Central control of cardiovascular adjustments to exercise

Voluntary heart rate (HR) control during moderate exercise on a bicycle ergometer was studied in 10 healthy physically conditioned men (5 experimental and 5 control). The results showed that subjects could learn to attenuate the tachycardia of exercise while exercising at a steady work level of 60-70% of maximum HR. Experimental subjects who saw beat-to-beat displays of HR and were instructed to slow HR showed 22% less increase in HR than did control subjects who exercised without HR displays or instruction to slow HR (42.6 vs. 54.6 beats/min). When the control subjects were given feedback in additional sessions, they also decreased HR significantly by 9% (54.6 vs. 49.9 beats/min). Analyses of concomitant respiratory and metabolic data showed that HR attenuation was accompanied by decreased O2 consumption (P less than 0.06) and pulmonary ventilation (P less than 0.01). Rate pressure product also fell, indicating a decrease in myocardial O2 consumption. Comparisons among pre- and postsubmaximal and cardiovascular pulmonary and humoral responses during maximal test sessions suggested that the improvement in cardiopulmonary function during feedback training occurred with no sacrifice to working muscle requirements because blood lactate concentrations were similar. The attenuation of the HR response obtained in the present study indicates that feedback training in physically conditioned subjects can influence cardiovascular responses even under conditions of heavy local demands imposed by working muscles.     

The role of behavioral conditioning in the cardiovascular adjustment to exercise

The purpose of this study was to determine if normal subjects could be trained to attenuate their cardiovascular responses while exercising on a bicycle ergometer. Ten young, untrained subjects exercised on a bicycle ergometer for five sessions. Half of the group was asked to slow their heart rate while exercising with heart rate feedback during exercise. Their average heart rate increase was 20% less than that of the control subjects, who exercised without feedback. The control subjects subsequently also received feedback during exercise and they were able to attenuate their heart rate responses comparably. Systolic blood pressure was not affected by feedback training. Changes in rate-pressure product paralleled changes in heart rate. These data show that autonomically mediated adjustments to exercise can be brought under experimental control through the use of appropriate behavioral techniques.     

Reflex cardiovascular responses originating in exercising muscles of mice.

The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 +/- 1.9 mmHg) and heart rate (33.5 +/- 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 +/- 3.5, 20.9 +/- 4.0, 21.7 +/- 2.6, and 25.8 +/- 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O(2)-90% N(2)) elicits increases in blood pressure (11.7 +/- 2.6 mmHg) and heart rate (42.7 +/- 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.     

Improved estimation of total oxygen uptake in exercise by evaluation of aerobic fitness

The purpose of the present study was to contrive a new practical method for estimating total O2 uptake during exercise from total heart beats after individual evaluation of aerobic fitness levels. Twenty healthy male subjects participated in cycle ergometer tests, maximal O2 uptake (VO2max) tests and various simple tests including simple endurance tests. From the cycle ergometer results, the following formula for estimating total O2 uptake in exercise was determined: TVO2 (ml X kg-1) = SR125 X (45.8 X mean HR + 4268) X THB X 10(-4) where TVO2, THB, and mean HR are total O2 uptake, total heart beats, and mean heart rate (beats X min-1) in exercise, respectively, and SR125 is the slope of the regression line between accumulated heart beats and accumulated O2 uptake during exercise at 125 beats X min-1 of mean HR. SR125 had a significant correlation not only with VO2max but also with each score (X) in any simple endurance tests such as, for example, a step test for 2 min. In this case, accordingly, SR125 can be found as; SR125 = -0.00118X + 0.3478. These formulae indicate that the total O2 uptake of any exercising subject can be estimated from his total heart beats regardless of intensities of exercise when his aerobic fitness level is evaluated by the simple endurance test. The total O2 uptake estimated by our method was compared to that measured by the Douglas bag method, and the discrepancy between the two results was less than the errors of values estimated by traditional methods.     

A practical method for estimating total oxygen uptake during exercise in elderly men

In the present study, after a total of 51 observations of a 30-min cycle exercise performed by 17 men ranging in age from 60 to 65 years, the following formula was finally obtained for evaluating total O2 uptake (TVO2) during exercise: TVO2 (ml.kg-1) = SR125 X (49.5 X mean HR + 3760) X THB X 10(-4), where mean HR and THB are mean heart rate (beats.min-1) and total heart beats in exercise, respectively, and SR125 is the slope of the regression line of accumulative O2 uptake on accumulative heart beats during exercise at a mean HR of 125 beats.min-1. SR125 was significantly correlated not only to predicted VO2max but also score (X) in the step test for 2 min (25 steps.min-1 on 35-cm stool), yielding a formula, SR125 = -0.00131X + 0.3660. Consequently, both formulae indicate that total O2 uptake of any exercising elderly man can be estimated from total heart beats and mean HR during exercise, regardless of intensity of exercise when SR125 was determined by the step test. The discrepancy between total O2 uptake evaluated by the estimation method for elderly men and that determined by the Douglas bag method was 10.2 +/- 7.3%.     

