Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity

The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C—40 min of rest), low- (E40%—40% of 1 repetition maximum, RM), and high-intensity (E80%—80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF_R–Rnu) and high-frequency (HF_R–Rnu) components of the R–R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (−6 ± 1 and −8 ± 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (−0.4 ± 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (−11 ± 2 vs. −17 ± 2 ml/beat, and +17 ± 2 vs. +21 ± 2 bpm, P < 0.05). LF_R–Rnu increased, while ln HF_R–Rnu decreased in both exercise sessions. In conclusion: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.     

Artificial gravity training reduces bed rest-induced cardiovascular deconditioning

We studied 15 men (8 treatment, 7 control) before and after 21 days of 6o head-down tilt to determine whether daily, 1-h exposures to 1.0 G_z (at the heart) artificial gravity (AG) would prevent bed rest-induced cardiovascular deconditioning. Testing included echocardiographic analysis of cardiac function, plasma volume (PV), aerobic power (VO₂pk) and cardiovascular and neuroendocrine responses to 80o head-up tilt (HUT). Data collected during HUT were ECG, stroke volume (SV), blood pressure (BP) and blood for catecholamines and vasoactive hormones. Heart rate (HR), cardiac output (CO), total peripheral resistance, and spectral power of BP and HR were calculated. Bed rest decreased PV, supine and HUT SV, and indices of cardiac function in both groups. Although PV was decreased in control and AG after bed rest, AG attenuated the decrease in orthostatic tolerance [pre- to post-bed rest change; control: −11.8 ± 2.0, AG: −6.0 ± 2.8 min (p = 0.012)] and VO₂pk [pre- to post-bed rest change; control: −0.39 ± 0.11, AG: −0.17 ± 0.06 L/min (p = 0.041)]. AG prevented increases in pre-tilt levels of plasma renin activity [pre- to post-bed rest change; control: 1.53 ± 0.23, AG: −0.07 ± 0.34 ng/mL/h (p = 0.001)] and angiotensin II [pre- to post-bed rest change; control: 3.00 ± 1.04, AG: −0.63 ± 0.81 pg/mL (p = 0.009)] and increased HUT aldosterone [post-bed rest; control: 107 ± 30 pg/mL, AG: 229 ± 68 pg/mL (p = 0.045)] and norepinephrine [post-bed rest; control: 453 ± 107, AG: 732 ± 131 pg/mL (p = 0.003)]. We conclude that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.     

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.     

Influence of respiratory pressure support on hemodynamics and exercise tolerance in patients with COPD

Inspiratory pressure support (IPS) plus positive end-expiratory pressure (PEEP) ventilation might potentially interfere with the “central” hemodynamic adjustments to exercise in patients with chronic obstructive pulmonary disease (COPD). Twenty-one non- or mildly-hypoxemic males (FEV₁ = 40.1 ± 10.7% predicted) were randomly assigned to IPS (16 cmH₂O) + PEEP (5 cmH₂O) or spontaneous ventilation during constant-work rate (70–80% peak) exercise tests to the limit of tolerance (T _lim). Heart rate (HR), stroke volume (SV), and cardiac output (CO) were monitored by transthoracic cardioimpedance (Physioflow™, Manatec, France). Oxyhemoglobin saturation was assessed by pulse oximetry (SpO₂). At similar SpO₂, IPS₁₆ + PEEP₅ was associated with heterogeneous cardiovascular effects compared with the control trial. Therefore, 11 patients (Group A) showed stable or increased Δ “isotime” – rest SV [5 (0–29) mL], lower ΔHR but similar ΔCO. On the other hand, ΔSV [−10 (−15 to −3) mL] and ΔHR were both lower with IPS₁₆ + PEEP₅ in Group B (N = 10), thereby reducing ΔCO (p < 0.05). Group B showed higher resting lung volumes, and T _lim improved with IPS₁₆ + PEEP₅ only in Group A [51 (−60 to 486) vs. 115 (−210 to 909) s, respectively; p < 0.05]. We conclude that IPS₁₆ + PEEP₅ may improve SV and exercise tolerance in selected patients with advanced COPD. Impaired SV and CO responses, associated with a lack of enhancement in exercise capacity, were found in a sub-group of patients who were particularly hyperinflated at rest.     

