Search

Estimation of cardiac output by impedance cardiography (QZ) in exercise during normal breathing (NB) has been limited by motion artifact. Our objective was to obtain readable impedance cardiograms on five subjects during upright cycle exercise at 0, 50, 100, 150, and 200 W to permit comparisons of QZ during NB, expiratory breath hold (EXP) and inspiratory breath hold (INSP). Q was also determined using an equilibration CO2 rebreathing method [Q(RB)]. QZ during NB exceeded EXP QZ at 100, 150, and 200 W, and exceeded INSP QZ at 100 W (P less than 0.05). The low EXP QZ values were due to a significantly lower stroke volume at 100, 150, and 200 W (P less than 0.05). For the INSP QZ at 100 W, heart rate was lower than during EXP (P less than 0.05). Regression of QZ (NB) against Q(RB) resulted in a linear relationship (r = 0.93) over the range of Q = 7-26 1/min. The slope of the regression differed significantly from 1.0 (P less than 0.05). We conclude that QZ values obtained during EXP or INSP should not be assumed to represent QZ during NB, at least at work rates greater than 50 W. A consequence of the linear relationship between QZ(NB) and Q(RB) over the range of 0-200 W is that estimates of CO2 rebreathing cardiac output can be obtained by impedance cardiography if QZ is adjusted using an appropriate empirical factor.

The power-endurance time curve described for cycle ergometry has been examined with respect to high velocity treadmill running to exhaustion. On a cycle ergometer, a hyperbolic function has been described that can be linearized by expressing power relative to the inverse of time to exhaustion. The mathematical relationship of this linear function is P = W'/t + theta f, where P = power output, W' = slope of regression, and theta f = fatigue threshold (intercept of power output). Six cross-country runners took part as subjects. Each ran to exhaustion with the treadmill at 6 different velocities between 19.2 and 22.4 km/h. The linear regressions fitted to velocity versus 1/time had correlation coefficients between r = 0.979 and 0.997. It was concluded that the treadmill velocity-endurance time relationship for runs of 2-12 min duration conformed to a similar hyperbolic function as that described for cycle ergometry. The two parameters W' and theta f might provide valuable indices of physical performance potential, which can be used to monitor training responses in competitive runners.

A CO2 rebreathing technique was used to assess possible changes in the ventilatory response to CO2 in rats following a 14-week swim training program. Over the final 9 weeks, the rats swam 1 hr per day with a weight of 2.5% of the body weight attached to the tail. Ventilation was measured by a barometric method in awake, restrained rats in a total body plethysmography at CO2 concentrations of 0, 2, 4, 6, and 8%, with an initial O2 concentration of approximately 100%. Ventilation increased in the trained rats with increasing CO2 from 775ml . min-1 . kg-1 at 0% CO2 to 1,387 ml . min-1 . kg-1 at 8% CO2. This increase was a consequence of a 34% increase in tidal volume and a 32% increase in breathing frequency. In comparison with a group of sedentary control rats, there was a significantly higher ventilation and tidal volume at 0% CO2; however, this difference disappeared with increasing levels of CO2. A significantly lower resting heart rate was observed in the exercised (296 +/- 44 beats . min-1, mean +/- SD) compared to the sedentary control rats 380 +/- 42). It was concluded that, while the normal training response of resting bradycardia was observed following this duration and intensity of training, endurance swimming had no significant effect on the ventilatory response to CO2 in the rat.

To examine the significance of endogenous stores of glycogen in specific fiber types (I, IIa, IIb) of the costal region of the diaphragm, adult male Wistar rats performed continuous running (25 m/min, 8 degrees grade) exercise for either 30 min or until fatigue. At 30 min of exercise, glycogen loss, as measured microphotometrically using the periodic acid-Schiff technique averaged between 73 and 80% (P less than 0.05) in the different fiber types. When exercise was performed to exhaustion, representing an additional 94 min, no further reduction in glycogen was observed in any fiber type. Biochemical determinations of glycogen from the diaphragm confirmed the extensive reduction in glycogen concentration with exercise. Large reductions (P less than 0.05) in glycogen were also noted in the soleus, plantaris, and vastus lateralis red. Although significant depletion (P less than 0.05) occurred in the vastus lateralis white, it was not as pronounced as in these other muscles. Repletion to preexercise glycogen concentration was complete by 4 h of recovery in all muscles except the vastus lateralis white. It is concluded that endogenous glycogen is a significant substrate in all muscles sampled regardless of fiber composition. In the case of the costal region of the diaphragm, the increased work of breathing resulting from heavy exercise leads to the recruitment of all fiber types, and each fiber type depends on glycogen as a substrate at least early in the exercise.

