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Biomedical subjects

H Hoppeler

Publications and source records attributed to H Hoppeler.

At least 19 recordsLinked to original sources

Fiber type dependent upregulation of human skeletal muscle UCP2 and UCP3 mRNA expression by high-fat diet.

OBJECTIVE: To test the hypothesis that consumption of a high-fat diet leads to an increase in UCP mRNA expression in human skeletal muscle. In a group of endurance athletes, with a range in fiber type distribution, we hypothesized that the effect of the high-fat diet on UCP2 and UCP3 mRNA expression is more pronounced in muscle fibers which are known to have a high capacity to shift from carbohydrate to fat oxidation (type IIA fibers). DESIGN: Ten healthy trained athletes (five males, five females) consumed a low-fat diet (17+/-0.9 en% of fat) and high-fat diet (41.4+/-1.4 en% fat) for 4 weeks, separated by a 4 week wash-out period. Muscle biopsies were collected at the end of both dietary periods. MEASUREMENTS: Using RT-PCR, levels of UCP2 and UCP3 mRNA expression were measured and the percentage of type I, IIA and IIB fibers were determined using the myofibrillar ATPase method in all subjects. RESULTS: UCP3L mRNA expression tended to be higher on the high-fat diet, an effect which reached significance when only males were considered (P=0.037). Furthermore, diet-induced change in mRNA expression of UCP3T (r: 0.66, P=0.037), UCP3L (r: 0.61, P=0.06) and UCP2 (r: 0.70, P=0.025), but not UCP3S, correlated significantly with percentage dietary fat on the high-fat diet. Plasma FFA levels were not different during the two diets. Finally, the percentage of type IIA fibers was positively correlated with the diet-induced change in mRNA expression for UCP2 (r: 0.7, P=0.03), UCP3L (r: 0.73, P=0.016) and UCP3T (r: 0.68, P=0.03) but not with UCP3S (r: 0.06, NS). CONCLUSION: UCP2 and UCP3 mRNAs are upregulated by a high-fat diet. This upregulation is more pronounced in humans with high proportions of type IIA fibers, suggesting a role for UCPs in lipid utilization.

Adult↗

Training high--living low: changes of aerobic performance and muscle structure with training at simulated altitude.

This study was undertaken to test the hypothesis that endurance training in hypoxia is superior to training of the same intensity in normoxia. To avoid adaptation to hypoxia, the subjects lived under normoxic conditions when not training. A secondary objective of this study was to compare the effect of high- vs. moderate-intensity training on aerobic performance variables. Thirty-three men without prior endurance training underwent a cycle ergometer training of 6 weeks, 5 d/week, 30 minutes/d. The subjects were assigned to 4 groups, N-high, N-low, H-high and H-low based on the training criteria normoxia (N; corresponding to a training altitude of 600 m), vs. hypoxia (H; training altitude 3850 m) and intensity (high; corresponding to 80% and low: corresponding to 67% of VO2max). VO2max measured in normoxia increased between 8.5 to 11.1%, independent of training altitude or intensity. VO2max measured in hypoxia increased between 2.9 and 7.2%. Hypoxia training resulted in significantly larger increases than normoxia training. Maximal power that subjects could maintain over a thirty-minute period (measured in normoxia or hypoxia) increased from 12.3 - 26.8% independent of training altitude. However, subjects training at high intensity increased performance more than subjects training at a low intensity. Muscle volume of the knee-extensors as measured by magnetic resonance imaging increased significantly in the H-high group only (+ 5.0%). Mitochondrial volume density measured by EM-morphometry in biopsy samples of m. vastus lat. increased significantly in all groups with the highest increase seen in the H-high group (+ 59%). Capillary length density increased significantly in the H-high group only (+ 17.2%). The main finding of this study is that in previously untrained people, training in hypoxia while living at low altitude increases performance in normoxia to the same extent as training in normoxia, but leads to larger increases of aerobic performance variables when measured under hypoxic conditions. Training intensity had no effect on the gain of VO2max. On the level of skeletal muscle tissue, the combination of hypoxia with high training intensity constitutes the most effective stimulus for increasing muscle oxidative capacity.