Relevance of individual characteristics for thermoregulation during exercise in a hot-dry environment

The aim of this study was to investigate the relevance of individual characteristics for thermoregulation during prolonged cycling in the heat. For this purpose, 28 subjects cycled for 60 min at 60% VO_2peak in a hot-dry environment (36 ± 1°C; 25 ± 2% relative humidity, airflow 2.5 m/s). Subjects had a wide range of body mass (99–43 kg), body surface area (2.2–1.4 m²), body fatness (28–5%) and aerobic fitness level (VO_2peak = 5.0–2.1 L/min). At rest and during exercise, rectal and mean skin temperatures were measured to calculate the increase in body temperature (ΔT _body) during the trial. Net metabolic heat production (M _NET) and potential heat loss (by means of evaporation, radiation and convection) were calculated. Although subjects exercised at the same relative intensity, ΔT _body presented high between-subjects variability (range from 0.44 to 1.65°C). ΔT _body correlated negatively with body mass (r = −0.49; P < 0.01), body surface area (r = −0.47; P < 0.01) and T_body at rest (r = −0.37; P < 0.05), but it did not significantly correlate with body fatness (r = 0.12; P > 0.05). ΔT _body positively correlated with the body surface area/mass ratio (r = 0.46; P < 0.01) and the difference between M _NET and potential heat loss (r = 0.56; P < 0.01). In conclusion, a large body size (mass and body surface area) is beneficial to reduce ΔT _body during cycling exercise in the heat. However, subjects with higher absolute heat production (more aerobically fit) accumulate more heat because heat production may exceed potential heat loss (uncompensability).     

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.     

Kinetics of skeletal muscle O2 delivery and utilization at the onset of heavy-intensity exercise in pulmonary arterial hypertension

Impaired O₂ delivery relative to O₂ demands at the onset of exercise might influence the response profile of muscle fractional O₂ extraction (≅Δ[deoxy-Hb/Mb] by near-infrared spectroscopy) either by accelerating its rate of increase or creating an “overshoot” (OS) in patients with pulmonary arterial hypertension (PAH). We therefore assessed the kinetics of O₂ uptake ( [(V)\dot]\textO₂ ), \left( {\dot{V}{\text{O}}_{2} } \right), Δ[deoxy-Hb/Mb] in the vastus lateralis, and heart rate (HR) at the onset of heavy-intensity exercise in 14 females with PAH (connective tissue disease, IPAH, portal hypertension, and acquired immunodeficiency syndrome) and 11 age- and gender-matched controls. Patients had slower [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} and HR dynamics than controls (τ [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2}  = 62.7 ± 15.2 s vs. 41.0 ± 13.8 s and t ^1/2-HR = 61.3 ± 16.6 s vs. 43.4 ± 8.8 s, respectively; p < 0.01). No study participant had a significant reduction in oxyhemoglobin saturation. In OS(−) subjects (6 patients and 7 controls), the kinetics of Δ[deoxy-Hb/Mb] relative to [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} were faster in patients (p = 0.05). Larger area under the OS and slower kinetics (MRT) of the “downward” component indicated greater O₂ delivery-to-utilization mismatch in OS(+) patients versus OS(+) controls (477.4 ± 330.0 vs. 78.1 ± 65.6 a.u. and 74.6 ± 18.8 vs. 46.0 ± 17.0 s, respectively; p < 0.05). Resting pulmonary vascular resistance was higher in OS(+) than OS(−) patients (23.1 ± 12.0 vs. 10.7 ± 4.0 Woods, respectively; p < 0.05). We conclude that microvascular O₂ delivery-to-utilization inequalities slowed the rate of adaptation of aerobic metabolism at the start of heavy-intensity exercise in women with PAH.     

