Wavelet-Based System Identification of Short-Term Dynamic Characteristics of Arterial Baroreflex

The assessment of arterial baroreflex function in cardiovascular diseases requires quantitative evaluation of dynamic and static baroreflex properties because of the frequent modulation of baroreflex properties with unstable hemodynamics. The purpose of this study was to identify the dynamic baroreflex properties from transient changes of step pressure inputs with background noise during a short-duration baroreflex test in anesthetized rabbits with isolated carotid sinuses, using a modified wavelet-based time-frequency analysis. The proposed analysis was able to identify the transfer function of baroreflex as well as static properties from the transient input-output responses under normal [gain at 0.04 Hz from carotid sinus pressure (CSP) to arterial pressure (n = 8); 0.29 ± 0.05 at low (40–60 mmHg), 1.28 ± 0.12 at middle (80–100 mmHg), and 0.38 ± 0.07 at high (120–140 mmHg) CSP changes] and pathophysiological [gain in control vs. phenylbiguanide (n = 8); 0.32 ± 0.07 vs. 0.39 ± 0.09 at low, 1.39 ± 0.15 vs. 0.59 ± 0.09 (p < 0.01) at middle, and 0.35 ± 0.04 vs. 0.15 ± 0.02 (p < 0.01) at high CSP changes] conditions. Subsequently, we tested the proposed wavelet-based method under closed-loop baroreflex responses; the simulation study indicates that it may be applicable to clinical situations for accurate assessment of dynamic baroreflex function. In conclusion, the dynamic baroreflex property to various pressure inputs could be simultaneously extracted from the step responses with background noise.     

Cardiovascular time courses during prolonged immersed static apnoea

To define the dynamics of cardiovascular adjustments to apnoea during immersion, beat-to-beat heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures were recorded in six divers during and after prolonged apnoeas while resting fully immersed in 27°C water. Apnoeas lasted 215 ± 35 s. Compared to control values, HR decreased by 20 beats min⁻¹ and SBP and DBP increased by 23 and 17 mmHg, respectively, in the initial 20 ± 3 s (phase I). Both HR and BP remained stable during the following 92 ± 15 s (phase II). Subsequently, during the final 103 ± 29 s, SBP and DBP increased linearly to values about 60% higher than control, whereas HR remained unchanged (phase III). Cardiac output (Q′) decreased by 35% in phase I and did not further change in phases II and III. Compared to control, total peripheral resistances were twice and three times higher than control, respectively, at the end of phases I and III. After resumption of breathing, HR and BP returned to control values in 5 and 30 s, respectively. The time courses of cardiovascular adjustments to immersed breath-holding indicated that cardiac response took place only at the beginning of apnoea. In contrast, vascular responses showed two distinct adjustments. This pattern suggests that the chronotropic control via the baroreflex is modified during apnoea. These cardiovascular changes during immersed static apnoea are in agreement with those already reported for static dry apnoeas.     

Resetting of the arterial baroreflex increases orthostatic sympathetic activation and prevents postural hypotension in rabbits

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP–SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA–AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP–AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

Signaling pathways involved with the stimulatory effect of Angiotensin II on vacuolar H+-ATPase in proximal tubule cells

It has been documented that angiotensin II (ANG II) (10⁻⁹ M) stimulates proton extrusion via H⁺-adenosine triphosphatase (ATPase) in proximal tubule cells. In the present study, we investigated the signaling pathways involved in the effects of ANG II on H⁺-ATPase activity and on the cytosolic free calcium concentration in immortalized rat proximal tubule cells, a permanent cell line derived from rat proximal tubules. The effects of ANG on pH_i and [Ca⁺²]_i were assessed by the fluorescent probes, 2′,7-bis (2-carboxyethyl)-5(6)-carboxyfluorescein-acetoxy-methyl ester and fluo-4-acetoxy-methyl ester, in the absence of Na⁺ to block the Na⁺/H⁺ exchanger. In the control situation, the pH recovery rate following intracellular acidification with NH₄Cl was 0.073±0.011 pH units/min (n=12). This recovery was significantly increased with ANG II (10⁻⁹ M), to 0.12±0.015 pH units/min, n=10. This last effect was also followed by a significant increase of Ca⁺² _i, from 99.72±1.704 nM (n=21) to 401.23±33.91 nM (n=39). The stimulatory effect of ANG II was blocked in the presence of losartan, an angiotensin II subtype 1 (AT₁) receptor antagonist. H89 [protein kinase A (PKA) inhibitor] plus ANG II had no effect on the pH recovery. Staurosporine [protein kinase C (PKC) inhibitor] impaired the effect of ANG II. Phorbol myristate acetate (PKC activator) mimicked in part the stimulatory effect of ANG II, but reduced Ca⁺² _i. 1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (intracellular calcium chelator) alone reduced the pH_i recovery rate below control levels and impaired the effect of ANG II, in a way similar to that of trimethoxy benzoate (a blocker of Ca⁺² _i mobilization). We conclude that ANG II regulates rat proximal tubule vacuolar H⁺-ATPase by a PKA-independent mechanism and that PKC and intracellular calcium play a critical role in this regulation.     

