Muscle Oxygenation Responses to Low-intensity Steady Rate Concentric and Eccentric Cycling

2018 ◽  
Vol 39 (03) ◽  
pp. 173-180 ◽  
Author(s):  
Mark Rakobowchuk ◽  
Laurie Isacco ◽  
Ophélie Ritter ◽  
Alicia Represas ◽  
Malika Bouhaddi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Exercise Bout ◽  
Systolic Arterial Pressure ◽  
Muscle Oxygenation ◽  
Exercise Session ◽  
Metabolic Demand ◽  
Low Intensity ◽  
Mechanical Power Output ◽  
Training Impulse

AbstractMuscle deoxygenation responses provide information about the training impulse of an exercise session enabling adaptation to be predicted. Our aim was to investigate muscle oxygenation profiles during prolonged low-intensity eccentric and concentric cycling. Twelve healthy men performed two 45-min exercise sessions of concentric (CON) and eccentric (ECC) cycling, matched for the same heart rate at the start of each session. Mechanical power output during ECC was ~2.5 times that of CON (210±40 W vs. 82±16 W). Oxygen uptake, blood lactate, cardiac output and systolic arterial pressure responses did not differ between exercises. Heart rate was similar at 5 min of each exercise bout but progressively increased during ECC and was higher at 15, 30 and 45 min of ECC compared to CON (+10 bpm), with a trend for a lower stroke volume. Diastolic and mean blood pressures were higher during ECC. No significant differences were observed in muscle oxygenation profiles. Muscle oxygenation responses during prolonged low-intensity exercise were not affected by the type of muscle action at the same metabolic demand and cardiac output.

Low-intensity exercise training decreases cardiac output and hypertension in spontaneously hypertensive rats

1997 ◽  
Vol 273 (6) ◽  
pp. H2627-H2631 ◽  
Author(s):  
Acácio Salvador Véras-Silva ◽  
Katt Coelho Mattos ◽  
Nilo Sérgio Gava ◽  
Patricia Chakur Brum ◽  
Carlos Eduardo Negrão ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Exercise Training ◽  
High Intensity ◽  
Peripheral Resistance ◽  
High Intensity Exercise ◽  
Spontaneously Hypertensive ◽  
Low Intensity ◽  
Low Intensity Exercise

The decrease in cardiac sympathetic tone and heart rate after low-intensity exercise training may have hemodynamic consequences in spontaneously hypertensive rats (SHR). The effects of exercise training of low and high intensity on resting blood pressure, cardiac output, and total peripheral resistance were studied in sedentary ( n = 17), low- ( n = 17), and high-intensity exercise-trained ( n = 17) SHR. Exercise training was performed on a treadmill for 60 min, 5 times per week for 18 weeks, at 55% or 85% maximum oxygen uptake. Blood pressure was evaluated by a cannula inserted into the carotid artery, and cardiac output was evaluated by a microprobe placed around the ascending aorta. Low-intensity exercise-trained rats had a significantly lower mean blood pressure than sedentary and high-intensity exercise-trained rats (160 ± 4 vs. 175 ± 3 and 173 ± 2 mmHg, respectively). Cardiac index (20 ± 1 vs. 24 ± 1 and 24 ± 1 ml ⋅ min−1 ⋅ 100 g−1, respectively) and heart rate (332 ± 6 vs. 372 ± 14 and 345 ± 9 beats/min, respectively) were significantly lower in low-intensity exercise-trained rats than in sedentary and high-intensity exercise-trained rats. No significant difference was observed in stroke volume index and total peripheral resistance index in all groups studied. In conclusion, low-intensity, but not high-intensity, exercise training decreases heart rate and cardiac output and, consequently, attenuates hypertension in SHR.

scholarly journals Lack of Correlation between Accelerometers and Heart-Rate Monitorization during Exercise Session in Older Adults

2020 ◽  
Vol 17 (15) ◽  
pp. 5518
Author(s):  
Laura Carbonell-Hernández ◽  
Diego Pastor ◽  
Alejandro Jiménez-Loaisa ◽  
Juan Arturo Ballester-Ferrer ◽  
Carlos Montero-Carretero ◽  
...  
Keyword(s):  
Older Adults ◽  
Heart Rate ◽  
Physical Exercise ◽  
Older People ◽  
The Other ◽  
Exercise Session ◽  
Active Aging ◽  
Low Intensity ◽  
Indispensable Tool ◽  
Highly Correlated

Aging is increasing worldwide; hence, aging-related health is also more relevant. Well-programmed physical exercise is now an indispensable tool to achieve active aging and preserve older people’s health. Such “well-programmed” exercise requires efficient and useful tools to measure the activity. The objective of this study is to evaluate the effectiveness of accelerometers to estimate two different intensities of physical exercise in older people. Thirty-eight subjects (64.5 ± 5.3 years) were measured during two different sessions of physical exercise: one moderate in intensity, the other of low intensity. Heart rate and accelerometry were recorded and analyzed. The results showed that the two variables in the physical exercise sessions were not highly correlated, and that accelerometry did not seem useful to assess low-intensity sessions not based on walking.

