Effect of two different intense training regimens on skeletal muscle ion transport proteins and fatigue development

This study examined the effect of two different intense exercise training regimens on skeletal muscle ion transport systems, performance, and metabolic response to exercise. Thirteen subjects performed either sprint training [ST; 6-s sprints (n = 6)], or speed endurance training [SET; 30-s runs approximately 130% Vo(2 max), n = 7]. Training in the SET group provoked higher (P < 0.05) plasma K(+) levels and muscle lactate/H(+) accumulation. Only in the SET group was the amount of the Na(+)/H(+) exchanger isoform 1 (31%) and Na(+)-K(+)-ATPase isoform alpha(2) (68%) elevated (P < 0.05) after training. Both groups had higher (P < 0.05) levels of Na(+)-K(+)-ATPase beta(1)-isoform and monocarboxylate transporter 1 (MCT1), but no change in MCT4 and Na(+)-K(+)-ATPase alpha(1)-isoform. Both groups had greater (P < 0.05) accumulation of lactate during exhaustive exercise and higher (P < 0.05) rates of muscle lactate decrease after exercise. The ST group improved (P < 0.05) sprint performance, whereas the SET group elevated (P < 0.05) performance during exhaustive continuous treadmill running. Improvement in the Yo-Yo intermittent recovery test was larger (P < 0.05) in the SET than ST group (29% vs. 10%). Only the SET group had a decrease (P < 0.05) in fatigue index during a repeated sprint test. In conclusion, turnover of lactate/H(+) and K(+) in muscle during exercise does affect the adaptations of some but not all related muscle ion transport proteins with training. Adaptations with training do have an effect on the metabolic response to exercise and specific improvement in work capacity.     

Effects of sprint training on extrarenal potassium regulation with intense exercise in Type 1 diabetes.

Effects of sprint training on plasma K+ concentration ([K+]) regulation during intense exercise and on muscle Na+-K+-ATPase were investigated in subjects with Type 1 diabetes mellitus (T1D) under real-life conditions and in nondiabetic subjects (CON). Eight subjects with T1D and seven CON undertook 7 wk of sprint cycling training. Before training, subjects cycled to exhaustion at 130% peak O2 uptake. After training, identical work was performed. Arterialized venous blood was drawn at rest, during exercise, and at recovery and analyzed for plasma glucose, [K+], Na+ concentration ([Na+]), catecholamines, insulin, and glucagon. A vastus lateralis biopsy was obtained before and after training and assayed for Na+-K+-ATPase content ([3H]ouabain binding). Pretraining, Na+-K+-ATPase content and the rise in plasma [K+] ([K+]) during maximal exercise were similar in T1D and CON. However, after 60 min of recovery in T1D, plasma [K+], glucose, and glucagon/insulin were higher and plasma [Na+] was lower than in CON. Training increased Na+-K+-ATPase content and reduced [K+] in both groups (P < 0.05). These variables were correlated in CON (r = -0.65, P < 0.05) but not in T1D. This study showed first that mildly hypoinsulinemic subjects with T1D can safely undertake intense exercise with respect to K+ regulation; however, elevated [K+] will ensue in recovery unless insulin is administered. Second, sprint training improved K+ regulation during intense exercise in both T1D and CON groups; however, the lack of correlation between plasma delta[K+] and Na+-K+-ATPase content in T1D may indicate different relative contributions of K+-regulatory mechanisms.     

Exercise-induced regulation of muscular Na+-K+ pump, FXYD1, and NHE1 mRNA and protein expression: importance of training status, intensity, and muscle type