Haemodynamic responses to angiotensin II in conscious lambs: role of nitric oxide and prostaglandins

It was hypothesized that nitric oxide (NO) and prostaglandins (PGs) play a synergistic role in modulating haemodynamic responses to angiotensin II (ANG II) in an age-dependent manner. To this end, experiments were carried out in conscious, chronically instrumented lambs aged ∼1 week (N = 9) and ∼6 weeks (N = 10) to evaluate the haemodynamic responses to ANG II, before and after treatment with the l-arginine analogue, N-nitro-l-arginine methyl ester (l-NAME), as well as the cyclooxygenase inhibitor, indomethacin (INDO). Pressor and renal blood flow responses to ANG II were measured before (control) and after administration of l-NAME (20 mg kg⁻¹), following pretreatment with either vehicle (VEH) (experiment 1) or INDO (1 mg kg⁻¹, experiment 2). The two experiments were carried out at minimum intervals of 48 h. In both age groups, the pressor and renal vasoconstrictor responses to ANG II were augmented by pretreatment with INDO, the effects being similar at 1 and 6 weeks. The haemodynamic responses to ANG II were, however, not altered after l-NAME following pretreatment with either VEH or INDO. These data provide new evidence that soon after birth, endogenously produced PGs, but not endogenously produced NO, balance the vasoconstrictor actions of ANG II. There is, however, no apparent interaction between PGs and NO in modulating the responses to ANG II postnatally.     

Baroreflex control of sinus node during dynamic exercise in humans: effect of muscle mechanoreflex

Aim: This study evaluated the influence of muscle mechanical afferent stimulation on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Methods: Systolic blood pressure (SBP) and pulse interval (PI) were measured continuously and non‐invasively in 15 subjects at rest and during passive cycling. The arterial baroreflex was evaluated with the cross‐correlation method (xBRS) for the computation of time‐domain baroreflex sensitivity on spontaneous blood pressure and PI variability. xBRS computes the greatest positive correlation between beat‐to‐beat SBP and PI, and when significant at P = 0.01, slope and delay are recorded as one xBRS value. Heart rate variability (HRV) was evaluated in the frequency domain. Results: Compared with rest, passive exercise resulted in a parallel increase in heart rate (67 ± 3.2 vs. 70 ± 3.6 beats min^?1; P < 0.05) and mean arterial pressure (87 ± 2 vs. 95 ± 2 mmHg; P < 0.05), and a significant decrease in xBRS (13.1 ± 1.8 vs. 10.5 ± 1.7 ms mmHg^?1; P < 0.01) with an apparent rightward shift in the regression line relating SBP to PI. Also low frequency power of HRV increased while high frequency power decreased (56.7 ± 3.5 vs. 62.7 ± 4.8 and 43.2 ± 3.4 vs. 36.9 ± 4.9 normalized units respectively; P < 0.05). Conclusion: These data suggest that the stimulation of mechanosensitive stretch receptors is capable of modifying the integrated baroreflex control of sinus node function by decreasing the cardiac vagal outflow during exercise.     

