Peak Twitch Amplitude Research Articles

Performance fatigability during isometric vs. concentric quadriceps fatiguing tasks in men and women

In the present study, we aimed to provide a robust comparison of the fatigability of the knee extensors following isometric (ISO) and concentric (CON) tasks. Twenty young adults (25 ± 4 yr, 10 women) randomly performed the ISO and CON quadriceps intermittent fatigue test, consisting of ten (5 s on/5-s off, ISO) or one-hundred (0.5-s on/0.5-s off, CON) contractions with 10 % increments per stage until exhaustion. Performance fatigability was quantified as maximal isometric (MVIC) and concentric (MVCC) torque loss. Voluntary activation and contractile function (peak-twitch) were investigated using peripheral nerve stimulation. Number of stages (6.2 ± 0.7 vs. 4.9 ± 0.8; P < 0.001) and torque-time integral (20,166 ± 7,821 vs. 11,285 ± 4,933 Nm.s; P < 0.001) were greater for ISO than CON. MVIC, MVCC and voluntary activation decreased similarly between sessions (P > 0.05) whereas peak-twitch amplitude decreased more for CON (P < 0.001). The number of contractions was similar across sexes (ISO: men = 62 ± 8, women = 61 ± 5; CON: men = 521 ± 67, women = 458 ± 76, P > 0.05). MVCC was more reduced in women for both sessions (all P < 0.05), while MVIC loss was similar between sexes. We concluded that, despite greater torque-time integral and duration for ISO, both sessions induced a similar performance fatigability at exhaustion. Contractile function was more altered in CON. Finally, sex-related difference in fatigability depends on the contraction mode used during testing.

Acute effect of tendon vibration applied during isometric contraction at two knee angles on maximal knee extension force production

The aim of the current study was to investigate the effect of a single session of prolonged tendon vibration combined with low submaximal isometric contraction on maximal motor performance. Thirty-two young sedentary adults were assigned into two groups that differed based on the knee angle tested: 90° or 150° (180° = full knee extension). Participants performed two fatigue-inducing exercise protocols: one with three 10 min submaximal (10% of maximal voluntary contraction) knee extensor contractions and patellar tendon vibration (80 Hz) another with submaximal knee extensor contractions only. Before and after each fatigue protocol, maximal voluntary isometric contractions (MVC), voluntary activation level (assessed by the twitch interpolation technique), peak-to-peak amplitude of maximum compound action potentials of vastus medialis and vastus lateralis (assessed by electromyography with the use of electrical nerve stimulation), peak twitch amplitude and peak doublet force were measured. The knee extensor fatigue was significantly (P<0.05) greater in the 90° knee angle group (-20.6% MVC force, P<0.05) than the 150° knee angle group (-8.3% MVC force, P = 0.062). Both peripheral and central alterations could explain the reduction in MVC force at 90° knee angle. However, tendon vibration added to isometric contraction did not exacerbate the reduction in MVC force. These results clearly demonstrate that acute infrapatellar tendon vibration using a commercial apparatus operating at optimal conditions (i.e. contracted and stretched muscle) does not appear to induce knee extensor neuromuscular fatigue in young sedentary subjects.

Six weeks of localized heat therapy does not affect muscle mass, strength and contractile properties in healthy active humans.

Animal and human studies have shown that repeated heating may induce skeletal muscle adaptations, increasing muscle strength. The aim of this study is to investigate the effect of 6weeks of localized heating on skeletal muscle strength, volume and contractile properties in healthy humans. Fifteen active participants (8 males/7 females, 35 ± 6 years, 70 ± 14kg, 173 ± 7cm, average training of 87min per week) were subjected to 6weeks of single-leg heat therapy. Heat pads were applied for 8h/day, 5days/week, on one randomly selected calf of each participant, while the contralateral leg acted as control. The heat pads increased muscle temperature by 4.6 ± 1.2°C (p < 0.001). Every 2weeks, participants were tested for morphological (MRI), architectural (ultrasound), contractile (electrically evoked twitch), and force (isometric and isokinetic) adaptations. Repeated localized heating did not affect the cross-sectional area (p = 0.873) or pennation angle (p = 0.345) of the gastrocnemius muscles; did not change the evoked peak twitch amplitude (p = 0.574) or rate of torque development (p = 0.770) of the plantar flexors; and did not change maximal voluntary isometric (p = 0.214) or isokinetic (p = 0.973) plantar flexor torque. Whereas previous studies have observed improved skeletal muscle function following whole-body and localized heating in active and immobilized humans, respectively, the current data suggested that localized heating may not be a potent stimulus for muscle adaptations in active humans.