The relationship between arterialized blood lactate concentration [( La-]) and O2 uptake (VO2) was examined during a total of 23 tests by eight subjects. Exercise was on a cycle ergometer with work rate incremented from loadless pedaling to exhaustion as a 50-W/min ramp function. Two different mathematical models were studied. One model employed a log-log transformation of [La-] and VO2 to yield [La-] threshold as proposed by Beaver et al. (J. Appl. Physiol. 59: 1936-1940, 1985). The other model was a continuous exponential plus constant of the form La- = a + b[exp(cVO2)]. In 21 of 23 data sets, the mean square error (MSE) of the continuous model was less than that of the log-log model (P less than 0.001). The MSE was on average 3.5 times greater in the log-log model than in the continuous model. The residuals were randomly distributed about the line of best fit for the continuous model. In contrast, the log-log model showed a nonrandom pattern indicating an inappropriate model. As an index of the position of the [La-]-VO2 continuous model, the VO2 at which the rate of increase of [La-] equaled the rate of increase of VO2 (d[La-]/dVO2 = 1) was determined. This VO2 was 2.241 +/- 0.081 l/min, which averaged 64.6% of maximal VO2. It is proposed that this lactate slope index could be used as a relative indicator of fitness instead of the previously applied threshold concept. The change in [La-] could be better described mathematically by a continuous model rather than the threshold model of Beaver et al.

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.

1. The blood flow in the forearm and the calf of six healthy volunteers was measured at rest and after exercise by impedance plethysmography using pulsatile (QZp) and venous occlusion (QZocc) methods, and by venous occlusion strain gauge plethysmography (Qsg). 2. At rest, the impedance QZp method gave values slightly higher than those of Qsg. In the forearm, the ratio QZp to Qsg was 1.26 in the supine position and 1.97 in the upright sitting position. For the calf muscle, the ratios were 1.08 in the supine position and 1.23 in the upright position. 3. Immediately after exercise, Qsg increased from resting values of approximately 2-4 ml min-1 100 ml-1 to mean values of 16-25 ml min-1 100 ml-1 in upright and supine arm or leg exercise. In contrast, the QZp values after exercise increased to only 3.1-4.6 ml min-1 100 ml-1. QZocc likewise failed to show increases in flow except in the supine leg exercise, where flow increased to 8.7 ml min-1 100 ml-1. 4. In an additional subject, it was shown that electrode position had no significant effect on the QZp blood flow measurement after exercise. 5. The failure of QZp to accurately follow the change in Qsg with exercise was probably due in part to pulsatile venous outflow. In addition, changes in microvessel packed cell volume and shear rate may influence the observed QZp. It is concluded that impedance plethysmography is not valid for estimation of limb blood flow during reactive hyperaemia after exercise.

The effects of oral propranolol (2 x 80 mg/day) on the contractile responses to twitch and tetanic electrical stimulation were examined in the tibialis anterior (TA) muscle of seven healthy young males. The TA muscle was fatigued by four forms of repeated isometric contractions: (1) maximal voluntary contractions (MVC), (2) MVC with circulation occluded, (3) electrically evoked contractions with 20 Hz supramaximal voltage stimulation and (4) electrically evoked contractions with circulation occluded. Each contraction was sustained for 10 s with 5 s recovery. Duration of exercise was 10 min for intact circulation and 4 min for circulatory occlusion. Pre-exercise, both the twitch contraction time and the 1/2 relaxation time were significantly (P less than 0.05) longer with beta-blockade than placebo. beta-blockade did not affect torque output during tetanic stimulation or MVC. Immediately post-exercise, the peak twitch torque was reduced in all beta-blocked and placebo conditions except electrically induced exercise with intact circulation. The 1/2 relaxation time was significantly lengthened by repeated MVC with circulation intact; beta-blockade caused a greater lengthening than placebo (P less than 0.05). The tetanic torque was reduced immediately post-exercise at each of 10, 20, 50 and 100 Hz for both beta-blockade and placebo for each form of exercise. There were no significant beta-blockade effects. Torque output at 10 Hz was still reduced up to 10 min post-exercise. In contrast, 100 Hz torque output recovered by 5 min post-exercise. The changes in tetanic responses were qualitatively similar with intact circulation and with circulatory occlusion. In the tibialis anterior muscle, the effects of fatiguing exercise are not accentuated by beta-blockade. These data in the TA are notably different from those in the triceps surae, where greater fatigue has been shown with beta-blockade.

