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

1985 ◽  
Vol 59 (2) ◽  
pp. 320-327 ◽  
Author(s):  
H. Hoppeler ◽  
H. Howald ◽  
K. Conley ◽  
S. L. Lindstedt ◽  
H. Claassen ◽  
...  

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).

1989 ◽  
Vol 66 (2) ◽  
pp. 695-703 ◽  
Author(s):  
K. J. Mikines ◽  
B. Sonne ◽  
P. A. Farrell ◽  
B. Tronier ◽  
H. Galbo

Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] were subjected to three sequential hyperinsulinemic euglycemic clamps 15 h after having performed their last training session (T). Results were compared with findings in seven untrained subjects (VO2max 44 +/- 2 ml.min-1.kg-1) studied both at rest (UT) and after 60 min of bicycle exercise at 150 W (UT-ex). In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Furthermore, responsiveness was higher (P less than 0.05) in T than in UT-ex. Insulin-stimulated O2 uptake and maximal glucose oxidation rate were higher in T than in UT and UT-ex. Insulin-stimulated conversion or glucose to glycogen and muscle glycogen synthase was higher in T than in UT and UT-ex. However, glycogen storage in vastus lateralis muscle was found only in UT-ex. No change in any glucoregulatory hormone or metabolite could explain the increased insulin action in trained subjects. It is concluded that physical training induces an adaptive increase in insulin responsiveness of whole-body glucose uptake, which does not reflect increased glycogen deposition in muscle.(ABSTRACT TRUNCATED AT 250 WORDS)


2007 ◽  
Vol 103 (1) ◽  
pp. 177-183 ◽  
Author(s):  
Andrew W. Subudhi ◽  
Andrew C. Dimmen ◽  
Robert C. Roach

To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% FiO2) and acute hypoxic (Hypox: 12% FiO2) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (μM) changes of oxy- and deoxyhemoglobin (Δ[O2Hb], Δ[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Δ[THb] = Δ[O2Hb] + Δ[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (α = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Powerpeak; increased (inc) Δ[O2Hb], inc. Δ[HHb], inc. Δ[THb]}, but fell from 75 to 100% Powerpeak {decreased (dec) Δ[O2Hb], inc. Δ[HHb], no change Δ[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Δ[O2Hb], inc. Δ[HHb]), whereas Δ[THb] again rose up to 75% Powerpeak and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Δ[O2Hb], inc. Δ [HHb], inc. Δ[THb]), although Δ[O2Hb] was unchanged between 75 and 100% Powerpeak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Lejun Wang ◽  
Yuting Wang ◽  
Aidi Ma ◽  
Guoqiang Ma ◽  
Yu Ye ◽  
...  

The increased popularization of cycling has brought an increase in cycling-related injuries, which has been suggested to be associated with muscle fatigue. However, it still remains unclear on the utility of different EMG indices in muscle fatigue evaluation induced by cycling exercise. In this study, ten cyclist volunteers performed a 30-second all-out cycling exercise after a warm-up period. Surface electromyography (sEMG) from vastus lateralis muscle (VL) and power output and cadence were recorded and EMG RMS, MF and MPF based on Fourier Transform, MDF and MNF based on wavelet packet transformation, and C(n) based on Lempel–Ziv complexity algorithm were calculated. Utility of the indices was compared based on the grey rational grade of sEMG indices and power output and cadence. The results suggested that MNF derived from wavelet packet transformation was significantly higher than other EMG indices, indicating the potential application for fatigue evaluation induced by all-out cycling exercise.


2019 ◽  
Vol 14 (8) ◽  
pp. 1103-1109
Author(s):  
Tiago Turnes ◽  
Rafael Penteado dos Santos ◽  
Rafael Alves de Aguiar ◽  
Thiago Loch ◽  
Leonardo Trevisol Possamai ◽  
...  

Purpose: To compare the intensity and physiological responses of deoxygenated hemoglobin breaking point ([HHb]BP) and anaerobic threshold (AnT) during an incremental test and to verify their association with 2000-m rowing-ergometer performance in well-trained rowers. Methods: A total of 13 male rowers (mean [SD] age = 24 [11] y and  = 63.7 [6.1] mL·kg−1·min−1) performed a step incremental test. Gas exchange, vastus lateralis [HHb], and blood lactate concentration were measured. Power output, , and heart rate of [HHb]BP and AnT were determined and compared with each other. A 2000-m test was performed in another visit. Results: No differences were found between [HHb]BP and AnT in the power output (236 [31] vs 234 [31] W; Δ = 0.7%), 95% confidence interval [CI] 6.7%), (4.2 [0.5] vs 4.3 [0.4] L·min−1; Δ = −0.8%, 95% CI 4.0%), or heart rate (180 [16] vs 182 [12] beats·min−1; Δ = −1.6%, 95% CI 2.1%); however, there was high typical error of estimate (TEE) and wide 95% limits of agreement (LoA) for power output (TEE 10.7%, LoA 54.1–50.6 W), (TEE 5.9%, LoA −0.57 to 0.63 L·min−1), and heart rate (TEE 2.4%, LoA −9.6 to 14.7 beats·min−1). Significant correlations were observed between [HHb]BP (r = .70) and AnT (r = .89) with 2000-m mean power. Conclusions: These results demonstrate a breaking point in [HHb] of the vastus lateralis muscle during the incremental test that is capable of distinguishing rowers with different performance levels. However, the high random error would compromise the use of [HHb]BP for training and testing in rowing.