Oxygen availability affects exercise capacity, but not neuromuscular fatigue characteristics of knee extensors, during exhaustive intermittent cycling.

To compare the effects of different hypoxia severities on exercise capacity, cardio-respiratory, tissue oxygenation and neuromuscular fatigue characteristics in response to exhaustive intermittent cycling. Eleven well-trained cyclists, repeated supra-maximal cycling efforts of 15s (30% of anaerobic power reserve, 609 ± 23W), interspersed with 45s of passive rest until task failure. The exercise was performed on separate days in normoxia (SL; simulated altitude/end-exercise arterial oxygen saturation = 0m/~ 96%), moderate (MH; 2200m/~ 90%) and severe (SH; 4200m/~ 79%) hypoxia in a cross-over design. Neuromuscular tests, including brief (5s) and sustained (30s) maximal isometric voluntary contractions of the knee extensors, were performed at baseline and exhaustion. Exercise capacity decreased with hypoxia severity (23 ± 9, 16 ± 6 and 9 ± 3 cycle efforts in SL, MH and SH, respectively; P < 0.001; η2 = 0.72). Both cerebral (P < 0.001; η2 = 0.86) and muscle (P < 0.01; η2 = 0.54) oxygenation decreased throughout the exercise, independent of condition (P ≥ 0.45; η2 ≥ 0.14). Compared to SL, muscle oxygenation was globally lower in MH and SH (P = 0.011; η2 = 0.36). Cardiovascular solicitation neared maximal values at exhaustion in all conditions. Peak twitch amplitude with single and paired electrical stimuli (P < 0.001; η2 ≥ 0.87), maximal torque (P < 0.001; η2 ≥ 0.48) and voluntary activation measured using transcranial magnetic stimulation (P ≤ 0.034; η2 ≥ 0.31) during brief and sustained MVCs were all reduced at exhaustion, independent of condition (P ≥ 0.196; η2 ≥ 0.15). Despite reduced exercise capacity with increasing severity of hypoxia during exhaustive intermittent cycling, neuromuscular fatigue characteristics were not different at task failure and cardiovascular solicitation neared maximum values.

Passive heat acclimation improves skeletal muscle contractility in humans.

The aim of this study was to investigate the effect of repeated passive heat exposure (i.e., acclimation) on muscle contractility in humans. Fourteen nonheat-acclimated males completed two trials including electrically evoked twitches and voluntary contractions in thermoneutral conditions [Cool: 24°C, 40% relative humidity (RH)] and hot ambient conditions in the hyperthermic state (Hot: 44-50°C, 50% RH) on consecutive days in a counterbalanced order. Rectal temperature was ~36.5°C in Cool and was maintained at ~39°C throughout Hot. Both trials were repeated after 11 days of passive heat acclimation (1 h per day, 48-50°C, 50% RH). Heat acclimation decreased core temperature in Cool (-0.2°C, P < 0.05), increased the time required to reach 39°C in Hot (+9 min, P < 0.05) and increased sweat rate in Hot (+0.7 liter/h, P < 0.05). Moreover, passive heat acclimation improved skeletal muscle contractility as evidenced by an increase in evoked peak twitch amplitude both in Cool (20.5 ± 3.6 vs. 22.0 ± 4.0 N·m) and Hot (20.5 ± 4.7 vs. 22.0 ± 4.0 N·m) (+9%, P < 0.05). Maximal voluntary torque production was also increased both in Cool (145 ± 42 vs. 161 ± 36 N·m) and Hot (125 ± 36 vs. 145 ± 30 N·m) (+17%, P < 0.05), despite voluntary activation remaining unchanged. Furthermore, the slope of the relative torque/electromyographic linear relationship was improved postacclimation (P < 0.05). These adjustments demonstrate that passive heat acclimation improves skeletal muscle contractile function during electrically evoked and voluntary muscle contractions of different intensities both in Cool and Hot. These results suggest that repeated heat exposure may have important implications to passively maintain or even improve muscle function in a variety of performance and clinical settings.

