Progressive effect of endurance training on metabolic adaptations in working skeletal muscle

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.

1992 ◽  
Vol 73 (6) ◽  
pp. 2701-2708 ◽  
Author(s):  
H. J. Green ◽  
J. R. Sutton ◽  
E. E. Wolfel ◽  
J. T. Reeves ◽  
G. E. Butterfield ◽  
...  

To determine whether the working muscle is able to sustain ATP homeostasis during a hypoxic insult and the mechanisms associated with energy metabolic adaptations during the acclimatization process, seven male subjects [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg] were given a prolonged exercise challenge (45 min) at sea level (SL), within 4 h after ascent to an altitude of 4,300 m (acute hypoxia, AH), and after 3 wk of sustained residence at 4,300 m (chronic hypoxia, CH). The prolonged cycle test conducted at the same absolute intensity and representing 51 +/- 1% of SL maximal aerobic power (VO2 max) and between 64 +/- 2 (AH) and 66 +/- 1% (CH) at altitude was performed without a reduction in ATP concentration in the working vastus lateralis regardless of condition. Compared with rest, exercise performed during AH resulted in a greater increase (P < 0.05) in muscle lactate concentration (5.11 +/- 0.68 to 22.3 +/- 6.1 mmol/kg dry wt) than exercise performed either at SL (5.88 +/- 0.85 to 11.5 +/- 3.1) or CH (5.99 +/- 0.88 to 12.4 +/- 2.1). These differences in lactate concentration have been shown to reflect differences in arterial lactate concentration and glycolysis (Brooks et al. J. Appl. Physiol. 71: 333–341, 1991). The reduction in glycolysis at least between AH and CH appears to be accompanied by a tighter metabolic control. During CH, free ADP was lower and the ATP-to-free ADP ratio was increased (P < 0.05) compared with AH.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 269 (2) ◽  
pp. E222-E230 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
S. M. Grant

This study investigated the hypothesis that training-induced reductions in exercise blood glucose utilization can occur independently of increases in muscle mitochondrial potential. To induce a training adaptation, eight active participants (23 +/- 1 yr, 80.6 +/- 3.7 kg, mean +/- SE) with a maximal oxygen consumption (VO2max) of 45.5 +/- 2.4 ml.kg-1.min-1, cycled at 59% VO2max for 2 h per day for 10 consecutive days. Measurements of blood glucose appearance (Ra) and disappearance (Rd), using a primed continuous infusion of [6,6-2H2]glucose, were made during 90 min of cycle exercise (59% VO2max) performance before and after training. Training resulted in a 25% decrease (P < 0.01) in mean glucose Ra during exercise (43.0 +/- 3.7 to 34.4 +/- 2.8 mumol.kg-1.min-1). Since blood glucose concentration was not different between training conditions, glucose metabolic clearance rate was also depressed (P < 0.05). Exercise-induced glycogen depletion in vastus lateralis muscle was reduced (P < 0.05) with training. Calculation of carbohydrate and fat oxidation based on the respiratory exchange ratio supported a shift toward greater preference for fat. Because training did not elicit changes in the maximal activities of citrate synthase and malate dehydrogenase, two enzymes of the citric acid cycle, it would appear that increases in mitochondrial potential are not necessary for the adaptations that occurred.


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.


1995 ◽  
Vol 78 (1) ◽  
pp. 138-145 ◽  
Author(s):  
H. J. Green ◽  
S. Jones ◽  
M. Ball-Burnett ◽  
B. Farrance ◽  
D. Ranney

In previous research we established using a short-term (5–7 days) training model that increases in muscle oxidative potential are not a prerequisite for the characteristic energy metabolic adaptations (lower lactate, glycogen depletion, and phosphocreatine hydrolysis) observed during prolonged exercise. To investigate whether increased muscle aerobic potential further potentiates the metabolic adaptive response, seven healthy male volunteers [maximal O2 uptake (VO2max) = 45.1 +/- 1.1 (SE) ml.kg-1.min-1] engaged in an 8-wk training program consisting of 2 h of cycle exercise at 62% of pretraining VO2max 5–6 times/wk. Analysis of tissue samples obtained from the vastus lateralis after 60 min of exercise revealed that by 4 wk of training muscle lactate concentration, phosphocreatine hydrolysis, and glycogen depletion were depressed (all P < 0.05). Further training for 4 wk had no additional effect (P < 0.05). The ratio of fructose 6-phosphate to fructose 1,6-phosphate, an index of phosphofructokinase activity, was not altered with training. Muscle oxidative potential as estimated from the maximal activity of succinic dehydrogenase increased by 31% by 4 wk of training (P <0.05) before plateauing during the final 4 wk of training. The increase in VO2max of 15.6% (P < 0.05) noted with training was also primarily expressed during the initial 4 wk. O2 uptake during submaximal exercise was unchanged. Because the metabolic response was similar in magnitude to that previously observed with short-term training, we conclude that, at least for the conditions of this study, the development of increased muscle aerobic potential is of minimal consequence on the magnitude of the energy metabolic adaptations examined.


