Systolic and diastolic function during cycling at the respiratory threshold between elderly and young healthy individuals.

The hemodynamic consequences of aging have been extensively investigated during maximal incremental exercise. However, less is known about the effects of aging on hemodynamics during submaximal steady-state exercise. The aim of the present investigation was to compare the hemodynamics of healthy elderly and young subjects during an exercise bout conducted at the gas threshold (GET) intensity. Two groups of healthy, physically active subjects were studied: the elderly group-EG (n = 11; > 60 years old) and the young group-YG (n = 13; < 35 years old). Both groups performed a 5-min rectangular exercise test at the GET intensity. Hemodynamics were measured using echocardiography. The main finding was that stroke volume responses were higher in the YG than the EG (72.5 ± 16.7 vs. 52.4 ± 8.4 ml, respectively). The increased stroke volume capacity in the YG was the consequence of a greater capacity to increase cardiac preload and contractility and, to a lesser extent, to reduce systemic vascular resistance. Importantly, the atrial contribution to ventricular diastolic filling was substantially higher in the YG when compared to the EG.

Ischemic preconditioning of the muscle reduces the metaboreflex response of the knee extensors.

PURPOSE: This study investigated the effect of ischemic preconditioning (IP) on metaboreflex activation following dynamic leg extension exercise in a group of healthy participants. METHOD: Seventeen healthy participants were recruited. IP and SHAM treatments (3 × 5 min cuff occlusion at 220 mmHg or 20 mmHg, respectively) were administered in a randomized order to the upper part of exercising leg's thigh only. Muscle pain intensity (MP) and pain pressure threshold (PPT) were monitored while administrating IP and SHAM treatments. After 3 min of leg extension exercise at 70% of the maximal workload, a post-exercise muscle ischemia (PEMI) was performed to monitor the discharge group III/IV muscle afferents via metaboreflex activation. Hemodynamics were continuously recorded. MP was monitored during exercise and PEMI. RESULTS: IP significantly reduced mean arterial pressure compared to SHAM during metaboreflex activation (mean ± SD, 109.52 ± 7.25 vs. 102.36 ± 7.89 mmHg) which was probably the consequence of a reduced end diastolic volume (mean ± SD, 113.09 ± 14.25 vs. 102.42 ± 9.38 ml). MP was significantly higher during the IP compared to SHAM treatment, while no significant differences in PPT were found. MP did not change during exercise, but it was significantly lower during the PEMI following IP (5.10 ± 1.29 vs. 4.00 ± 1.54). CONCLUSION: Our study demonstrated that IP reduces hemodynamic response during metaboreflex activation, while no effect on MP and PPT were found. The reduction in hemodynamic response was likely the consequence of a blunted venous return.

A brief bout of exercise in hypoxia reduces ventricular filling rate and stroke volume response during muscle metaboreflex activation.

PURPOSE: The hemodynamic consequences of exercise in hypoxia have not been completely investigated. The present investigation aimed at studying the hemodynamic effects of contemporary normobaric hypoxia and metaboreflex activation. METHODS: Eleven physically active, healthy males (age 32.7 ± 7.2 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed two randomly assigned exercise sessions (3 minutes pedalling at 30% of Wmax): (1) one in normoxia (NORMO), and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia (PEMI) to study the metaboreflex, or (2) a control exercise recovery session, i.e., without metaboreflex activation. Hemodynamics were assessed with impedance cardiography. RESULTS: The main result was that the HYPO session impaired the ventricular filling rate (measured as stroke volume/diastolic time) response during PEMI versus control condition in comparison to the NORMO test (31.33 ± 68.03 vs. 81.52 ± 49.23 ml·s-1,respectively, p = 0.003). This caused a reduction in the stroke volume response (1.45 ± 9.49 vs. 10.68 ± 8.21 ml, p = 0.020). As a consequence, cardiac output response was impaired during the HYPO test. CONCLUSIONS: The present investigation suggests that a brief exercise bout in hypoxia is capable of impairing cardiac filling rate as well as stroke volume during the metaboreflex. These results are in good accordance with recent findings showing that among hemodynamic modulators, ventricular filling is the most sensible variable to hypoxic stimuli.

Mechanisms Involved in Cardioprotection Induced by Physical Exercise.