Acclimatization↗

Postexercise fat intake repletes intramyocellular lipids but no faster in trained than in sedentary subjects.

The hypotheses that postexercise replenishment of intramyocellular lipids (IMCL) is enhanced by endurance training and that it depends on fat intake were tested. Trained and untrained subjects exercised on a treadmill for 2 h at 50% peak oxygen consumption, reducing IMCL by 26-22%. During recovery, they were fed 55% (high fat) or 15% (low fat) lipid energy diets. Muscle substrate stores were estimated by (1)H (IMCL)- and (13)C (glycogen)-magnetic resonance spectroscopy in tibialis anterior muscle before and after exercise. Resting IMCL content was 71% higher in trained than untrained subjects and correlated significantly with glycogen content. Both correlated positively with indexes of insulin sensitivity. After 30 h on the high-fat diet, IMCL concentration was 30-45% higher than preexercise, whereas it remained 5-17% lower on the low-fat diet. Training status had no significant influence on IMCL replenishment. Glycogen was restored within a day with both diets. We conclude that fat intake postexercise strongly promotes IMCL repletion independently of training status. Furthermore, replenishment of IMCL can be completed within a day when fat intake is sufficient.

Adult↗

Molecular adaptations in human skeletal muscle to endurance training under simulated hypoxic conditions.

This study was performed to explore changes in gene expression as a consequence of exercise training at two levels of intensity under normoxic and normobaric hypoxic conditions (corresponding to an altitude of 3,850 m). Four groups of human subjects trained five times a week for a total of 6 wk on a bicycle ergometer. Muscle biopsies were taken, and performance tests were carried out before and after the training period. Similar increases in maximal O(2) uptake (8.3-13.1%) and maximal power output (11.4-20.8%) were found in all groups. RT-PCR revealed elevated mRNA concentrations of the alpha-subunit of hypoxia-inducible factor 1 (HIF-1) after both high- (+82.4%) and low (+78.4%)-intensity training under hypoxic conditions. The mRNA of HIF-1alpha(736), a splice variant of HIF-1alpha newly detected in human skeletal muscle, was shown to be changed in a similar pattern as HIF-1alpha. Increased mRNA contents of myoglobin (+72.2%) and vascular endothelial growth factor (+52.4%) were evoked only after high-intensity training in hypoxia. Augmented mRNA levels of oxidative enzymes, phosphofructokinase, and heat shock protein 70 were found after high-intensity training under both hypoxic and normoxic conditions. Our findings suggest that HIF-1 is specifically involved in the regulation of muscle adaptations after hypoxia training. Fine-tuning of the training response is recognized at the molecular level, and with less sensitivity also at the structural level, but not at global functional responses like maximal O(2) uptake or maximal power output.

Acyl-CoA Dehydrogenase↗

Muscle tissue adaptations to hypoxia.

This review reports on the effects of hypoxia on human skeletal muscle tissue. It was hypothesized in early reports that chronic hypoxia, as the main physiological stress during exposure to altitude, per se might positively affect muscle oxidative capacity and capillarity. However, it is now established that sustained exposure to severe hypoxia has detrimental effects on muscle structure. Short-term effects on skeletal muscle structure can readily be observed after 2 months of acute exposure of lowlanders to severe hypoxia, e.g. during typical mountaineering expeditions to the Himalayas. The full range of phenotypic malleability of muscle tissue is demonstrated in people living permanently at high altitude (e.g. at La Paz, 3600-4000 m). In addition, there is some evidence for genetic adaptations to hypoxia in high-altitude populations such as Tibetans and Quechuas, who have been exposed to altitudes in excess of 3500 m for thousands of generations. The hallmark of muscle adaptation to hypoxia in all these cases is a decrease in muscle oxidative capacity concomitant with a decrease in aerobic work capacity. It is thought that local tissue hypoxia is an important adaptive stress for muscle tissue in exercise training, so these results seem contra-intuitive. Studies have therefore been conducted in which subjects were exposed to hypoxia only during exercise sessions. In this situation, the potentially negative effects of permanent hypoxic exposure and other confounding variables related to exposure to high altitude could be avoided. Training in hypoxia results, at the molecular level, in an upregulation of the regulatory subunit of hypoxia-inducible factor-1 (HIF-1). Possibly as a consequence of this upregulation of HIF-1, the levels mRNAs for myoglobin, for vascular endothelial growth factor and for glycolytic enzymes, such as phosphofructokinase, together with mitochondrial and capillary densities, increased in a hypoxia-dependent manner. Functional analyses revealed positive effects on V(O(2)max) (when measured at altitude) on maximal power output and on lean body mass. In addition to the positive effects of hypoxia training on athletic performance, there is some recent indication that hypoxia training has a positive effect on the risk factors for cardiovascular disease.