1995 ◽  
Vol 73 (4) ◽  
pp. 474-482 ◽  
Author(s):  
H. J. Green ◽  
M. Ball-Burnett ◽  
G. Jamieson ◽  
J. Cadefau ◽  
R. Cussó

In previous studies we have been able to demonstrate tighter metabolic control of muscle metabolism during prolonged steady-state exercise 5 to 6 days after the initiation of training and well before changes in oxidative potential. To examine whether the metabolic adaptations are manifested during the non-steady-state adjustment to submaximal exercise, 11 male subjects ([Formula: see text] peak, 45 ± 2.4 mL∙kg−1∙min−1, [Formula: see text]) performed 98 min of cycle exercise at 67% of [Formula: see text] peak prior to and following 3 to 4 days of training for 2 h per day. Analysis of lactate concentration (mmol/kg dry weight) in samples rapidly extracted from vastus lateralis indicated reductions (p < 0.05) of 44% at 3 min (42.1 ± 7.1 vs. 23.6 ± 7.7), 29% at 15 min (35.4 ± 6.4 vs. 25.0 ± 6.0), and 32% at 98 min (22.9 ± 6.9 vs. 15.6 ± 3.2) with training. Training also resulted in higher phosphocreatine and lower creatine and Pi values that were not specific to any exercise time point. In addition, [Formula: see text] was not altered either during the non-steady state or during the steady-state phases of exercise. These results suggest that at least part of the tightening of the metabolic control and the apparent reduction in glycogenolysis and glycolysis in response to short-term training occurs during the adjustment phase to steady-state exercise.Key words: training, metabolic control, nonsteady state.


2002 ◽  
Vol 282 (1) ◽  
pp. E154-E160 ◽  
Author(s):  
H. Green ◽  
A. Halestrap ◽  
C. Mockett ◽  
D. O'Toole ◽  
S. Grant ◽  
...  

To investigate the effects of a single session of prolonged cycle exercise [60% peak O2 uptake (V˙o 2 peak) for 5–6 h] on metabolic adaptations in working vastus lateralis muscle, nine untrained males (peak O2 uptake = 47.2 ± 1.1 ml · kg−1 · min−1, means ± SE) were examined before (Pre) and at 2 (Post-2), 4 (Post-4), and 6 (Post-6) days after the training session. On the basis of 15 min of cycle exercise at 59% V˙o 2 peak, it was found that training reduced ( P < 0.05) exercise muscle lactate (mM) at Post-2 (6.65 ± 0.69), Post-4 (7.74 ± 0.63), and Post-6 (7.78 ± 1.2) compared with Pre (10.9 ± 1.3). No effect of training was observed on exercise ATP, phosphocreatine, and glycogen levels. After the single session of training, plasma volumes were elevated ( P < 0.05) at Post-2 (6.7 ± 1.7%), Post-4 (5.86 ± 1.9), and Post-6 (5.13 ± 2.5). The single exercise session also resulted in elevations ( P< 0.05) in the monocarboxylate transporters MCT1 and MCT4 throughout the 6 days after exercise. Although epinephrine and norepinephrine both increased with exercise, only norepinephrine was reduced ( P < 0.05) with training and only at Post-4. These results indicate that regulation of cellular lactate levels occurs rapidly and independently of other metabolic adaptations. It is proposed that increases in MCT and plasma volume are at least partly involved in the lower muscle lactate content observed after the training session by increasing lactate membrane transport and removal, respectively.


2000 ◽  
Vol 278 (1) ◽  
pp. E118-E126 ◽  
Author(s):  
H. Green ◽  
R. Tupling ◽  
B. Roy ◽  
D. O'Toole ◽  
M. Burnett ◽  
...  