Stressor-induced increase in muscle fatigability of young men and women is predicted by strength but not voluntary activation

This study investigated mechanisms for the stressor-induced changes in muscle fatigability in men and women. Participants performed an isometric-fatiguing contraction at 20% maximal voluntary contraction (MVC) until failure with the elbow flexor muscles. Study one (n = 55; 29 women) involved two experimental sessions: 1) a high-stressor session that required a difficult mental-math task before and during a fatiguing contraction and 2) a control session with no mental math. For some participants (n = 28; 14 women), cortical stimulation was used to examine mechanisms that contributed to muscle fatigability during the high-stressor and control sessions. Study two (n = 23; nine women) determined the influence of a low stressor, i.e., a simple mental-math task, on muscle fatigability. In study one, the time-to-task failure was less for the high-stressor session than control (P < 0.05) for women (19.4%) and men (9.5%): the sex difference response disappeared when covaried for initial strength (MVC). MVC force, voluntary activation, and peak-twitch amplitude decreased similarly for the control and high-stressor sessions (P < 0.05). In study two, the time-to-task failure of men or women was not influenced by the low stressor (P > 0.05). The greater fatigability, when exposed to a high stressor during a low-force task, was not exclusive to women but involved a strength-related mechanism in both weaker men and women that accelerated declines in voluntary activation and slowing of contractile properties.

External anal sphincter fatigue is not improved by N‐acetylcysteine in an animal model

Oxidative stress is associated with skeletal muscle fatigue. This study tests the hypotheses that N-acetylcysteine (NAC) reduces fatigue and accelerates recovery of the rat external anal sphincter (EAS). Fifteen female Wistar rats were killed humanely. The EAS was mounted as a ring preparation and electrically stimulated with 50 Hz trains of 200 ms in duration every 4 s for three and a half minutes. Three groups were analysed: a control group (n = 5), a group pretreated with NAC (10(-4) mol L(-1); n = 5) and a group pretreated with NAC (10(-3) mol L(-1); n = 5). A novel fatigue index was formulated and was compared to a conventional method of expressing fatigue. There was no significant difference at concentrations of NAC (10(-4) mol L(-1); P > 0.05). At high concentrations of NAC (10(-3) mol L(-1)) there was a significant depression in peak twitch amplitude before fatigue (P = 0.04). N-acetylcysteine in both concentrations used, did not alter fatigue or recovery of the rat EAS. There was a significant positive correlation between the two methods of expressing fatigue but the conventional method produced a higher fatigue index (22.4% on average). N-acetylcysteine does not ameliorate fatigue or accelerate recovery of the EAS and may not be a useful medical therapy for faecal incontinence.

