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Biomedical subjects

S L Lindstedt

Publications and source records attributed to S L Lindstedt.

At least 19 recordsLinked to original sources
PubMed1998

Exercise training in chronic hypoxia has no effect on ventilatory muscle function in humans.

At the highest altitude, aerobic work is limited by environmental oxygen availability. We therefore reasoned that the hyperpnea associated with endurance training at altitude should provide a strong stimulus for adaptation of the ventilatory muscles. We measured peak inspiratory muscle pressure-flow characteristics (inspiring through graded resistors) and maximum sustainable ventilation capacity in ten permanent residents of La Paz, Bolivia (3600 m) prior to and immediately following 6 weeks of incremental endurance training. Additionally, eight local residents did no training and functioned as controls for the capacity test. While V(O2)max measured in hypoxia increased by 19% (Favier et al., 1995b. J. Appl Physiol. 78, 2286-2293.), none of the tested ventilatory variables showed significant changes. The values for the group mean slopes of maximum inspiratory pressure-flow pairs (- 10.5 vs. - 9.8 cm H2O x sec x L(-1), P=0.301; before versus after training, respectively), maximum inspiratory pressure (112.1+/-8.9 vs. 106.9+/-8.6 cmH2O, P=0.163), peak inspiratory flow (9.8+/-0.41 vs. 10.2+/-0.55 L x sec(-1) P=0.172) and the maximum volitional volume in 12 sec (43.9+/-2.4 vs. 45.6+/-2.4 L in 12 sec, P=0.133) were unchanged with exercise training. Likewise, maximal sustainable minute volume was not different between post-training and control subjects (177.4+/-7.9 vs. 165.4+/-8.4 L x min(-1), P=0.141). These data support the concept that endurance training fails to elicit functional adaptations in ventilatory muscles in humans, even when exercise is done in hypoxia.

Acclimatization↗
PubMed1998

Task-specific design of skeletal muscle: balancing muscle structural composition.

Skeletal muscle fibers are composed of three structural elements, each contributing a unique aspect of muscle function, yet each 'competing' in a sense for space inside the cell. The volume occupied by myofibrils determines the force of contraction, the volume of sarcoplasmic reticulum sets the rate of onset and relaxation of a fiber's contraction and hence contraction frequency, and the volume of mitochondria sets the level of sustained performance. The entirety of functional outcomes in muscle, from sustained isometric to high frequency contractions, and from high power output to high endurance, are all primarily attributable to shifts in the proportions (and relationships) of those three structures. This paper examines and reviews these components of muscle first to identify and summarize structure-function 'rules', and second to examine the balance between sometimes competing demands. In particular, we focus on those muscles in which power, endurance and frequency are all simultaneously high (flight muscles), and examine how muscle has 'solved' problems of space and energy demand. From these results and observations it would appear that for flight to have evolved in small animals, the double packing of inner mitochondrial membranes may be expected in animals under 50-80 g in mass, and asynchronous muscle is structurally essential for flight in small insects with wing beat frequencies above about 100 Hz.

Animals↗
PubMed1996

Minimal cost per twitch in rattlesnake tail muscle.

Sound production is one of the most energetically costly activities in animals. Minimizing contraction costs is one means of achieving the activation rates necessary for sound production (20-550 Hz) (refs 1-3) without exceeding energy supplies. Rattlesnakes produce a sustained, high-frequency warning sound by extremely rapid contraction of their tailshaker muscles (20-90 Hz) (refs 4,5). The ATP cost per twitch is only 0.015 micromol ATP per g muscle per twitch during rattling, as measured by in vivo magnetic resonance. The reduced volume density of myofibre (32%) in tailshaker muscle is consistent with contraction cost being minimized (crossbridge cycling), in contrast to the contractile costs of vertebrate locomotory and asynchronous insect flight muscle. Thus tailshaker muscle is an example of sound-producing muscle designed for 'high frequency, minimal cost'. The high rates of rattling are achieved by minimizing contractile use of ATP, which reduces the cost per twitch to among the lowest found for striated muscle.

Adenosine Triphosphate↗
PubMed1996

The whistle and the rattle: the design of sound producing muscles.

