scholarly journals Human muscle metabolism during intermittent maximal exercise

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.

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.


1996 ◽  
Vol 270 (2) ◽  
pp. E265-E272 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
G. J. Heigenhauser ◽  
S. M. Grant

We investigated the hypothesis that a program of prolonged endurance training, previously shown to decrease metabolic perturbations to acute exercise within 5 days of training, would result in greater metabolic adaptations after a longer training duration. Seven healthy male volunteers [O2 consumption = 3.52 +/- 0.20 (SE) l/min] engaged in a training program consisting of 2 h of cycle exercise at 59% of pretraining peak O2 consumption (VO2peak) 5-6 times/wk. Responses to a 90-min submaximal exercise challenge were assessed pretraining (PRE) and after 5 and 31 days of training. On the basis of biopsies obtained from the vastus lateralis muscle, it was found that, after 5 days of training, muscle lactate concentration, phosphocreatine (PCr) hydrolysis, and glycogen depletion were reduced vs. PRE (all P < 0.01). Further training (26 days) showed that, at 31 days, the reduction in PCr and the accumulation of muscle lactate was even less than at 5 days (P < 0.01). Muscle oxidative potential, estimated from the maximal activity of succinate dehydrogenase, was increased only after 31 days of training (+41%; P < 0.01). In addition, VO2peak was only increased (10%) by 31 days (P < 0.05). The results show that a period of short-term training results in many characteristic training adaptations but that these adaptations occurred before increases in mitochondrial potential. However, a further period of training resulted in further adaptations in muscle metabolism and muscle phosphorylation potential, which were linked to the increase in muscle mitochondrial capacity.


2012 ◽  
Vol 113 (6) ◽  
pp. 917-928 ◽  
Author(s):  
David Morales-Alamo ◽  
Jesús Gustavo Ponce-González ◽  
Amelia Guadalupe-Grau ◽  
Lorena Rodríguez-García ◽  
Alfredo Santana ◽  
...  

AMP-activated protein kinase (AMPK) is a major mediator of the exercise response and a molecular target to improve insulin sensitivity. To determine if the anaerobic component of the exercise response, which is exaggerated when sprint is performed in severe acute hypoxia, influences sprint exercise-elicited Thr172-AMPKα phosphorylation, 10 volunteers performed a single 30-s sprint (Wingate test) in normoxia and in severe acute hypoxia (inspired Po2: 75 mmHg). Vastus lateralis muscle biopsies were obtained before and immediately after 30 and 120 min postsprint. Mean power output and O2 consumption were 6% and 37%, respectively, lower in hypoxia than in normoxia. O2 deficit and muscle lactate accumulation were greater in hypoxia than in normoxia. Carbonylated skeletal muscle and plasma proteins were increased after the sprint in hypoxia. Thr172-AMPKα phosphorylation was increased by 3.1-fold 30 min after the sprint in normoxia. This effect was prevented by hypoxia. The NAD+-to-NADH.H+ ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia ( P < 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia ( P < 0.05). This could have led to lower liver kinase B1 (LKB1) activation by SIRT1 and, hence, blunted Thr172-AMPKα phosphorylation. Ser485-AMPKα1/Ser491-AMPKα2 phosphorylation, a known negative regulating mechanism of Thr172-AMPKα phosphorylation, was increased by 60% immediately after the sprint in hypoxia, coincident with increased Thr308-Akt phosphorylation. Collectively, our results indicate that the signaling response to sprint exercise in human skeletal muscle is altered in severe acute hypoxia, which abrogated Thr172-AMPKα phosphorylation, likely due to lower LKB1 activation by SIRT1.