Acclimatization↗

Effect of diet on the replenishment of intramyocellular lipids after exercise.

BACKGROUND: Muscle triglycerides are important as a source of energy and in relation to metabolic sensitivity. However, the classic biopsy method does not distinguish intra- from extracellular fat, and their regulation by exercise and diet is largely unknown. Magnetic resonance spectroscopy (MRS) is available to assess the intramyocellular lipid (IMCL) pool non-invasively in humans. AIM OF THE STUDY: The aim of this work was to use sequential MRS measurements of IMCL and glycogen to explore the role of three levels of dietary fat on the replenishment of these energy stores after exercise. METHODS: Following 2 h of exercise, two subjects (S1, S2) were fed one of three diets (15%, 40% or 70% fat energy), each on a separate occasion. IMCL and glycogen were measured by MRS in the tibialis anterior muscle before, after exercise, and at 10 and at 32 h of recovery. RESULTS: Initial IMCL concentration (mmol.kg-1: 3.0 in S1 and 1.8 in S2) was reduced to 70% after exercise. The rate of replenishment was minimal with the low-fat (mmol.kg-1.24 h-1: 0.7 and 0.0) and much higher with both higher fat diets (mmol.kg-1.24 h-1: 3.1 and 3.2 in S1, 0.7 and 0.9 in S2). Glycogen and IMCL replenishments were inversely correlated. CONCLUSIONS: IMCL and glycogen can vary acutely in response to diet after exercise. Studies are needed to determine if such variations occur within the range of ordinary diets and to clarify the functional significance of IMCL in differently active individuals.

Adult↗

Structural and functional limits for oxygen supply to muscle.

Environmental oxygen is transported by the respiratory cascade to the site of oxidation in active tissues. Under conditions of heavy exercise it is ultimately the working skeletal muscle cells that determine the aerobic demand as over 90% of energy is spent in muscle cells. Oxygen is transported in the circulation bound to haemoglobin of erythrocytes while substrates are transported in the plasma. The supply of oxygen must be continuous because there are only minimal oxygen stores in the body of most mammalian species while substrates are stored in significant quantities both within muscle cells as also in organismic substrate stores. The pathways for oxygen and substrates ultimately converge in muscle mitochondria. In mammals, a structural limitation of carbohydrate and lipid transfer from the microvascular system to muscle cells is reached at a moderate work intensity (i.e. at less than 50% of VO2max). At higher work rates intracellular substrate stores must be used for oxidation. It is therefore not surprising to find larger intramyocellular carbohydrate and lipid stores in 'athletic' species as well as in endurance-trained human athletes. The transfer limitations for carbohydrates and lipids presumably occur on the level of the sarcolemma. These findings imply that the design of the respiratory cascade from lungs to muscle mitochondria has to be analysed with regard to satisfying the demand for oxygen of the working muscle cells. Substrate stores are replenished at low flux rates during periods of rest and are stored intracellularly. They are therefore locally available to mitochondria for aerobic work at high intensities.

Animals↗

Effects of creatine supplementation on muscle weakness in patients with rheumatoid arthritis.

