Inaccuracy of the HR reserve vs. V˙O2 reserve relationship during prone arm-paddling exercise in surfboard riders

Previous studies have demonstrated that during lower-body exercise the percentage of heart rate reserve (%HRR) is equivalent to the percentage of the oxygen consumption reserve (%V˙O(2R)) but not to a percentage of the peak oxygen consumption (%V˙O(2peak)). The current study examined these relationships in trained surfboard riders (surfers) during upper-body exercise. Thirteen well-trained competitive surfers performed a stepwise, incremental, prone arm-paddling exercise test to exhaustion. For each subject, data obtained at the end of each stage (i.e., HR and V˙O(2) values) were expressed as a percentage of HRR, V˙O(2peak), and V˙O(2R) respectively and used to determine the individual %HRR-%V˙O(2peak) and %HRR-%V˙O(2R) relationships. Mean slope and intercept were calculated and compared with the line of identity (slope=1, intercept=0). The %HRR versus %V˙O(2R) regression mean slope (0.88±0.06) and intercept (20.82±4.57) were significantly different (p<0.05) from 1 and 0, respectively. Similarly, the regression of %HRR versus %V˙O(2peak) resulted in a line that differed in the slope (p<0.05) but not in the intercept (p=0.94) from the line of identity. Predicted values of %HRR were significantly higher (p<0.05) from indicated values of %V˙O(2R) for all the intensities ranging from 35% to 95% V˙O(2R). Unlike results found for lower-body exercise, a given %HRR during prone upper-body exercise was not equivalent to its corresponding %V˙O(2R). Thus, to ensure more targeted exercise intensity during arm-paddling exercise, individual HR-V˙O(2) equations should be used.     

Estimation of oxygen uptake from heart rate and ratings of perceived exertion in young soccer players

The objective of this study was to estimate the oxygen uptake (&OV0312;O2) in elite youth soccer players using measures of heart rate (HR) and ratings of perceived exertion (RPEs). Forty-six regional-level male youth soccer players (～13 years) participated in 2 VO(2)max tests. Data for HR, RPE, and VO(2) were simultaneously recorded during the VO(2)max tests with incremental running speed. Regression equations were derived from the first VO(2)max test. Two weeks later, all players performed the same VO(2)max test to validate the developed regression equations. There were no significant differences between the estimated values in the first test and actual values in the second test. During the continuous endurance exercise, the combination of percentage of maximal HR (%HRmax) and RPE measures gave similar estimation of %VO(2)max (R = 83%) in comparison to %HRmax alone (R = 81%). However, the estimation of VO(2) using combined %HRmax and RPE was not satisfactory (R = 45-46%). Therefore, the use of %HRmax (without RPE) to estimate %VO(2)max could be a useful tool in young soccer players during field-based continuous endurance testing and training. Specifically, coaches can use the %HRmax to quantify internal loads (%VO(2)max) and subsequently implement continuous endurance training at appropriate intensities. Furthermore, it seems that RPE is more useful as a measure of internal load during noncontinuous (e.g., intermittent and sprint) exercises but not to estimate %VO(2)max during continuous aerobic exercise (R = 59%).     

Pulmonary diffusing capacity for nitric oxide during exercise in morbid obesity

Morbidly obese individuals may have altered pulmonary diffusion during exercise. The purpose of this study was to examine pulmonary diffusing capacity for nitric oxide (DLNO) and carbon monoxide (DLCO) during exercise in these subjects. Ten morbidly obese subjects (age = 38 +/- 9 years, BMI = 47 +/- 7 kg/m(2), peak oxygen consumption or VO(2peak) = 2.4 +/- 0.4 l/min) and nine nonobese controls (age = 41 +/- 9 years, BMI = 23 +/- 2 kg/m(2), VO(2peak) = 2.6 +/- 0.9 l/min) participated in two sessions: the first measured resting O(2) and VO(2peak) for determination of wattage equating to 40, 75, and 90% oxygen uptake reserve (VO(2)R). The second session measured pulmonary diffusion from single-breath maneuvers of 5 s each, as well as heart rate (HR) and VO(2) over three workloads. DLNO, DLCO, and pulmonary capillary blood volume were larger in obese compared to nonobese groups (P 0.10). The morbidly obese have increased pulmonary diffusion per unit increase in VA compared with nonobese controls which may be due to a lower rise in VA per unit increase in VO(2) in the obese during exercise.     