Vertebrate sound producing muscles often operate at frequencies exceeding 100 Hz, making them the fastest vertebrate muscles. Like other vertebrate muscle, these sonic muscles are "synchronous," necessitating that calcium be released and resequestered by the sarcoplasmic reticulum during each contraction cycle. Thus to operate at such high frequencies, vertebrate sonic muscles require extreme adaptations. We have found that to generate the "boatwhistle" mating call (approximately 200 Hz), the swimbladder muscle fibers of toadfish have evolved (i) a large and very fast calcium transient, (ii) a fast crossbridge detachment rate, and (iii) probably a fast kinetic off-rate of Ca2+ from troponin. The fibers of the shaker muscle of rattlesnakes have independently evolved similar traits, permitting tail rattling at approximately 90 Hz.

Air Sacs↗
PubMed1995

Fatigue and the design of the respiratory system.

One source of muscle fatigue may be the failure to provide the required oxygen by any step in the oxygen transport cascade or a lack of the necessary machinery to utilize that oxygen. We favor abandoning the concept of a single rate-limiting step for the concept of tuned resistors, each contributing to the overall resistance to oxygen flow. However, because some of these steps have considerably less phenotypic plasticity than others, these are the component parts of the respiratory system that must be built with adequate "reserve" to accommodate adaptive increases in the other steps (Lindstedt et al., 1988; Weibel et al., 1992; Lindstedt et al., 1994). These structures will usually appear to be over built except in those rare individual animals at the species-specific limit of VO2 in which these less malleable structures may be limiting.

Animals↗
PubMed1994

Does peak inspiratory flow contribute to setting VO2max? A test of symmorphosis.

Symmorphosis predicts that animal design is optimized in such a way that structure 'statisfies but does not exceed' functional requirements. To provide one test of this hypothesis, we examined peak inspiratory flow and its relation to maximum oxygen uptake in humans. We measured maximal forced (peak) inspiratory flow (VImax) and maximum oxygen uptake (VO2max) via cycle ergometry in well trained (VO2max > 65 ml O2.kg-1.min-1) and untrained (VO2max < 45 ml O2.kg-1.min-1) male subjects. Tests of VImax and peak oxygen uptake (VO2peak) were made while the subjects were breathing through inspiratory orifices differing in area. VImax varied as an identical function of orifice diameter in both groups of subjects. However, VO2peak was more sensitive to decreasing orifice diameter in trained endurance athletes than it was in untrained individuals. The diameter of the largest orifice that caused a reduction in oxygen uptake was over two times larger for trained than for untrained subjects, corresponding to about a four-fold difference in resistance at any flow rate. These results suggest that the structures setting VImax (airway resistance and inspiratory muscle strength) are not matched to oxygen demand (VO2max) in humans. While these structures seem to be 'over-built' and hence do not likely contribute to setting the limits to aerobic performance in most humans, they may be among the primary limiting factors in the most elite endurance athletes.

Adaptation, Physiological↗
PubMed1994

Capillary blood transit time in muscles in relation to body size and aerobic capacity.

The mean minimal transit time for blood in muscle capillaries (tc) was estimated in six species, spanning two orders of magnitude in body mass and aerobic capacity: horse, steer, dog, goat, fox and agouti. Arterial (CaO2) and mixed venous (CvO2) blood O2 concentrations, blood hemoglobin concentrations ([Hb]) and oxygen uptake rates were measured while the animals ran on a treadmill at a speed that elicited the maximal oxygen consumption rate (VO2max) from each animal. Blood flow to the muscles (Qm) was assumed to be 85% of cardiac output, which was calculated using the Fick relationship. Total muscle capillary blood volume (Vc) and total muscle mitochondrial volume were estimated by morphometry, using a whole-body muscle sampling scheme. The tc was computed as Vc/Qm. The tc was 0.3-0.5 s in the 4 kg foxes and agoutis, 0.7-0.8 s in the 25 kg dogs and goats, and 0.8-1.0 s in the 400 kg horses and steers. The tc was positively correlated with body mass and negatively correlated with transcapillary O2 release rate per unit capillary length. Mitochondrial content was positively correlated with VO2max and with the product of Qm and [Hb]. These data suggested that Qm, Vc, maximal hemoglobin flux, and consequently tc, are co-adjusted to result in muscle O2 supply conditions that are matched to the O2 demands of the muscles at VO2max.

