Reduction In VO2max Research Articles

Dynamic exercise in senescent beagles: oxygen consumption and hemodynamic responses.

Seven senescent beagles and seven younger mature beagles were studied at rest, as well as during maximal and submaximal exercise on a motor-driven treadmill. Maximal exercise capacity was significantly (P less than 0.05) reduced, and maximal total body O2 consumption (VO2 max) was 31% lower in senescent beagles. VO2 was also significantly reduced in old dogs, when directly compared at the same relative workloads in old and younger mature dogs. However, VO2 was very similar in both groups during each of the absolute levels of directly comparable exercise. The observed age-related reduction in VO2 max was associated with a significant 25% reduction in maximal cardiac output (CO) in senescent beagles, and with an 11% reduction in maximal arteriovenous O2 difference. CO was also significantly reduced in old dogs at the same relative levels of submaximal exercise evaluated. Combined effects of reductions in stroke volume and in heart rate both contributed to the observed reductions in CO observed in senescent dogs during maximal exercise, as well as during relative levels of submaximal exercise. However, CO responses at each absolute level of submaximal exercise were similar in senescent and younger mature beagles, and the relationship between CO and VO2 was also similar in both groups. Increases in stroke volume significantly contributed to observed increases in CO beginning at the same relative level of exercise in both old and young dogs. Results of this study demonstrate that significant age-related changes in VO2max and in other associated hemodynamic parameters occur during maximal exercise. Many of these changes are also apparent when relative levels of submaximal exercise are directly compared in senescent and in younger mature beagles. However, most hemodynamic responses during absolute levels of exercise are similar in both groups, unless these parameters reflect the relative workload performed, indicating that these responses are appropriate for each absolute level of work that can be performed in the senescent dogs.

The effect of detraining and reduced training on the physiological adaptations to aerobic exercise training.

In previously sedentary individuals, regularly performed aerobic exercise results in significant improvements in exercise capacity. The development of peak exercise performance, as typified by competitive endurance athletes, is dependent upon several months to years of aerobic training. The physiological adaptations associated with these improvements in both maximal exercise performance, as reflected by increases in maximal oxygen uptake (VO2max), and submaximal exercise endurance include increases in both cardiovascular function and skeletal muscle oxidative capacity. Despite prolonged periods of aerobic training, reductions in maximal and submaximal exercise performance occur within weeks after the cessation of training. These losses in exercise performance coincide with declines in cardiovascular function and muscle metabolic potential. Significant reductions in VO2max have been reported to occur within 2 to 4 weeks of detraining. This initial rapid decline in VO2max is likely related to a corresponding fall in maximal cardiac output which, in turn, appears to be mediated by a reduced stroke volume with little or no change in maximal heart rate. A loss in blood volume appears to, at least partially, account for the decline in stroke volume and VO2max during the initial weeks of detraining, although changes in cardiac hypertrophy, total haemoglobin content, skeletal muscle capillarisation and temperature regulation have been suggested as possible mediating factors. When detraining continues beyond 2 to 4 weeks, further declines in VO2max appear to be a function of corresponding reductions in maximal arterial-venous (mixed) oxygen difference. Whether reductions in oxygen delivery to and/or extraction by working muscle regulates this progressive decline is not readily apparent. Changes in maximal oxygen delivery may result from decreases in total haemoglobin content and/or maximal muscle blood flow and vascular conductance. The declines in skeletal muscle oxidative enzyme activity observed with detraining are not causally linked to changes in VO2max but appear to be functionally related to the accelerated carbohydrate oxidation and lactate production observed during exercise at a given intensity. Alternatively, reductions in submaximal exercise performance may be related to changes in the mean transit time of blood flow through the active muscle and/or the thermoregulatory response (i.e. degree of thermal strain) to exercise. In contrast to the responses observed with detraining, currently available research indicates that the adaptations to aerobic training may be retained for at least several months when training is maintained at a reduced level. Reductions of one- to two-thirds in training frequency and/or duration do not significantly alter VO2max or submaximal endurance time provided the intensity of each exercise session is maintained.(ABSTRACT TRUNCATED AT 400 WORDS)

Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects

Conflicting data on the alterations in the maximal exercise response to beta blockade (BB) may be the result of differences in the length of time the subject has been on medication, i.e., hours vs days. The purpose of this study was to examine maximal exercise responses during acute and chronic administration of BB. Twenty-eight healthy males, 14 untrained (UT) and 14 involved in a personal training regimen (TR), performed maximal treadmill tests after 1 d and 9 d under three double-blind, randomized conditions: a placebo (PLAC), propranolol (PROP) 80 mg b.i.d., and atenolol (ATEN) 100 mg o.d. Maximal heart rate (HR), oxygen consumption (VO2), ventilation (VE), and treadmill time were significantly reduced by PROP and ATEN after an acute and chronic dose when compared to PLAC (P less than 0.05) in both groups of subjects. Maximal HR was decreased more after 1 d of BB than after 9 d of BB with both PROP and ATEN in the UT subjects and with PROP only in the TR group. VO2max, VEmax, and treadmill time were also less attenuated after 9 d of BB; however, this trend did not reach statistical significance. The nonselective beta blocker, PROP, caused greater reductions in VO2max compared to the selective beta blocker, ATEN, in both groups of subjects. These data indicate that, other than a small change in maximal HR, there is no difference in the exercise response to acute and chronic BB in normal and highly conditioned individuals.

