Approximation equation for oxygen uptake kinetics in decrement-load exercise starting from low exercise intensity.
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The purpose of the present study was to determine the degree of fitting an approximation equation for oxygen uptake (Vo(2)) in decrement-load exercise (DLE). Work rate was started from 120 watts and was decreased by a rate of 15 watts per min. The initial work rate of DLE corresponded to 72+/-10% of the work rate at anaerobic threshold determined in incremental-load exercise (ILE). Vo(2) in DLE increased rapidly, reached a peak, and decreased linearly until the end of the exercise. Vo(2) in DLE was higher than that in ILE at the same work rate except in the early periods in ILE and DLE. This difference ranged from 300 to 400 ml/min. This difference is a result of repayment of oxygen debt in DLE and from the oxygen deficit induced by the delay of response of Vo(2) in ILE. As work rate in DLE can be obtained by the difference between work rates in constant-load exercise (CLE) and ILE, we postulated that the approximation equation for Vo(2) kinetics in DLE could be expressed by a combination of approximation equations in CLE and in ILE. When time delay was taken into consideration in this equation, the fitting of data obtained by using the equation was better than that of data obtained by using the equation without a parameter of time delay. The degree of fitting ranged from 94 to 98% (r(2)). Thus, it seems that Vo(2) including oxygen debt in DLE can be approximated by the equation used in this study. (+info)
Beta-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans.
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Acute hypoxia increases heart rate (HR) and cardiac output (Qt) at a given oxygen consumption (VO2) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac beta receptors. Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and Qt during hypoxic exercise. To test this, we separately blocked the beta-sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean +/- S.E.M. age = 31.7+/-1.6 years, normoxic maximal VO2 (VO2,max)=3.1+/-0.3 l min(-1)) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction=0.125) to VO2,max. Data were collected on different days under the following conditions: (1)control, (2) after 8.0 mg propranolol i.v. and (3) after 0.8 mg glycopyrrolate i.v. Qt was measured using open-circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a given VO2 (P<0.05, P<0.01 and P=0.2, respectively). HR/VO2 and Qt/VO2 increased during hypoxia in all three conditions (P<0.05). Unexpectedly, the effects of hypoxia on HR and Qt were not significantly different from control with either beta-sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and Qt do not necessarily require intact cardiac muscarinic and beta receptors. It may be that cardiac alpha receptors play a primary role in elevating HR and Qt during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked. (+info)
Effects of short-term training on plasma acid-base balance during incremental exercise in man.
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The present study examined the effect of short-term submaximal training on plasma acid-base balance during exercise. The influence of water and ion exchange between plasma, active muscles and erythrocytes in the response to training were also studied. The contributions of independent physicochemical variables (i.e. strong ion difference ([SID]), total concentration of weak acids ([Atot]) and PO2) to changes in arterial (a) and femoral venous (v) plasma [H+] were examined in six subjects (age 24+/-1.5 years; maximum oxygen consumption rate (VO2,max), 3.67+/-0.24 l min(-1)) during steady-state cycling for 15 min at each of 30, 65 and 75% of VO2,max before (pre) and after (post) training for 7 days on a cycle ergometer (2 h daily at 60 % VO2,max). The rise in [H+]a during exercise was attenuated post-training by 3 and 5 nequiv l(-1) (P<0.05) at 65 and 75% VO2,max, respectively, due first to less decrease in [SID]a, secondary to lower [Cl-]a and [Lac-]a; and second, to a reduction in [Atot]a, due to greater plasma volume and less plasma water flux (Jv) into leg muscle (P<0.05). The rise in [H+]v was also less in post-training by 4.5 and 6 nequiv l(-1) (P<0.05) at 65 and 75% VO2,max, respectively, and attributed solely to lower [Atot]v (P<0.05). Attenuation of exercise induced decreases in plasma [SID]a and [SID]v from rest to 75 % VO2,max was accompanied by reductions in erythrocyte Lac- and Cl- uptake (P<0.05), and smaller increases in erythrocyte K+ release (P<0.05). We conclude that the training-induced attenuation of the rise in plasma [H+]a and [H+]v during incremental exercise resulted from adaptive changes within muscles (less Lac- production and less water uptake) and erythrocytes (less uptake of Lac-, Cl- and K+), leading to greater [SID] and lower [Atot] in both arterial and femoral venous plasma. (+info)
Cutaneous active vasodilation in humans during passive heating postexercise.
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The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact alpha-adrenergic vasoconstrictor activity (untreated) and one infused with bretylium tosylate (bretylium treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption followed by 20 min of seated recovery. A liquid-conditioned suit was used to increase mean skin temperature ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 +/- 0.01, 0.39 +/- 0.02, and 0.53 +/- 0.02 degrees C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly, there was an increase of 0.20 +/- 0.01, 0.37 +/- 0.02, and 0.53 +/- 0.02 degrees C for the treated site for the 55, 70, and 85% exercise trials, respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity. (+info)
Paradoxical effects of prior activity on human sarcoplasmic reticulum Ca2+-ATPase response to exercise.
