Origins of [H+] Changes in Exercising Skeletal Muscle

1995 ◽  
Vol 20 (3) ◽  
pp. 357-368 ◽  
Author(s):  
Michael I. Lindinger

This brief review describes the main physicochemical factors that contribute to increases in intracellular hydrogen ion concentration ([H+]i) in mammalian skeletal muscle during high intensity exercise. High intensity exercise results in changes in the three main independent physicochemical variables: PCO2, the strong ion difference ([SID]), and total concentration of weak acids and bases ([Atot]), within the intracellular fluid compartment of contracting muscle that result in increased [H+]i. The decrease in [SID] contributes 62% to the increase in [H+]i, due to decreased [K+]i and increased [lactate]i; the decrease in phosphocreatine ([PCr2−]i) exerts an alkalinizing effect. The increase in [Atot], resulting primarily from increases in inorganic phosphate and creatine as a result of PCr2− breakdown, contributes 19% to the increase in [H+]i. An increase in the apparent proton dissociation constant (KA) for [Atot] contributes 7% to the increase in [H+]i. PCO2 is a relatively poor effector of changes in [H+]i, such that a 50-mmHg increase in PCO2 contributes only 12% to the increase in [H+]i during high intensity exercise. Key words: acid-base balance, strong ion difference, phosphocreatine, potassium, carbon dioxide, metabolism

2001 ◽  
Vol 280 (2) ◽  
pp. R481-R487 ◽  
Author(s):  
Robert J. Preston ◽  
Aaron P. Heenan ◽  
Larry A. Wolfe

In accordance with Stewart's physicochemical approach, the three independent determinants of plasma hydrogen ion concentration ([H+]) were measured at rest and during exercise in the follicular (FP) and luteal phase (LP) of the human menstrual cycle. Healthy, physically active women with similar physical characteristics were tested during either the FP ( n = 14) or LP ( n = 14). Arterialized blood samples were obtained at rest and after 5 min of upright cycling at both 70 and 110% of the ventilatory threshold (TVent). Measurements included plasma [H+], arterial carbon dioxide tension (PaCO2 ), total weak acid ([ATot]) as reflected by total protein, and the strong-ion difference ([SID]). The transition from rest to exercise in both groups resulted in a significant increase in [H+] at 70% TVentversus rest and at 110% TVent versus both rest and 70% TVent. No significant between-group differences were observed for [H+] at rest or in response to exercise. At rest in the LP, [ATot] and PaCO2 were significantly lower (acts to decrease [H+]) compared with the FP. This effect was offset by a reduction in [SID] (acts to increase [H+]). After the transition from rest to exercise, significantly lower [ATot] during the LP was again observed. Although the [SID] and PaCO2 were not significantly different between groups, trends for changes in these two variables were similar to changes in the resting state. In conclusion, mechanisms regulating [H+] exhibit phase-related differences to ensure [H+] is relatively constant regardless of progesterone-mediated ventilatory changes during the LP.


2005 ◽  
Vol 2 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Amanda Waller ◽  
Michael I Lindinger

AbstractThe present study used the physicochemical approach to characterize the changes in acid–base status that occur in Standardbred racehorses during recovery from high-intensity exercise. Jugular venous blood was sampled from nine Standardbreds in racing condition, at rest and for 2 h following a high-intensity training workout. Plasma [H+] increased from 39.1±1.0 neq l−1 at rest to 44.8±2.7 neq l−1 at 1 min of recovery. A decreased strong ion difference ([SID]) was the primary contributor to the increased [H+] immediately at the end of exercise, while increased plasma weak ion concentration ([Atot]) was a minor contributor to the acidosis. A decreased partial pressure of carbon dioxide (PCO2) at 1 min of recovery had a slight alkalinizing effect. The decreased [SID] at 1 min of recovery was a result of a 15.1±3.1 meq l−1 increase in [lactate−], as [Na+] and [K+] were also increased by 6.5±0.7 and 1.14±0.06 meq l−1, respectively, at 1 min of recovery. It is concluded that high-intensity exercise and recovery is associated with significant changes in acid–base balance, and that full recovery of many parameters that determine acid–base status requires 60–120 min.


1982 ◽  
Vol 100 (1) ◽  
pp. 23-40 ◽  
Author(s):  
R G O'Regan ◽  
S Majcherczyk

Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.


2014 ◽  
Vol 116 (5) ◽  
pp. 553-559 ◽  
Author(s):  
Audrey Baguet ◽  
Inge Everaert ◽  
Benito Yard ◽  
Verena Peters ◽  
Johannes Zschocke ◽  
...  