1982 ◽  
Vol 63 (1) ◽  
pp. 87-92 ◽  
Author(s):  
G. R. Ward ◽  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. The activity of pyruvate dehydrogenase in its active and inactive forms was measured in biopsy samples obtained from the vastus lateralis muscle of healthy subjects before and after exercise. 2. At rest, 40 ± 4% (mean ± sem) of the enzyme was in the active form. 3. After progressive aerobic exercise to exhaustion (n = 5), 88 ± 2·3% was in the active form. 4. After intermittent supramaximal short-term exercise (1 min exercise, 3 min rest) to exhaustion (n = 6), 60 ± 2·2% was in the active form. 5. After isometric maximal exercise of 65 ± 3·6 s duration (n = 3), only 39 ± 1% of the enzyme was in the active form. 6. Muscle glycogen depletion was greatest with intermittent exercise and least with isometric maximal exercise; in contrast, the increase in muscle lactate was least with progressive exercise (1·3 to 9·4 μmol/g), intermediate in intermittent maximal exercise (1·2 to 13·1 μmol/g) and greatest after isometric exercise (1·8 to 17·6 μmol/g). There were no significant differences between the three studies in the changes in lactate/pyruvate ratios. 7. In three subjects who exercised with one leg, activation of the enzyme was twice as great in the exercised as in the inactive leg. 8. The ratio of active to total enzyme in biopsies of resting muscle was greater in four well-trained athletes than in four untrained control subjects (70% compared with 41% respectively). 9. The activation of pyruvate dehydrogenase appears to play an important part in regulating the use of glycogen and glucose during exercise in man.


2016 ◽  
Vol 8 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Pantelis T. Nikolaidis ◽  
Beat Knechtle

SummaryStudy aim: The aim of the present study was to examine the effect of two different recovery durations (2 min versus 5 min) on the physiological responses (power output, stretch-shortening cycle and lactate concentration) to a 5×6 s repeated cycling sprint exercise protocol in pre-pubescent soccer players. Materials and methods: Twelve male soccer players (age 12.23 ± 0.55 yrs, body mass 43.6 ± 5.5 kg and height 156.1 ± 5.8 cm) performed 5 × 6 s sprints on a cycle ergometer (Ergomedic 874E, Monark, Sweden) against 0.075 times their body mass resistance on two occasions within a week. In one session there was a 2 min recovery and in the other there was a 5 min recovery in a counterbalanced order. A squat jump (SJ) and a countermovement jump (CMJ) were tested before and after each trial, and the eccentric utilisation ratio (EUR) was calculated as CMJ/SJ. Results: No significant trial × recovery interaction was observed in the participants’ peak power (p = 0.891, η2 = 0.118), mean power (p = 0.910, η2 = 0.106), SJ (p = 0.144, η2 = 0.630), CMJ (p = 0.616, η2 = 0.347) and EUR (p = 0.712, η2 = 0.295). However, a main effect of the trial on the CMJ of a large magnitude (p = 0.006, η2 = 0.862) was found, in which a higher score was recorded in the third trial than in the first trial (23.3 versus 21.8 cm). No differences were found in the lactate concentrations examined 5 min after the end of the protocol between the two recovery conditions (6.7 ± 1.8 vs. 6.0 ± 1.6 mmol · L–1, in the 2 and 5 min recovery, respectively, Cohen’s d = 0.4). Conclusions: The duration of the passive recovery time (2 min vs. 5 min) in trials of repeated sprints did not induce important changes either to the indices of the jumping performance or to the power output in pre-pubescent participants.


1992 ◽  
Vol 73 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
J. P. Kirwan ◽  
D. M. Bier ◽  
...  

The purpose of this study was to test the hypothesis that the rate of plasma glucose oxidation during exercise is inversely related to muscle respiratory capacity. To this end, 14 subjects were studied: in 7 of these subjects, the blood lactate threshold (LT) occurred at a relatively high intensity [i.e., at 65 +/- 2% of peak cycle ergometer oxygen uptake (VO2 peak)], whereas in the other 7 subjects, LT occurred at a relatively low intensity (i.e., at 45 +/- 2% of VO2 peak). VO2peak did not differ between the two groups, but citrate synthase activity in the vastus lateralis muscle was 53% higher (P < 0.05) in the high LT group. A primed continuous infusion of [U-13C]glucose was used to quantify rates of glucose appearance (Ra), disappearance (Rd), and oxidation (R(ox)) during 90 min of exercise at 55% VO2peak. Although both absolute and relative rates of oxygen uptake during exercise were similar in the two groups, mean Ra and Rd were 17% lower (P < 0.001) in the high LT group, and mean R(ox) was 25% lower (21.0 +/- 2.6 vs. 27.9 +/- 2.6 mumol.min-1.kg-1; P < 0.001). The percentage of total energy derived from glucose oxidation was inversely related to muscle citrate synthase activity (r = -0.85; P < 0.01). These data support the concept that skeletal muscle respiratory capacity has a major role in determining the metabolic response to submaximal exercise.