It is investigated if exercise-induced mRNA changes cause similar protein expression changes of Na(+)-K(+) pump isoforms (α(1), α(2), β(1), β(2)), FXYD1, and Na(+)/K(+) exchanger (NHE1) in rat skeletal muscle. Expression was evaluated (n = 8 per group) in soleus and extensor digutorum longus after 1 day, 3 days, and 3 wk (5 sessions/wk) of either sprint (4 × 3-min sprint + 1-min rest) or endurance (20 min) running. Two hours after exercise on day 1, no change in protein expression was apparent in either training group or muscle, whereas sprint exercise increased the mRNA of soleus α(2) (4.9 ± 0.8-fold; P < 0.05), β(2) (13.2 ± 4.4-fold; P < 0.001), and NHE1 (12.0 ± 3.1-fold; P < 0.01). Two hours after sprint exercise, protein expression normalized to control samples was higher on day 3 than day 1 for soleus α(1) (41 ± 18% increase vs. 15 ± 8% reduction; P < 0.05), α(2) (64 ± 35% increase vs. 37 ± 12% reduction; P < 0.05), β(1) (17 ± 21% increase vs. 14 ± 29% reduction; P < 0.05), and FXYD1 (35 ± 16% increase vs. 13 ± 10% reduction; P < 0.05). In contrast, on day 3, soleus α(1) (0.1 ± 0.1-fold; P < 0.001), α(2) (0.2 ± 0.1-fold; P < 0.001), β(1) (0.4 ± 0.1-fold; P < 0.05), and β(2)-mRNA (2.9 ± 1.7-fold; P < 0.001) expression was lower than after exercise on day 1. After 3 wk of training, no change in protein expression relative to control existed. In conclusion, increased expression of Na(+)-K(+) pump subunits, FXYD1 and NHE1 after 3 days exercise training does not appear to be an effect of increased constitutive mRNA levels. Importantly, sprint exercise can reduce mRNA expression concomitant with increased protein expression.     

Downregulation of Na+-K+-ATPase pumps in skeletal muscle with training in normobaric hypoxia.

To investigate the effects of training in normoxia vs. training in normobaric hypoxia (fraction of inspired O2 = 20.9 vs. 13.5%, respectively) on the regulation of Na+-K+-ATPase pump concentration in skeletal muscle (vastus lateralis), 9 untrained men, ranging in age from 19 to 25 yr, underwent 8 wk of cycle training. The training consisted of both prolonged and intermittent single leg exercise for both normoxia (N) and hypoxia (H) during a single session (a similar work output for each leg) and was performed 3 times/wk. Na+-K+-ATPase concentration was 326 +/- 17 (SE) pmol/g wet wt before training (Control), increased by 14% with N (371 +/- 18 pmol/g wet wt; P < 0.05), and decreased by 14% with H (282 +/- 20 pmol/g wet wt; P < 0.05). The maximal activity of citrate synthase, selected as a measure of mitochondrial potential, showed greater increases (P < 0.05) with H (1.22 +/- 0.10 mmol x h-1 x g wet wt-1; 70%; P < 0.05) than with N (0.99 +/- 0.10 mmol x h-1 x g wet wt-1; 51%; P < 0.05) compared with pretraining (0.658 +/- 0.09 mmol x h-1 x g wet wt-1). These results demonstrate that normobaric hypoxia induced during exercise training represents a potent stimulus for the upregulation in mitochondrial potential while at the same time promoting a downregulation in Na+-K+-ATPase pump expression. In contrast, normoxic training stimulates increases in both mitochondrial potential and Na+-K+-ATPase concentration.     

Human neuromuscular fatigue is associated with altered Na+-K+-ATPase activity following isometric exercise.

The purpose of this study was to investigate the hypothesis that reductions in Na+-K+- ATPase activity are associated with neuromuscular fatigue following isometric exercise. In control (Con) and exercised (Ex) legs, force and electromyogram were measured in 14 volunteers [age, 23.4 +/- 0.7 (SE) yr] before and immediately after (PST0), 1 h after (PST1), and 4 h after (PST4) isometric, single-leg extension exercise at ~60% of maximal voluntary contraction for 30 min using a 0.5 duty cycle (5-s contraction, 5-s rest). Tissue was obtained from vastus lateralis muscle before exercise in Con and after exercise in both the Con (PST0) and Ex legs (PST0, PST1, PST4), for the measurements of Na+-K+-ATPase activity, as determined by the 3-O-methylfluorescein phosphatase (3-O-MFPase) assay. Voluntary (maximal voluntary contraction) and elicited (10, 20, 50, 100 Hz) force was reduced 30-55% (P < 0.05) at PST0 and did not recover by PST4. Muscle action potential (M-wave) amplitude and area (measured in the vastus medialis) and 3-O-MFPase activity at PST0-Ex were less than that at PST0-Con (P < 0.05) by 37, 25, and 38%, respectively. M-wave area at PST1-Ex was also less than that at PST1-Con (P < 0.05). Changes in 3-O-MFPase activity correlated to changes in M-wave area across all time points (r = 0.38, P < 0.05, n = 45). These results demonstrate that Na+-K+- ATPase activity is reduced by sustained isometric exercise in humans from that in a matched Con leg and that this reduction in Na+-K+-ATPase activity is associated with loss of excitability as indicated by M-wave alterations.     