The influence of priming exercise on oxygen uptake, cardiac output, and muscle oxygenation kinetics during very heavy-intensity exercise in 9- to 13-yr-old boys

2010 ◽  
Vol 109 (2) ◽  
pp. 491-500 ◽  
Author(s):  
Alan R. Barker ◽  
Andrew M. Jones ◽  
Neil Armstrong
Keyword(s):  
Cardiac Output ◽  
Phase Ii ◽  
Near Infrared ◽  
Slow Component ◽  
Exercise Bout ◽  
Muscle Oxygenation ◽  
Heavy Exercise ◽  
Total Phase ◽  
Priming Exercise ◽  
Component Amplitude

The present study examined the effect of priming exercise on O2 uptake (V̇o2) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O2 delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II V̇o2 τ, 3) elevate the phase II V̇o2 total amplitude, and 4) reduce the magnitude of the V̇o2 slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests V̇o2, muscle oxygenation (near infrared spectroscopy), and cardiac output (Q̇) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q̇ at baseline and throughout the second exercise bout. The phase II V̇o2 τ was not altered by priming exercise ( bout 1: 22 ± 7 s vs. bout 2: 20 ± 4 s; P = 0.30). However, the time constant describing the entire V̇o2 response from start to end of exercise was accelerated ( bout 1: 43 ± 8 s vs. bout 2: 36 ± 5 s; P = 0.002) due to an increased total phase II V̇o2 amplitude ( bout 1: 1.73 ± 0.33 l/min vs. bout 2: 1.80 ± 0.59 l/min; P = 0.002) and a reduced V̇o2 slow component amplitude ( bout 1: 0.18 ± 0.08 l/min vs. bout 2: 0.12 ± 0.09 l/min; P = 0.048). These results suggest that phase II V̇o2 kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the V̇o2 total phase II and slow component amplitudes may be O2 delivery sensitive.

Cardiovascular drift and cerebral and muscle tissue oxygenation during prolonged cycling at different pedalling cadences

2012 ◽  
Vol 37 (3) ◽  
pp. 407-417 ◽  
Author(s):  
Stylianos N. Kounalakis ◽  
Nickos D. Geladas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Cerebral Oxygenation ◽  
Vastus Lateralis ◽  
Muscle Oxygenation ◽  
Peak Oxygen Consumption ◽  
Electromyographic Activity ◽  
Cardiovascular Drift

We hypothesized that a faster cycling cadence could exaggerate cardiovascular drift and affect muscle and cerebral blood volume and oxygenation. Twelve healthy males (mean age, 23.4 ± 3.8 years) performed cycle ergometry for 90 min on 2 separate occasions, with pedalling frequencies of 40 and 80 r·min–1, at individual workloads corresponding to 60% of their peak oxygen consumption. The main measured variables were heart rate, ventilation, cardiac output, electromyographic activity of the vastus lateralis, and regional muscle and cerebral blood volume and oxygenation. Cardiovascular drift developed at both cadences, but it was more pronounced at the faster than at the slower cadence, as indicated by the drop in cardiac output by 1.0 ± 0.2 L·min–1, the decline in stroke volume by 9 ± 3 mL·beat–1, and the increase in heart rate by 9 ± 1 beats·min–1 at 80 r·min–1. At the faster cadence, minute ventilation was higher by 5.0 ± 0.5 L·min–1, and end-tidal CO2 pressure was lower by 2.0 ± 0.1 torr. Although higher electromyographic activity in the vastus lateralis was recorded at 80 r·min–1, muscle blood volume did not increase at this cadence, as it did at 40 r·min–1. In addition, muscle oxygenation was no different between cadences. In contrast, cerebral regional blood volume and oxygenation at 80 r·min–1 were not as high as at 40 r·min–1 (p < 0.05). Faster cycling cadence exaggerates cardiovascular drift and seems to influence muscle and cerebral blood volume and cerebral oxygenation, without muscle oxygenation being radically affected.

scholarly journals Exercise with End-expiratory Breath Holding Induces Large Increase in Stroke Volume

2020 ◽  
Vol 42 (01) ◽  
pp. 56-65
Author(s):  
Xavier Woorons ◽  
Frederic Lemaitre ◽  
Guido Claessen ◽  
Cloé Woorons ◽  
Henri Vandewalle
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Exercise Bout ◽  
Left Ventricular ◽  
Breath Holding ◽  
Early Recovery ◽  
Normal Breathing ◽  
Filling Time ◽  
First Session