Syncope is unrelated to supine and postural hypotension following prolonged exercise

Syncope is widely reported following prolonged exercise. It is often assumed that the magnitude of exercise-induced hypotension (post-exercise hypotension; PEH), and the hypotensive response to postural change (initial orthostatic hypotension; IOH) are predictors of syncope post-exercise. The aim of this study was to determine the relationship between PEH, IOH, the residual IOH and syncope following prolonged exercise. Blood pressure (BP; Finometer) was measured continuously in 19 athletes (47 ± 20 years; BMI: 23.2 ± 2.2 kg m²; [(V)\dot] \dot{V} O₂ max: 51.3 ± 10.8 mL kg⁻¹ min⁻¹) whilst supine and during head-up tilt (HUT) to 60° for 15 min (or to syncope), prior to and following 4 h of running at 70–80% maximal heart rate. Syncope developed in 15 of 19 athletes post-exercise [HUT-time completed, Pre: 14:39 (min:s) ± 0:55; Post: 5:59 ± 4:53; P < 0.01]. PEH was apparent (−7 ± 7 mmHg; −8 ± 8%), but was unrelated to HUT-time completed (r ² = 0.09; P > 0.05). Although the magnitude of IOH was similar to post-exercise [−28 ± 12 vs. −20 ± 14% (pre-exercise); P > 0.05], the BP recovery following IOH was incomplete [−9 ± 9 vs. −1 ± 11 (pre-exercise); P < 0.05]; however, neither showed a relation to HUT-time completed (r ² = 0.18, r ² = 0.01; P > 0.05, respectively). Although an inability to maintain BP is a common feature of syncope post-exercise, the magnitude of PEH, IOH and residual IOH do not predict time to syncope. Practically, endurance athletes who present with greater hypotension are not necessarily at a greater risk of syncope than those who present with lesser reductions in BP.     

The effect of 48?weeks of aerobic exercise training on cutaneous vasodilator function in post-menopausal females

Skin blood flow (SkBF) and endothelial-dependent vasodilatation decline with ageing and can be reversed with exercise training. We tested whether 48 weeks of training could improve SkBF and endothelial function in post-menopausal females; 20 post-menopausal subjects completed the study. SkBF was measured by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Resting CVC was measured at 32°C and peak CVC at 42°C. Cutaneous endothelial-dependent and -independent vasodilatations were determined by the iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. All assessments described were performed at entry (week 0), and after 6, 12, 24, 36, and 48 weeks of training. Resting CVC measures did not change (P > 0.05) throughout the study. Peak CVC increased (P < 0.05) after 24 weeks (7.2 ± 1.2 vs. 11.6 ± 1.4 AU mmHg⁻¹) and at the 36- and 48-week assessments (13.0 ± 1.7 and 14.9 ± 2.1 AU mmHg⁻¹, respectively). Responses to ACh also increased (P < 0.05) at the 24-week assessment (5.1 ± 2.1 vs. 8.55 ± 2.3 AU mmHg⁻¹) and increased further at the 36 and 48-week assessments (11.6 ± 3.7 and 13.2 ± 3.9 AU mmHg⁻¹, respectively). Cutaneous responses to SNP increased (P < 0.05) after 36 weeks (8.7 ± 2.1 vs. 13.02 ± 2.23 AU mmHg⁻¹ at 36 weeks). VO_2max increased after 12 weeks (23.5 ± 0.7 vs. 25.4 ± 0.9 ml kg⁻¹ min⁻¹) and improved (P < 0.05) further throughout the study (31.6 ± 1.8 ml kg⁻¹ min⁻¹ at week 48). Aerobic exercise produces positive adaptations in the cutaneous vasodilator function to local heating as well as in cutaneous endothelial and endothelial-independent vasodilator mechanisms. Aerobic capacity was also significantly improved. These adaptations were further enhanced with progressive increases in exercise intensity.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CV_drift) during cycling. Twelve healthy males (23.4 ± 0.5 years, mean ± SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CV_drift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (ΔSV = −16.2 ± 2.0 and −17.1 ± 1.0 ml beat⁻¹; ΔHR = 18.3 ± 2.0 and 17.5 ± 3.0 beats min⁻¹ for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO₂ rebreathing) was 14.7 ± 0.3 l min⁻¹ and 15.0 ± 0.3 l min⁻¹, and mean arterial pressure was 100.0 ± 1.0 mmHg and 96.7 ± 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 ± 1.2% and 11.0 ± 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 ± 0.8 (AU) for 40 rpm and 53.0 ± 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CV_drift during cycling, at least under the present experimental conditions.     