Four weeks of speed endurance training reduces energy expenditure during exercise and maintains muscle oxidative capacity despite a reduction in training volume

We studied the effect of an alteration from regular endurance to speed endurance training on muscle oxidative capacity, capillarization, as well as energy expenditure during submaximal exercise and its relationship to mitochondrial uncoupling protein 3 (UCP3) in humans. Seventeen endurance-trained runners were assigned to either a speed endurance training (SET; n = 9) or a control (Con; n = 8) group. For a 4-wk intervention (IT) period, SET replaced the ordinary training ( approximately 45 km/wk) with frequent high-intensity sessions each consisting of 8-12 30-s sprint runs separated by 3 min of rest (5.7 +/- 0.1 km/wk) with additional 9.9 +/- 0.3 km/wk at low running speed, whereas Con continued the endurance training. After the IT period, oxygen uptake was 6.6, 7.6, 5.7, and 6.4% lower (P < 0.05) at running speeds of 11, 13, 14.5, and 16 km/h, respectively, in SET, whereas remained the same in Con. No changes in blood lactate during submaximal running were observed. After the IT period, the protein expression of skeletal muscle UCP3 tended to be higher in SET (34 +/- 6 vs. 47 +/- 7 arbitrary units; P = 0.06). Activity of muscle citrate synthase and 3-hydroxyacyl-CoA dehydrogenase, as well as maximal oxygen uptake and 10-km performance time, remained unaltered in both groups. In SET, the capillary-to-fiber ratio was the same before and after the IT period. The present study showed that speed endurance training reduces energy expenditure during submaximal exercise, which is not mediated by lowered mitochondrial UCP3 expression. Furthermore, speed endurance training can maintain muscle oxidative capacity, capillarization, and endurance performance in already trained individuals despite significant reduction in the amount of training.     

Muscle Na+-K+-ATPase activity and isoform adaptations to intense interval exercise and training in well-trained athletes.

The Na+ -K+ -ATPase enzyme is vital in skeletal muscle function. We investigated the effects of acute high-intensity interval exercise, before and following high-intensity training (HIT), on muscle Na+ -K+ -ATPase maximal activity, content, and isoform mRNA expression and protein abundance. Twelve endurance-trained athletes were tested at baseline, pretrain, and after 3 wk of HIT (posttrain), which comprised seven sessions of 8 x 5-min interval cycling at 80% peak power output. Vastus lateralis muscle was biopsied at rest (baseline) and both at rest and immediately postexercise during the first (pretrain) and seventh (posttrain) training sessions. Muscle was analyzed for Na+ -K+ -ATPase maximal activity (3-O-MFPase), content ([3H]ouabain binding), isoform mRNA expression (RT-PCR), and protein abundance (Western blotting). All baseline-to-pretrain measures were stable. Pretrain, acute exercise decreased 3-O-MFPase activity [12.7% (SD 5.1), P < 0.05], increased alpha1, alpha2, and alpha3 mRNA expression (1.4-, 2.8-, and 3.4-fold, respectively, P < 0.05) with unchanged beta-isoform mRNA or protein abundance of any isoform. In resting muscle, HIT increased (P < 0.05) 3-O-MFPase activity by 5.5% (SD 2.9), and alpha3 and beta3 mRNA expression by 3.0- and 0.5-fold, respectively, with unchanged Na+ -K+ -ATPase content or isoform protein abundance. Posttrain, the acute exercise induced decline in 3-O-MFPase activity and increase in alpha1 and alpha3 mRNA each persisted (P < 0.05); the postexercise 3-O-MFPase activity was also higher after HIT (P < 0.05). Thus HIT augmented Na+ -K+ -ATPase maximal activity despite unchanged total content and isoform protein abundance. Elevated Na+ -K+ -ATPase activity postexercise may contribute to reduced fatigue after training. The Na+ -K+ -ATPase mRNA response to interval exercise of increased alpha- but not beta-mRNA was largely preserved posttrain, suggesting a functional role of alpha mRNA upregulation.     

