Maximal metabolic rate (MMR) of mammals scales differently from basal metabolic rate (BMR). This is first shown by scrutinizing data reported on exercise-induced
V
̇
O
2
max in 34 eutherian mammalian ...species covering a body mass range of 7
g–500
kg.
V
̇
O
2
max was found to scale with the 0.872 (±0.029, 95% confidence limits 0.813–0.932) power of body mass which is significantly different from the 3/4 power reported for basal metabolic rate. The aerobic scope is higher in athletic than non-athletic species, and it is also higher in large than in small species. Integrated structure-function studies on a subset of 11 species (body mass 20
g–450
kg) show that the variation of
V
̇
O
2
max with body size is tightly associated with the aerobic capacity of the locomotor musculature: the scaling exponents for
V
̇
O
2
max, the total volume of mitochondria, and the volume of capillaries are nearly identical. The higher
V
̇
O
2
max of athletic species is tightly linked to proportionally larger mitochondrial and capillary volumes in animals of the same size class. As a result
V
̇
O
2
max is linearly related to both total mitochondrial and capillary erythrocyte volumes. We conclude that the scaling of maximal metabolic rate is explained by features and mechanisms different from those determining basal metabolic rate.
Following tendon tear, the musculo-tendinous unit retracts permanently, looses muscle fibre volume and is infiltrated with fat. This is currently considered to be an unexplained degenerative process. ...In a sheep model of chronic tendon tear with delayed tendon repair (35 weeks after tendon release), we studied the nature of these muscle changes in eight experimental animals. At sacrifice (75 weeks after tendon release) the muscle had retracted by 1.7
±
0.5 cm (9% of entire length,
P<0.0001), the pennation angle had increased from 22
±
2.5° to 50
±
11° (
P<0.0001) and the mean muscle fibre length had shortened from 32
±
3 to 16
±
5 mm (50%,
P<0.0001). In electron and light microscopy, we found essentially normal muscle fibres with an unaltered fibre diameter and myofibrillar structure, while interstitial fat and fibrous tissue had increased from 3.9% to 45.9% (
P<0.0001) of the muscle volume.
Geometric modelling showed that the increase of the pennation angle separates the muscle fibre bundles mechanically like limbs of a parallelogram. Infiltrating fat cells fill the created space between the reoriented muscle fibres which may be quantitatively calculated without affecting the structural properties of the muscle cells. Fatty infiltration is therefore not seen as a degenerative process but a necessary rearrangement of the tissue after macroarchitectural changes caused by musculo-tendinous retraction.
Mitochondria in skeletal muscle tissue can undergo rapid and characteristic changes as a consequence of manipulations of muscle use and environmental conditions. Endurance exercise training leads to ...increases of mitochondrial volume of up to 50% in training interventions of a few weeks in previously untrained subjects. Additionally, a shift of substrate metabolism toward a higher reliance on lipids is observed, structurally reflected as a doubling of the intramyocellular lipid content. A similar increase in intramyocellular lipids without an increase in mitochondrial volume is observed as a consequence of a high-fat diet. Strength training has a major impact on muscle myofibrillar volume, however the mitochondrial compartment appears relatively unchanged. Bedrest and microgravity conditions lead to losses of both myofibrillar and mitochondrial volume, likely as a consequence of the decrease in metabolic and mechanical stress on muscle tissue. Permanent severe hypoxia leads to a loss of muscle mass and muscle oxidative capacity; however, hypoxia signaling events are triggered, which lead to distinct reprogramming phenomena of the transcriptome of the muscle cells. The molecular mechanisms that orchestrate the plasticity of skeletal muscle mitochondria are just beginning to unfold. The present data indicate that transcriptional events largely contribute to increases in mitochondrial mass in human skeletal muscle with endurance training. Expression of mitochondrial proteins from the nuclear and mitochondrial genomes is coordinated and involves the nuclear-encoded transcription factors NRF-1 and TFAM. Transcription of genes encoding the mitochondrial proteins involved in beta oxidation can be regulated separately from the genes of the Krebs cycle and the respiratory chain. Transcription factors AP-1 and PPARalpha/gamma and the protein kinase AMPK are signaling molecules that transduce the metabolic and mechanical factors sensed during endurance training into the complex transcriptional adaptations of mitochondrial proteins.