Insulin inhibits β-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection

Sympathetic overactivity is closely connected with cell injury and contractile dysfunction during myocardial ischemia/reperfusion (MI/R). Insulin exerts protection for the I/R heart and the underlying mechanisms remain unclear. This study aimed to investigate the ability of insulin to modulate beta-adrenergic actions on myocardial contraction and post-ischemic injury in acute MI/R and the underlying mechanism. Isolated hearts from adult SD rats were subjected to MI/R (30 min/2 h) and treated with isoproterenol (ISO) or/and insulin. Myocardial contraction, cardiomyocyte apoptosis, myocardial injury and infarction were assessed. In a separate study, isolated ventricular myocytes were subjected to simulated I/R (15/30 min) and myocyte shortening and intracellular Ca2+ transient in response to ISO during reperfusion were assessed with presence or absence of insulin. In isolated I/R hearts, insulin largely reversed the ISO-associated contractile functional impairment at 2 h after MI/R, inhibiting ISO-induced declines in heart rate and left ventricular systolic pressure by 34.0% and 23.0% and preventing ISO-induced elevation in left ventricular end-diastolic pressure by 28.7% respectively (all P < 0.05). In addition, ISO alone resulted in enlarged infarct size, elevated CK and LDH activity and increased apoptotic index in I/R hearts compared with vehicle, which were inhibited by treatment of insulin (all P < 0.05). Interestingly, in SI/R cardiomyocytes, insulin alone at 10(-7 )mol/l increased cell contraction whereas attenuated the positive inotropic response to ISO (10(-9 )mol/l) during R as evidenced by a 18.7% reduction in peak twitch amplitude and a 23.9% reduction in calcium transient amplitude (both P < 0.05). Moreover, insulin blunted ISO-mediated increase in PKA activity, enhanced the PKA-dependent phosphorylation of phospholamban (PLB), resulting in increased sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity. Insulin attenuated the contractile response to beta-AR stimulation and suppressed ISO-elicited cardiac dysfunction and cell injury in MI/R. The inhibitory effect of insulin on the beta-adrenergic action involved the inhibition of PKA-mediated Ca2+ transient and promotion of post-ischemic Ca2+ handling.

Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties

This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.

Diminished cardiac contractile response to tetrahydropapaveroline in hypertension: role of β-adrenoceptors and intracellular Ca 2+

Tetrahydropapaveroline (THP), a condensation product of ethanol-derived acetaldehyde, potentiates cardiac function through a β-adrenergic mechanism. It is well established that β-adrenergic activity is markedly depressed in hypertension. However, little is known about the myocardial action of THP in hypertension. In this study, the effect of THP was examined using left ventricular papillary muscles and ventricular myocytes from 10-week-old normotensive (WKY) and spontaneously hypertensive (SHR) rats. The mechanical parameters evaluated include: peak tension developed (PTD), peak twitch amplitude (PTA), time-to-PTD/PTA (TPT/TPS), time-to-90% relaxation/relengthening (RT 90/TR 90), and the maximal velocities of contraction/shortening and relaxation/relengthening (±VT/±d L/d t). Intracellular Ca 2+ transients were measured as fura-2 fluorescence intensity changes (ΔFFI). THP (0.01–100 μM) produced a concentration-dependent increase in myocardial contraction on muscles and myocytes from both groups of animals. However, preparations from the SHR group were generally less responsive to THP than their normotensive counterparts. The increase in contractility by THP was associated with increases in ΔFFI and ±VT, and shortening of TPT/TPS and RT 90/TR 90. The role of β-adrenoceptor(s) in the mechanism of action of THP was explored using specific β-receptor subtype antagonists CGP 207.12A (β 1) and ICI 118,551 (β 2). In preparations from both WKY and SHR hearts, the THP-induced increase in cardiac contractility was either attenuated or blocked by CGP 207.12A and ICI 118,551. These results indicate that THP exhibits a positive action on myocardial contraction that is mediated, in part, through both β 1 and β 2 adrenergic receptors. This cardiac inotropic response, however, is markedly diminished in hypertension, which is due possibly to alterations in β-adrenergic signal transduction.

Influence of age on contractile response to insulin-like growth factor 1 in ventricular myocytes from spontaneously hypertensive rats.