Relationship between performance at different exercise intensities and skeletal muscle characteristics

The hypothesis investigated whether exercise performance over a broad range of intensities is determined by specific skeletal muscle characteristics. Seven subjects performed 8-10 exhaustive cycle trials at different workloads, ranging from 150 to 700 W (150 min to 20 s). No relationships between the performance times at high and low workloads were observed. A relationship (P < 0.05) was noticed between the percentage of fast-twitch x fibers and the exercise time at 579 ± 21 W (～30 s; r(2) = 0.88). Capillary-to-fiber-ratio (r(2): 0.58-0.85) was related (P < 0.05) to exercise time at work intensities ranging from 395 to 270 W (2.5-21 min). Capillary density was correlated (r(2) = 0.68; P < 0.05) with the net rate of plasma K(+) accumulation during an ～3-min bout and was estimated to explain 50-80% (P < 0.05) of the total variance observed in exercise performances lasting ～30 s to 3 min. The Na(+)-K(+) pump β(1)-subunit expression was found to account for 13-34% (P < 0.05) during exhaustive exercise of ～1-4 min. In conclusion, exercise performance at different intensities is related to specific physiological variables. A large distribution of fast-twitch x fibers may play a role during very intense efforts, i.e., ～30 s. Muscle capillaries and the Na(+)-K(+) pump β(1)-subunit seem to be important determinants for performance during exhaustive high-intensity exercises lasting between 30 s and 4 min.     

Four weeks of normobaric "live high-train low" do not alter muscular or systemic capacity for maintaining pH and K⁺ homeostasis during intense exercise

It was investigated if athletes subjected to 4 wk of living in normobaric hypoxia (3,000 m; 16 h/day) while training at 800-1,300 m ["live high-train low" (LHTL)] increase muscular and systemic capacity for maintaining pH and K(+) homeostasis as well as intense exercise performance. The design was double-blind and placebo controlled. Mean power during 30-s all-out cycling was similar before and immediately after LHTL (650 ± 31 vs. 628 ± 32 W; n = 10) and placebo exposure (658 ± 22 vs. 660 ± 23 W; n = 6). Supporting the performance data, arterial plasma pH, lactate, and K(+) during submaximal and maximal exercise were also unaffected by the intervention in both groups. In addition, muscle buffer capacity (in mmol H(+)·kg dry wt(-1)·pH(-1)) was similar before and after in both the LHTL (140 ± 12 vs. 140 ± 16) and placebo group (145 ± 2 vs. 140 ± 3). The expression of sarcolemmal H(+) transporters (Na(+)/H(+) exchanger 1, monocarboxylate transporters 1 and 4), as well as expression of Na(+)-K(+) pump subunits-α(1), -α(2), and -β(1) was also similar before and after the intervention. In conclusion, muscular and systemic capacity for maintaining pH and K(+) balance during exercise is similar before and after 4 wk of placebo-controlled normobaric LHTL. In accordance, 30-s all-out sprint ability was similar before and after LHTL.     

Effect of exercise and training on phospholemman phosphorylation in human skeletal muscle