BACKGROUND AND OBJECTIVES: Patients with rheumatoid arthritis (RA) frequently suffer from muscle weakness. Oral administration of creatine has been shown to improve muscle strength in healthy subjects. The objective of this study was to examine the effect of oral creatine supplementation on muscle weakness, disease activity and activities of daily living in patients with RA. METHODS: During a period of 3 weeks, 12 patients with RA were treated with creatine monohydrate (20 g/day for 5 days followed by 2 g/day for 16 days). They were examined on entry and at the end of the study. The patients were investigated clinically, blood and urine samples were obtained, muscle biopsies were performed before and after treatment, muscle strength was determined, and self-administered patient questionnaires were completed. RESULTS: From all patients we were able to obtain full clinical and questionnaire data, while biopsies were taken from 12 patients at the start and from nine patients at the end of the study. Muscle strength, as determined by the muscle strength index, increased in eight of 12 patients. In contrast, physical functional ability and disease activity did not change significantly. The creatine concentration in serum and skeletal muscle increased significantly, while creatine phosphate and total creatine did not increase in skeletal muscle. The skeletal muscle creatine content was associated with muscle strength at baseline but not after administration of creatine. The changes in muscle strength were not associated with the changes in skeletal muscle creatine or creatine phosphate. CONCLUSION: Although the skeletal muscle creatine content and muscle strength increased with creatine administration in some patients with RA, a clear clinical benefit could not be demonstrated for this treatment when the patients were considered as one group.

Adult↗

Eccentric ergometry: increases in locomotor muscle size and strength at low training intensities.

Lengthening (eccentric) muscle contractions are characterized by several unusual properties that may result in unique skeletal muscle adaptations. In particular, high forces are produced with very little energy demand. Eccentrically trained muscles gain strength, but the specific nature of fiber size and composition is poorly known. This study assesses the structural and functional changes that occur to normal locomotor muscle after chronic eccentric ergometry at training intensities, measured as oxygen uptake, that do not influence the muscle when exercised concentrically. Male subjects trained on either eccentric or concentric cycle ergometers for 8 wk at a training intensity starting at 54% and ending at 65% of their peak heart rates. The isometric leg strength increased significantly in the eccentrically trained group by 36%, as did the cross-sectional area of the muscle fiber by 52%, but the muscle ultrastructure remained unchanged. There were no changes in either fiber size, composition, or isometric strength in the concentrically trained group. The responses of muscle to eccentric training appear to be similar to resistance training.

Adult↗

Structural changes in arm muscles after microgravity.

Disuse muscle atrophy is a well-known consequence of spaceflight. However, most of the available muscle data concern lower limb muscles of rats and primates exposed to microgravity aboard Russian Cosmos biosatellites and American Space Shuttles. The purpose of our study was, therefore, to provide information concerning the effects of a 14-day spaceflight on two upper limb muscles of rhesus monkeys (Macaca mulatta). Our objective was to compare structural adaptations after 14 days of microgravity in a slow-twitch extensor muscle, i.e., the triceps, with a fast-twitch flexor muscle, i.e., the biceps. We hypothesize that muscle responses will be muscle specific, i.e., slow will differ from fast muscles, flexors will differ from extensors, and arms will differ from legs.

Animals↗

Vascular growth in hypoxic skeletal muscle.

The critical role of skeletal muscle capillaries is the supply of oxygen to skeletal muscle fibers during conditions of maximal aerobic work. The supply of substrates under these conditions is not limited by the vascular bed but rather by the capacity of the sarcolemmal transporter systems. Because of this dominant role of oxygen supply in muscle tissue, hypoxia has generally been considered to be an important stimulus for capillary neo-formation in skeletal muscle. Early morphometric work seemed to indicate that animals exposed to permanent hypoxia had in fact a significantly improved vascular supply in muscle tissue. Later work questioned these early findings and it was concluded that hypoxia per se was not a sufficient stimulus for capillary neo-formation but that additional stimuli such as cold-exposure needed to be present. In humans exposed to severe hypoxia during simulated or real ascents to Mt. Everest an increase in capillary density was in fact found. However, this increase could be shown to result from a reduction of muscle fiber volume and not from capillary growth. Broadly compatible results were obtained in animal experiments in which changes in capillarity were assessed in muscles with limited blood supply which were exposed to chronic electrical stimulation. Recently we have shown that endurance exercise training in humans results in a rise in mRNA of vascular endothelial growth factor (VEGF) only when carried out vigorously and in hypoxia. These results indicate that molecular techniques will allow in the near future to delineate the role played by hypoxia in capillary neo-formation.