Aerobiosis↗
PubMed1994

Exercise performance of mammals: an allometric perspective.

We have examined aerobic exercise performance among the mammals with particular attention to the constraints that body size places on all aspects of muscle biomechanics, aerobic energetics, tissue oxygen diffusion, cardiovascular oxygen delivery, and pulmonary oxygen uptake. Several body-size-dependent patterns emerge that seemingly govern aerobic performance in mammals, with the caveat that at any given body size there is a range of aerobic capacities, the result of natural selection operating on the size-dependent "default values" of structure and function. Among these default values, the following apparent functional clusters surface: 1. In general, concentrations and pressures (e.g., of proteins and gases) are roughly independent of body size. Inspiratory and expiratory ventilation pressures, blood pressure and the partial pressures of O2 and CO2 in lungs, blood, and tissues do not vary with body size. Likewise, concentrations of hemoglobin, myoglobin, and hematocrit are independent of body size. 2. Most volumes and capacities scale linearly with body size (i.e., as a constant function of body mass). In addition to heart, lung, and total blood volumes, important examples relevant to exercise performance are the diffusing capacities for oxygen in the lung and, apparently, in the tissues. 3. Finally, most time-dependent variables related to oxygen delivery scale allometrically with body mass; they are of shorter duration in small animals than in large ones. Biological rates, for example, Vmax of working muscle, heart and respiratory rates, and transit times of blood through the muscles and lungs, all vary roughly as the -1/5 to -1/4 power of body mass.

Animals↗
PubMed1993

Limits to maximal performance.

Body size fundamentally affects maximal locomotor performance in mammals. Comparisons of performances of different-sized animals yield different results if made using relative, rather than absolute scales. Absolute speed may be a reasonable way to evaluate the locomotor performance of an animal that must escape predators in real time. However, comparisons of metabolic power in animals of different size can only be made meaningfully on a mass-specific basis. Numerous factors associated with the mechanics, energetics, and storage of elastic energy during locomotion change with body size, which results in allometric relationships that make the energetic cost of locomotion (alpha Mb-0.3) more expensive for small mammals than for large mammals. Small mammals have lower enzymatic capacities for anaerobic glycolysis (alpha Mb0.15) and higher specific aerobic capacities (alpha Mb-0.13) than large mammals. However, the energetic cost of transport increases more than aerobic power as mammals get smaller. The higher ratio of cost to available power in small mammals may explain why they run more slowly than large mammals, as a rule. Maximum aerobic capacity is allometrically related to body size. Limits to VO2max can be imposed by mitochondrial oxidative capacity, as in goats, or by the O2 transport system, as in humans and horses. No single step in the O2 transport system can limit the flux of O2 by itself; however, in an average non-athletic species of mammal, any of the steps in the system might appear to be the weakest link. In highly aerobic athletic species, and possibly elite athletic individuals of other species (e.g. humans), the malleable elements of the O2 transport system may develop to the point that their O2 transport capacities approach that of the least malleable element in the system, the lung. VO2max is very high in such individuals, and appears to be limited by simultaneous failure of all components of the O2 transport system.

Animals↗
PubMed1992

Estimating transit time for capillary blood in selected muscles of exercising animals.

The mean minimal capillary transit time was estimated in muscles of various animals using a combination of physiological and morphometric methods. Radioactive microspheres were injected intravascularly in various animals running on a treadmill at maximum oxygen consumption rate (VO2,max) to label blood flow to individual muscles. The muscles were then removed and preserved by standard methods for electron microscopy. The volume density of mitochondria was measured to assess muscle oxidative capacity. Capillary densities in muscle cross-sections, capillary diameters and tortuosities were incorporated into an estimate of capillary volume per unit muscle mass. Mean capillary transit time (tc) in the exercising muscles was estimated by dividing mass-specific capillary volume by mass-specific blood flow. Estimates of tc ranged from values near 1 s in horse heart and thigh muscles to 0.2 s in duck gastrocnemius. The relationship between muscle blood flow and tc was hyperbolic. The experimental data indicate a limiting value of 0.2 s for transit times at very high blood flows. There was no correlation between tc and body-mass-specific VO2,max.