Evidence suggests a pathophysiological role of insulin-like growth factor 1 (IGF-1) in hypertension. Cardiac function is altered with advanced age, similar to hypertension. Accordingly, the effects of IGF-1 on cardiac myocyte shortening and intracellular Ca(2+) were evaluated in hypertension at different ages. Ventricular myocytes were isolated from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), aged 12 and 36 weeks. Mechanical and intracellular Ca(2+) properties were examined by edge-detection and fluorescence microscopy. At 12 weeks, IGF-1 (1 to 500 ng/mL) increased peak twitch amplitude (PTA) and FFI changes (DeltaFFI) in a dose-dependent manner in WKY myocytes, with maximal increases of 27.5% and 35.2%, respectively. However, IGF-1 failed to exert any action on PTA and DeltaFFI in the age-matched SHR myocytes. Interestingly, at 36 weeks, IGF-1 failed to exert any response in WKY myocytes but depressed both PTA and DeltaFFI in a dose-dependent manner in SHR myocytes, with maximal inhibitions of 40.5% and 16.1%, respectively. Myocytes from SHR or 36-week WKY were less sensitive to norepinephrine (1 micromol/L) and KCl (30 mmol/L). Pretreatment with nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 micromol/L) did not alter the IGF-1-induced response in 12-week WKY myocytes but unmasked a positive action in 12-week SHR and 36-week WKY myocytes. L-NAME also significantly attenuated IGF-1-induced depression in 36-week SHR myocytes. In addition, the Ca(2+) channel opener Bay K8644 (1 micromol/L) abolished IGF-1-induced cardiac depression in 36-week SHR myocytes. Collectively, these results suggest that the IGF-1-induced cardiac contractile response was reduced with advanced age as well as with hypertension. Alterations in nitric oxide and intracellular Ca(2+) modulation may underlie, in part, the resistance to IGF-1 in hypertension and advanced age.

Hypertension Augments Ethanol-Induced Depression of Cell Shortening and Intracellular Ca2+ Transients in Adult Rat Ventricular Myocytes

Ethanol, a risk factor for myocardial dysfunction, depresses myocardial contraction. This study was to determine whether ethanol-induced myocardial depression is affected by hypertension. Mechanical properties of ventricular myocytes isolated from both normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were evaluated using a video edge-detection system. Myocytes were electrically stimulated to contract at 0.5 Hz. Contractile properties analyzed include peak twitch amplitude (PTA), time-to-PTA (TPS), time-to-90% relengthening (TR90), and maximal velocities of shortening/relengthening (±dL/dt). Intracellular Ca2+ transients were measured as fura-2 fluorescence intensity (ΔFFI) changes. Acute ethanol exposure (80-640 mg/dl) caused a concentration-dependent inhibition of PTA and ΔFFI in both WKY and SHR myocytes. The extent of maximal inhibition of PTA and FFI was significantly greater in SHRs (53.7 and 38.9%) compared to the WKY group (21.0 and 25.4%). Ethanol did not affect TPS but shortened TR90 and slowed ±dL/dt at high concentration ranges. Interestingly, the augmented ethanol-induced inhibition of cell shortening in hypertension was greatly attenuated by Ca2+ channel opener BayK 8644 (1 μM). These results suggest that ethanol-induced myocardial depression may be augmented in hypertension, possibly due to mechanism(s) involving sarcolemmal Ca2+ channels.

Augmentation of the inotropic response to insulin in diabetic rat hearts

Insulin participates in the modulation of myocardial function, but its inotropic action in diabetes mellitus is not fully clear. In the present study, we examined contractile responses to insulin in left-ventricular papillary muscles and ventricular myocytes isolated from hearts of normal or short-term (5–7 days) streptozotocin-induced (65 mg kg ) diabetic rats. Mechanical properties of papillary muscles and ventricular myocytes were evaluated using a force transducer and an edge-detector, respectively. Contractile properties of papillary muscles or cardiac myocytes, electrically stimulated at 0.5 Hz, were analyzed in terms of peak tension development (PTD) or peak twitch amplitude (PTA), time-to-peak contraction (TPT) and time-to-90% relaxation (RT 90). Intracellular Ca 2+ transients were measured as fura-2 fluorescence intensity change (ΔFFI). Insulin (1–500 nM) had no effect on PTD in normal myocardium, whereas it produced a positive inotropic response in preparations from diabetic animals, with a maximal increase of 11%. Insulin did not modify TPT or RT 90 in either group. Further studies revealed that insulin enhanced cell shortening in diabetic but not normal myocytes, with a maximal increase of 21%. Consistent with its action on the mechanical properties of papillary muscles and cardiac myocytes, insulin also induced a dose-dependent increase in the intracellular Ca 2+ transient in diabetic but not normal myocytes. Collectively, these data suggest that the myocardial contractile response to insulin may be altered in diabetes.