Effect of moderate intensity resistance training during weight loss on body composition and physical performance in overweight older adults

The impact of resistance training has not been thoroughly examined in overweight older adults undergoing weight loss. Subjects (n = 27) were overweight and obese (BMI 31.7 ± 3.6 kg/m²) older (age 67 ± 4 years) adults and were randomized into either a 10-week Dietary Approaches to Stop Hypertension for weight loss diet (DASH, n = 12) or DASH plus moderate intensity resistance training (DASH-RT, n = 15). Outcomes included weight loss, total body and mid-thigh composition, muscle and physical function. There were no significant weight loss differences between the DASH-RT and DASH groups (−3.6 ± 0.8 vs. −2.0 ± 0.9%, p = 0.137). The DASH-RT group had a greater reduction in body fat than the DASH group (−4.1 ± 0.9 vs. −0.2 ± 1.0 kg, p = 0.005). The DASH-RT group had greater changes in lean mass (+0.8 ± 0.4 vs. −1.4 ± 0.4 kg, p = 0.002) and strength (+60 ± 18 vs. −5 ± 9 N, p = 0.008) than the DASH group. There were favorable changes in mid-thigh composition variables in the DASH-RT group that were different than the lack of changes observed in the DASH group, except for intermuscular adipose tissue. Both groups experienced decreases in 400-m walk times showed (DASH −36 ± 11 s, DASH-RT −40 ± 7 s) with no differences between groups. Moderate intensity resistance training during weight loss appears to improve fat mass and thigh composition, but weight loss only does not. However, global measures of physical functioning may improve with a weight loss-only program.     

The intraocular pressure response to dehydration: a pilot study

The aim of this study was to determine the intraocular pressure response to differing levels of dehydration. Seven males participated in 90 min of treadmill walking (5 km h⁻¹ and 1% grade) in both temperate (22°C) and hot (43°C) conditions. At baseline and 30 min intervals intraocular pressure, nude body mass, body temperature and heart rate were recorded. Statistically significant interactions (p < 0.05) were observed for intraocular pressure (hot condition: baseline 17.0 ± 2.9, 30 min 15.6 ± 3.5, 60 min 14.5 ± 3.7 and 90 min 13.6 ± 2.9 mmHg; temperate condition: baseline 16.8 ± 2.7, 30 min 16.5 ± 2.6, 60 min 15.8 ± 2.5 and 90 min 15.7 ± 1.8 mmHg) and body mass loss (hot condition: 30 min −1.07 ± 0.35, 60 min −2.17 ± 0.55 and 90 min −3.13 ± 0.74%; temperate condition: 30 min −0.15 ± 0.11, 60 min −0.47 ± 0.18 and 90 min −0.78 ± 0.25%). Significant linear regressions (p < 0.05) were observed for intraocular pressure and body mass loss (adjusted r ² = 0.24) and intraocular pressure change and body mass loss (adjusted r ² = 0.51). In conclusion, intraocular pressure was progressively reduced during a period of exercise causing dehydration, but remained relatively stable when hydration was maintained. The present study revealed a moderate relationship between dehydration (body mass loss) and intraocular pressure change.     

Short-term cardiovascular responses to rapid whole-body tilting during exercise

Our objective was to characterize the responses of heart rate (HR) and arterial blood pressure (BP) to changes in posture during concomitant dynamic leg exercise. Ten men performed dynamic leg exercise at 50, 100, and 150 W and were rapidly and repeatedly tilted between supine (0°) and upright (80°) positions at 2-min intervals. Continuous recordings of BP and HR were made, and changes in central blood volume were estimated from transthoracic impedance. Short-lasting increases in BP were observed immediately upon tilting from the upright to the supine position (down-tilt), averaging +18 mmHg (50 W) to +31 mmHg (150 W), and there were equally short-lasting decreases in BP, ranging from −26 to −38 mmHg upon tilting from supine to upright (up-tilt). These components occurred for all pressure parameters (systolic, mean, diastolic, and pulse pressures). We propose that these transients reflect mainly tilt-induced changes in total peripheral resistance resulting from decreases and increases of the efficiency of the venous muscle pump. After 3–4 s (down-tilt) and 7–11 s (up-tilt) there were large HR transients in a direction opposite to the pressure transients. These HR transients were larger during the down-tilt (−15 to −26 beats · min⁻¹) than during the up-tilt (+13 to +17 beats · min⁻¹), and increased in amplitude with work intensity during the down-tilt. The tilt-induced HR fluctuations could be modelled as a basically linear function of an arterial baroreflex input from a site half-way between the heart and the carotid sinus, and with varying contributions of fast vagal and slow sympathetic HR responses resulting in attenuated tachycardic responses to hypotensive stimuli during exercise. Accepted: 24 August 1999     