AbstractEight well-trained male cyclists participated in two testing sessions each including two sets of 10 cycle exercise bouts at 150% of maximal aerobic power. In the first session, subjects performed the exercise bouts with end-expiratory breath holding (EEBH) of maximal duration. Each exercise bout started at the onset of EEBH and ended at its release (mean duration: 9.6±0.9 s; range: 8.6–11.1 s). At the second testing session, subjects performed the exercise bouts (same duration as in the first session) with normal breathing. Heart rate, left ventricular stroke volume (LVSV), and cardiac output were continuously measured through bio-impedancemetry. Data were analysed for the 4 s preceding and following the end of each exercise bout. LVSV (peak values: 163±33 vs. 124±17 mL, p<0.01) was higher and heart rate lower both in the end phase and in the early recovery of the exercise bouts with EEBH as compared with exercise with normal breathing. Cardiac output was generally not different between exercise conditions. This study showed that performing maximal EEBH during high-intensity exercise led to a large increase in LVSV. This phenomenon is likely explained by greater left ventricular filling as a result of an augmented filling time and decreased right ventricular volume at peak EEBH.

Cardiovascular and Metabolic Responses to Electrical Stimulation-Induced Leg Exercise in Spinal Cord Injury

1997 ◽  
Vol 36 (04/05) ◽  
pp. 372-375 ◽  
Author(s):  
J. R. Sutton ◽  
A. J. Thomas ◽  
G. M. Davis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Cardiac Output ◽  
Electrical Stimulation ◽  
Knee Flexion ◽  
Flexion Extension ◽  
Cord Injury ◽  
Leg Exercise ◽  
Leg Muscle

Abstract:Electrical stimulation-induced leg muscle contractions provide a useful model for examining the role of leg muscle neural afferents during low-intensity exercise in persons with spinal cord-injury and their able-bodied cohorts. Eight persons with paraplegia (SCI) and 8 non-disabled subjects (CONTROL) performed passive knee flexion/extension (PAS), electrical stimulation-induced knee flexion/extension (ES) and voluntary knee flexion/extension (VOL) on an isokinetic dynamometer. In CONTROLS, exercise heart rate was significantly increased during ES (94 ± 6 bpm) and VOL (85 ± 4 bpm) over PAS (69 ± 4 bpm), but no changes were observed in SCI individuals. Stroke volume was significantly augmented in SCI during ES (59 ± 5 ml) compared to PAS (46 ± 4 ml). The results of this study suggest that, in able-bodied humans, Group III and IV leg muscle afferents contribute to increased cardiac output during exercise primarily via augmented heart rate. In contrast, SCI achieve raised cardiac output during ES leg exercise via increased venous return in the absence of any change in heart rate.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

CARDIAC OUTPUT RESPONSE TO CHANGES IN CONTRACTILITY, PRELOAD AND HEART RATE DURING ENELURANE ANESTHESIA

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A499
Author(s):  
M. Sato ◽  
S. Hoka ◽  
H. Arintura ◽  
K. Ono ◽  
J. Yoshitake
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Output Response

Cardiac output in muscular exercise at 5,800 m (19,000 ft)

1964 ◽  
Vol 19 (3) ◽  
pp. 441-447 ◽  
Author(s):  
L. G. C. E. Pugh
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sea Level ◽  
Indirect Evidence ◽  
Mean Value ◽  
Muscular Exercise ◽  
Maximum Output ◽  
Work Intensity ◽  
Maximum Heart Rate ◽  
Sea Level Pressure

Cardiac output during muscular exercise was estimated by the acetylene technique on four members of the Himalayan Scientific and Mountaineering expedition 1960–1961 at sea level and 5,800 m (19,000 ft). The output for a given work intensity at 5,800 m (19,000 ft) was comparable with the output at the same work intensity at sea level, but the maximum output was reduced, the mean value being 16 liters/min, compared with 23 liters/min at sea level. Heart rates during light and moderate exercise were higher than the rates observed at the same work intensity at sea level. The maximum heart rate during exercise was limited to 130–150 beats/min compared with 180–196 beats/min at sea level. The stroke volume at altitude was lower than at sea level at each work rate. On breathing oxygen at sea-level pressure, heart rate for a given work intensity was reduced; but the maximum heart rate increased. Indirect evidence suggested that maximum cardiac output increased but probably not to the sea-level values because of the increased hemoglobin and lower heart rate. altitude acclimatization; cardiac function, work and altitude; hypoxia and cardiac output Submitted on July 29, 1963

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