Effects of feeding on muscle blood flow during prolonged exercise in miniature swine

Eight exercise-trained miniature swine were studied during prolonged treadmill runs (100 min) under fasting and preexercise feeding conditions. Each animal ran at identical external work loads that corresponded to 65% of the heart rate reserve (210-220 beats/min) for the two exercise bouts. Cardiac outputs and stroke volumes were higher and heart rates lower for fed than for fasting runs (P less than 0.05). Preexercise feeding did not alter oxygen consumption, core temperature, mean arterial pressure, and arterial-mixed venous oxygen difference during prolonged exercise; however, mixed venous lactate concentration was lower at end exercise than during fasting conditions (1.2 vs. 2.6 mM, P less than 0.05). Microsphere measurements of regional blood flow revealed significantly higher total gastrointestinal flow (23%) for fed than for fasting conditions. Throughout the exercise bout, blood flow to the biceps femoris, semitendinosus, and tibialis anterior muscles was lower in fed than in fasted animals (P less than 0.05). Combined hindlimb muscle blood flow averaged 15 ml.min-1.100 g-1 (18%, P less than 0.05) lower under feeding than fasting run conditions. These findings provide further evidence that cardiovascular reflexes originate in the gut after feeding to increase cardiac output and redistribute a portion of the blood flow away from active muscle to the gastrointestinal tract during prolonged exercise.     

Muscle pump and central command during recovery from exercise in humans.

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.     

Plateau in muscle blood flow during prolonged exercise in miniature swine

Cardiovascular, metabolic, and thermoregulatory responses were studied in eight male miniature swine during a prolonged treadmill run. Each animal underwent 8-10 wk of exercise training, thoracic surgery, and 3 wk of retraining before the experimental run. This regimen enabled the animals to run at 65% of the heart rate range (210-220 beats/min) for approximately 100 min. Skin wetting and a fan were used to cool the pigs during the run. Regional blood flow was significantly altered with the onset of exercise; however, hindlimb muscle and total gastrointestinal blood flow were unchanged throughout the exercise period. Compared with 5-min values, heart rate and cardiac output were significantly elevated by 17 beats/min and 31 ml.min-1.kg-1 at 60 min and by 20 beats/min and 33 ml.min-1.kg-1 at end exercise, respectively. Core temperatures increased between 5 and 30 min of exercise (39.4 vs. 39.9 degrees C) but then remained unchanged to the end of exercise. Mean arterial pressure, O2 consumption, and blood lactate did not change during the exercise bout. These data indicate that limiting increases in core temperature during prolonged exercise was associated with a plateau in active muscle blood flow.     

Exercise, dobutamine, and combined atropine, norepinephrine, and epinephrine compared

We compared the cardiovascular effects evoked in conscious dogs by 1) submaximal exercise; 2) infusion of dobutamine (40 micrograms X kg-1 X min-1); and 3) infusion of a combination of atropine (0.15 mg/kg), norepinephrine (0.19 micrograms X kg-1 X min-1), and epinephrine (0.05 micrograms X kg-1 X min-1). Myocardial O2 demand, as estimated by the double product (heart rate X systolic blood pressure), was similar during all three interventions. Cardiac output and heart rate increased significantly (P less than 0.05) during each of the three interventions. Arteriovenous O2 difference and total body O2 consumption, however, increased only during submaximal exercise. Although myocardial blood flow increased similarly during each of the three interventions, blood flow to skeletal muscle and the tongue increased only during exercise. Exercise and the combined infusion of atropine, norepinephrine, and epinephrine produced similar increases in blood flow to the diaphragm and similar decreases in blood flow to the stomach. These changes in blood flow were associated with appropriate changes in vascular resistance. Additionally, blood flow to the brain, kidney, adrenal glands, liver, and intestine did not change during any of the three interventions. Thus, in dogs, submaximal exercise, infusion of dobutamine, and infusion of a combination of atropine, norepinephrine, and epinephrine to evoke a given level of estimated myocardial O2 consumption produce similar increases in cardiac output, heart rate, and myocardial blood flow. In contrast, the changes in total body O2 consumption, arteriovenous O2 difference, regional blood flow, and regional vascular resistance that occur during each of these three interventions are different.     