Skeletal muscle lipid metabolism with obesity

The objectives of this study were to 1). examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2). determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [n = 8; body mass index (BMI) 23.8 +/- 0.58 kg/m(2)], overweight/obese (n = 8; BMI 30.2 +/- 0.81 kg/m(2)), and extremely obese (n = 8; BMI 53.8 +/- 3.5 kg/m(2)) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58 and 83% lower in skeletal muscle from extremely obese (44.9 +/- 5.2 nmol x g(-1) x h(-1)) patients compared with normal-weight (71.0 +/- 5.0 nmol x g(-1) x h(-1)) and overweight/obese (82.2 +/- 8.7 nmol x g(-1) x h(-1)) patients, respectively. Palmitate oxidation was negatively (R = -0.44, P = 0.003) associated with BMI. Long-chain fatty acyl-CoA content was higher in both the overweight/obese and extremely obese patients compared with normal-weight patients, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long-chain fatty acyl-CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity and that the accumulation of intramyocellular long-chain fatty acyl-CoAs is not solely a result of reduced fatty acid oxidation.     

The physiological effects of caffeine in women during treadmill walking

Although the effects of caffeine ingestion on athletic performance in men have been studied extensively, there is limited previous research examining caffeine's effects on women of average fitness levels participating in common modes of physical activity. The purpose of this study was to determine the effect of 2 levels of caffeine dosage on the metabolic and cardiorespiratory responses to treadmill walking in women. Subjects were 20 women (19-28 years of age) of average fitness, not habituated to caffeine. Each subject was assigned randomly a 3-mg x kg(-1) dose of caffeine, 6-mg x kg(-1) dose of caffeine, and placebo for 3 trials of moderate steady-state treadmill walking at 94 m x min(-1) (3.5 mph). Steady-state rating of perceived exertion (RPE), heart rate (HR), respiratory exchange ratio (RER), weight-relative VO2, %VO2max reserve (%VO2R), and rate of energy expenditure (REE) were measured during each trial. Repeated measures analysis of variance revealed that a 6-mg x kg(-1), but not a 3-mg x kg(-1) dose of caffeine increased VO2 (p = 0.04), REE (p = 0.03), and %VO2R (p = 0.03), when compared to the placebo. Caffeine had no effect on RPE, HR, or RER. No significant differences were observed between the placebo trials and the 3-mg x kg(-1) dose trials. Although a 6-mg x kg(-1) dose of caffeine significantly increased REE during exercise, the observed increase (approximately 0.23 kcal x min(-1)) would not noticeably affect weight loss. Because caffeine had no effect on RPE, it would not be prudent for a trainer to recommend caffeine in order to increase a woman's energy expenditure or to decrease perception of effort during mild exercise. These data also demonstrate that caffeine intake should not interfere with monitoring walking intensity by tracking exercise heart rate in women.     

Metabolic and thermoregulatory responses to a simulated American football practice in the heat