2011 ◽  
Vol 111 (5) ◽  
pp. 1422-1430 ◽  
Author(s):  
R. A. Jacobs ◽  
P. Rasmussen ◽  
C. Siebenmann ◽  
V. Díaz ◽  
M. Gassmann ◽  
...  

Human endurance performance can be predicted from maximal oxygen consumption (V̇o2max), lactate threshold, and exercise efficiency. These physiological parameters, however, are not wholly exclusive from one another, and their interplay is complex. Accordingly, we sought to identify more specific measurements explaining the range of performance among athletes. Out of 150 separate variables we identified 10 principal factors responsible for hematological, cardiovascular, respiratory, musculoskeletal, and neurological variation in 16 highly trained cyclists. These principal factors were then correlated with a 26-km time trial and test of maximal incremental power output. Average power output during the 26-km time trial was attributed to, in order of importance, oxidative phosphorylation capacity of the vastus lateralis muscle ( P = 0.0005), steady-state submaximal blood lactate concentrations ( P = 0.0017), and maximal leg oxygenation (sO2LEG) ( P = 0.0295), accounting for 78% of the variation in time trial performance. Variability in maximal power output, on the other hand, was attributed to total body hemoglobin mass (Hbmass; P = 0.0038), V̇o2max ( P = 0.0213), and sO2LEG ( P = 0.0463). In conclusion, 1) skeletal muscle oxidative capacity is the primary predictor of time trial performance in highly trained cyclists; 2) the strongest predictor for maximal incremental power output is Hbmass; and 3) overall exercise performance (time trial performance + maximal incremental power output) correlates most strongly to measures regarding the capability for oxygen transport, high V̇o2max and Hbmass, in addition to measures of oxygen utilization, maximal oxidative phosphorylation, and electron transport system capacities in the skeletal muscle.


1993 ◽  
Vol 75 (2) ◽  
pp. 712-719 ◽  
Author(s):  
G. C. Gaitanos ◽  
C. Williams ◽  
L. H. Boobis ◽  
S. Brooks

Eight male subjects volunteered to take part in this study. The exercise protocol consisted of ten 6-s maximal sprints with 30 s of recovery between each sprint on a cycle ergometer. Needle biopsy samples were taken from the vastus lateralis muscle before and after the first sprint and 10 s before and immediately after the tenth sprint. The energy required to sustain the high mean power output (MPO) that was generated over the first 6-s sprint (870.0 +/- 159.2 W) was provided by an equal contribution from phosphocreatine (PCr) degradation and anaerobic glycolysis. Indeed, within the first 6-s bout of maximal exercise PCr concentration had fallen by 57% and muscle lactate concentration had increased to 28.6 mmol/kg dry wt, confirming significant glycolytic activity. However, in the tenth sprint there was no change in muscle lactate concentration even though MPO was reduced only to 73% of that generated in the first sprint. This reduced glycogenolysis occurred despite the high plasma epinephrine concentration of 5.1 +/- 1.5 nmol/l after sprint 9. In face of a considerable reduction in the contribution of anaerobic glycogenolysis to ATP production, it was suggested that, during the last sprint, power output was supported by energy that was mainly derived from PCr degradation and an increased aerobic metabolism.


2013 ◽  
Vol 114 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Scott Trappe ◽  
Erik Hayes ◽  
Andrew Galpin ◽  
Leonard Kaminsky ◽  
Bozena Jemiolo ◽  
...  