Effects of chronic and acute exercise on cardiovascular beta-adrenergic responses.

beta-Adrenergic receptor density and responsiveness may be increased in experimental animals by physical conditioning, and the opposite effects have been observed after a single bout of exercise. To determine whether the chronic and acute effects of exercise include similar alterations in cardiovascular function in humans, we characterized heart rate, blood pressure, and distal lower extremity blood flow responses to graded-dose isoproterenol infusion in 15 young healthy subjects before and after exercise training and with and without a single preceding bout of prolonged exercise of either low or high intensity (61 +/- 1 or 82 +/- 1% maximal heart rate). VO2max was increased 18% after exercise training (43.2 +/- 2.7 to 51.1 +/- 3.3 ml.kg-1.min-1; P less than 0.001). Despite a concomitant fall in resting heart rate (59 +/- 3 to 50 +/- 2 beats/min; P less than 0.001), chronotropic and lower extremity blood flow responses to isoproterenol remained unchanged. Similarly, 1 h of acute high-intensity treadmill exercise altered baseline heart rate (58 +/- 4 to 74 +/- 5 beats/min; P less than 0.02), but neither low- nor high-intensity acute exercise influenced heart rate or lower extremity blood flow responses to isoproterenol. In contrast, the systolic pressure response to isoproterenol was blunted after high- but not low-intensity prolonged exercise (P less than 0.02). These data indicate that cardiac chronotropic (primarily beta 1) and vascular (beta 2) adrenergic agonist responses are not altered in humans by training or acute exercise. The systolic blood pressure response to beta-adrenergic stimulation is decreased by a single bout of high-intensity prolonged exercise by mechanisms that remain to be defined.     

Operation Everest II: preservation of cardiac function at extreme altitude

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.     

Differential contribution of central command to the cardiovascular responses during static exercise of ankle dorsal and plantar flexion in humans

To examine whether central command contributes differently to the cardiovascular responses during voluntary static exercise engaged by different muscle groups, we encouraged healthy subjects to perform voluntary and electrically evoked involuntary static exercise of ankle dorsal and plantar flexion. Each exercise was conducted with 25% of the maximum voluntary force of the right ankle dorsal and plantar flexion, respectively, for 2 min. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and stroke volume, cardiac output (CO), and total peripheral resistance were calculated. With voluntary exercise, HR, MAP, and CO significantly increased during dorsal flexion (the maximum increase, HR: 12 ± 2.3 beats/min; MAP: 14 ± 2.0 mmHg; CO: 1 ± 0.2 l/min), whereas only MAP increased during plantar flexion (the maximum increase, 6 ± 2.0 mmHg). Stroke volume and total peripheral resistance were unchanged throughout the two kinds of voluntary static exercise. With involuntary exercise, there were no significant changes in all cardiovascular variables, irrespective of dorsal or plantar flexion. Furthermore, before the force onset of voluntary static exercise, HR and MAP started to increase without muscle contraction, whereas they had no significant changes with involuntary exercise at the moment. The present findings indicate that differential contribution of central command is responsible for the different cardiovascular responses to static exercise, depending on the strength of central control of the contracting muscle.     

Hypoxia potentiates exercise-induced sympathetic neural activation in humans.

Our purpose was to test the hypothesis that hypoxia potentiates exercise-induced sympathetic neural activation in humans. In 15 young (20-30 yr) healthy subjects, lower leg muscle sympathetic nerve activity (MSNA, peroneal nerve; microneurography), venous plasma norepinephrine (PNE) concentrations, heart rate, and arterial blood pressure were measured at rest and in response to rhythmic handgrip exercise performed during normoxia or isocapnic hypoxia (inspired O2 concn of 10%). Study I (n = 7): Brief (3-4 min) hypoxia at rest did not alter MSNA, PNE, or arterial pressure but did induce tachycardia [17 +/- 3 (SE) beats/min; P less than 0.05]. During exercise at 50% of maximum, the increases in MSNA (346 +/- 81 vs. 207 +/- 14% of control), PNE (175 +/- 25 vs. 120 +/- 11% of control), and heart rate (36 +/- 2 vs. 20 +/- 2 beats/min) were greater during hypoxia than during normoxia (P less than 0.05), whereas the arterial pressure response was not different (26 +/- 4 vs. 25 +/- 4 mmHg). The increase in MSNA during hypoxic exercise also was greater than the simple sum of the separate responses to hypoxia and normoxic exercise (P less than 0.05). Study II (n = 8): In contrast to study I, during 2 min of exercise (30% max) performed under conditions of circulatory arrest and 2 min of postexercise circulatory arrest (local ischemia), the MSNA and PNE responses were similar during systemic hypoxia and normoxia. Arm ischemia without exercise had no influence on any variable during hypoxia or normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of airflow and work load on cardiovascular drift and skin blood flow