Animals↗
PubMed1991

Running energetics in the pronghorn antelope.

The pronghorn antelope (Antilocapra americana) has an alleged top speed of 100 km h-1, second only to the cheetah (Acionyx jubatus) among land vertebrates, a possible response to predation in the exposed habitat of the North American prairie. Unlike cheetahs, however, pronghorn antelope are distance runners rather than sprinters, and can run 11 km in 10 min, an average speed of 65 km h-1. We measured maximum oxygen uptake in pronghorn antelope to distinguish between two potential explanations for this ability: either they have evolved a uniquely high muscular efficiency (low cost of transport) or they can supply oxygen to the muscles at unusually high levels. Because the cost of transport (energy per unit distance covered per unit body mass) varies as a predictable function of body mass among terrestrial vertebrates, we can calculate the predicted cost to maintain speeds of 65 and 100 km h-1 in an average 32-kg animal. The resulting range of predicted values, 3.2-5.1 ml O2 kg-1 s-1, far surpasses the predicted maximum aerobic capacity of a 32-kg mammal (1.5 ml O2 kg-1 s-1). We conclude that their performance is achieved by an extraordinary capacity to consume and process enough oxygen to support a predicted running speed greater than 20 ms-1 (70 km h-1), attained without unique respiratory-system structures.

Animals↗
PubMed1989

Total muscle mitochondrial volume in relation to aerobic capacity of horses and steers.

The relationship between maximal oxygen consumption rate (VO2max) and mitochondrial content of skeletal muscles was examined in horses and steers (n = 3 each). Samples of the heart left ventricle, diaphragm, m. vastus medialis, m. semitendinosus, m. cutaneous thoracicus and m. masseter, as well as samples of muscles collected in a whole-body sampling procedure, were analyzed by electron microscopy. VO2max per kilogram body mass was 2.7 x greater in horses than steers. This higher VO2max was in proportion to the higher total volume of mitochondria in horse versus steer muscle when analyzed from the whole-body samples and from the locomotor muscle samples. In non-locomotor muscles, total mitochondrial volume was greater in horses than steers, but not in proportion to their differences in VO2max. The VO2max of the mitochondria was estimated to be close to 4.5 ml O2.ml-1 mitochondria in both species. It is concluded that in a comparison of a highly aerobic to a less aerobic mammalian species of similar body size, a higher oxidative potential may be found in all muscles of the more aerobic species. This greater oxidative potential is achieved by a greater total volume of skeletal muscle mitochondria.

Animals↗
PubMed1988

Skeletal muscle mitochondria: the aerobic gate?

At an animal's maximum aerobic capacity (VO2max), the O2 flowing through the respiratory system is consumed by a functionally exclusive sink, skeletal muscle mitochondria. Thus, O2 consumption will never exceed the muscles O2 demand. If the system is ideally designed, structures upstream to the skeletal muscle O2 sink must be built to insure adequate O2 delivery to the working muscle. There are a number of structure-function solutions available to supply the demanded O2 to the muscle; these have been found to vary, often ontogenetically, with hypoxia, training, etc. But there is one relationship that is invariant: Total O2 uptake can be predicted by the total (active) skeletal muscle mitochondrial volume. In aerobic and sedentary animals, across a range of body sizes, maximum (in vivo) mitochondrial O2 consumption is constant among mammals (at approximately 2000 O2 molecules per square micron of inner mitochondrial membrane per second). Because the volume of mitochondria is one of the most plastic of all respiratory structures, we interpret this relationship as suggesting that skeletal muscle mitochondria alone sets the demand for O2 and, thus, the volume of skeletal muscle mitochondria dictates an animal's maximum aerobic capacity.

Animals↗
PubMed1988

Limitations to aerobic performance in mammals: interaction of structure and demand.