Role of muscle loss in the age-associated reduction in VO2 max.

A progressive decline in maximal O2 consumption (VO2max) expressed traditionally as per kilogram body weight generally occurs with advancing age. To investigate the extent to which this decline could be attributable to the age-associated loss of metabolically active tissue, i.e., muscle, we measured 24-h urinary creatinine excretion, an index of muscle mass, in 184 healthy nonobese volunteers, ages 22-87 yr, from the Baltimore Longitudinal Study of Aging who had achieved a true VO2max during graded treadmill exercise. A positive correlation was found between VO2max and creatinine excretion in both men (r = 0.64, P less than 0.001) and women (r = 0.47, P less than 0.001). As anticipated, VO2max showed a strong negative linear relationship with age in both men and women. Creatinine excretion also declined with age in men and women. When VO2max was normalized for creatinine excretion, the variance in the VO2max decline attributable to age declined from 60 to 14% in men and from 50 to 8% in women. Thus comparing the standard age regression of VO2max per kilogram body weight with that in which VO2max is normalized per milligram creatinine excretion, the decline in VO2max between a hypothetical 30 yr old and a 70 yr old was reduced from 39 to 18% in men and from 30 to 14% in women. We conclude that in both sexes, a large portion of the age-associated decline in VO2max in non-endurance-trained individuals is explicable by the loss of muscle mass, which is observed with advancing age.

Physical fitness of blind and sighted children.

Twenty-seven children (age 7-17 years) with varying degrees of blindness but with no other known disorder were assessed for physical fitness. Twenty-seven randomly selected children with normal eyesight were also assessed. Maximum oxygen uptake (VO2max) was measured directly during a progressive exercise test on a treadmill. There was a significant and substantial reduction in VO2max in totally blind children (mean +/- standard deviation 35.0 +/- 7.5 ml X min-1 X kg-1) compared with normal children (45.9 +/- 6.6 ml X min-1 X kg-1). Partially sighted children had a significant but smaller reduction in VO2max. Fitness assessed by a step-test was significantly reduced in the visually impaired children, and skin-fold thickness was also significantly greater in totally blind children. The level of habitual physical activity for each child, as assessed by a questionnaire, correlated with VO2max (r = 0.53, p less than 0.0001). Blind children were significantly less active than normal children, and the difference between mean VO2max for blind and normal children became non-significant when their different activity levels were taken into account. It is concluded that totally blind children are less fit than other children at least partly because of their lower level of habitual activity.

Ventilation threshold and aging.

The ventilation threshold (VeT) in 60 healthy men ages 22 to 65 years was determined on a maximal treadmill test. The VeT was identified as the highest VO2 before the ventilatory equivalent for oxygen began to increase without a corresponding increase in the ventilatory equivalent for carbon dioxide. The VO2 max was significantly lower in the 60 compared with the 20-year-old group (with age, r = -.81). The VeT was significantly lower in the oldest compared with the youngest group (with age, r = -.69); however, the VeT as a percentage of VO2 max was significantly greater in the oldest group, (with age, r = .37). The reserve capacity (VO2 max minus VeT) was significantly lower in the older men (with age, r = -.75) and was due to a greater reduction in VO2 max than in VeT. With multiple regression analysis, the variability in VeT was determined primarily by VO2 max (65.8%) and not age. Decrease in strenuous activity with age may account for the large reduction in VO2 max, whereas maintained submaximal activity may attenuate the reduction in VO2 at the ventilation threshold, thus resulting in a large loss in functional reserve above the level of the VeT.

Influence of heat stress and acclimation on maximal aerobic power.

Thirteen male volunteers performed cycle ergometer maximal oxygen uptake (VO2max tests) in moderate (21 degrees C, 30% rh) and hot (49 degrees C, 20% rh) environments, before and after a 9-day heat acclimation program. This program resulted in significantly decreased (P less than 0.01) final heart rate (24 bt X min-1) and rectal temperature (0.4 degrees C) from the first to last day of acclimation. The VO2max was lower (P less than 0.01) in the hot environment relative to the moderate environment both before (8%) and after (7%) acclimation with no significant difference (P greater than 0.05) shown for maximal power output (PO max, watts) between environments either before or after acclimation. The VO2max was higher (P less than 0.01) by 4% after acclimation in both environments. Also, PO max was higher (P less than 0.05) after acclimation in both the moderate (4%) and hot (2%) environments. The reduction in VO2max in the hot compared to moderate environment was not related to the difference in core temperature at VO2max between moderate and hot trials, nor was it strongly related with aerobic fitness level. These findings indicate that heat stress, per se, reduced the VO2max. Further, the reduction in VO2max due to heat was not affect be state of heat acclimation, the degree of elevation in core temperature, or level of aerobic fitness.