Cardiovascular drift (CVD) can be defined as a progressive increase in heart rate (HR), decreases in stroke volume (SV) and mean arterial pressure (MAP), and a maintained cardiac output (Q) during prolonged exercise. To test the hypothesis that the magnitude of CVD would be related to changes in skin blood flow ( SkBF ), eight healthy, moderately trained males performed 70-min bouts of cycle ergometry in a 2 X 2 assortment of airflows (less than 0.2 and 4.3 m X s-1) and relative work loads (43.4% and 62.2% maximal O2 uptake). Ambient temperature and relative humidity were controlled to mean values of 24.2 +/- 0.8 degrees C and 39.5 +/- 2.4%, respectively. Q, HR, MAP, SkBF , skin and rectal temperatures, and pulmonary gas exchange were measured at 10-min intervals during exercise. Between the 10th and 70th min during exercise at the higher work load with negligible airflow, HR and SkBF increased by 21.6 beats X min-1 and 14.0 ml X 100 ml-1 X min-1, respectively, while SV and MAP decreased by 16.4 ml and 11.3 mmHg. The same work load in the presence of 4.3 m X s-1 airflow resulted in nonsignificant changes of 7.6 beats X min-1, 4.0 ml X (100 ml-1 X min)-1, -2.7 ml, and -1.7 mmHg for HR, SkBF , SV, and MAP. Since nonsignificant changes in HR, SkBF , SV, and MAP were observed at the lower work load in both airflow conditions, the results emphasize that CVD occurs only in conditions which combine high metabolic and thermal circulatory demands.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of chronic beta-adrenergic blockade on exercise training in dogs

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

The cardiovascular adaptation at the onset of voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one is central command descending from higher brain centers, and the other is a muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in producing the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous administration of gadolinium (55 micromol/kg), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of voluntary static exercise (pressing a bar with a forelimb) in conscious cats. HR increased by 31 +/- 5 beats/min and MAP increased by 15 +/- 1 mmHg at the onset of voluntary static exercise. Gadolinium affected neither the baseline values nor the initial increases of HR and MAP at the onset of exercise, although the peak force applied to the bar tended to decrease to 65% of the control value before gadolinium. Furthermore, we examined the effect of gadolinium on the reflex responses in HR and MAP (18 +/- 7 beats/min and 30 +/- 6 mmHg, respectively) during passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted the passive stretch-induced increases in HR and MAP, suggesting that gadolinium blocks the stretch-activated ion channels and thereby attenuates the reflex cardiovascular responses to passive mechanical stretch of a limb. We conclude that the initial cardiovascular adaptation at the onset of voluntary static exercise is predominantly induced by feedforward control of central command descending from higher brain centers but not by a muscle mechanoreflex.     

Neurohumoral and cardiopulmonary response to sustained submaximal exercise in the dog

Neurohumoral, cardiovascular, and respiratory parameters were evaluated during sustained submaximal exercise (3.2 km/h, 15 degrees elevation) in normal adult mongrel dogs. At the level of activity achieved (fivefold elevation of total body O2 consumption and threefold elevation of cardiac output), significant (P less than 0.05) increases in plasma norepinephrine and epinephrine concentration (from 150 +/- 23 to 341 +/- 35 and from 127 +/- 27 to 222 +/- 31 pg/ml, respectively) were present, as well as smaller but significant increases in plasma renin activity and plasma aldosterone concentration (from 2.2 +/- 0.3 to 3.1 +/- 0.6 ng X ml-1 X h-1 and from 98 +/- 8 to 130 +/- 6 pg/ml, respectively). Plasma arginine vasopressin increased variably and insignificantly. The cardiovascular response (heart rate, systemic arterial and pulmonary arterial pressures, left ventricular filling pressure, and calculated total peripheral and pulmonary arteriolar resistance) closely paralleled that of human subjects. Increased hemoglobin concentration was induced by exercise in the dogs. The ventilatory response of the animals was characterized by respiratory alkalosis. These data suggest similarities between canine and human subjects in norepinephrine, plasma renin activity, and plasma aldosterone responses to submaximal exercise. Apparent species differences during submaximal exertion include greater alterations of plasma epinephrine concentration and a respiratory alkalosis in dogs.     