Energy cost is a major factor influencing the tolerable thermal load, particularly during exercise in the heat. However, no data exist on the metabolic cost of football practice, although a value of 35% of maximal aerobic capacity (VO(2)max) has been estimated. The energy cost and thermoregulatory response of offensive linemen (OL) was measured wearing different American football ensembles during a simulated half of football practice in the heat. Five collegiate offensive linemen (133 kg, 20% fat, 42 ml x kg(-1) x min(-1) maximal oxygen uptake) completed each of four 60-minute test sessions in an environmental chamber (28 degrees C, 55% relative humidity [RH]) wearing shorts (S), helmet (H), helmet and shoulder pads (HS), and full gear (FUL). Core temperature in the digestive tract (TGI) was obtained using an ingestible sensor. During simulated football drills (e.g., repetitions of drive blocking), exercise intensity ranged from 30 to 81% VO(2)max but averaged 55%VO(2)max (6.7 METS) overall. Blood lactate remained >5 mmol x L(-1), and heart rate (HR) averaged 79%HRmax. Equipment had a significant effect on %VO(2)max but only during recovery between drills with HS (61.4 +/- 3.7%) compared with H (53.3 +/- 6.9%) and S (40.1 +/- 8.5%). The TGI was higher (p < 0.05) with HS compared with H at several time-points after 30 minutes. Football practice for OL elicits a significantly higher overall metabolic cost (>6 METS, >50%VO(2)max) than assumed in previous studies. The addition of shoulder pads increases core temperature and energy cost, especially during recovery between active drills in unacclimatized linemen.     

Ventilatory and perceptual responses to cycle exercise in obese women.

The main purpose of this study was to examine the relative contribution of respiratory mechanical factors and the increased metabolic cost of locomotion to exertional breathlessness in obese women. We examined the relationship of intensity of breathlessness to ventilation (VE) when exertional oxygen uptake (VO2) of obesity was minimized by cycle exercise. Eighteen middle-aged (54+/-8 yr, mean+/-SD) obese [body mass index (BMI) 40.2+/-7.8 kg/m2] and 13 age-matched normal-weight (BMI 23.3+/-1.7 kg/m2) women were studied. Breathlessness at higher submaximal cycle work rates was significantly increased (by>or=1 Borg unit) in obese compared with normal-weight women, in association with a 35-45% increase in Ve and a higher metabolic cost of exercise. Obese women demonstrated greater resting expiratory flow limitation, reduced resting end-expiratory lung volume (EELV)(by 20%), and progressive increases in dynamic EELV during exercise: peak inspiratory capacity (IC) decreased by 16% (0.39 liter) of the resting value. VE/VO2 slopes were unchanged in obesity. Breathlessness ratings at any given VE or VO2 were not increased in obesity, suggesting that respiratory mechanical factors were not contributory. Our results indicate that in obese women, recruitment of resting IC and dynamic increases in EELV with exercise served to optimize operating lung volumes and to attenuate expiratory flow limitation so as to accommodate the increased ventilatory demand without increased breathlessness.     

Reduced stroke volume during exercise in postural tachycardia syndrome.

Postural tachycardia syndrome (POTS) is characterized by excessive tachycardia without hypotension during orthostasis. Most POTS patients also report exercise intolerance. To assess cardiovascular regulation during exercise in POTS, patients (n = 13) and healthy controls (n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter), heart rate (HR; measured by ECG), and cardiac output (open-circuit acetylene breathing) were measured. In both positions, mean arterial pressure, cardiac output, and total peripheral resistance at rest and during exercise were similar in patients and controls (P > 0.05). However, supine stroke volume (SV) tended to be lower in the patients than controls at rest (99 +/- 5 vs. 110 +/- 9 ml) and during 75-W exercise (97 +/- 5 vs. 111 +/- 7 ml) (P = 0.07), and HR was higher in the patients than controls at rest (76 +/- 3 vs. 62 +/- 4 beats/min) and during 75-W exercise (127 +/- 3 vs. 114 +/- 5 beats/min) (both P < 0.01). Upright SV was significantly lower in the patients than controls at rest (57 +/- 3 vs. 81 +/- 6 ml) and during 75-W exercise (70 +/- 4 vs. 94 +/- 6 ml) (both P < 0.01), and HR was much higher in the patients than controls at rest (103 +/- 3 vs. 81 +/- 4 beats/min) and during 75-W exercise (164 +/- 3 vs. 131 +/- 7 beats/min) (both P < 0.001). The change (upright - supine) in SV was inversely correlated with the change in HR for all participants at rest (R(2) = 0.32), at 25 W (R(2) = 0.49), 50 W (R(2) = 0.60), and 75 W (R(2) = 0.32) (P < 0.01). These results suggest that greater elevation in HR in POTS patients during exercise, especially while upright, was secondary to reduced SV and associated with exercise intolerance.     