The anaerobic threshold has generally been determined by simple visual inspection of ventilation or other gas-exchange data obtained during incremental exercise. To establish objective criteria for the determination of anaerobic threshold, a computer algorithm has been developed that models the ventilatory response to exercise using multisegment linear regression. The best-fit regression model is chosen by minimizing the pooled residual sum of squares . The anaerobic threshold is reported as the first break point in that model. The computer-determined anaerobic threshold values for 37 subjects were compared with subjectively determined values as chosen by four independent observers. The observers' estimates, when pooled to yield a single a single value for each subject, gave a mean value for the gas-exchange anaerobic threshold of 2.26 +/- 0.69 l/min. The estimates by the computer method averaged 2.21 +/- 0.65 l/min. The correlation coefficient for these two methods was 0.94.

The effects of dynamic exercise on the acute recovery blood pressure (BP) were studied in normotensive and hypertensive subjects. Three groups [eight normotensives, age 19 to 29 yr (N1); eight normotensives, age 35 to 62 yr (N2); and eight hypertensives, age 44 to 57 yr (H)] were tested over three separate sessions. The first two sessions were for familiarization with the protocol and test procedures. Resting systolic BP decreased (P less than 0.01) in all groups from sessions 1 to 3: N1 = 126 to 121 mm Hg; N2 = 127 to 120; H = 155 to 142. Resting diastolic BP decreased (P less than 0.05) in the N1 and H groups from 77 to 73 and 98 to 95 mm Hg, respectively. On the third day, each subject followed the protocol of Wilcox et al. (8) of 15 min of seated rest, five 10-min periods of treadmill walking with a 3-min rest between each period, and 60 min of seated recovery. Exercise was performed at 67% of estimated maximal heart rate. In all three groups, significant (P less than 0.05) reductions in both systolic BP (N1 = -12 +/- 1; N2 = -10 +/- 2; H = -12 +/- 3) and diastolic BP (N1 = -5 +/- 2; N2 = -5 +/- 1; H = -7 +/- 2) occurred from pre-exercise rest to post-exercise rest. Systolic BP remained lower following 60-min recovery (P less than 0.02), while diastolic BP returned to pre-exercise levels in all three groups. No between-group differences were observed in the magnitude of reduction of BP post-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

This article is divided into two parts: Part 1 consists of the position stand of The Canadian Association of Applied Sport Sciences on the involvement of children in competitive sports, and Part II presents scientific background and rationale pertinent to the position statements. Each part is divided into major categories reflecting the multi-disciplinary concerns of the participation of pre- and post-pubescent children in sport situations at all levels. Psychological considerations focus on the child learning a sense of competence and control through sport participation. Success in a sport should not be based solely on winning, but on one's own performance and attained goals. Sport involvement can provide one important avenue for a child's social development. Non-aggressive behaviour and a constructive problem-solving approach should be encouraged. Any form of discrimination towards sport participation or competition should be discouraged. From the physiological and medical point of view, it should be recognized that each child is different in his/her response and tolerance to exercise due to a great range of variability in growth rates, anthropometric indices, gender and state of health, even in children of a similar chronological age. Younger prepubertal children should be encouraged to participate in a wide variety of motor skills, whereas older post-pubertal children can become more specialized in their training and sport participation. A child's performance and adaptation to training should not be directly compared to an adult's as significant differences exist, especially during the years of accelerated growth. Environmental exercise tolerance is also more limited to children than adults. In younger children repetitive heavy loading of the musculoskeletal system should be approached with caution. With proper equipment design and usage, and rule modifications, serious injuries can be avoided. Medical disabilities should be evaluated on an individual basis and should not necessarily preclude a child's participation. Teachers, parents and coaches should have a thorough understanding of the implications of children involved in sports and adhere to the recommendations reviewed in this statement.

This study examined the involvement of the hormones aldosterone and prolactin in sweat gland function during heat acclimatization. Two groups of male subjects (n = 8) were tested - one receiving a placebo (control), the other receiving bromocriptine. Both groups performed cycle ergometer exercise at 50% of maximal oxygen uptake over 10 consecutive days in an environmental chamber maintained at 39 degrees C and 30% relative humidity. Duration of exercise was 90 min on days 2-4 and 6-9, and 45 min on test days 1, 5 and 10. Electrolyte concentrations were determined by total body washdown. Prolactin increased (p less than 0.001) during exercise on day 1 in the control group but not on days 5 and 10. In contrast, prolactin was suppressed by bromocriptine and did not rise in response to exercise or heat exposure. Plasma aldosterone increased during exercise in both groups, showing no differences between groups. The sodium concentration in sweat decreased significantly (p less than 0.05) in the control group from day 1 to 10 but was unchanged in the treatment group. These data suggest that acclimatization-related changes in sweat gland function may be attenuated by increases in central dopaminergic activity and implicate prolactin in control of sweat gland function.