Significance: Regular exercise training can reduce myocardial damage caused by acute ischemia/reperfusion (I/R). Exercise can reproduce the phenomenon of ischemic preconditioning, due to the capacity of brief periods of ischemia to reduce myocardial damage caused by acute I/R. In addition, exercise may also activate the multiple kinase cascade responsible for cardioprotection even in the absence of ischemia. Recent Advances: Animal and human studies highlighted the fact that, besides to reduce risk factors related to cardiovascular disease, the beneficial effects of exercise are also due to its ability to induce conditioning of the heart. Exercise behaves as a physiological stress that triggers beneficial adaptive cellular responses, inducing a protective phenotype in the heart. The factors contributing to the exercise-induced heart preconditioning include stimulation of the anti-radical defense system and nitric oxide production, opioids, myokines, and adenosine-5'-triphosphate (ATP) dependent potassium channels. They appear to be also involved in the protective effect exerted by exercise against cardiotoxicity related to chemotherapy. Critical Issues and Future Directions: Although several experimental evidences on the protective effect of exercise have been obtained, the mechanisms underlying this phenomenon have not yet been fully clarified. Further studies are warranted to define precise exercise prescriptions in patients at risk of myocardial infarction or undergoing chemotherapy.

Effects of exercise in normobaric hypoxia on hemodynamics during muscle metaboreflex activation in normoxia.

PURPOSE: Little is known about the cardiovascular effects of the transition from exercise in hypoxia (EH) to normoxia. This investigation aimed to assess hemodynamics during the metaboreflex elicited in normoxia after EH. METHODS: Ten trained athletes (four females and six males, age 35.6 ± 8.4 years) completed a cardiopulmonary test to determine the workload at anaerobic threshold (AT). On separate days, participants performed three randomly assigned exercise sessions (10 min pedalling at 80% of AT): (1) one in normoxia (EN); (2) one in normobaric hypoxia with FiO2 15.5% (EH15.5%); and (3) one in normobaric hypoxia with FiO2 13.5% (EH13.5%). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia after cycling for 3 min, to study the metaboreflex, or (2) a control exercise recovery (CER) session, without any metaboreflex stimulation. RESULTS: The main result were that both EH15.5% and EH13.5% impaired (p < 0.05) the ventricular filling rate response during the metaboreflex (- 18 ± 32 and - 20 ± 27 ml s-1), when compared to EN (+ 29 ± 32 ml s-1), thereby causing a reduction in stroke volume response (- 9.1 ± 3.2, - 10.6 ± 8.7, and + 5 ± 5.7 ml for EH15.5%, EH13.5% and EN test, respectively, p < 0.05). Moreover, systemic vascular resistance was increased after the EH15.5% and the EH13.5% in comparison with the EN test. CONCLUSIONS: These data demonstrate that moderate exercise in hypoxia impairs the capacity to enhance venous return during the metaboreflex stimulated in normoxia. Overall, there is a functional shift from a flow to vasoconstriction-mediated mechanism for maintaining the target blood pressure during the metaboreflex.

Cardio-metabolic responses during horse riding at three different speeds.

PURPOSE: The purpose of the present investigation was to study the metabolic demand and cardiovascular response during a typical horse riding session. METHODS: To this aim, 19 (9 male, 10 female) riders, regularly participating in competitions, were enrolled. They underwent a preliminary, incremental exercise test on a cycle-ergometer to assess their anaerobic threshold (AT) and VO2max. Then, participants underwent a riding training session, which comprised periods of walking, trotting, and cantering for a total of 20 min. Oxygen uptake (VO2), carbon dioxide production (VCO2), and heart rate (HR) were obtained throughout the preliminary and riding test by means of a portable metabolic system. Moreover, excess of CO2 production (CO2excess) and oxygen pulse (OP) were also calculated to obtain an estimate of anaerobic glycolysis and stroke volume. RESULTS: The main result was that all collected parameters remained below the AT level throughout the riding session, with the exception of HR that approached the AT level only during cantering. In detail, during cantering, average VO2, VCO2, HR, CO2excess, and OP values were 1289 ± 331 mL min(-1), 1326 ± 266 mL min(-1), 158 ± 22 bpm, 215 ± 119 mL min(-1), and 7.8 ± 1.6 mL/bpm, respectively. CONCLUSIONS: It was concluded that riding imposes only light to moderate stress on the aerobic and anaerobic energy systems. Moreover, cardiovascular reserve is only moderately recruited in terms of inotropism, while chronotropism can be stimulated more.

Diving response after a one-week diet and overnight fasting.