Lung density is not altered following intense normobaric hypoxic interval training in competitive female cyclists.

Noninvasive imaging techniques have been used to assess pulmonary edema following exercise but results remain equivocal. Most studies examining this phenomenon have used male subjects while the female response has received little attention. Some suggest that women, by virtue of their smaller lungs, airways, and diffusion surface areas may be more susceptible to pulmonary limitations during exercise. Accordingly, the purpose of this study was to determine if intense normobaric hypoxic exercise could induce pulmonary edema in women. Baseline lung density was obtained in eight highly trained female cyclists (mean +/- SD: age = 26 +/- 7 yr; height = 172.2 +/- 6.7 cm; mass = 64.1 +/- 6.7 kg; Vo(2max) = 52.2 +/- 2.2 ml.kg(-1).min(-1)) using computed tomography (CT). CT scans were obtained at the level of the aortic arch, the tracheal carina, and the superior end plate of the tenth thoracic vertebra. While breathing 15% O(2), subjects then performed five 2.5-km cycling intervals [mean power = 212 +/- 31 W; heart rate (HR) = 94.5 +/- 2.2%HRmax] separated by 5 min of recovery. Throughout the intervals, subjects desaturated to 82 +/- 4%, which was 13 +/- 2% below resting hypoxic levels. Scans were repeated 44 +/- 8 min following exercise. Mean lung density did not change from pre (0.138 +/- 0.014 g/ml)- to postexercise (0.137 +/- 0.011 g/ml). These findings suggest that pulmonary edema does not occur in highly trained females following intense normobaric hypoxic exercise.     

Effect of positive-pressure breathing on cardiovascular and thermoregulatory responses to exercise

Five healthy male volunteers performed 20 min of both seated and supine cycle-ergometer exercise (intensity, 50% maximal O2 uptake) in a warm environment (Tdb = 30 degrees C, relative humidity = 40-50%) with and without breathing 10 cmH2O of continuous positive airway pressure (CPAP). The final esophageal temperature (Tes) at the end of 20 min of seated exercise was significantly higher during CPAP (mean difference = 0.18 +/- 0.04 degree C, P less than 0.05) compared with control breathing (C). The Tes threshold for forearm vasodilation was significantly higher (P less than 0.05) during seated CPAP exercise than C (C = 37.16 +/- 0.13 degrees C, CPAP = 37.38 + 0.12 degree C). The highest forearm blood flow (FBF) at the end of exercise was significantly lower (P less than 0.05) during seated exercise with CPAP (mean +/- SE % difference from C = -30.8 +/- 5.8%). During supine exercise, there were no significant differences in the Tes threshold, highest FBF, or final Tes with CPAP compared with C. The added strain on the cardiovascular system produced by CPAP during seated exercise in the heat interacts with body thermoregulation as evidenced by elevated vasodilation thresholds, reduced peak FBF, and slightly higher final esophageal temperatures.     

Heart rate response to onset of exercise: evidence for enhanced cardiac sympathetic activity in animals susceptible to ventricular fibrillation

A large heart rate (HR) increase at the onset of exercise has been linked to an increased risk for adverse cardiovascular events, including cardiac death. However, the relationship between changes in cardiac autonomic regulation induced by exercise onset and the confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, a retrospective analysis of the HR response to exercise onset was made in mongrel dogs with healed myocardial infarctions that were either susceptible (S, n = 131) or resistant (R, n = 114) to VF (induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise). The ECG was recorded, and time series analysis of HR variability (vagal activity index, the 0.24-1.04-Hz frequency component of R-R interval variability) was measured before and 30, 60, and 120 s after the onset of exercise (treadmill running). Exercise elicited significantly (ANOVA, P < 0.0001) greater increases in HR in susceptible dogs at all three times (e.g., at 60 s: R, 46.8 +/- 2.3 vs. S, 57.1 +/- 2.2 beats/min). However, the vagal activity index decreased to a similar extent in both groups of dogs (at 60 s: R, -2.8 +/- 0.1 vs. S, -3.0 +/- 0.2 ln ms2). Beta-adrenoceptor blockade (BB, propranolol 1.0 mg/kg iv) reduced the HR increase and eliminated the differences noted between the groups [at 60 s: R (n = 26), 40.4 +/- 3.2 vs. S (n = 31), 37.5 +/- 2.4 beats/min]. After BB, exercise once again elicited similar declines in vagal activity in both groups (at 60 s: R, -3.6 +/- 0.5 vs. S, -3.2 +/- 0.4 ln ms2). When considered together, these data suggest that at the onset of exercise HR increases to a greater extent in animals prone to VF compared with dogs resistant to this malignant arrhythmia due to an enhanced cardiac sympathetic activation in the susceptible dogs.     

