Double-blind intervention trial on modulation of ozone effects on pulmonary function by antioxidant supplements.
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The aim of this study was to investigate whether the acute effects of ozone on lung function could be modulated by antioxidant vitamin supplementation in a placebo-controlled study. Lung function was measured in Dutch bicyclists (n = 38) before and after each training session on a number of occasions (n = 380) during the summer of 1996. The vitamin group (n = 20) received 100 mg of vitamin E and 500 mg of vitamin C daily for 15 weeks. The average ozone concentration during exercise was 77 microg/m3 (range, 14-186 microg/m3). After exclusion of subjects with insufficient compliance from the analysis, a difference in ozone exposure of 100 microg/m3 decreased forced expiratory volume in 1 second (FEV1) 95 ml (95% confidence interval (CI) -265 to -53) in the placebo group and 1 ml (95% CI -94 to 132) in the vitamin group; for forced vital capacity, the change was -125 ml (95% CI -384 to -36) in the placebo group and -42 ml (95% CI -130 to 35) in the vitamin group. The differences in ozone effect on lung function between the groups were statistically significant. The results suggest that supplementation with the antioxidant vitamins C and E confers partial protection against the acute effects of ozone on FEV1 and forced vital capacity in cyclists. (+info)
Heart rate during exercise with leg vascular occlusion in spinal cord-injured humans.
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Feed-forward and feedback mechanisms are both important for control of the heart rate response to muscular exercise, but their origin and relative importance remain inadequately understood. To evaluate whether humoral mechanisms are of importance, the heart rate response to electrically induced cycling was studied in participants with spinal cord injury (SCI) and compared with that elicited during volitional cycling in able-bodied persons (C). During voluntary exercise at an oxygen uptake of approximately 1 l/min, heart rate increased from 66 +/- 4 to 86 +/- 4 (SE) beats/min in seven C, and during electrically induced exercise at a similar oxygen uptake in SCI it increased from 73 +/- 3 to 110 +/- 8 beats/min. In contrast, blood pressure increased only in C (from 88 +/- 3 to 99 +/- 4 mmHg), confirming that, during exercise, blood pressure control is dominated by peripheral neural feedback mechanisms. With vascular occlusion of the legs, the exercise-induced increase in heart rate was reduced or even eliminated in the electrically stimulated SCI. For C, heart rate tended to be lower than during exercise with free circulation to the legs. Release of the cuff elevated heart rate only in SCI. These data suggest that humoral feedback is of importance for the heart rate response to exercise and especially so when influence from the central nervous system and peripheral neural feedback from the working muscles are impaired or eliminated during electrically induced exercise in individuals with SCI. (+info)
Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise.
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To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate. (+info)
Evidence of O2 supply-dependent VO2 max in the exercise-trained human quadriceps.
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Maximal O2 delivery and O2 uptake (VO2) per 100 g of active muscle mass are far greater during knee extensor (KE) than during cycle exercise: 73 and 60 ml. min-1. 100 g-1 (2.4 kg of muscle) (R. S. Richardson, D. R. Knight, D. C. Poole, S. S. Kurdak, M. C. Hogan, B. Grassi, and P. D. Wagner. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H1453-H1461, 1995) and 28 and 25 ml. min-1. 100 g-1 (7.5 kg of muscle) (D. R. Knight, W. Schaffartzik, H. J. Guy, R. Predilleto, M. C. Hogan, and P. D. Wagner. J. Appl. Physiol. 75: 2586-2593, 1993), respectively. Although this is evidence of muscle O2 supply dependence in itself, it raises the following question: With such high O2 delivery in KE, are the quadriceps still O2 supply dependent at maximal exercise? To answer this question, seven trained subjects performed maximum KE exercise in hypoxia [0.12 inspired O2 fraction (FIO2)], normoxia (0.21 FIO2), and hyperoxia (1.0 FIO2) in a balanced order. The protocol (after warm-up) was a square wave to a previously determined maximum work rate followed by incremental stages to ensure that a true maximum was achieved under each condition. Direct measures of arterial and venous blood O2 concentration in combination with a thermodilution blood flow technique allowed the determination of O2 delivery and muscle VO2. Maximal O2 delivery increased with inspired O2: 1.3 +/- 0.1, 1.6 +/- 0.2, and 1.9 +/- 0.2 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Maximal work rate was affected by variations in inspired O2 (-25 and +14% at 0.12 and 1.0 FIO2, respectively, compared with normoxia, P < 0.05) as was maximal VO2 (VO2 max): 1.04 +/- 0.13, 1. 24 +/- 0.16, and 1.45 +/- 0.19 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Calculated mean capillary PO2 also varied with FIO2 (28.3 +/- 1.0, 34.8 +/- 2.0, and 40.7 +/- 1.9 Torr at 0.12, 0.21, and 1.0 FIO2, respectively, P < 0.05) and was proportionally related to changes in VO2 max, supporting our previous finding that a decrease in O2 supply will proportionately decrease muscle VO2 max. As even in the isolated quadriceps (where normoxic O2 delivery is the highest recorded in humans) an increase in O2 supply by hyperoxia allows the achievement of a greater VO2 max, we conclude that, in normoxic conditions of isolated KE exercise, KE VO2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O2 supply. (+info)
Pyruvate dehydrogenase activation in inactive muscle during and after maximal exercise in men.