The effects of short recovery duration on <Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript> and muscle deoxygenation during intermittent exercise

This study compared the oxygen uptake (VO₂) and muscle deoxygenation (∆HHb) of two intermittent protocols to responses during continuous constant load cycle exercise in males (24 year ± 2, n = 7). Subjects performed three protocols: (1) 10 s work/5 s active recovery (R), R at 20 W (INT1): (2) 10 s work/5 s R, R at moderate intensity (INT2); and (3) continuous exercise (CONT), all for 10 min, on separate days. The work rate of CONT and the 10 s work of INT1 and INT2 were set within the heavy intensity domain. VO₂ and ∆HHb data were filtered and averaged to 5 s bins. Average VO₂ (80–420 s) was highest during CONT (3.77 L/min), lower in INT2 (3.04 L/min), and lowest during INT1 (2.81 L/min), all (p < 0.05). Average ∆HHb (80–420 s) was higher during CONT (p < 0.05) than both INT exercise protocols (CONT; 25.7 ± 0.9 a.u. INT1; 16.4 ± 0.8 a.u., and INT2; 15.8 ± 0.8 a.u.). The repeated changes in metabolic rate elicited oscillations in ΔHHb in both intermittent protocols, whereas oscillations in VO₂ were only observed during INT1. The greater ΔHHb during CONT suggests a reduction in oxygen delivery compared to oxygen consumption relative to INT. The higher VO₂ for INT 2 versus INT 1 and similar ΔHHb during INT suggests an increase in oxygen delivery during INT 2. Thus the different demands of INT1, INT2, and CONT protocols elicited differing physiological responses to a similar heavy intensity power output. These intermittent exercise models seem to elicit an elevated O₂ delivery condition compared to CONT.     

Skin microvascular reactivity in trained adolescents

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 55 ± 6 mL kg⁻¹ min⁻¹) and nine age- and maturation-matched untrained controls ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 43 ± 5 mL kg⁻¹ min⁻¹) aged 13–15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 ± 4 vs. 9 ± 3 perfusion units (PU), p < 0.05; SkBF_max: 282 ± 120 vs. 204 ± 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC_max: 3 ± 1 vs. 2 ± 1 PU mmHg⁻¹, p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 ± 21 vs. 35 ± 15 PU, p < 0.05; area under curve: 1596 ± 739 vs. 962 ± 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.     

Are the parameters of VO2, heart rate and muscle deoxygenation kinetics affected by serial moderate-intensity exercise transitions in a single day?

This study compared the parameter estimates of pulmonary oxygen uptake (VO_2p), heart rate (HR) and muscle deoxygenation (Δ[HHb]) kinetics when several moderate-intensity exercise transitions (MODs) were performed during a single visit versus several MODs performed during separate visits. Nine subjects (24 ± 5 years, mean ± SD) each completed two successive cycling MODs on six occasions (1-6A and 1-6B) from 20 W to a work rate corresponding to 80% estimated lactate threshold with 6 min recovery at 20 W. During one visit, subjects completed two series of three MODs (6A-F), separated by 20 min rest. VO_2p time constants (τVO_2p; 27 ± 10 s, 25 ± 12 s, 25 ± 11 s) were similar (p > 0.05) for MODs 1-6A, 1-6B and 6A-F, respectively. τVO_2p had reproducibility 95% confidence intervals (CI₉₅) of 8.3, 8.2, 4.7, 4.9 and 4.7 s when comparing single (1A vs. 2A), the average of two (1-2A vs. 3-4A), three (1-3A vs. 4-6A), four (1-2AB vs. 3-4AB) and six (1-3AB vs. 4-6AB) MODs, respectively. The effective Δ[HHb] response time (τ′Δ[HHb]) was unaffected across conditions (1-6A: 19 ± 2 s, 1-6B: 19 ± 3 s, 6A-F: 17 ± 4 s) with reproducibility CI₉₅ of 5.3, 4.5, 3.1, 2.9 and 3.3 s when a single, two, three, four and six MODs were compared, respectively. τHR was reduced in MODs 6A-F compared to 1-6A and 1-6B (23 ± 5 s, 25 ± 5 s, 27 ± 6 s, respectively). This study showed that parameter estimates of VO_2p, HR and Δ[HHb] kinetics are largely unaffected by data collection sequence, and the day-to-day reproducibility of τVO_2p and τ′Δ[HHb] estimates, as determined by the CI₉₅, was appreciably improved by averaging of at least three MODs.     

<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.     

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.     