Phospholemman (PLM, FXYD1) is a partner protein and regulator of the Na(+)-K(+)-ATPase (Na(+)-K(+) pump). We explored the impact of acute and short-term training exercise on PLM physiology in human skeletal muscle. A group of moderately trained males (n = 8) performed a 1-h acute bout of exercise by utilizing a one-legged cycling protocol. Muscle biopsies were taken from vastus lateralis at 0 and 63 min (non-exercised leg) and 30 and 60 min (exercised leg). In a group of sedentary males (n = 9), we determined the effect of a 10-day intense aerobic cycle training on Na(+)-K(+)-ATPase subunit expression, PLM phosphorylation, and total PLM expression as well as PLM phosphorylation in response to acute exercise (1 h at ～72% Vo(2peak)). Biopsies were taken at rest, immediately following, and 3 h after an acute exercise bout before and at the conclusion of the 10-day training study. PLM phosphorylation was increased both at Ser(63) and Ser(68) immediately after acute exercise (75%, P < 0.05, and 30%, P < 0.05, respectively). Short-term training had no adaptive effect on PLM phosphorylation at Ser(63) and Ser(68), nor was the total amount of PLM altered posttraining. The protein expressions of α(1)-, α(2)-,and β(1)-subunits of Na(+)-K(+)-ATPase were increased after training (113%, P < 0.05, 49%, P < 0.05, and 27%, P < 0.05, respectively). Whereas an acute bout of exercise increased the phosphorylation of PKCα/βII on Thr(638/641) pre- and posttraining, phosphorylation of PKCζ/λ on Thr(403/410) was increased in response to acute exercise only after the 10-day training. In conclusion, we show that only acute exercise, and not short-term training, increases phosphorylation of PLM on Ser(63) and Ser(68), and data from one-legged cycling indicate that this effect of exercise on PLM phosphorylation is not due to systemic factors. Our results provide evidence that phosphorylation of PLM may play a role in the acute regulation of the Na(+)-K(+)-ATPase response to exercise.     

Chronic intermittent hypoxia and incremental cycling exercise independently depress muscle in vitro maximal Na+-K+-ATPase activity in well-trained athletes.

Athletes commonly attempt to enhance performance by training in normoxia but sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia reduces muscle Na(+)-K(+)-ATPase content, whereas fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair performance. We examined whether LHTL and intense exercise would decrease muscle Na(+)-K(+)-ATPase activity and whether these effects would be additive and sufficient to impair performance or plasma K(+) regulation. Thirteen subjects were randomly assigned to two fitness-matched groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate altitude (3,000 m, inspired O(2) fraction = 15.48%) for 23 nights and lived and trained by day under normoxic conditions in Canberra (altitude approximately 600 m). Con lived, trained, and slept in normoxia. A standardized incremental exercise test was conducted before and after LHTL. A vastus lateralis muscle biopsy was taken at rest and after exercise, before and after LHTL or Con, and analyzed for maximal Na(+)-K(+)-ATPase activity [K(+)-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase)] and Na(+)-K(+)-ATPase content ([(3)H]ouabain binding sites). 3-O-MFPase activity was decreased by -2.9 +/- 2.6% in LHTL (P < 0.05) and was depressed immediately after exercise (P < 0.05) similarly in Con and LHTL (-13.0 +/- 3.2 and -11.8 +/- 1.5%, respectively). Plasma K(+) concentration during exercise was unchanged by LHTL; [(3)H]ouabain binding was unchanged with LHTL or exercise. Peak oxygen consumption was reduced in LHTL (P < 0.05) but not in Con, whereas exercise work was unchanged in either group. Thus LHTL had a minor effect on, and incremental exercise reduced, Na(+)-K(+)-ATPase activity. However, the small LHTL-induced depression of 3-O-MFPase activity was insufficient to adversely affect either K(+) regulation or total work performed.     

Membrane leakage and increased content of Na+ -K+ pumps and Ca2+ in human muscle after a 100-km run.

During prolonged exercise, changes in the ionic milieu in and surrounding the muscle fibers may lead to fatigue or damage of the muscle and thereby impair performance. In 10 male subjects, we investigated the effects of 100 km running on muscle and plasma electrolyte contents, muscle Na+ -K+ pump content, and plasma concentrations of creatine kinase (CK) and lactate dehydrogenase (LDH). After completion of a 100-km run, significant increases were found in plasma K+ (from 4.0 +/- 0.1 to 5.5 +/- 0.2 mM, P < 0.001), muscle Na+ -K+ pump content (from 334 +/- 11 to 378 +/- 17 pmol/g, P < 0.05), and total muscle Ca2+ content (from 0.84 +/- 0.03 to 1.02 +/- 0.04 micromol/g, P < 0.001). There was also a large increase in the plasma levels of the muscle-specific enzymes CK and LDH, which reached peak values at the end of the run and lasted several days after the run, indicating that a significant degree of muscle membrane leakage was present. The simultaneous occurrence of raised cellular Ca2+ content and muscle membrane leakage supports the theory that Ca2+ plays a role in the initiation of degenerative processes in muscles after severe exercise.     

