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Physical inactivity is a global health risk that can be addressed through application of exercise training suitable for an individual's health and age. People's willingness to participate in physical activity is often limited by an initially poor physical capability and early onset of fatigue. One factor associated with muscle fatigue during intense contractions is an inexcitability of skeletal muscle cells, reflecting impaired transmembrane Na+/K+ exchange and membrane depolarization, which are regulated via the transmembranous protein Na+-K+-ATPase (NKA). This short review focuses on the plasticity of NKA in skeletal muscle in humans after periods of altered usage, exploring NKA upregulation with exercise training and downregulation with physical inactivity. In human skeletal muscle, the NKA content quantified by [³H]ouabain binding site content shows robust, yet tightly constrained, upregulation of 8-22% with physical training, across a broad range of exercise training types. Muscle NKA content in humans undergoes extensive downregulation with injury that involves substantial muscular inactivity. Surprisingly, however, no reduction in NKA content was found in the single study that investigated short-term disuse. Despite clear findings that exercise training and injury modulate NKA content, the adaptability of the individual NKA isoforms in muscle (α1-3 and β1-3) and of the accessory and regulatory protein FXYD1 are surprisingly inconsistent across studies, for exercise training as well as for injury/disuse. Potential reasons for this are explored. Finally, we provide suggestions for future studies to provide greater understanding of NKA regulation during exercise training and inactivity in humans. [ABSTRACT FROM AUTHOR]

Muscle oxygen kinetics at onset of intense dynamic exercise in humans. Am J Physiol Regulatory Integrative Comp Physiol 279: R899-R906, 2000.--The present study examined the onset and the rate of rise of muscle oxidation during intense exercise in humans and whether oxygen availability limits muscle oxygen uptake in the initial phase of intense exercise. Six subjects performed 3 min of intense one-legged knee-extensor exercise [65.3 [+ or -] 3.7 (means [+ or -] SE) W]. The femoral arteriovenous blood mean transit time (MTT) and time from femoral artery to muscle microcirculation was determined to allow for an examination of the oxygen uptake at capillary level. MTT was 15.3 [+ or -] 1.8 s immediately before exercise, 10.4 [+ or -] 0.7 s after 6 s of exercise, and 4.7 [+ or -] 0.5 s at the end of exercise. Arterial venous [0.sub.2] difference ([a-v.sub.diff] [O.sub.2]) of 18 [+ or -] 5 ml/l before the exercise was unchanged after 2 s, but it increased (P [is less than] 0.05) after 6 s of exercise to 43 [+ or -] 10 ml/l and reached 146 [+ or -] 4 ml/l at the end of exercise. Thigh oxygen uptake increased (P [is less than] 0.05) from 32 [+ or -] 8 to 102 [+ or -] 28 ml/min after 6 s of exercise and to 789 [+ or -] 88 ml/min at the end of exercise. The time to reach half-peak [a-v.sub.diff] [O.sub.2] and thigh oxygen uptake was 13 [+ or -] 2 and 25 [+ or -] 3 s, respectively. The difference between thigh oxygen delivery (blood flow x arterial oxygen content) and thigh oxygen uptake increased (P [is less than] 0.05) after 6 s and returned to preexercise level after 14 s. The present data suggest that, at the onset of exercise, oxygen uptake of the exercising muscles increases after a delay of only a few seconds, and oxygen extraction peaks after ~50 s of exercise. The limited oxygen utilization in the initial phase of intense exercise is not caused by insufficient oxygen availability. blood flow; mean transit time; oxygen delivery

Juel, C., H. Pilegaard, J. J. Nielsen, and J. Bangsbo. Interstitial [K.sup.+] in human skeletal muscle during and after dynamic graded exercise determined by microdialysis. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 278: R400-R406, 2000.--Interstitial [K.sup.+] concentrations were measured during one-legged knee-extensor exercise by use of microdialysis with probes inserted in the vastus lateralis muscle of the subjects. [K.sup.+] in the dialysate was measured either by flame photometry or a [K.sup.+]-sensitive electrode placed in the perfusion outlet. The correction for fractional [K.sup.+] recovery was based on the assumption of identical fractional thallium loss. The interstitial [K.sup.+] was 4.19 [+ or -] 0.09 mM at rest and increased to 6.17 [+ or -] 0.19, 7.48 [+ or -] 1.18, and 9.04 [+ or -] 0.74 mM at 10, 30, and 50 W exercise, respectively. The individual probes demonstrated large variations in interstitial [K.sup.+], and values [is greater than] 10 mM were obtained. The observed interstitial [K.sup.+] was markedly higher than previously found for venous [K.sup.+] concentrations at similar work intensities. The present data support a potential role for interstitial [K.sup.+] in regulation of blood flow and development of fatigue. fatigue; regulation of blood flow

Due to a high prevalence of asthma and exercise‐induced bronchoconstriction in elite athletes, there is a high use of beta2‐adrenoceptor agonists (beta2‐agonists) in the athletic population. While anabolic in rodents, no study has been able to detect hypertrophy in humans after chronic beta2‐agonist inhalation. We investigated whether inhaled beta2‐agonist, terbutaline, alters body composition and metabolic rate with and without concurrent exercise training in healthy young men. Sixty‐seven participants completed a 4‐week intervention of daily terbutaline (8 × 0.5 mg) or placebo treatment without concurrent training (habitual; n = 23), with resistance (n = 23) or endurance (n = 21) training 3 times weekly. Before and after the interventions, participant's body composition was determined by dual‐energy X‐ray absorptiometry and resting metabolic rate and substrate oxidation by indirect calorimetry. Terbutaline increased lean body mass by 1.03 kg (95% CI 0.29‐1.76; P < .05) and 1.04 kg (95% CI 0.16‐1.93; P < .05) compared to placebo in the habitual and resistance training group, respectively, but had no effect compared to placebo in the endurance training group [−0.56 kg (95% CI −1.74‐0.62; P > .05)]. Fat mass, bone mineral content, and resting metabolic rate did not change differently between treatments with the intervention. Daily inhalation of terbutaline in near‐therapeutic doses induces skeletal muscle growth. This observation should be a concern for antidoping authorities. [ABSTRACT FROM AUTHOR]

Key points: Low‐volume high‐intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high‐volume moderate‐intensity exercise training. These training‐induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high‐intensity exercise is still incompletely understood. Here we show that, by comparing different work‐matched low‐volume high‐intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis‐related muscle mRNA responses. Furthermore, when compared with high‐volume moderate‐intensity exercise, only the low‐volume high‐intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses. The present results, besides improving our understanding of the mechanisms mediating exercise‐induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals. Abstract: The aim of the present study was to examine the impact of exercise‐induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance‐trained men performed three cycling exercise protocols characterized by different metabolic profiles in a randomized, counter‐balanced order. Specifically, two work‐matched low‐volume supramaximal‐intensity intermittent regimes, consisting of repeated‐sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high‐volume continuous moderate‐intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3 h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post‐exercise plasma adrenaline levels in comparison with RS and CM. Exercise‐induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise‐induced PGC‐1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF‐2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise‐induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high‐intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations. [ABSTRACT FROM AUTHOR]