Occlusion of the nonworking leg muscles prior to the onset of supine arm exercise was examined for an effect on the kinetics of respiratory gas exchange (VO2 and VCO2), ventilation (VE), and heart rate (HR). Seven subjects performed arm cycling at 40 W (two females) or 50 W (five males) for 8 min following 4 min of "0" W pedaling. Six repetitions of each of uncuffed and cuffed leg conditions were averaged for individual subject analysis. The VO2 kinetics were significantly faster in the cuffed than the uncuffed condition (mean response time 66.0 +/- 26.4 vs 81.2 +/- 37.5 s, P less than 0.04). The kinetics of VCO2, VE, and HR were not affected by occlusion. It is concluded that the faster VO2 kinetics with the prior occlusion of nonworking leg muscles was a consequence of increased availability of oxygen to the working arm muscles at the onset of exercise.

Chronic, as well as acute, exercise increases circulating PRL in females. The response of males to repeated exercise, however, is unknown. The purpose of the present study was to examine the effects of acute and chronic exercise on plasma PRL levels in untrained males. Eight male subjects performed cycle ergometer exercise at 50% of their maximal oxygen uptake on 10 consecutive days. The subjects exercised in an environmental chamber maintained at 39 degrees C and 30% relative humidity. PRL levels were measured on days 1, 5, and 10 before exercise, and after 20 and 45 minutes of exercise. Acute exercise increased PRL levels. However, plasma levels did not significantly increase during exercise on days 5 and 10. This suggests a similarity in the PRL response to acute exercise in males and females, but a sex difference in the response to chronic exercise.

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.

The effect of work rate increase in ramp work tests was studied in six healthy subjects. Each subject exercised on a cycle ergometer with the work rate incremented by either 65.4 W . min-1 and 49.0 W . min-1 for the fast ramps or 8.2 W . min-1 and 6.1 W . min-1 for the slow ramps for male and female subjects, respectively. Gas exchange was monitored by open-circuit spirometry. Arterialized venous blood samples were obtained from a dorsal hand vein. The peak VO2 was not significantly different for fast (3218 +/- 602 ml . min-1, X +/- SD) and slow (3237 +/- 601 ml . min-1) ramp tests. Gas-exchange anaerobic threshold, determined by multi-segment linear regression of VE vs VO2, was similar for fast and slow ramp tests (1742 +/- 415 and 1925 +/- 639 ml O2 . min-1, P greater than 0.05). The VO2 at which blood lactate increased 0.5 mM above resting levels was lower (1463 +/- 259 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the slow ramp test. The VO2 at which blood lactate reached 2.0 mM was greater (2383 +/- 247 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the fast ramp test. In addition to these lactate differences, blood pH and HCO3- did not change in direct proportion to the lactate concentration in either test. Blood PCO2 was significantly (P less than 0.05) greater at the point of exhaustion in the fast ramp test (42.2 +/- 2.3 mmHg) than in the slow ramp test (26.7 +/- 2.1 mmHg). It is concluded that the gas-exchange anaerobic threshold can be clearly dissociated from the blood lactate threshold by altering the work rate forcing function. Other mechanisms, such as H+ efflux and CO2 storage capacity, are more likely explanations for the gas-exchange anaerobic threshold.

Cardiac output (Q) was estimated in supine rest and in upright cycling at several work rates up to 200 W in five male and one female subjects. At least four repetitions of both the CO2-rebreathing plateau method (Collier, J. Appl. Physiol. 9:25-29, 1956) and the Kim et al. (J. Appl. Physiol. 21: 1338-1344, 1966) single-breath method were performed at each work rate, in a steady state of O2 consumption and heart rate. At supine rest and low work rates, estimates of Q were similar by the two methods. However, at higher work rates, the single-breath method significantly (P less than 0.05) underestimated the value obtained by CO2 rebreathing. The reason for the difference in estimates of Q by the two methods was traced to the determination of arterial partial pressure of CO2 (PaCO2) and mixed venous partial pressure of CO2 (PvCO2). The estimate of PaCO2 from the single-breath method was approximately 88.5% of the estimate from end-tidal PCO2 used with the rebreathing method (P less than 0.001). The oxygenated PvCO2 calculated from the single-breath Q averaged approximately 92.5% of the PvCO2 from CO2 rebreathing (P less than 0.0001). The difference in estimates of Q was not eliminated by using a logarithmic form of the CO2 dissociation curve with the single-breath method.