Altitude↗

Carnitine homeostasis in patients with rheumatoid arthritis.

Myopathy is a frequent finding in patients with rheumatoid arthritis (RA). Since carnitine is important for skeletal muscle energy metabolism, carnitine metabolism was investigated in patients with RA and myopathy. Muscle strength was estimated by determination of a muscle strength index (MSI) which is derived from isometric measurements of muscle strength at knees and elbows. Carnitine was determined by a radioenzymatic method and 3-methylhistidine by high-performance liquid chromatography. In comparison to control subjects, patients had a reduced MSI. Both the 24-h creatinine and 3-methylhistidine excretions were reduced in patients. The plasma carnitine pool was not different between patients and control subjects, except for a higher long-chain acylcarnitine concentration in patients. Urinary excretion of carnitine was decreased in patients, also after normalization for body weight. Accordingly, renal carnitine clearance and excretion fraction were both decreased in patients. Skeletal muscle free- and total carnitine levels were increased in patients, whereas the long-chain acylcarnitine content was markedly decreased. The total skeletal muscle carnitine content showed a negative correlation with the MSI and no association with disease activity. Carnitine deficiency does not explain reduced skeletal muscle strength in patients with RA. Decreased renal carnitine excretion in patients is most likely due to reduced carnitine biosynthesis, leading to more efficient tubular carnitine reabsorption for maintaining the carnitine body stores.

Adult↗

Skeletal muscle substrate metabolism.

Endurance power of muscles is determined largely by the capacities to oxidize substrates in mitochondria in the process of making ATP by oxidative phosphorylation. This review explores physiological and morphological factors that may cause limitation of carbohydrate and fat utilization by muscle cells. The pathways for oxygen and substrates converge in muscle mitochondria. In mammals, a structural limitation of carbohydrate and lipid transfer from the microvascular system to muscle cells is reached at a moderate work intensity (that is, at 40-50% of VO2max). At higher work rates intracellular substrate stores must be used for oxidation. Because of the importance of these intracellular stores for aerobic work we find larger intramyocellular substrate stores in endurance trained athletes. The transfer limitations for carbohydrates and lipids on the level of the sarcolemma implies that the design of the respiratory cascade from lungs to muscle mitochondria reflects primarily oxygen demand.

Animals↗

Muscle structure with low- and high-fat diets in well-trained male runners.

Endurance capacity, maximal oxygen uptake capacity (VO2max) and quantitative muscle ultrastructural composition was analyzed in 7 well-trained male runners (mean age 37.1 years, mean VO2max 60 ml/min/kg) after a one month period of a low-fat diet (dietary fat intake 18.4% and a similar period of a high-fat diet (dietary fat intake 40.6%). Between these two interventional periods a washout period of one month was interspersed in which the nutritional fat content was approx. 32%; close to the average American Diet. During all three periods protein content of the nutrition was kept nearly constant at 15%. After the high-fat diet time to exhaustion in the endurance test increased significantly by 21% while VO2max remained unchanged. Muscle mitochondrial volume density remained unchanged while the intramyocellular fat content increased by 60%. Due to large interindividual differences in this variable this difference did not become statistically significant. While some 20% of the mitochondria are located in a subsarcolemmal location, only 10% of the lipid stores are associated with these mitochondria. Less than 2% of the mitochondrial outer surface are in contact with lipid droplets whereas 25-35% of the lipid surface is in contact with mitochondria. None of these variables is significantly altered after a high-fat diet. It is concluded that the change in endurance capacity of the subjects cannot be explained based on the structural changes observed in skeletal muscle tissue. This may be related to methodological problems associated with the determination of intramyocellular fat content.

Adult↗

Creatine supplementation--part I: performance, clinical chemistry, and muscle volume.