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Pyruvate dehydrogenase activity (PDHa) and acetyl-group accumulation were examined in the inactive deltoid muscle in response to maximal leg exercise in men. Seven subjects completed three consecutive 30-s bouts of maximal isokinetic cycling, with 4-min rest intervals between bouts. Biopsies of the deltoid were obtained before exercise, after bouts 1 and 3, and after 15 min of rest recovery. Inactive muscle lactate (LA) and pyruvate (PYR) contents increased more than twofold (P < 0.05) after exercise (bout 3) and remained elevated after 15 min of recovery (P < 0.05). Increased PYR accumulation secondary to LA uptake by the inactive deltoid was associated with greater PDHa, which progressively increased from 0.71 +/- 0.23 mmol. min-1. kg wet wt-1 at rest to a maximum of 1.83 +/- 0.30 mmol. min-1. kg wet wt-1 after bout 3 (P < 0.05) and remained elevated after 15 min of recovery (1.63 +/- 0.24 mmol. min-1. kg wet wt-1; P < 0.05). Acetyl-CoA and acetylcarnitine accumulations were unaltered. Increased PDHa allowed and did not limit the oxidation of LA and PYR in inactive human skeletal muscle after maximal exercise. (+info)
High-resistance training and muscle metabolism during prolonged exercise.
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To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance training (HRT), active but untrained males (age 20 +/- 0.7 yr; mean +/- SE) performed lower-limb weight training 3 days/wk for 12 wk using three sets of 6-8 repetitions maximal (RM)/day. Muscle metabolism was examined at different stages of training (4, 7, and 12 wk) using a two-stage continuous cycle test performed at the same absolute power output and duration (56.4 +/- 2.9 min) and representing 57 and 72% of pretraining peak aerobic power (VO2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher (P < 0.05) phosphocreatine (PCr; 27.4 +/- 6. 7 vs. 38.0 +/- 1.9 mmol/kg dry wt), a lower lactate (38.9 +/- 8.5 vs. 24.4 +/- 6.1 mmol/kg dry wt), and a higher (P < 0.05) glycogen content (132 +/- 11 vs. 181 +/- 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72% VO2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found on VO2 peak with training (41.2 +/- 2.9 vs. 41.0 +/- 2.1 ml. kg-1. min-1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy. (+info)
Peripheral muscle ergoreceptors and ventilatory response during exercise recovery in heart failure.
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Recent studies have suggested that the increased ventilatory response during exercise in patients with chronic heart failure was related to the activation of muscle metaboreceptors. To address this issue, 23 patients with heart failure and 7 normal subjects performed arm and leg bicycle exercises with and without cuff inflation around the arms or the thighs during recovery. Obstruction slightly reduced ventilation and gas exchange variables at recovery but did not change the kinetics of recovery of these parameters compared with nonobstructed recovery: half-time of ventilation recovery was 175 +/- 54 to 176 +/- 40 s in patients and 155 +/- 66 to 127 +/- 13 s in controls (P < 0.05, patients vs. controls, not significant within each group from baseline to obstructed recovery). We conclude that muscle metaboreceptor activation does not seem to play a role in the exertion hyperventilation of patients with heart failure. (+info)
Breathing patterns during slow and fast ramp exercise in man.
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Breathing frequency (fb), tidal volume (VT), and respiratory timing during slow (SR, 8 W min-1) and fast (FR, 65 W min-1) ramp exercise to exhaustion on a cycle ergometer was examined in seven healthy male subjects. Expiratory ventilation (VE), pulmonary gas exchange (VO2 and VCO2) and end-tidal gas tensions (PET,O2 and PET,CO2) were determined using breath-by-breath techniques. Arterialized venous blood was sampled from a dorsal hand vein at 2 min intervals during SR and 30 s intervals during FR and analysed for arterial plasma PCO2 (PaCO2). PET,CO2 increased with increasing work rates (WRs) below the ventilatory threshold (VT); at WRs > or = 90% VO2,max, PET,CO2 was reduced (P < 0.05) below 0 W values in SR but not in FR.fb and VT were similar for SR and FR at all submaximal WRs, resulting in a similar VE. At exhaustion VE was similar but fb was higher (P < 0.05) and VT was lower (P < 0.05) in SR (fb, 51 +/- 10 breaths min-1; VT, 2590 +/- 590 ml) than in FR (fb, 42 +/- 8 breaths min-1; VT, 3050 +/- 470 ml). The time of expiration (TE) decreased with increasing WR, but there was no difference between SR and FR. The time of inspiration (TI) decreased at exercise intensities > or = VT; at exhaustion, TI was shorter (P < 0.05) during SR (0.512 +/- 0.097 s) than during FR (0.753 +/- 0.100 s). The TI to total breath duration (TI/TTot) and the inspiratory flow (VT/TI) were similar during SR and FR at all submaximal exercise intensities; at VO2,max, TI/TTot was lower (P < 0.05) and VT/TI was higher (P < 0.05) during SR (TI/TTot, 0.473 +/- 0.030; VT/TI, 5.092 +/- 0.377 l s-1) than during FR (TI/TTot, 0.567 +/- 0.050; VT/TI, 4.117 +/- 0.635 l s-1). These results suggest that during progressive exercise, breathing pattern and respiratory timing may be determined, at least at submaximal work rates, independently of alveolar and arterial PCO2. (+info)