1995 ◽  
Vol 269 (3) ◽  
pp. E458-E468 ◽  
Author(s):  
C. T. Putman ◽  
N. L. Jones ◽  
L. C. Lands ◽  
T. M. Bragg ◽  
M. G. Hollidge-Horvat ◽  
...  

The regulation of the active form of pyruvate dehydrogenase (PDHa) and related metabolic events were examined in human skeletal muscle during repeated bouts of maximum exercise. Seven subjects completed three consecutive 30-s bouts of maximum isokinetic cycling, separated by 4 min of recovery. Biopsies of the vastus lateralis were taken before and immediately after each bout. PDHa increased from 0.45 +/- 0.15 to 2.96 +/- 0.38, 1.10 +/- 0.11 to 2.91 +/- 0.11, and 1.28 +/- 0.18 to 2.82 +/- 0.32 mmol.min-1.kg wet wt-1 during bouts 1, 2, and 3, respectively. Glycolytic flux was 13-fold greater than PDHa in bouts 1 and 2 and 4-fold greater during bout 3. This discrepancy between the rate of pyruvate production and oxidation resulted in substantial lactate accumulation to 89.5 +/- 11.6 in bout 1, 130.8 +/- 13.8 in bout 2, and 106.6 +/- 10.1 mmol/kg dry wt in bout 3. These events coincided with an increase in the mitochondrial oxidation state, as reflected by a fall in mitochondrial NADH/NAD, indicating that muscle lactate production during exercise was not an O2-dependent process in our subjects. During exercise the primary factor regulating PDHa transformation was probably intracellular Ca2+. In contrast, the primary regulatory factors causing greater PDHa during recovery were lower ATP/ADP and NADH/NAD and increased concentrations of pyruvate and H+. Greater PDHa during recovery facilitated continued oxidation of the lactate load between exercise bouts.


1999 ◽  
Vol 87 (3) ◽  
pp. 1083-1086 ◽  
Author(s):  
G. McConell ◽  
R. J. Snow ◽  
J. Proietto ◽  
M. Hargreaves

Eight endurance-trained men cycled to volitional exhaustion at 69 ± 1% peak oxygen uptake on two occasions to examine the effect of carbohydrate supplementation during exercise on muscle energy metabolism. Subjects ingested an 8% carbohydrate solution (CHO trial) or a sweet placebo (Con trial) in a double-blind, randomized order, with vastus lateralis muscle biopsies ( n = 7) obtained before and immediately after exercise. No differences in oxygen uptake, heart rate, or respiratory exchange ratio during exercise were observed between the trials. Exercise time to exhaustion was increased by ∼30% when carbohydrate was ingested [199 ± 21 vs. 152 ± 9 (SE) min, P < 0.05]. Plasma glucose and insulin levels during exercise were higher and plasma free fatty acids lower in the CHO trial. No differences between trials were observed in the decreases in muscle glycogen and phosphocreatine or the increases in muscle lactate due to exercise. Muscle ATP levels were not altered by exercise in either trial. There was a small but significant increase in muscle inosine monophosphate levels at the point of exhaustion in both trials, and despite the subjects in CHO trial cycling 47 min longer, their muscle inosine monophosphate level was significantly lower than in the Con trial (CHO: 0.16 ± 0.08, Con: 0.23 ± 0.09 mmol/kg dry muscle). These data suggest that carbohydrate ingestion may increase endurance capacity, at least in part, by improving muscle energy balance.


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