrenal response to high-intensity dynamic exercise.