Enhanced neural drive after maximal strength training in multiple sclerosis patients

Multiple sclerosis (MS) patients suffer from impaired muscle activation and lower limb strength. Strength training enhances muscle activation and muscle strength, but neural adaptations to strength training remain unexplored in MS patients. The hypothesis was that maximal strength training (MST) using high loads and few repetitions would improve central neural drive and thus strength capacity of MS patients. 14 MS patients staying at a national MS rehabilitation center were randomly assigned to a MST group or a control group (CG). Both groups received “today’s treatment”. In addition, the MST group trained 4 × 4 repetitions of unilateral dynamic leg press and plantar flexion 5 days a week for 3 weeks. Neural adaptations of the soleus muscle were assessed by surface electromyography (EMG) activity, and by superimposed H-reflexes and V-waves obtained during maximum voluntary isometric plantar flexor contractions (MVCs). H-reflexes and V-waves were normalized by the M-wave (H _SUP/M _SUP, V/M _SUP, respectively). In the MST group, MVC increased by 20 ± 9% (P < 0.05). Soleus EMG activity and V/M _SUP ratio increased by 40 and 55%, respectively, in the MST group compared to the CG (P ≤ 0.05). The H _SUP/M _SUP ratio remained unchanged. No change was apparent in the CG. MST group subjects were able to complete all training sessions. No adverse effects were reported. This randomized study provides evidence that MST is effective of augmenting the magnitude of efferent motor output of spinal motor neurons in MS patients, alleviating some neuromuscular symptoms linked to the disease.     

Estimation of cardiomyocyte transmembrane potential with potential-sensitive fluorescent probes

Transmembrane potentials on the plasma (Δφ₄) and mitochondrial (Δφ_m) membrane of isolated rat cardiomyocytes were estimated using the potential-sensitive fluorescent probe DSM. The values were −93±4 and −196±11 mV, respectively. Sufan significantly decreased the reduction of Δφ_m induced by chemical hypoxia. The effects of antiarrhythmic drugs on changes in Δφ_p were studied using the fluorescent probe dis-C₃-(5). Lidocaine, novocainamide, richlocaine, and leocaine blocked depolarization of the myocyte plasma membrane induced by electrical stimulation and did not affect the Δφ_m. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 11, pp. 594–597, November, 1998     

The contribution of haemoglobin mass to increases in cycling performance induced by simulated LHTL

We sought to determine whether improved cycling performance following ‘Live High-Train Low’ (LHTL) occurs if increases in haemoglobin mass (Hb_mass) are prevented via periodic phlebotomy during hypoxic exposure. Eleven, highly trained, female cyclists completed 26 nights of simulated LHTL (16 h day⁻¹, 3000 m). Hb_mass was determined in quadruplicate before LHTL and in duplicate weekly thereafter. After 14 nights, cyclists were pair-matched, based on their Hb_mass response (ΔHb_mass) from baseline, to form a response group (Response, n = 5) in which Hb_mass was free to adapt, and a Clamp group (Clamp, n = 6) in which ΔHb_mass was negated via weekly phlebotomy. All cyclists were blinded to the blood volume removed. Cycling performance was assessed in duplicate before and after LHTL using a maximal 4-min effort (MMP_4min) followed by a ride time to exhaustion test at peak power output (T _lim). VO_2peak was established during the MMP_4min. Following LHTL, Hb_mass increased in Response (mean ± SD, 5.5 ± 2.9%). Due to repeated phlebotomy, there was no ΔHb_mass in Clamp (−0.4 ± 0.6%). VO_2peak increased in Response (3.5 ± 2.3%) but not in Clamp (0.3 ± 2.6%). MMP_4min improved in both the groups (Response 4.5 ± 1.1%, Clamp 3.6 ± 1.4%) and was not different between groups (p = 0.58). T _lim increased only in Response, with Clamp substantially worse than Response (−37.6%; 90% CL −58.9 to −5.0, p = 0.07). Our novel findings, showing an ~4% increase in MMP_4min despite blocking an ~5% increase in Hb_mass, suggest that accelerated erythropoiesis is not the sole mechanism by which LHTL improves performance. However, increases in Hb_mass appear to influence the aerobic contribution to high-intensity exercise which may be important for subsequent high-intensity efforts.     