Introduction
We aimed to manipulate physiological determinants of severe exercise performance. We hypothesized that (1) beta-alanine supplementation would increase intramuscular carnosine and ...buffering capacity and dampen acidosis during severe cycling, (2) that high-intensity interval training (HIT) would enhance aerobic energy contribution during severe cycling, and (3) that HIT preceded by beta-alanine supplementation would have greater benefits.
Methods
Sixteen active men performed incremental cycling tests and 90-s severe (110 % peak power) cycling tests at three time points: before and after oral supplementation with either beta-alanine or placebo, and after an 11-days HIT block (9 sessions, 4 × 4 min), which followed supplementation. Carnosine was assessed via MR spectroscopy. Energy contribution during 90-s severe cycling was estimated from the O
2
deficit. Biopsies from
m. vastus lateralis
were taken before and after the test.
Results
Beta-alanine increased leg muscle carnosine (32 ± 13 %,
d
= 3.1). Buffering capacity and incremental cycling were unaffected, but during 90-s severe cycling, beta-alanine increased aerobic energy contribution (1.4 ± 1.3 %,
d
= 0.5), concurrent with reduced O
2
deficit (−5.0 ± 5.0 %,
d
= 0.6) and muscle lactate accumulation (−23 ± 30 %,
d
= 0.9), while having no effect on pH. Beta-alanine also enhanced motivation and perceived state during the HIT block. There were no between-group differences in adaptations to the training block, namely increased buffering capacity (+7.9 ± 11.9 %,
p
= 0.04,
d
= 0.6,
n
= 14) and glycogen storage (+30 ± 47 %,
p
= 0.04,
d
= 0.5,
n
= 16).
Conclusions
Beta-alanine did not affect buffering considerably, but has beneficial effects on severe exercise metabolism as well as psychological parameters during intense training phases.
1 Département de Physiologie et des Explorations Fonctionnelles, Hôpital Civil, and Faculté de Médicine, Institut de Physiologie, Unité Propre de Recherche de l'Enseignement Supérieur Équipe ...d'Accueil 3072, Strasbourg, France; 2 Institute of Anatomy, University of Bern, Bern, Switzerland; 3 Laboratoire d'Etudes Physiologiques à l'Exercice, Département des Sciences du Sport et de l'Exercice, Équipe d'Accueil 3872, Université d'Evry Val d'Essonne, Evry, France; and 4 Service de Cardiologie, Hôpitaux Civils de Colmar, Colmar, France
Submitted 22 June 2005
; accepted in final form 27 July 2005
This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia Nor group; n = 9; maximal oxygen uptake ( O 2 max ) = 61.5 ± 1.1 ml·kg 1 ·min 1 or intermittently in hypoxia (Hyp group; n = 9; O 2 max = 64.2 ± 1.2 ml·kg 1 ·min 1 ). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (2440 min) training sessions, performed either in normoxia inspired O 2 fraction (F I O 2 ) = 20.9% or in normobaric hypoxia (F I O 2 = 14.5%). Before and after training, all athletes realized 1 ) a normoxic and hypoxic incremental test to determine O 2 max and ventilatory thresholds (first and second ventilatory threshold), and 2 ) an all-out test at the pretraining minimal velocity eliciting O 2 max to determine their time to exhaustion (T lim ) and the parameters of O 2 uptake ( O 2 ) kinetics. Only the Hyp group significantly improved O 2 max (+5% at both F I O 2 , P < 0.05), without changes in blood O 2 -carrying capacity. Moreover, T lim lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of O 2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged O 2 max (+1%, nonsignificant), T lim (+10%, nonsignificant), and O 2 kinetics. In addition, T lim improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including O 2 max or O 2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.