Exercise performance and beta-blockade.

beta-Adrenoceptor blockers (beta-blockers) are common first-choice drugs in the treatment of various cardiovascular disorders. Physical exercise performed during single-dose administration of beta-blockers, however, is associated with an increased rate of perceived exertion; an effect which appears to be partly reduced with long term treatment. Although clinical doses of beta-blockade may reduce heart rate by 30 to 35%, during maximal exercise cardiac output is not equally reduced. Accordingly, most studies have demonstrated increased stroke volume after beta-blockade. This reduction in heart rate is typically accompanied by a decreased VO2max (5 to 15%) in both patients and healthy, trained subjects. This smaller reduction in VO2max, as compared with the decrease in cardiac output, is the result of a partly compensating increased arteriovenous O2 difference. Work capacity as reflected by the ability to perform intense short term or more prolonged steady-state exercise is also impaired following beta-blockade. beta-Adrenoceptors can be subdivided into types beta 1- and beta 2. Blockers which are specific for either beta 1-receptors (beta 1-selective blockers) or both beta 1- and beta 2 receptors (non-selective blockers) differ with regard to their effect on exercise performance. Exercise performance ability, irrespective of exercise intensity and duration, is impaired to a greater extent following non-selective than beta 1-selective blockade at equal reductions in heart rate. This response stems from a decreased energy flux through glycogenolysis during non-selective blockade treatment. Individuals receiving beta-blockade medication therefore show greater adaptive response to physical conditioning during treatment with beta 1-selective than non-selective blockade probably because of greater training intensity with the former therapy. Neither psychomotor performance nor muscular strength and power is negatively affected by beta-blockade. Nevertheless, the ability to perform athletic events requiring high levels of motor control under emotional stress but not high levels of aerobic or anaerobic energy release, is probably increased during beta-blockade.

Blood volume and hemoglobin concentration as determinants of maximal aerobic power

Changes in blood volume (BV) and hemoglobin concentration ( [Hb] ) were induced in five healthy young men. After acute hypovolemic anemia was achieved by blood withdrawal, VO2max values decreased, while the same [Hb] due to acute plasma volume expansion (6% dextran) did not alter VO2max. After reinfusion of red blood cells, leading to hypervolemia and increased [Hb], VO2max increased. Plasma volume expansion in this situation, leading to hypervolemia at normal [Hb], resulted in a slight reduction in VO2max, which, however, remained elevated (approximately 4%) above control values. Physical performance, measured as time to exhaustion, corresponded to the changes in VO2max except for the hypervolemic anemic situation, where it decreased. Changes in peak heart rate were inversely related to BV changes, but were also influenced by [Hb]. The results point to a significant influence of the total amount of Hb rather than the blood hemoglobin concentration for obtaining a high maximal aerobic power. Thus, a reduced [Hb], concomitantly with an elevated blood volume (plasma volume), may result in an unchanged VO2max, but reduced performance time.

Exercise and cardiac performance capacity in rats with partial sympathectomy.

This study was undertaken to examine maximal oxygen uptake (VO2 max) and heart rate (HR) during exercise, in situ derived cardiac contractile capacity, and Ca2+ regulation of cardiac myofibril ATPase in normal female rats and in rats with partial sympathectomy (SYMX) induced by chronic injections of guanethidine. Also, normal control (NC) rats were studied during exercise with and without the beta 1-blocking drug atenolol. The results show that SYMX did not have any effect on Ca2+-regulated cardiac myofibril ATPase activity. Also similar cardiac functional capacity, as reflected in left ventricular pressure development and +dP/dtmax, was observed for both groups when the heart was stressed by either exogenous norepinephrine or maximal afterload (aortic constriction). Exercise VO2 max was reduced by 15% (P less than 0.05) in the SYMX compared to the NC group. Although this reduction in VO2 max corresponded to a parallel reduction in HRmax, NC rats with cardiac beta-blockade attained normal VO2 max even though their exercise HRmax was below the SYMX group. These findings suggest that normal rats with attenuated HR and contractility have a better capacity to acutely maintain VO2 max during exercise than rats with chemical sympathectomy.

Decrease in maximum consumption of oxygen after blockage of beta-andrenergic receptors

VO2 max, maximum oxygen uptake, has been measured in 4 normal young men, before and after beta-adrenergic blockade (0.5 to 5 mg Pindolol by mouth). Pindolol induces bradycardia and reduces VO2 max. A statistically significant positive correlation appears between posology of Pindolol and bradycardia, this posology and reduction of VO2 max, and finally between bradycardia and reduction of VO2 max. These correlations indicate that the reduction of VO2 max is best explained by a circulatory limitation of oxygen supply to active muscles.