The purpose of this study was to investigate the hypothesis that a single, extended session of heavy exercise would be effective in inducing adaptations in energy metabolism during exercise in the absence of increases in oxidative potential. Ten healthy males [maximal aerobic power (V˙o 2 peak) = 43.4 ± 2.2 (SE) ml ⋅ kg−1 ⋅ min−1] participated in a 16-h training session involving cycling for 6 min each hour at ∼90% of maximal oxygen consumption. Measurements of metabolic changes were made on tissue extracted from the vastus lateralis during a two-stage standardized submaximal cycle protocol before (Pre) and 36–48 h after (Post) the training session. At Pre, creatine phosphate (PCr) declined ( P < 0.05) by 32% from 0 to 3 min and then remained stable until 20 min of exercise at 60%V˙o 2 peak before declining ( P < 0.05) by a further 35% during 20 min of exercise at 75%V˙o 2 peak. Muscle lactate (mmol/kg dry wt) progressively increased ( P < 0.05) from 4.59 ± 0.64 at 0 min to 17.8 ± 2.7 and 30.9 ± 5.3 at 3 and 40 min, respectively, whereas muscle glycogen (mmol glucosyl units/kg dry wt) declined ( P < 0.05) from a rest value of 360 ± 24 to 276 ± 31 and 178 ± 36 at similar time points. During exercise after the training session, PCr and glycogen were not as depressed ( P < 0.05), and increases in muscle lactate were blunted ( P < 0.05). All of these changes occurred in the absence of increases in oxidative potential as measured by the maximal activities of citrate synthase and malate dehydrogenase. These findings are consistent with other studies, namely, that muscle metabolic adaptations to regular exercise are an early adaptive event that occurs before increases in oxidative potential.


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.


Sensors ◽  
2019 ◽  
Vol 19 (21) ◽  
pp. 4729 ◽  
Author(s):  
Taha Khan ◽  
Lina E. Lundgren ◽  
Eric Järpe ◽  
M. Charlotte Olsson ◽  
Pelle Viberg

Blood lactate accumulation is a crucial fatigue indicator during sports training. Previous studies have predicted cycling fatigue using surface-electromyography (sEMG) to non-invasively estimate lactate concentration in blood. This study used sEMG to predict muscle fatigue while running and proposes a novel method for the automatic classification of running fatigue based on sEMG. Data were acquired from 12 runners during an incremental treadmill running-test using sEMG sensors placed on the vastus-lateralis, vastus-medialis, biceps-femoris, semitendinosus, and gastrocnemius muscles of the right and left legs. Blood lactate samples of each runner were collected every two minutes during the test. A change-point segmentation algorithm labeled each sample with a class of fatigue level as (1) aerobic, (2) anaerobic, or (3) recovery. Three separate random forest models were trained to classify fatigue using 36 frequency, 51 time-domain, and 36 time-event sEMG features. The models were optimized using a forward sequential feature elimination algorithm. Results showed that the random forest trained using distributive power frequency of the sEMG signal of the vastus-lateralis muscle alone could classify fatigue with high accuracy. Importantly for this feature, group-mean ranks were significantly different (p < 0.01) between fatigue classes. Findings support using this model for monitoring fatigue levels during running.


1978 ◽  
Vol 45 (6) ◽  
pp. 852-857 ◽  
Author(s):  
P. D. Gollnick ◽  
J. Karlsson ◽  
K. Piehl ◽  
B. Saltin

Experiments were conducted to examine the conversions of phosphorylase b to phosphorylase a in human skeletal muscle during bicycle exercise or isometric contractions. Muscle biopsies were obtained from the vastus lateralis with the needle technique at rest and either during or immediately after activity and frozen in liquid nitrogen within 2--4 s. Total phosphorylase and phosphorylase a activities were differentiated by measurement in the presence and absence of AMP, respectively. At rest 8.5% of the total phosphorylase activity existed in the a form. Little or no change in the percent of phosphorylase in the a form occurred during voluntary dynamic or static muscular activity that produced muscle lactate concentrations in excess of 18 mmol.kg-1 wet muscle. Electrical stimulation of the vastus lateralis muscle also failed to produce an increase in the percentage of phosphorylase a. These data suggest that during exercise the conversion of phosphorylase to the a form is of minor importance. An increased activity of phosphorylase b due to changes in muscle concentrations of ATP, AMP, and inorganic phosphate may regulate glycogenolysis during voluntary exercise in man.


Sign in / Sign up

Export Citation Format

Share Document