Given the ergogenic properties of β-alanyl-L-histidine (carnosine) in skeletal muscle, it can be hypothesized that elevated levels of circulating carnosine could equally be advantageous for high-intensity exercises. Serum carnosinase (CN1), the enzyme hydrolyzing the dipeptide, is highly active in the human circulation. Consequently, dietary intake of carnosine usually results in rapid degradation upon absorption, yet this is less pronounced in subjects with low CN1 activity. Therefore, acute carnosine supplementation before high-intensity exercise could be ergogenic in these subjects. In a cross-sectional study, we determined plasma CN1 activity and content in 235 subjects, including 154 untrained controls and 45 explosive and 36 middle- to long-distance elite athletes. In a subsequent double-blind, placebo-controlled, crossover study, 12 men performed a cycling capacity test at 110% maximal power output (CCT 110%) following acute carnosine (20 mg/kg body wt) or placebo supplementation. Blood samples were collected to measure CN1 content, carnosine, and acid-base balance. Both male and female explosive athletes had significantly lower CN1 activity (14% and 21% lower, respectively) and content (30% and 33% lower, respectively) than controls. Acute carnosine supplementation resulted only in three subjects in carnosinemia. The CCT 110% performance was not improved after carnosine supplementation, even when accounting for low/high CN1 content. No differences were found in acid-base balance, except for elevated resting bicarbonate following carnosine supplementation and in low CN1 subjects. In conclusion, explosive athletes have lower serum CN1 activity and content compared with untrained controls, possibly resulting from genetic selection. Acute carnosine supplementation does not improve high-intensity performance.


2005 ◽  
Vol 2 (4) ◽  
pp. 209-217 ◽  
Author(s):  
Michael I. Lindinger

AbstractThe fatigue of high-intensity exercise is now believed to reside primarily within the excitation–contraction coupling processes associated with the plasma membrane of skeletal muscle (sarcolemm) and calcium-mediated events leading to myofilament sliding. This paper summarizes recent developments and advances in the identification of factors that contribute to changes in sarcolemmal excitability of mammalian skeletal muscle as a consequence of high-intensity exercise. There is an increasing recognition of the probable role that is played by the transverse tubular system (T-system), a system that comprises c. 80% of the total sarcolemmal surface capable of ion exchange. Furthermore, the fluid within the T-system has limited access to interstitial fluid bathing myofibres; hence, T-system fluid is probably markedly different from interstitial fluid during high-intensity exercise. Mechanically skinned fibre preparation is providing many new insights into functions of the surface membrane and T-system in fatigue. A scenario is developed whereby accumulation of potassium within the T-system ([K+]o) contributes to reduced membrane excitability, as well as lowering of T-system sodium and chloride, concomitant with loss of intracellular potassium ([K+]i) and accumulation of intracellular sodium ([Na+]) and chloride ([Cl−]). Lowering the [Na+]o/[Na+]i ratio and raising myoplasmic [Na+]i have been shown to decrease membrane excitability and impair action potential propagation. Maintained high [Cl−]o may also have a protective effect in maintaining membrane excitability, and this effect appears to be very pronounced in the presence of raised [K+]o. In contrast to dogma associating high [H+] to fatigue, recent studies have also shown that induced acidosis that results in increased [H+]o and [H+]i restores force production in muscles and skinned fibres fatigued by intermittent tetanic stimulation. This effect may be due to a decrease in surface membrane Cl− permeability that serves to restore membrane excitability. During high-intensity exercise, simultaneous changes in trans-membrane ion concentrations and membrane ion conductances may serve to reduce impairment of membrane excitability that provides for a maintained, though reduced, contractile function.


Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghan

Normal metabolism results in a net acid production of approximately 1 mmol/kg day−1. Physiological pH is regulated by excretion of this acid load (as carbon dioxide) by the kidneys and the lungs. A series of buffers in the body reduces the effects of metabolic acids on body and urine pH. For acid–base disorders to occur, there must be excessive intake (or loss) of acid (or base) or, alternatively, an inability to excrete acid. For these changes to result in a substantially abnormal pH, the various buffer systems must been overwhelmed. The pH scale is logarithmic, so relatively small changes in pH signify large differences in hydrogen ion concentration. Most minor perturbations in acid–base balance are asymptomatic, as small changes in acid or base levels are rapidly controlled through consumption of buffers or through changes in respiratory rate. Alterations in renal acid excretion take some time to occur. Only when these compensatory mechanisms are overwhelmed do symptoms related to changes in pH develop. This chapter reviews the causes and consequences of acid–base disorders.


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