PURPOSE: Our purpose was to study the effects and side effects of creatine (Cr) supplementation on high-intensity, short-term muscle work, on biochemical parameters related to Cr metabolism in blood and urine, and on muscle volume of the lower limb muscles. METHODS: A cycling ergometer was used in a double-blind, cross-over study on 10 well-trained male physical education students to measure physical performance with 10 repetitive ergometer sprints (6-s duration, 30-s rest) before and after supplementation (5 d, 20 g x d(-1), washout period 61 +/- 8 d, mean +/- SEM, minimum 28 d) with Cr or placebo. Before and after supplementation, blood and urine were taken and the muscle volume of the lower limb was determined by magnetic resonance imaging (MRI). RESULTS: A significant (P << 0.05) increase in performance (+7%) at the end [4-6 s] of the later sprints (4-7 and 8-10) was observed combined with a lower production of blood lactate (-1 mmol x L(-1)) with Cr supplementation. The concentration of Cr was increased significantly in urine (P < 0.001) and serum (P = 0.005), whereas creatinine (Crn) was increased in serum (P < 0.001). Crn in urine and Crn clearance did not change significantly with Cr intake. There were no significant changes in the analyzed blood enzyme activities. A significant gain of body weight (pre-Cr 76.5 +/- 1.7 kg to 77.9 +/- 1.7 kg post-Cr) with Cr supplementation was measured, but no accompanying increase of muscle mass in a limited volume of the lower limb was observed by MRI. CONCLUSION: Cr supplementation is effective in improving short-term performance, and the methods used show no detrimental side effects with this supplementation protocol.

Adult↗

Creatine supplementation--part II: in vivo magnetic resonance spectroscopy.

PURPOSE: Our purpose was to study effects of creatine (Cr) supplementation on muscle metabolites noninvasively by means of magnetic resonance spectroscopy (MRS) before and after supplementation with Cr or placebo. METHODS: 1H-MRS was used in a comprehensive, double-blind, cross-over study in 10 volunteers to measure Cr in m. tibialis anterior and m. rectus femoris at rest. PCr/ATP was observed in m. quadriceps femoris by 31P-MRS at rest and after exercise. RESULTS: A significant increase in total Cr was observed with Cr intake in m. tibialis anterior (+9.6 +/- 1.7%, P = 0.001) and in m. rectus femoris (+18.0 +/- 1.8%, P < 0.001). PCr/ATP showed a significant increase (+23.9 +/- 2.3%, P < 0.001) in m. quadriceps femoris at rest with Cr supplementation. Post-Cr supplementation recovery rates from exercise were significantly lower (k = 0.029 s(-1), P < 0.01) compared with postplacebo consumption (k = 0.034 s(-1)) and presupplementation (k = 0.037 s(-1)). However, higher levels of PCr/ATP at rest compensate for this reduction of the recovery rate after Cr supplementation. The increase of PCr/ATP determined by 31P-MRS correlates with the increase of Cr observed by 1H-MRS (r = 0.824, P < 0.001). CONCLUSION: Noninvasive observation of Cr and PCr after Cr supplementation shows an increase in a muscle specific manner. Higher preexercise levels of PCr/ATP at rest compensate for significantly slower recovery rates of PCr/ATP after Cr supplementation.

Adenosine Triphosphate↗

Chronic eccentric exercise: improvements in muscle strength can occur with little demand for oxygen.

Eccentric contractions, the lengthening of muscle while producing force, are a common part of our everyday movements. This study presents a challenge to the accepted notion that eccentric work causes obligatory muscle injury while demonstrating that an increase in muscle strength, via eccentric work, can occur with little demand for oxygen. Nine healthy subjects, ages 18-34, were randomly placed in either an eccentric or a concentric training group. Both groups trained for 6 wk while progressively increasing training frequency and duration. Significant gains in isometric leg strength were seen in the eccentrically trained subjects only. While training, the oxygen consumption required to do the eccentric work was equal to or less than that required to do the concentric work. The results demonstrate that by progressively increasing the eccentric work rate, significant isometric strength gains can be made without muscle injury and with minimal increase in metabolic demand for oxygen. The potential clinical implications of an eccentric training program that uncouples skeletal muscle strength improvements from the demand for oxygen are alluring.

Adolescent↗

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↗