In this paper we have explored the linked series of structures that collectively comprise the respiratory system. In examining each of these structural resistors, some seem to be primarily fixed, for example, the trachea, while others must be primarily variable or adaptable, for example, the cardiovascular system. Those structures that are truly variable will not be maintained with structural capacity in excess of their functional demand. As a consequence, these structures are the ones that may most often appear to be limiting O2 uptake. However, we question under which in vivo circumstances the most plastic steps in the cascade of resistances will impart the single-step limitation to O2 uptake. When reviewed in this context, available experimental evidence suggests that among the most athletic animals (those with the greatest weight-specific VO2), the respiratory resistors are likely tuned rather than dominated by a single-step limitation. Skeletal muscle must set the demand for O2 in exercising animals; hence, the relationship between total skeletal muscle mitochondria and maximum O2 consumption is quantitatively consistent, spanning broad differences in body size and aerobic capacity. Those respiratory structures that are primarily nonadaptable must be built with enough "excess structure" to accommodate potential adaptation in an animal's aerobic capacity during its lifetime. Consequently, the least aerobic animals will always appear to experience a limitation to VO2max in one of the most plastic or adaptable structures. We suggest that the adaptable structures upstream to the muscle mitochondria are built and maintained at a cost-benefit maximum ("structural efficiency") in all species. This differs from the concept of optimal structural design or symmorphosis.

Animals↗
PubMed1985

Estimate of muscle-shortening rate during locomotion.

All skeletal muscle can produce roughly the same maximal cross-sectional force; however, the power (energy X time-1) required to develop and maintain that force increases with increasing contraction velocity. Thus the rate of muscle tension development may be of primary importance in setting the energy demand of contracting muscle. We have estimated the rate of muscle shortening during terrestrial locomotion in mammals as a function of body mass. The rate of muscle shortening of the knee extensors is much faster in small than large mammals, scaling in proportion to the -0.23 power of mass. This exponent suggests a constant body size-independent relation among skeletal muscle: O2 consumption, mitochondria content, myosin ATPase activity, and in vivo shortening velocity.

Animals↗
PubMed1985

Endurance training in humans: aerobic capacity and structure of skeletal muscle.

The adaptation of muscle structure, power output, and mass-specific rate of maximal O2 consumption (VO2max/Mb) with endurance training on bicycle ergometers was studied for five male and five female subjects. Biopsies of vastus lateralis muscle and VO2max determinations were made at the start and end of 6 wk of training. The power output maintained on the ergometer daily for 30 min was adjusted to achieve a heart rate exceeding 85% of the maximum for two-thirds of the training session. It is proposed that the observed preferential proliferation of subsarcolemmal vs. interfibrillar mitochondria and the increase in intracellular lipid deposits are two possible mechanisms by which muscle cells adapt to an increased use of fat as a fuel. The relative increase of VO2max/Mb (14%) with training was found to be smaller by more than twofold than the relative increase in maximal maintained power (33%) and the relative change in the volume density of total mitochondria (+40%). However, the calculated VO2 required at an efficiency of 0.25 to produce the observed mass-specific increase in maximal maintained power matched the actual increase in VO2max/Mb (8.0 and 6.5 ml O2 X min-1 X kg-1, respectively). These results indicate that despite disparate relative changes the absolute change in aerobic capacity at the local level (maintained power) can account for the increase in aerobic capacity observed at the general level (VO2max).

Adipose Tissue↗
PubMed1985

Malleability of skeletal muscle in overcoming limitations: structural elements.

The quantitative structural composition of skeletal muscle tissue shows a wide range of variability among different species of animals and in any one species among muscles with a different function. Moreover, experimental manipulations such as exercise training or chronic electrical stimulation can dramatically change the ultrastructural appearance of the muscles involved. Both in endurance exercise and in chronic electrical stimulation the volume density of mitochondria can be increased greatly (by more than three-fold in the stimulation experiments). This happens without an apparent change of the internal architecture of the mitochondria, since the surface density of the inner mitochondrial membranes remains constant. In situations where both the mitochondrial volume and the maximal rate of oxygen consumption of the muscle tissue are known, these two variables are found to be linearly related. It can be calculated that the 'maximal' oxygen consumption of a unit volume of mitochondria in muscle is close to 5 ml O2 min-1 cm-3 under comparable conditions in man, mouse and a series of African mammals. It is hypothesized that there is a constant volume of oxygen metabolized per unit volume of mitochondria and unit time under limiting conditions in working skeletal muscle tissue. Given the efficiency of muscular energy conversion, this would allow an estimate of the potential for aerobic power production of a muscle from measurement of its volume density of mitochondria.

Animals↗