Effects of fasting on insulin action and glucose kinetics in lean and obese men and women

The development of insulin resistance in the obese individual could impair the ability to appropriately adjust metabolism to perturbations in energy balance. We investigated a 12- vs. 48-h fast on hepatic glucose production (R(a)), peripheral glucose uptake (R(d)), and skeletal muscle insulin signaling in lean and obese subjects. Healthy lean [n = 14; age = 28.0 +/- 1.4 yr; body mass index (BMI) = 22.8 +/- 0.42] and nondiabetic obese (n = 11; age = 34.6 +/- 2.3 yr; BMI = 36.1 +/- 1.5) subjects were studied following a 12- and 48-h fast during 2 h of rest and a 3-h 40 mUxm(-2)xmin(-1) hyperinsulinemic-euglycemic clamp (HEC). Basal glucose R(a) decreased significantly from the 12- to 48-h fast (lean 1.96 +/- 0.23 to 1.63 +/- 0.15; obese 1.23 +/- 0.07 to 1.07 +/- 0.07 mgxkg(-1)xmin(-1); P = 0.004) and was equally suppressed during the HEC after both fasts. The increase in glucose R(d) during the HEC after the 12-h fast was significantly decreased in lean and obese subjects after the 48-h fast (lean 9.03 +/- 1.17 to 4.16 +/- 0.34, obese 6.10 +/- 0.77 to 3.56 +/- 0.30 mgxkg FFM(-1)xmin(-1); P < 0.001). After the 12- but not the 48-h fast, insulin-stimulated AKT Ser(473) phosphorylation was greater in lean than obese subjects. We conclude that 1) 48 h of fasting produces a marked decline in peripheral insulin action, while suppression of hepatic glucose production is maintained in lean and obese men and women; and 2) the magnitude of this decline is greater in lean vs. obese subjects.     

Work capacity during 30 days of bed rest with isotonic and isokinetic exercise training

The purpose was to test the hypothesis that twice daily, short-term, variable intensity isotonic and intermittent high-intensity isokinetic leg exercise would maintain peak O2 uptake (VO2) and muscular strength and endurance, respectively, at or near ambulatory control levels during 30 days of -6 degrees head-down bed rest (BR) deconditioning. Nineteen men (aged 32-42 yr) were divided into no exercise control (peak VO2 once/wk, n = 5), isokinetic (Lido ergometer, n = 7), and isotonic (Quinton ergometer, n = 7) groups. Exercise training was conducted in the supine position for two 30-min periods/day for 5 days/wk. Isotonic training was at 60-90% of peak VO2, and isokinetic training (knee flexion-extension) was at 100 degrees/s. Mean (+/- SE) changes (P less than 0.05) in peak VO2 (ml.m-1.kg-1) from ambulatory control to BR day 28 were 44 +/- 4 to 36 +/- 3, -18.2% (3.27-2.60 l/m) for no exercise, 39 +/- 4 to 40 +/- 3, +2.6% (3.13-3.14 l/min) for isotonic, and 44 +/- 3 to 40 +/- 2, -9.1% (3.24-2.90 l/min) for isokinetic. There were no significant changes in any groups in leg peak torque (right knee flexion or extension), leg mean total work, arm total peak torque, or arm mean total work. Mean energy costs for the isotonic and isokinetic exercise training were 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1) and 214 kcal/h (8.9 +/- 0.5 ml.m-1.kg-1), respectively. Thus near-peak, variable intensity, isotonic leg exercise maintains peak VO2 during 30 days of BR, while this peak, intermittent, isokinetic leg exercise protocol does not.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

Mild obesity does not limit change in end-expiratory lung volume during cycling in young women.