maximal oxygen uptake; time to exhaustion; competitive endurance runners
Address for reprint requests and other correspondence: J. Lonsdorfer, Hôpital de la Robertsau, 83 rue Himmerich, BP 426, 67091 Strasbourg Cedex, France (e-mail: jeanlonsdorfer{at}hotmail.fr )
A prolonged sojourn above 5500 m induces muscle deterioration and accumulation of lipofuscin in Caucasians, probably because of overproduction of reactive oxygen species (ROS). Because Sherpas, who ...live at high altitude, have very limited muscle damage, it was hypothesized that Himalayan natives possess intrinsic mechanisms protecting them from oxidative damage. This possibility was investigated by comparing the muscle proteomes of native Tibetans permanently residing at high altitude, second‐generation Tibetans born and living at low altitude, and Nepali control subjects permanently residing at low altitude, using 2D gel electrophoresis and mass spectrometry. Seven differentially regulated proteins were identified: glutathione‐S‐transferase P1‐1, which was 380% and 50% overexpressed in Tibetans born and living at high and low altitude, respectively; Δ2‐enoyl‐CoA‐hydratase, which was up‐regulated in both Tibetan groups; glyceraldehyde‐3‐phosphate dehydrogenase and lactate dehydrogenase, which were both slightly down‐regulated in Tibetans born and living at high altitude; phosphoglycerate mutase, which was 50% up‐regulated in the native Tibetans; NADH‐ubiquinone oxidoreductase, slightly overexpressed in Tibetans born and living at high altitude; and myoglobin, which was overexpressed in both Tibetan groups. We concluded that Tibetans at high altitude, and to some extent, those born and living at low altitude, are protected from ROS‐induced tissue damage and possess specific metabolic adaptations.
This review reports on the collaborative efforts of the Department of Physiology of the University of Geneva headed by Paolo Cerretelli, the Research Institute at the Federal School of Physical ...Education in Magglingen and the Department of Anatomy of the University of Bern to elucidate the functional and structural conditions for and consequences of climbing successfully at altitudes in excess of 8000 m. Using a combination of physiological whole body measurements with biochemical, histochemical and morphometric analyses of muscle biopsy samples we were able to establish specific phenotypical alterations of muscle tissue exposed to extreme hypoxia and stress for prolonged periods of time. The decline in aerobic work capacity could be shown to be a consequence of a loss of muscle mass as well as of muscle tissue oxidative capacity whereby muscle capillarity was found to be maintained. The degradation of muscle tissue was further characterized by an increase in muscle lipofuscin. The latter is believed to be the consequence of lipid peroxidation eventually related to mitochondrial loss. Current work ensuing from our long-term collaboration suggests that Sherpas might be protected against the damaging effect of hypoxia by antioxidant mechanisms protecting their muscles under the conditions of extreme altitude.
Supplementation with beta-alanine may have positive effects on severe-intensity, intermittent, and isometric strength-endurance performance. These could be advantageous for competitive alpine skiers, ...whose races last 45 to 150 s, require metabolic power above the aerobic maximum, and involve isometric muscle work. Further, beta-alanine supplementation affects the muscle force-frequency relationship, which could influence explosiveness. We explored the effects of beta-alanine on explosive jump performance, severe exercise energy metabolism, and severe-intensity ski-like performance.
Nine male elite alpine skiers consumed 4.8 g/d beta-alanine or placebo for 5 weeks in a double-blind fashion. Before and after, they performed countermovement jumps (CMJ), a 90-s cycling bout at 110% VO2max (CLT), and a maximal 90-s box jump test (BJ90).
Beta-alanine improved maximal (+7 ± 3%, d = 0.9) and mean CMJ power (+7 ± 2%, d = 0.7), tended to reduce oxygen deficit (-3 ± 8%, p = .06) and lactate accumulation (-12 ± 31%) and enhance aerobic energy contribution (+1.3 ± 2.9%, p = .07) in the CLT, and improved performance in the last third of BJ90 (+7 ± 4%, p = .02). These effects were not observed with placebo.
Beta-alanine supplementation improved explosive and repeated jump performance in elite alpine skiers. Enhanced muscle contractility could possibly explain improved explosive and repeated jump performance. Increased aerobic energy production could possibly help explain repeated jump performance as well.
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