Reversibility and partial reactions of the Na(+)-K+ pump of rat erythrocytes

An assay was developed to characterize the kinetic parameters of the Na(+)-K+ pump of rat erythrocytes under conditions as physiological as possible. Changes in the red cell Na+ and Rb+ content were determined in Na+ media (containing 2.5 mM inorganic phosphate (PO4) as a function of cell Na+ (2-8 mmol/l) and extracellular Rb+ (0.2-5 mM). Evaluation of the data revealed that under these conditions the Na(+)-K+ pump mediates, in addition to forward running 3 Nai+: 2 Rbo+ exchange, 1 Ki+:Rbo+ exchange and pump reversal (3 Nao+:2 Ki+ exchange). The two latter modes of Na(+)-K+ pump operation are accelerated by PO4 and lowering of cell Na+. At physiological cation and PO4 concentrations, 1Ki+:Rbo+ exchange contributes by 30-60% to total ouabain-sensitive Rb+ uptake. Thereby, the stoichiometry of ouabain-sensitive Na+ net-extrusion to Rb+ uptake is reduced to values between 1.0 and 0.5. Only at cell Na+ contents above 20 mmol/l the Na+:Rb+ stoichiometry approaches the value of 3:2 = 1.5. At certain constellations of Nai+ and Rbo+ the Na(+)-K+ pump cannot perform any net-transport of Na+ and K+ (Rb+). These equilibrium points are not far from those expected from thermodynamic considerations. The results demonstrate that in normal rat erythrocytes the reversible reaction cycle of the Na(+)-K+ pump runs in several modes of operation. The "abnormal" modes complicate the interpretation of unidirectional fluxes mediated by the Na(+)-K+ pump.     

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.     

The 10-20-30 training concept improves performance and health profile in moderately trained runners

The effect of an alteration from regular endurance to interval (10-20-30) training on the health profile, muscular adaptations, maximum oxygen uptake (Vo(2max)), and performance of runners was examined. Eighteen moderately trained individuals (6 females and 12 males; Vo(2max): 52.2 ± 1.5 ml·kg(-1)·min(-1)) (means ± SE) were divided into a high-intensity training (10-20-30; 3 women and 7 men) and a control (CON; 3 women and 5 men) group. For a 7-wk intervention period the 10-20-30 replaced all training sessions with 10-20-30 training consisting of low-, moderate-, and high-speed running (<30%, <60%, and >90% of maximal intensity) for 30, 20, and 10 s, respectively, in three or four 5-min intervals interspersed by 2 min of recovery, reducing training volume by 54% (14.0 ± 0.9 vs. 30.4 ± 2.3 km/wk) while CON continued the normal training. After the intervention period Vo(2max) in 10-20-30 was 4% higher, and performance in a 1,500-m and a 5-km run improved (P < 0.05) by 21 and 48 s, respectively. In 10-20-30, systolic blood pressure was reduced (P < 0.05) by 5 ± 2 mmHg, and total and low-density lipoprotein (LDL) cholesterol was lowered (P < 0.05) by 0.5 ± 0.2 and 0.4 ± 0.1 mmol/l, respectively. No alterations were observed in CON. Muscle membrane proteins and enzyme activity did not change in either of the groups. The present study shows that interval training with short 10-s near-maximal bouts can improve performance and Vo(2max) despite a ～50% reduction in training volume. In addition, the 10-20-30 training regime lowers resting systolic blood pressure and blood cholesterol, suggesting a beneficial effect on the health profile of already trained individuals.     