Effects of temperature, ionic strength and pH on the function of skeletal muscle myosin from a eurythermal fish, Fundulus heteroclitus

The mummichog, Fundulus heteroclitus, is an intertidal fish that exhibits little change in swimming ability despite large and rapid variations in environmental parameters. We therefore tested the hypothesis that this nearly constant function is due to Fundulus myosin being intrinsically insensitive to changes of temperature, ionic strength and pH. In vitro motility assays were used to quantify the speed of unregulated actin filaments on myosin purified from F. heteroclitus glycolytic skeletal muscle. Filament speed was 2.07±0.17 μm s⁻¹ at 26°C, ionic strength (Γ/2) of 0.08 M Γ/2 and pH 7.4. Speed increased as temperature increased over the range of 5–36°C with an activation energy (E _a) of 94.0±7.0 kJ mol⁻¹) and an enthalpy (ΔH ^‡) of 91.5±7.0 kJ mol⁻¹ at 20°C. A linear relationship between temperature and ATPase activity was also obtained with actin-activated myosin Mg²⁺-ATPase assays over the temperature range 5–35°C with E _a=59.9±2.4 kJ mol⁻¹ and ΔH ^‡=57.4±2.4 kJ mol⁻¹ at 20°C. There was little or no effect of ionic strength on filament speed over the range 0.19 M Γ/2–0.54 M Γ/2. Speed increased significantly at lower ionic strengths and was 7.9-fold higher at 0.08 M Γ/2 than at 0.19 M Γ/2. Speed increased with pH with a 16-fold increase between pH 6.7 and 7.4. These results indicate that changes in physiological parameters that include temperature, pH and ionic strength affect the function of unregulated F. heteroclitus myosin, and thus other factors must be responsible for the mummichog’s swimming performance being comparatively insensitive to environmental variation.     

Measurement of Solute Transport in the Endothelial Glycocalyx Using Indicator Dilution Techniques

A new method is presented to quantify changes in permeability of the endothelial glycocalyx to small solutes and fluid flow using techniques of indicator dilution. Following infusion of a bolus of fluorescent solutes (either FITC or FITC conjugated Dextran70) into the rat mesenteric circulation, its transient dispersion through post-capillary venules was recorded and analyzed offline. To represent dispersion of solute as a function of radial position in a microvessel, a virtual transit time (VTT) was calculated from the first moment of fluorescence intensity–time curves. Computer simulations and subsequent in vivo measurements showed that the radial gradient of VTT within the glycocalyx layer (ΔVTT/Δr) may be related to the hydraulic resistance within the layer along the axial direction in a post-capillary venule and the effective diffusion coefficient within the glycocalyx. Modeling the inflammatory process by superfusion of the mesentery with 10⁻⁷ M fMLP, ΔVTT/Δr was found to decrease significantly from 0.23 ± 0.08 SD s/μm to 0.18 ± 0.09 SD s/μm. Computer simulations demonstrated that ΔVTT/Δr is principally determined by three independent variables: glycocalyx thickness (δ), hydraulic resistivity (K _r) and effective diffusion coefficient of the solute (D _eff) within the glycocalyx. Based upon these simulations, the measured 20% decrease in ΔVTT/Δr at the endothelial cell surface corresponds to a 20% increase in D _eff over a broad range in K _r, assuming a constant thickness δ. The absolute magnitude of D _eff required to match ΔVTT/Δr between in vivo measurements and simulations was found to be on the order of 2.5 × 10⁻³ × D _free, where D _free is the diffusion coefficient of FITC in aqueous media. Thus the present method may provide a useful tool for elucidating structural and molecular alterations in the glycocalyx as occur with ischemia, metabolic and inflammatory events.     

Influences of a dietary supplement in combination with an exercise and diet regimen on adipocytokines and adiposity in women who are overweight