Mechanically versus electro-magnetically braked cycle ergometer: performance and energy cost of the Wingate Anaerobic Test

Performance and metabolic profiles of the Wingate Anaerobic Test (WAnT) were compared between a mechanically resisted (ME) and an electro-magnetically braked (EE) cycle ergometer. Fifteen healthy subjects (24.0±3.5 years, 180.5±6.1 cm, 75.4±11.9 kg) performed a WAnT on ME, and EE 3 days apart. Performance was measured as peak power (PP), minimum power (MP), mean power (AP), time to PP (TTPP), fatigue rate (FR), and maximum cadence (RPM_MAX). Lactic (W _LAC) and alactic (W _PCR) anaerobic energy were calculated from net lactate appearance and the fast component of post-exercise oxygen uptake. Aerobic metabolism (W _AER) was calculated from oxygen uptake during the WAnT. Total energy cost (W _TOT) was calculated as the sum of W _LAC, W _PCR, and W _AER. There was no difference between ME and EE in PP (873±159 vs. 931±193 W) or AP (633±89 vs. 630±89 W). In the EE condition TTPP (2.3±0.7 vs. 4.3±0.7 s) was longer (P<0.001), MP (464±78 vs. 388±57 W) was lower (P<0.001), FR (15.2±5.2 vs. 20.5±6.8%) was higher (P<0.005), and RPM_MAX (168±18 vs. 128±15 rpm) was slower (P<0.001). There was no difference in W _TOT (1,331±182 vs. 1,373±120 J kg⁻¹), W _AER (292±76 vs. 309±72 J kg⁻¹), W _PCR (495±153 vs. 515±111 J kg⁻¹) or W _LAC (545±132 vs. 549±141 J kg⁻¹) between ME and EE devices. The EE produces distinctly different performance measures but valid metabolic WAnT results that may be used to evaluate anaerobic fitness.     

Temporal association of elevations in serum cardiac troponin T and myocardial oxidative stress after prolonged exercise in rats

The objective of this study was to determine if prolonged exercise resulted in the appearance of cardiac troponin T (cTnT) in serum and whether this was associated with elevated levels of myocardial oxidative stress. Forty-five male Sprague–Dawley rats were randomized into four groups and killed before (PRE-EX), immediately (0HR), 2 (2HR) and 24 h (24HR) after a 3-h bout of swimming with 5% body weight attached to their tail. In all animals serum cTnT was assayed using 3rd generation electrochemiluminescence. In homogenized heart tissue myocardial malondialdehyde (MDA), a marker of lipid peroxidation, glutathione (GSH), and a non-enzymatic estimate of total antioxidant capacity (T-AOC) were assessed spectrophotometrically. At PRE-EX cTnT was undetectable in all animals. At 0HR (median, range: 0.055, 0.020–0.100) and 2HR post-exercise (0.036, 0.016–2.110) cTnT was detectable in all animals (P < 0.05). At 24HR post-exercise cTnT was undetectable in all animals. An elevation in MDA was observed 0HR (mean ± SD: 1.7 ± 0.2 nmol mgpro⁻¹) and 2HR (1.6 ± 0.3 nmol mgpro⁻¹) post-exercise compared with PRE-EX (1.3 ± 0.2 nmol mgpro⁻¹; P < 0.05). The antioxidant response to this challenge was a significant (P < 0.05) decrease in GSH 2HR and 24HR post-exercise. Despite this T-AOC did not alter across the trial (P > 0.05). The results indicated that prolonged and strenuous exercise in rats resulted in an elevation in cTnT, a biomarker of cardiomyocyte damage, in all animals 0HR and 2HR after exercise completion. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart.     

