The detrusor smooth muscle is the main muscle component of the urinary bladder wall. Its ability to contract over a large length interval and to relax determines the bladder function during filling and micturition. These processes are regulated by several external nervous and hormonal control systems, and the detrusor contains multiple receptors and signaling pathways. Functional changes of the detrusor can be found in several clinically important conditions, e.g., lower urinary tract symptoms (LUTS) and bladder outlet obstruction. The aim of this review is to summarize and synthesize basic information and recent advances in the understanding of the properties of the detrusor smooth muscle, its contractile system, cellular signaling, membrane properties, and cellular receptors. Alterations in these systems in pathological conditions of the bladder wall are described, and some areas for future research are suggested.

https://www.physiology.org/doi/pdf/10.1152/physrev.00038.2003

Urinary bladder contraction and relaxation: Physiology and pathophysiology

This article critically discusses whether accumulation of lactic acid, or in reality lactate and/or hydrogen (H+) ions, is a major cause of skeletal muscle fatigue, i.e. decline of muscle force or power output leading to impaired exercise performance. There exists a long history of studies on the effects of increased lactate/H+ concentrations in muscle or plasma on contractile performance of skeletal muscle. Evidence suggesting that lactate/H+ is a culprit has been based on correlation-type studies, which reveal close temporal relationships between intramuscular lactate or H+ accumulation and the decline of force during fatiguing stimulation in frog, rodent or human muscle. In addition, an induced acidosis can impair muscle contractility in non-fatigued humans or in isolated muscle preparations, and several mechanisms to explain such effects have been provided. However, a number of recent high-profile papers have seriously challenged the 'lactic acid hypothesis'. In the 1990s, these findings mainly involved diminished negative effects of an induced acidosis in skinned or intact muscle fibres, at higher more physiological experimental temperatures. In the early 2000s, it was conclusively shown that lactate has little detrimental effect on mechanically skinned fibres activated by artificial stimulation. Perhaps more remarkably, there are now several reports of protective effects of lactate exposure or induced acidosis on potassium-depressed muscle contractions in isolated rodent muscles. In addition, sodium-lactate exposure can attenuate severe fatigue in rat muscle stimulated in situ, and sodium lactate ingestion can increase time to exhaustion during sprinting in humans. Taken together, these latest findings have led to the idea that lactate/H+ is ergogenic during exercise. It should not be taken as fact that lactic acid is the deviant that impairs exercise performance. Experiments on isolated muscle suggest that acidosis has little detrimental effect or may even improve muscle performance during high-intensity exercise. In contrast, induced acidosis can exacerbate fatigue during whole-body dynamic exercise and alkalosis can improve exercise performance in events lasting 1-10 minutes. To reconcile the findings from isolated muscle fibres through to whole-body exercise, it is hypothesised that a severe plasma acidosis in humans might impair exercise performance by causing a reduced CNS drive to muscle.

Lactic acid and exercise performance : culprit or friend?

http://europepmc.org/articles/PMC1330274?pdf=render

Effects of pH on contraction of rabbit fast and slow skeletal muscle fibers.

Decline in intracellular free Mg2+ is associated with irreversible tissue injury after brain trauma.

Phosphorus nuclear magnetic resonance spectra and steady-state O2 consumption rates were obtained from ex vivo arterially perfused cat biceps brachii (fast twitch) and soleus (slow twitch) muscles during and after periods of isometric twitch stimulation at 30 degrees C. In the biceps muscles, steady-state O2 consumption increased and phosphocreatine (PCr) concentration decreased progressively with stimulation. PCr recovery after these stimulation periods followed first-order kinetics with a half time of 10 min. The results in the biceps could be explained by a feedback control of cellular respiration by ADP concentration. In the soleus, steady-state O2 consumption also increased and PCr concentration decreased as stimulation rates increased. The half time for PCr recovery in the soleus was approximately 5 min, but, in contrast to the pattern in the biceps, the kinetics was not first order. There was an overshoot during the recovery period in the PCr content of soleus and a corresponding undershoot of Pi compared with resting values. Mitochondrial regulation by ADP is not sufficient to account for respiratory control in slow-twitch soleus. The respiration rate in neither muscle was dependent on the Pi content. Thus we conclude that the mechanism of control of cellular respiration is both quantitatively and qualitatively different in fast- and slow-twitch skeletal muscle.

Regulation of oxygen consumption in fast- and slow-twitch muscle

31P NMR spectroscopy, chemical analysis, and free Mg2+ of rabbit bladder and uterine smooth muscle

Phosphocreatine (PCr) and intracellular pH changes were monitored by 31P-NMR spectroscopy in isolated, arterially perfused cat biceps and soleus muscles, while the pH of the CO2-bicarbonate buffered perfusate was decreased from 7.1-7.4 to 6.4-6.7 by increasing the CO2 in the equilibrating gas from 5 to up to 70%. In biceps (fast twitch) muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force decreased by 8%, but the rise and relaxation times of tetanic were not significantly changed. In soleus muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force was unchanged, but the rise and relaxation times of tetani were increased by 27 and 112%, respectively. In both muscles greater decreases in tetanic force were observed during repetitive or ischemic stimulation, which resulted in intracellular pH similar to that produced by hypercapnia. Contrary to previous reports, there was no significant decrease in PCr level in either muscle type with decreased intracellular pH. In the soleus at 30 degrees C there was a significant increase in PCr level with decreased pH.

J M Krisanda

Papers

31P NMR spectroscopy, chemical analysis, and free Mg2+ of rabbit bladder and uterine smooth muscle

Effect of decreased pH on force and phosphocreatine in mammalian skeletal muscle.