Human power output during repeated sprint cycle exercise: the influence of thermal stress

Thermal stress is known to impair endurance capacity during moderate prolonged exercise. However, there is relatively little available information concerning the effects of thermal stress on the performance of high-intensity short-duration exercise. The present experiment examined human power output during repeated bouts of short-term maximal exercise. On two separate occasions, seven healthy males performed two 30-s bouts of sprint exercise (sprints I and II), with 4 min of passive recovery in between, on a cycle ergometer. The sprints were performed in both a normal environment [18.7 (1.5) degrees C, 40 (7)% relative humidity (RH; mean SD)] and a hot environment [30.1 (0.5) degrees C, 55 (9)% RH]. The order of exercise trials was randomised and separated by a minimum of 4 days. Mean power, peak power and decline in power output were calculated from the flywheel velocity after correction for flywheel acceleration. Peak power output was higher when exercise was performed in the heat compared to the normal environment in both sprint I [910 (172) W vs 656 (58) W; P < 0.01] and sprint II [907 (150) vs 646 (37) W; P < 0.05]. Mean power output was higher in the heat compared to the normal environment in both sprint I [634 (91) W vs 510 (59) W; P < 0.05] and sprint II [589 (70) W vs 482 (47) W; P < 0.05]. There was a faster rate of fatigue (P < 0.05) when exercise was performed in the heat compared to the normal environment. Arterialised-venous blood samples were taken for the determination of acid-base status and blood lactate and blood glucose before exercise, 2 min after sprint I, and at several time points after sprint II. Before exercise there was no difference in resting acid-base status or blood metabolites between environmental conditions. There was a decrease in blood pH, plasma bicarbonate and base excess after sprint I and after sprint II. The degree of post-exercise acidosis was similar when exercise was performed in either of the environmental conditions. The metabolic response to exercise was similar between environmental conditions; the concentration of blood lactate increased (P < 0.01) after sprint I and sprint II but there were no differences in lactate concentration when comparing the exercise bouts performed in a normal and a hot environment. These data demonstrate that when brief intense exercise is performed in the heat, peak power output increases by about 25% and mean power output increases by 15%; this was due to achieving a higher pedal cadence in the heat.     

Effect of training on muscle metabolism during treadmill sprinting

Sixteen subjects volunteered for the study and were divided into a control (4 males and 4 females) and experimental group (4 males and 4 females, who undertook 8 wk of sprint training). All subjects completed a maximal 30-s sprint on a nonmotorized treadmill and a 2-min run on a motorized treadmill at a speed designed to elicit 110% of maximum oxygen uptake (110% run) before and after the period of training. Muscle biopsies were taken from vastus lateralis at rest and immediately after exercise. The metabolic responses to the 110% run were unchanged over the 8-wk period. However, sprint training resulted in a 12% (P less than 0.05) and 6% (NS) improvement in peak and mean power output, respectively, during the 30-s sprint test. This improvement in sprint performance was accompanied by an increase in the postexercise muscle lactate (86.0 +/- 26.4 vs. 103.6 +/- 24.6 mmol/kg dry wt, P less than 0.05) and plasma norepinephrine concentrations (10.4 +/- 5.4 vs. 12.1 +/- 5.3 nmol/l, P less than 0.05) and by a decrease in the postexercise blood pH (7.17 +/- 0.11 vs. 7.09 +/- 0.11, P less than 0.05). There was, however, no change in skeletal muscle buffering capacity as measured by the homogenate technique (67.6 +/- 6.5 vs. 71.2 +/- 4.5 Slykes, NS).     

Prolonged exercise to fatigue in humans impairs skeletal muscle Na+-K+-ATPase activity, sarcoplasmic reticulum Ca2+ release, and Ca2+ uptake.