Post-concurrent exercise hemodynamics and cardiac autonomic modulation

Concurrent training is recommended for health improvement, but its acute effects on cardiovascular function are not well established. This study analyzed hemodynamics and autonomic modulation after a single session of aerobic (A), resistance (R), and concurrent (A + R) exercises. Twenty healthy subjects randomly underwent four sessions: control (C:30 min of rest), aerobic (A:30 min, cycle ergometer, 75% of VO₂ peak), resistance (R:6 exercises, 3 sets, 20 repetitions, 50% of 1 RM), and concurrent (AR: A + R). Before and after the interventions, blood pressure (BP), heart rate (HR), cardiac output (CO), and HR variability were measured. Systolic BP decreased after all the exercises, and the greatest decreases were observed after the A and AR sessions (−13 ± 1 and −11 ± 1 mmHg, respectively, P < 0.05). Diastolic BP decreased similarly after all the exercises, and this decrease lasted longer after the A session. CO also decreased similarly after the exercises, while systemic vascular resistance increased after the R and AR sessions in the recovery period (+4.0 ± 1.7 and +6.3 ± 1.9 U, respectively, P < 0.05). Stroke volume decreased, while HR increased after the exercises, and the greatest responses were observed after the AR session (SV, A = −14.6 ± 3.6, R = −22.4 ± 3.5 and AR = −23.4 ± 2.4 ml; HR, A =+13 ± 2, R =+15 ± 2 vs. AR =+20 ± 2 bpm, P < 0.05). Cardiac sympathovagal balance increased after the exercises, and the greatest increase was observed after the AR session (A = +0.7 ± 0.8, R = +1.0 ± 0.8 vs. AR = +1.2 ± 0.8, P < 0.05). In conclusion, the association of aerobic and resistance exercises in the same training session did not potentiate post-exercise hypotension, and increased cardiac sympathetic activation during the recovery period.     

Changes in glucose tolerance and insulin sensitivity following 2 weeks of daily cinnamon ingestion in healthy humans

Cinnamon can improve fasting glucose in humans yet data on insulin sensitivity are limited and controversial. Eight male volunteers (aged 25 ± 1 years, body mass 76.5 ± 3.0 kg, BMI 24.0 ± 0.7 kg m⁻²; mean ± SEM) underwent two 14-day interventions involving cinnamon or placebo supplementation (3 g day⁻¹). Placebo supplementation was continued for 5 days following this 14 day period. Oral glucose tolerance tests (OGTT) were performed on days 0, 1, 14, 16, 18, and 20. Cinnamon ingestion reduced the glucose response to OGTT on day 1 (−13.1 ± 6.3% vs. day 0; P < 0.05) and day 14 (−5.5 ± 8.1% vs. day 0; P = 0.09). Cinnamon ingestion also reduced insulin responses to OGTT on day 14 (−27.1 ± 6.2% vs. day 0; P < 0.05), as well as improving insulin sensitivity on day 14 (vs. day 0; P < 0.05). These effects were lost following cessation of cinnamon feeding. Cinnamon may improve glycaemic control and insulin sensitivity, but the effects are quickly reversed.     

Indirect measures of human vagal withdrawal during head-up tilt with and without a respiratory acidosis

Human ECG records were analyzed during supine (SUP) rest and whole body 80° head-up tilt (HUT), with a respiratory acidosis (5%CO₂) and breathing room air (RA). HUT increased heart rate in both conditions (RA_SUP 60 ± 13 vs. RA_HUT 79 ± 16; 5%CO_2SUP 63 ± 12 vs. 5%CO_2HUT 79 ± 14 beats min⁻¹) and decreased mean R–R interval, with no changes in the R–R interval standard deviation. When corrected for changes in frequency spectrum total power (NU), the high frequency (0.15–0.4 Hz) component (HF_NU) of heart rate variability decreased (RA_SUP 44.01 ± 21.57 vs. RA_HUT 24.05 ± 13.09; 5%CO_2SUP 69.23 ± 15.37 vs. 5%CO_2HUT 47.64 ± 21.11) without accompanying changes in the low frequency (0.04–0.15 Hz) component (LF_NU) (RA_SUP 52.36 ± 21.93 vs. RA_HUT 66.58 ± 19.49; 5%CO_2SUP 22.97 ± 11.54 vs. 5%CO_2HUT 40.45 ± 21.41). Positive linear relations between the tilt-induced changes (Δ) in HF_NU and R–R interval were recorded for RA (ΔHF_NU = 0.0787(ΔR−R) − 11.3, R ² = 0.79, P < 0.05), and for 5%CO₂ (ΔHF_NU = 0.0334(ΔR−R) + 1.1, R ² = 0.82, P < 0.05). The decreased HF component suggested withdrawal of vagal activity during HUT. For both RA and 5%CO₂, the positive linear relations between ΔHF_NU and ΔR−R suggested that the greater the increase in heart rate with HUT, the greater the vagal withdrawal. However, a reduced range of ΔHF during HUT with respiratory acidosis suggested vagal withdrawal was lower with a respiratory acidosis.