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To investigate the effects of intermittent heavy exercise (HE) on sarcoplasmic reticulum (SR) maximal Ca2+-ATPase activity (Vmax) and Ca2+ uptake, a continuous two-stage standardized cycling test was performed before and after HE by untrained men [peak aerobic power (Vo -->Vo2 peak) = 42.9 +/- 2.7 ml. kg-1 x min-1]. The HE consisted of 16 bouts of cycling performed for 6 min each hour at 90% Vo2 peak. Tissue was obtained from the vastus lateralis by needle biopsy before and during each cycle test. Before HE, reductions (P < 0.05 micromol. g protein-1x min-1) of 16 and 31% were observed in Vmax and Ca2+ uptake, respectively, after 40 min of the standardized test. Resting Vmax and Ca2+ uptake were depressed (P < 0.05) by 19 and 30%, respectively, when measured 36-48 h after HE. During the standardized test, after HE, Vmax increased (P < 0.05) by 20%, whereas no change was observed in Ca2+ uptake. The HE protocol resulted in small increases (P < 0.05) and decreases (P < 0.05) in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) 2a and SERCA1 expression, respectively, as determined by Western blotting techniques. These results indicate that SR Ca2+-sequestering function in response to a prolonged exercise test depends on prior activity status, such that rested muscles exhibit a decrease and prior exercised muscles, an increase in Ca2+-ATPase activity. Moreover, it appears that changes in SERCA content can occur in response to a sustained session of intermittent exercise. (+info)
UCP3 protein regulation in human skeletal muscle fibre types I, IIa and IIx is dependent on exercise intensity.
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It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50%, respectively; protein: by 30 and 27%, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16%, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26%, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid beta oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content. (+info)
Gender differences in the regulation of amino acid metabolism.
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Exercising men, compared with women, have a greater increase in leucine oxidation but not lysine rate of appearance. The cause for this sexual dimorphism is unknown; however, an inhibition of beta-adrenoreceptor activity has previously been shown to mediate amino acid metabolism (Lamont LS, McCullough AJ, and Kalhan SC. Am J Physiol Endocrinol Metab 268: E910-E916, 1995; Lamont LS, Patel DG, and Kalhan SC. J Appl Physiol 67: 221-225, 1989). This study was a gender comparison of leucine and lysine kinetics during a beta-adrenoreceptor blockade (beta1,beta2-blockade) and a placebo control by using a double-blind crossover protocol. Subjects exercised at 50% of their trial-specific maximal O2 consumption (1 h) after 7 days of dietary control. During exercise with beta-blockade, men had an increased nonprotein respiratory exchange ratio (P < 0.001), whereas women had an increased circulation of free fatty acids (P < 0.001). The genders also displayed distinct differences in exercise amino acid kinetics. The men, but not the women, increased leucine oxidation (P < 0.005) and lysine rate of appearance (P < 0.009) when exercising during beta-adrenergic blockade. This study indicates that during beta-blockade, exercising men increase their need for amino acids (and carbohydrate) to fuel energy needs, whereas women increase their mobilization of fat, thereby requiring less alternative fuels such as carbohydrate and amino acids. Gender-specific fuel preferences during exercise are regulated by beta-adrenergic-receptor activity. Substrate availability during exercise appears to modulate the amino acid oxidation differences between genders. (+info)
Carotid baroreflex responsiveness to head-up tilt-induced central hypovolaemia: effect of aerobic fitness.
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This investigation examined the interaction between carotid baroreflex (CBR) responsiveness during head-up tilt (HUT)-induced central hypovolaemia and aerobic fitness. Seven average fit (AF) individuals, with a mean maximal oxygen uptake (VO2max) of 49 +/- 1 (ml O2) kg-1 min-1, and seven high fit (HF) individuals, with a VO2max of 61 +/- 1 (ml O2) kg-1 min-1, voluntarily participated in the investigation. After 10-15 min supine, each subject was exposed to nine levels of progressively increasing HUT by 10 deg increments from -20 deg to +60 deg. During the final 3 min of each stage of HUT, the CBR responsiveness was measured using a rapid pulse (500 ms) train of neck pressure (NP) and neck suction (NS) ranging from +40 to -80 Torr. The maximal gain of the carotid-HR (Gmax-HR) and carotid-MAP (Gmax-MAP) baroreflex function curves was identified as measures of CBR responsiveness. During HUT-induced decreases in thoracic admittance, an index of central blood volume (CBV), the Gmax-HR and Gmax-MAP of the AF subjects increased more than the Gmax-HR and Gmax-MAP of the HF subjects (P < 0.05). The data demonstrate that the increase in the CBR responsiveness during a tilt-induced progressive unloading of the cardiopulmonary baroreceptors was attenuated in endurance-trained subjects. These findings provide an explanation for the predisposition to orthostatic hypotension and intolerance in well-trained athletes. (+info)