Prolonged exhaustive submaximal exercise in humans induces marked metabolic changes, but little is known about effects on muscle Na+-K+-ATPase activity and sarcoplasmic reticulum Ca2+ regulation. We therefore investigated whether these processes were impaired during cycling exercise at 74.3 +/- 1.2% maximal O2 uptake (mean +/- SE) continued until fatigue in eight healthy subjects (maximal O2 uptake of 3.93 +/- 0.69 l/min). A vastus lateralis muscle biopsy was taken at rest, at 10 and 45 min of exercise, and at fatigue. Muscle was analyzed for in vitro Na+-K+-ATPase activity [maximal K+-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase) activity], Na+-K+-ATPase content ([3H]ouabain binding sites), sarcoplasmic reticulum Ca2+ release rate induced by 4 chloro-m-cresol, and Ca2+ uptake rate. Cycling time to fatigue was 72.18 +/- 6.46 min. Muscle 3-O-MFPase activity (nmol.min(-1).g protein(-1)) fell from rest by 6.6 +/- 2.1% at 10 min (P <0.05), by 10.7 +/- 2.3% at 45 min (P <0.01), and by 12.6 +/- 1.6% at fatigue (P <0.01), whereas 3[H]ouabain binding site content was unchanged. Ca2+ release (mmol.min(-1).g protein(-1)) declined from rest by 10.0 +/- 3.8% at 45 min (P <0.05) and by 17.9 +/- 4.1% at fatigue (P < 0.01), whereas Ca2+ uptake rate fell from rest by 23.8 +/- 12.2% at fatigue (P=0.05). However, the decline in muscle 3-O-MFPase activity, Ca2+ uptake, and Ca2+ release were variable and not significantly correlated with time to fatigue. Thus prolonged exhaustive exercise impaired each of the maximal in vitro Na+-K+-ATPase activity, Ca2+ release, and Ca2+ uptake rates. This suggests that acutely downregulated muscle Na+, K+, and Ca2+ transport processes may be important factors in fatigue during prolonged exercise in humans.     

Erythrocyte cations and Na+,K+-ATPase pump activity in athletes and sedentary subjects

The chronic effect of training on intraerythrocyte cationic concentrations and on red cell Na+,K+-ATPase pump activity was studied by comparing well-trained athletes with sedentary subjects at rest. Also the acute effect of a 50-min cross-country run on these erythrocyte measurements was studied in the athletes. At rest the intraerythrocyte potassium concentration was increased (P less than 0.01) in the athletes compared to that of the control subjects. The intraerythrocyte concentrations of sodium and magnesium and red cell Na+,K+-ATPase pump activity were, however, similar in the trained and the untrained subjects. As compared with the resting condition, the intraerythrocyte potassium concentration was decreased (P less than 0.05) after exercise in the athletes, and this was accompanied by a minor increase in the intraerythrocyte sodium concentration. Red cell Na+,K+-ATPase pump activity was slightly increased (P less than 0.05) after exercise.     

Ionic mechanisms of excitation-induced regulation of Na+-K+-ATPase mRNA expression in isolated rat EDL muscle

This study investigated the effects of electrical stimulation on Na+-K+-ATPase isoform mRNA, with the aim to identify factors modulating Na+-K+-ATPase mRNA in isolated rat extensor digitorum longus (EDL) muscle. Interventions designed to mimic exercise-induced increases in intracellular Na+ and Ca2+ contents and membrane depolarization were examined. Muscles were mounted on force transducers and stimulated with 60-Hz 10-s pulse trains producing tetanic contractions three times at 10-min intervals. Ouabain (1.0 mM, 120 min), veratridine (0.1 mM, 30 min), and monensin (0.1 mM, 30 min) were used to increase intracellular Na+ content. High extracellular K+ (13 mM, 60 min) and the Ca2+ ionophore A-23187 (0.02 mM, 30 min) were used to induce membrane depolarization and elevated intracellular Ca2+ content, respectively. Muscles were analyzed for Na+-K+-ATPase alpha1-alpha3 and beta1-beta3 mRNA (real-time RT-PCR). Electrical stimulation had no immediate effect on Na+-K+-ATPase mRNA; however at 3 h after stimulation, it increased alpha1, alpha2, and alpha3 mRNA by 223, 621, and 892%, respectively (P = 0.010), without changing beta mRNA. Ouabain, veratridine, and monensin increased intracellular Na+ content by 769, 724, and 598%, respectively (P = 0.001) but did not increase mRNA of any isoform. High intracellular K+ concentration elevated alpha1 mRNA by 160% (P = 0.021), whereas A-23187 elevated alpha3 mRNA by 123% (P = 0.035) but reduced beta1 mRNA by 76% (P = 0.001). In conclusion, electrical stimulation induced subunit-specific increases in Na+-K+-ATPase mRNA in isolated rat EDL muscle. Furthermore, Na+-K+-ATPase mRNA appears to be regulated by different stimuli, including cellular changes associated with membrane depolarization and increased intracellular Ca2+ content but not increased intracellular Na+ content.