To investigate the effects of obesity on the regulation of end-expiratory lung volume (EELV) during exercise we studied nine obese (41 +/- 6% body fat and 35 +/- 7 yr, mean +/- SD) and eight lean (18 +/- 3% body fat and 34 +/- 4 yr) women. We hypothesized that the simple mass loading of obesity would constrain the decrease in EELV in the supine position and during exercise. All subjects underwent respiratory mechanics measurements in the supine and seated positions, and during graded cycle ergometry to exhaustion. Data were analyzed between groups by independent t-test in the supine and seated postures, and during exercise at ventilatory threshold and peak. Total lung capacity (TLC) was reduced in the obese women (P < 0.05). EELV was significantly lower in the obese subjects in the supine (37 +/- 6 vs. 45 +/- 5% TLC) and seated (45 +/- 6 vs. 53 +/- 5% TLC) positions and at ventilatory threshold (41 +/- 4 vs. 49 +/- 5% TLC) (P < 0.01). In conclusion, despite reduced resting lung volumes and alterations in respiratory mechanics during exercise, mild obesity in women does not appear to constrain EELV during cycling nor does it limit exercise capacity. Also, these data suggest that other nonmechanical factors also regulate the level of EELV during exercise.     

The physiological demands of hitting and running in tennis on different surfaces

The aim of the study was to examine how the training surface (i.e., clay or carpet) affects the characteristics (i.e., ball velocity, running pressure, running volume, and physiological responses) of a tennis training session. Ten competitive healthy and nationally ranked male tennis players (mean ± SD: age 24.2 ± 1.7 years, weight 81.4 ± 7.6 kg, height 1.88 ± 0.05 m, body mass index 23.1 ± 1.8) participated in a maximal treadmill test and a field test (e.g., an on-court tennis training session, which consisted of 4 exercises). Subjects' oxygen uptake (VO2) and heart rate (HR) were recorded by portable analyzers, and the ball velocity was measured using a radar gun during the training sessions. We did not find any significant influence of the court surface on any of the variables analyzed under the standardized exercise conditions of the study, as suggested in previous studies conducted under match-play conditions. Moreover, data showed significant differences between maximal forehand and backhand stroke velocities, the forehand stroke being significantly faster (p = 0.01) and more energy demanding on both playing surfaces (clay: 122.0 ± 9.1 vs. 111.1 ± 7.5; carpet: 120.4 ± 6.0 vs 111.5 ± 7.0 km·h). Comparing the same stroke on the same court surface, but at different stroke velocities, we found significant differences (p < 0.05) in all the physiological measurements (e.g., HR, %HRmax; VO2; %VO2), which significantly increased with hitting velocity.     

Oxidation of nonplasma fatty acids during exercise is increased in women with abdominal obesity.

We evaluated plasma fatty acid availability and plasma and whole body fatty acid oxidation during exercise in five lean and five abdominally obese women (body mass index = 21 +/- 1 vs. 38 +/- 1 kg/m(2)), who were matched on aerobic fitness, to test the hypothesis that obesity alters the relative contribution of plasma and nonplasma fatty acids to total energy production during exercise. Subjects exercised on a recumbent cycle ergometer for 90 min at 54% of their peak oxygen consumption. Stable isotope tracer methods ([(13)C]palmitate) were used to measure fatty acid rate of appearance in plasma and the rate of plasma fatty acid oxidation, and indirect calorimetry was used to measure whole body substrate oxidation. During exercise, palmitate rate of appearance increased progressively and was similar in obese and lean groups between 60 and 90 min of exercise [3.9 +/- 0.4 vs. 4.0 +/- 0.3 micromol. kg fat free mass (FFM)(-1). min(-1)]. The rate of plasma fatty acid oxidation was also similar in obese and lean subjects (12.8 +/- 1.7 vs. 14.5 +/- 1.8 micromol. kg FFM(-1). min(-1); P = not significant). However, whole body fatty acid oxidation during exercise was 25% greater in obese than in lean subjects (21.9 +/- 1.2 vs. 17.5 +/- 1.6 micromol. kg FFM(-1). min(-1); P < 0.05). These results demonstrate that, although plasma fatty acid availability and oxidation are similar during exercise in lean and obese women, women with abdominal obesity use more fat as a fuel by oxidizing more nonplasma fatty acids.     

Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients.

We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean +/- SE; age: 53 +/- 3 years; years posttransplant: 6 +/- 4) and five age- and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (Vo(2)(p)), heart rate (HR), stroke volume (SV), cardiac output (Q), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve Vo(2)(p), Q, and systemic arterial-venous oxygen difference (a-vO(2diff)) were 23-52% lower (P < 0.05) in HTR. The reduced Q and a-vO(2diff) reserves were associated with lower HR and HHb reserves, respectively. The phase II Vo(2)(p) time delay was greater (HTR: 38 +/- 2 vs. CON: 25 +/- 1 s, P < 0.05), while time constants for phase II Vo(2)(p) (HTR: 54 +/- 8 vs. CON: 31 +/- 3 s), Q (HTR: 66 +/- 8 vs. CON: 28 +/- 4 s), and HHb (HTR: 27 +/- 5 vs. CON: 13 +/- 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 +/- 21 s) vs. CON (21 +/- 2 s, P < 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 +/- 8 s vs. CON 31 +/- 6 s). The lower peak Vo(2)(p) and prolonged Vo(2)(p) kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.     

VO₂ requirements of boxing exercises

The purpose of this study was to quantify the physiological requirements of various boxing exercises such as sparring, pad work, and punching bag. Because it was not possible to measure the oxygen uptake (VO?) of "true" sparring with a collecting gas valve in the face, we developed and validated a method to measure VO? of "true" sparring based on "postexercise" measurements. Nine experienced male amateur boxers (Mean ± SD: age = 22.0 ± 3.5 years, height = 176.0 ± 8.0 cm, weight = 71.4 ± 10.9 kg, number of fights = 13.0 ± 9.5) of regional and provincial level volunteered to participate in 3 testing sessions: (a) maximal treadmill test in the LAB, (b) standardized boxing training in the GYM, and (c) standardized boxing exercises in the LAB. Measures of VO?, heart rate (HR), blood lactate concentration [LA], rated perceived exertion level, and punching frequencies were collected. VO? values of 43.4 ± 5.9, 41.1 ± 5.1, 24.7 ± 6.1, 30.4 ± 5.8, and 38.3 ± 6.5 ml·kg?1·min?1 were obtained, which represent 69.7 ± 8.0, 66.1 ± 8.0, 39.8 ± 10.4, 48.8 ± 8.5, and 61.7 ± 10.3%VO?peak for sparring, pad work, and punching bag at 60, 120, and 180 b·min?1, respectively. Except for lower VO? values for punching the bag at 60 and 120 b·min?1 (p < 0.05), there was no VO? difference between exercises. Similar pattern was obtained for %HRmax with respective values of 85.5 ± 5.9, 83.6 ± 6.3, 67.5 ± 3.5, 74.8 ± 5.9, and 83.0 ± 6.0. Finally, sparring %HRmax and [LA] were slightly higher in the GYM (91.7 ± 4.3 and 9.4 ± 2.2 mmol·L?1) vs. LAB (85.5 ± 5.9 and 6.1 ± 2.3 mmol·L?1). Thus, in this study simulated LAB sparring and pad work required similar VO? (43-41 ml·kg?1·min?1, respectively), which corresponds to ~70%VO?peak. These results underline the importance of a minimum of aerobic fitness for boxers and draw some guidelines for the intensity of training.