Tendon vibration attenuates superficial venous vessel response of the resting limb during static arm exercise

Background

The superficial vein of the resting limb constricts sympathetically during exercise. Central command is the one of the neural mechanisms that controls the cardiovascular response to exercise. However, it is not clear whether central command contributes to venous vessel response during exercise. Tendon vibration during static elbow flexion causes primary muscle spindle afferents, such that a lower central command is required to achieve a given force without altering muscle force. The purpose of this study was therefore to investigate whether a reduction in central command during static exercise with tendon vibration influences the superficial venous vessel response in the resting limb.

Methods

Eleven subjects performed static elbow flexion at 35% of maximal voluntary contraction with (EX + VIB) and without (EX) vibration of the biceps brachii tendon. The heart rate, mean arterial pressure, and rating of perceived exertion (RPE) in overall and exercising muscle were measured. The cross-sectional area (CSA_vein) and blood velocity of the basilic vein in the resting upper arm were assessed by ultrasound, and blood flow (BF_vein) was calculated using both variables.

Results

Muscle tension during exercise was similar between EX and EX + VIB. However, RPEs at EX + VIB were lower than those at EX (P <0.05). Increases in heart rate and mean arterial pressure during exercise at EX + VIB were also lower than those at EX (P <0.05). CSA_vein in the resting limb at EX decreased during exercise from baseline (P <0.05), but CSA_vein at EX + VIB did not change during exercise. CSA_vein during exercise at EX was smaller than that at EX + VIB (P <0.05). However, BF_vein did not change during the protocol under either condition. The decreases in circulatory response and RPEs during EX + VIB, despite identical muscle tension, showed that activation of central command was less during EX + VIB than during EX. Abolishment of the decrease in CSA_vein during exercise at EX + VIB may thus have been caused by a lower level of central command at EX + VIB rather than EX.

Conclusion

Diminished central command induced by tendon vibration may attenuate the superficial venous vessel response of the resting limb during sustained static arm exercise.     

Menstrual cycle phase affects temperature regulation during endurance exercise.

We investigated whether menstrual cycle phase would affect temperature regulation during an endurance exercise bout performed at room temperature (Ta) of 22 degrees C and 60% relative humidity. Nine eumenorrheic women [age 27.2 +/- 3.7 yr, peak O2 uptake (VO2) 2.52 +/- 0.35 l/min] performed 60 min of cycle exercise at 65% of peak VO2. Subjects were tested in both midfollicular (F) and midluteal (L) phases, although one woman did not show a rise in serum progesterone (P4) that is typically evident 1 wk after ovulation. VO2, rectal (Tre) and skin (Tsk) temperatures, heart rates (HR), and ratings of perceived exertion (RPE) were measured throughout exercise. Sweat loss (SL) was estimated from pre- and postexercise body weight differences. VO2, SL, and Tsk were not affected by menstrual cycle phase. Preexercise Tre was 0.3 degrees C higher during L than during F conditions, and this difference increased to 0.6 degrees C by the end of exercise (P less than 0.01). Compared with F, HRs during L were approximately 10 beats/min greater (P less than 0.001) at all times, whereas RPE responses were significantly greater (P less than 0.01) by 50 min of cycling. No differences in any measured values were found in the subject whose P4 was low in both test conditions. Results indicate that thermoregulation (specifically, regulation of Tre), as well as cardiovascular strain and perception of exercise, was adversely affected during the L phase.     

Supramaximal exercise after training-induced hypervolemia. I. Gas exchange and acid-base balance

The effect of an exercise-induced reduction in blood O2-carrying capacity on ventilatory gas exchange and acid-base balance during supramaximal exercise was studied in six males [peak O2 consumption (VO2peak), 3.98 +/- 0.49 l/min]. Three consecutive days of supramaximal exercise resulted in a preexercise reduction of hemoglobin concentration from 15.8 to 14.0 g/dl (P less than 0.05). During exercise (120% VO2peak) performed intermittently (1 min work to 4 min rest); a small but significant (P less than 0.05) increase was found for both O2 consumption (VO2) (l X min) and heart rate (beats/min) on day 2 of the training. On day 3, VO2 (l/min) was reduced 3.2% (P less than 0.05) over day 1 values. No changes were found in CO2 output and minute ventilation during exercise between training days. Similarly, short-term training failed to significantly alter the changes in arterialized blood PCO2, pH, and [HCO-3] observed during exercise. It is concluded that hypervolemia-induced reductions in O2-carrying capacity in the order of 10-11% cause minimal impairment to gas exchange and acid-base balance during supramaximal non-steady-state exercise.