BACKGROUND: We hypothesized that overnight fasting after a short dietary period, especially with carbohydrates, could allow performing breath-hold diving with no restraint for diaphragm excursion and blood shift and without any increase of metabolism, and in turn improve the diving response. METHODS: During two separate sessions, 8 divers carried out two trials: (A) a 30-m depth dive, three hours after a normal breakfast and (B) a dive to the same depth, but after following a diet and fasting overnight. Each test consisted of 3 apnea phases: descent, static and ascent whose durations were measured by a standard chronometer. An impedance cardiograph, housed in an underwater torch, provided data on trans-thoracic fluid index (TFI), stroke volume (SV), heart rate (HR) and cardiac output (CO). Mean blood pressure (MBP), arterial O2 saturation (SaO2), blood glucose (Glu) and blood lactate (BLa) were also collected. RESULTS: In condition B, duration of the static phase of the dive was longer than A (37.8 ± 7.4 vs. 27.3 ± 8.4 s respectively, P < 0.05). In static phases, mean ∆ SV value (difference between basal and nadir values) during fasting was lower than breakfast one (-2.6 ± 5.1 vs. 5.7 ± 7.6 ml, P < 0.05). As a consequence, since mean ∆ HR values were equally decreased in both metabolic conditions, mean ∆ CO value during static after fasting was lower than the same phase after breakfast (-0.4 ± 0.5 vs. 0.4 ± 0.5 L · min(-1) respectively, P < 0.05). At emersion, despite the greater duration of dives during fasting, SaO2 was higher than A (92.0 ± 2.7 vs. 89.4 ± 2.9 % respectively, P < 0.05) and BLa was lower in the same comparison (4.2 ± 0.7 vs. 5.3 ± 1.1 mmol∙L(-1), P < 0.05). CONCLUSIONS: An adequate balance between metabolic and splancnic status may improve the diving response during a dive at a depth of 30 m, in safe conditions for the athlete's health.

Daily assessment of arterial distensibility in a pediatric population before and after smoking cessation.

OBJECTIVES: Cigarette smoking is an important modifiable cardiovascular risk factor associated with increased stiffness of the large arteries in adulthood. This study aimed to 1) evaluate arterial distensibility and echocardiographic measures in adolescent smokers before and after participation in a successful smoking cessation program and to 2) compare the findings obtained with data from a control population of healthy non-smokers. METHODS: A total of 31 young smoking subjects (58.1% male; range: 11-18 years old; mean: 16.5±1.4 years old; mean tobacco consumption: 2.6±0.6 years) were examined before commencing and after taking part for at least 1 year in a smoking cessation program (mean: 1.4±0.3 years). Arterial stiffness was measured using the previously validated QKd100-60 method. Twenty-four-hour ambulatory blood pressure monitoring and transthoracic echocardiography were also performed. RESULTS: (Smokers before abuse cessation vs. smokers after abuse cessation) systolic blood pressure: p<0.004; diastolic blood pressure: p<0.02; mean blood pressure: p<0.01; QKd100-60 value: 183±5 vs. 196±3 msec, p<0.009; p = ns for all echocardiographic parameters. (Smokers after abuse cessation vs. controls) systolic blood pressure: p<0.01; diastolic blood pressure: p<0.03; mean blood pressure: p<0.02; QKd100-60 value: 196±3 vs. 203±2 msec, p<0.04; p<0.02, p<0.01, and p<0.05 for the interventricular septum, posterior wall, and left ventricular mass, respectively. CONCLUSIONS: Despite successful participation in a smoking cessation program, arterial distensibility improved but did not normalize. This finding underlines the presence of the harmful effect of arterial rigidity in these individuals, despite their having quit smoking and their young ages, thus resulting in the subsequent need for a lengthy follow-up period.

Daily assessment of arterial distensibility in a pediatric population before and after smoking cessation

OBJECTIVES: Cigarette smoking is an important modifiable cardiovascular risk factor associated with increased stiffness of the large arteries in adulthood. This study aimed to 1) evaluate arterial distensibility and echocardiographic measures in adolescent smokers before and after participation in a successful smoking cessation program and to 2) compare the findings obtained with data from a control population of healthy non-smokers. METHODS: A total of 31 young smoking subjects (58.1% male; range: 11-18 years old; mean: 16.5±1.4 years old; mean tobacco consumption: 2.6±0.6 years) were examined before commencing and after taking part for at least 1 year in a smoking cessation program (mean: 1.4±0.3 years). Arterial stiffness was measured using the previously validated QKd100-60 method. Twenty-four-hour ambulatory blood pressure monitoring and transthoracic echocardiography were also performed. RESULTS: (Smokers before abuse cessation vs. smokers after abuse cessation) systolic blood pressure: p<0.004; diastolic blood pressure: p<0.02; mean blood pressure: p<0.01; QKd100-60 value: 183±5 vs. 196±3 msec, p<0.009; p = ns for all echocardiographic parameters. (Smokers after abuse cessation vs. controls) systolic blood pressure: p<0.01; diastolic blood pressure: p<0.03; mean blood pressure: p<0.02; QKd100-60 value: 196±3 vs. 203±2 msec, p<0.04; p<0.02, p<0.01, and p<0.05 for the interventricular septum, posterior wall, and left ventricular mass, respectively. CONCLUSIONS: Despite successful participation in a smoking cessation program, arterial distensibility improved but did not normalize. This finding underlines the presence of the harmful effect of arterial rigidity in these individuals, despite their having quit smoking and their young ages, thus resulting in the subsequent need for a lengthy follow-up period. .