The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynex™, Imagenetix, Inc., San Diego, CA 92127, USA) on adipocytokine and regional body composition responses to a weight loss program was examined. Twenty-two women (Supplement group (S) (n = 11): age = 36.8 ± 7.2 years; weight = 87.1 ± 6.2 kg; % body fat = 43.4 ± 4.1; Placebo group (P) (n = 11): age = 38.3 ± 6.8 years; weight = 86.9 ± 4.7 kg; % body fat = 44.3 ± 2.0) completed an 8-week placebo-controlled, double-blind study consisting of a caloric restricted diet and cardiovascular exercise. Body composition and serum insulin, leptin, and adiponectin were assessed at pre-, mid-, and post-intervention. From pre- to post-intervention, significant decreases (P < 0.05) were observed for body weight (S: 87.1 ± 6.2–77.9 ± 5.1 kg; P: 86.9 ± 4.7–82.7 ± 3.8 kg) (P < 0.05 S vs. P), % body fat (S: 43.4 ± 4.1–36.1 ± 3.6; P: 44.3 ± 2.0–40.6 ± 1.2) (P < 0.05 S vs. P), leptin (S: 28.3 ± 3.5–16.2 ± 2.6 ng ml⁻¹; P: 29.4 ± 3.2–19.9 ± 1.1 ng ml⁻¹) (P < 0.05 S vs. P), and insulin (S: 7.3 ± 0.8–5.1 ± 0.2 mU l⁻¹; P: 7.7 ± 0.9–5.1 ± 0.3 mU l⁻¹). Serum adiponectin increased (P < 0.05) (S: 12.2 ± 2.4–26.3 ± 3.0 μg ml⁻¹: 12.6 ± 2.0–21.8 ± 3.1 μg ml⁻¹) (P < 0.05 for S vs. P). Supplementation with a proprietary blend of modified cellulose and cetylated fatty acids during an 8-week weight loss program exhibited favorable effects on adipocytokines and regional body composition.     

Change in body mass accurately and reliably predicts change in body water after endurance exercise

This study tested the hypothesis that the change in body mass (ΔBM) accurately reflects the change in total body water (ΔTBW) after prolonged exercise. Subjects (4 men, 4 women; 22–36 year; 66 ± 10 kg) completed 2 h of interval running (70% VO_2max) in the heat (30°C), followed by a run to exhaustion (85% VO_2max), and then sat for a 1 h recovery period. During exercise and recovery, subjects drank fluid or no fluid to maintain their BM, increase BM by 2%, or decrease BM by 2 or 4% in separate trials. Pre- and post-experiment TBW were determined using the deuterium oxide (D₂O) dilution technique and corrected for D₂O lost in urine, sweat, breath vapor, and nonaqueous hydrogen exchange. The average difference between ΔBM and ΔTBW was 0.07 ± 1.07 kg (paired t test, P = 0.29). The slope and intercept of the relation between ΔBM and ΔTBW were not significantly different from 1 and 0, respectively. The intraclass correlation coefficient between ΔBM and ΔTBW was 0.76, which is indicative of excellent reliability between methods. Measuring pre- to post-exercise ΔBM is an accurate and reliable method to assess the ΔTBW.     

In a hot–dry environment racewalking increases the risk of hyperthermia in comparison to when running at a similar velocity

The purpose of this study was to determine if in a hot–dry environment, racewalking increases intestinal temperature (T_int) above the levels observed when running either at the same velocity or at a similar rate of heat production. Nine trained racewalkers exercised for 60 min in a hot–dry environment (30.0 ± 1.4°C; 33 ± 8% relative humidity; 2.4 m s⁻¹ air speed) on three separate occasions: (1) racewalking at 10.9 ± 1.0 km h⁻¹ (Walk), (2) running at the same velocity (RunVel) and (3) running at 13 ± 1.8 km h⁻¹ to obtain a similar [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} than during Walk (Run [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} ). As designed, energy expenditure rate was similar during Walk and Run [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} , but lower during RunVel (842 ± 78 and 827 ± 75 vs. 713 ± 55 W; p < 0.01). Final T_int was lower during RunVel than during both Walk and Run [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} (38.4 ± 0.3 vs. 39.2 ± 0.4 and 39.0 ± 0.4°C; p < 0.01). Heart rate and sweat rate were also lower during RunVel than during Walk and Run [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} (i.e. heart rate 159 ± 13 vs. 179 ± 11 and 181 ± 11 beats min⁻¹ and sweat rate 0.8 ± 0.3 vs. 1.1 ± 0.3 and 1.1 ± 0.3 L h⁻¹; p < 0.01). However, we could not detect differences in skin temperature among trials. In conclusion, our data indicate that in a hot–dry environment racewalking increases the risk of hyperthermia in comparison with when running at a similar velocity. However, exercise mode (walking vs. running) had no measurable impact on T_INT or heat dissipation when matched for energy expenditure.