We examined whole body aerobic capacity and myocellular markers of oxidative metabolism in lifelong endurance athletes [ n = 9, 81 ± 1 yr, 68 ± 3 kg, body mass index (BMI) = 23 ± 1 kg/m2] and age-matched, healthy, untrained men ( n = 6; 82 ± 1 y, 77 ± 5 kg, BMI = 26 ± 1 kg/m2). The endurance athletes were cross-country skiers, including a former Olympic champion and several national/regional champions, with a history of aerobic exercise and participation in endurance events throughout their lives. Each subject performed a maximal cycle test to assess aerobic capacity (V̇o2max). Subjects had a resting vastus lateralis muscle biopsy to assess oxidative enzymes (citrate synthase and βHAD) and molecular (mRNA) targets associated with mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam)]. The octogenarian athletes had a higher ( P < 0.05) absolute (2.6 ± 0.1 vs. 1.6 ± 0.1 l/min) and relative (38 ± 1 vs. 21 ± 1 ml·kg−1·min−1) V̇o2max, ventilation (79 ± 3 vs. 64 ± 7 l/min), heart rate (160 ± 5 vs. 146 ± 8 beats per minute), and final workload (182 ± 4 vs. 131 ± 14 W). Skeletal muscle oxidative enzymes were 54% (citrate synthase) and 42% (βHAD) higher ( P < 0.05) in the octogenarian athletes. Likewise, basal PGC-1α and Tfam mRNA were 135% and 80% greater ( P < 0.05) in the octogenarian athletes. To our knowledge, the V̇o2max of the lifelong endurance athletes is the highest recorded in humans >80 yr of age and comparable to nonendurance trained men 40 years younger. The superior cardiovascular and skeletal muscle health profile of the octogenarian athletes provides a large functional reserve above the aerobic frailty threshold and is associated with lower risk for disability and mortality.


2000 ◽  
Vol 278 (4) ◽  
pp. E571-E579 ◽  
Author(s):  
Hervé Dubouchaud ◽  
Gail E. Butterfield ◽  
Eugene E. Wolfel ◽  
Bryan C. Bergman ◽  
George A. Brooks

To evaluate the effects of endurance training on the expression of monocarboxylate transporters (MCT) in human vastus lateralis muscle, we compared the amounts of MCT1 and MCT4 in total muscle preparations (MU) and sarcolemma-enriched (SL) and mitochondria-enriched (MI) fractions before and after training. To determine if changes in muscle lactate release and oxidation were associated with training-induced changes in MCT expression, we correlated band densities in Western blots to lactate kinetics determined in vivo. Nine weeks of leg cycle endurance training [75% peak oxygen consumption (V˙o 2 peak)] increased muscle citrate synthase activity (+75%, P < 0.05) and percentage of type I myosin heavy chain (+50%, P < 0.05); percentage of MU lactate dehydrogenase-5 (M4) isozyme decreased (−12%, P < 0.05). MCT1 was detected in SL and MI fractions, and MCT4 was localized to the SL. Muscle MCT1 contents were consistent among subjects both before and after training; in contrast, MCT4 contents showed large interindividual variations. MCT1 amounts significantly increased in MU, SL, and MI after training (+90%, +60%, and +78%, respectively), whereas SL but not MU MCT4 content increased after training (+47%, P < 0.05). Mitochondrial MCT1 content was negatively correlated to net leg lactate release at rest ( r = −0.85, P < 0.02). Sarcolemmal MCT1 and MCT4 contents correlated positively to net leg lactate release at 5 min of exercise at 65%V˙o 2 peak ( r = 0.76, P < 0.03 and r = 0.86, P < 0.01, respectively). Results support the conclusions that 1) endurance training increases expression of MCT1 in muscle because of insertion of MCT1 into both sarcolemmal and mitochondrial membranes, 2) training has variable effects on sarcolemmal MCT4, and 3) both MCT1 and MCT4 participate in the cell-cell lactate shuttle, whereas MCT1 facilitates operation of the intracellular lactate shuttle.


1998 ◽  
Vol 23 (1) ◽  
pp. 74-86 ◽  
Author(s):  
Philip D. Chilibeck ◽  
Gordon J. Bell ◽  
Teresa Socha ◽  
Tom Martin

We evaluated the effect of endurance training (cycling 3 times per week for 12 weeks) on succinate dehydrogenase (SDH) activity in the subsarcolemmal (SS) and intermyofibrillar (IMF) regions of vastus lateralis muscle fibres in 7 individuals (4 females and 3 males). SDH activity of the SS region increased 9.4% and 12.8% in type I and II fibres, respectively (p < .05). SDH activity of the IMF region increased 4.7% and 6.7% in type I and II fibres, respectively (p < .05). This was less than the increase in the SS region (p < .O5). No significant changes were observed in a control group (4 females and 3 males). These data suggest that mitochondria in the SS and IMF regions of human vastus lateralis muscle fibres are sensitive to endurance training. The greater response in the SS region suggests that the metabolic requirements of SS mitochondria were stressed to a greater extent than IMF mitochondria with endurance training. Key words: subsarcolemmal mitochondria, intermyofibrillar mitochondria


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