Altered inotropic response to IGF-I in diabetic rat heart: influence of intracellular Ca2+ and NO.

Normally, insulin-like growth factor I (IGF-I) exerts positive effects on cardiac growth and myocardial contractility, but resistance to its action has been reported in diabetes. This study was designed to determine whether IGF-I-induced myocardial contractile action is altered in diabetes as a result of an intrinsic alteration of contractile properties at the cellular level. Contractile responses to IGF-I were examined in left ventricular papillary muscles and ventricular myocytes from normal and short-term (5-7 days) streptozotocin-induced diabetic rats. Mechanical properties of muscles and myocytes were evaluated using a force transducer and an edge detector, respectively. Preparations were electrically stimulated at 0.5 Hz, and contractile properties analyzed include peak tension development (PTD) or peak twitch amplitude (PTA), time to peak contraction/shortening, and time to 90% relaxation/relengthening. Intracellular Ca2+ transients were measured as fura 2 fluorescence intensity changes. IGF-I (1-500 ng/ml) caused a dose-dependent increase in PTD and PTA in preparations from normal but not diabetic animals. IGF-I did not alter time to peak contraction/shortening or time to 90% relaxation/relengthening. Pretreatment with the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (100 microM) attenuated IGF-I-induced increases in PTD in normal myocardium but unmasked a positive inotropic action in diabetic animals. Pretreatment with Nomega-nitro-L-arginine methyl ester blocked IGF-I-induced increases in PTA in single myocytes. Consistent with its inotropic actions on muscles and myocytes, IGF-I induced a dose-dependent increase in Ca2+ transients in normal but not diabetic myocytes. These results suggest that the IGF-I-induced inotropic response is depressed in diabetes because of an intrinsic alteration at the myocyte level. Mechanisms underlying this alteration in IGF-I-induced myocardial response may be related to changes in intracellular Ca2+ and/or NO production in diabetes.

Diabetes rapidly induces contractile dysfunctions in isolated ventricular myocytes.

To determine whether diabetes-induced cardiac dysfunction is due to contractile dysfunction at the single-cell level, mechanical properties and Ca2+ transients were evaluated in ventricular myocytes isolated from diabetic rats. Rats were made diabetic by injection with streptozotocin and killed either 4-6 days or 8 wk after treatment. Shortening and relengthening (twitch) properties were evaluated in isolated myocytes with a high-resolution (120-Hz) video-based edge-detection system during electrical stimulation between 0.1 and 5 Hz. A separate cohort of myocytes was loaded with fura 2 to assess intracellular Ga2+ transients. Long-term (8-wk) but not short-term (4- to 6-day) diabetes depressed peak twitch amplitude. Diabetes markedly prolonged both the contraction and relaxation phases from both diabetic models. Additionally, 35% of the long-term diabetic myocytes could not pace at 5 Hz, and 48% of the short-term diabetic myocytes developed a hypercontracture at that frequency. Intracellular Ca2+ measurements showed slower Ca(2+)-transient decays in myocytes from short-term diabetic rats. These data demonstrate that contractile dysfunction seen in the diabetic heart is due, in part, to abnormalities of the myocyte. Furthermore, these abnormalities are present after only 4-6 days of diabetes, suggesting a rapid alteration in the processes regulating myocyte shortening and relengthening, which likely include impaired Ca2+ sequestration or extrusion.

Strength training alters contractile properties of the triceps brachii in men aged 65-78 years.

Voluntary and electrically evoked contractile properties were studied in the triceps brachii following a 24-week dynamic strength training program in ten men aged 65-78 years. Eight men of a similar age were control subjects. A resistance overload program was undertaken three times per week with subjects performing four sets of six to eight repetitions at 80% of their one repetition on maximum (1RM). Maximum voluntary contraction (MVC) and contractile properties were measured at 0, 12, and 24 weeks in the exercise group and at 0 and 24 weeks in the controls. The 1RM was used to assess dynamic strength at 0 and 24 weeks in the exercise group. Contractile measures consisted of supramaximal isometric twitch and post-activation twitch parameters. Muscle size was estimated from anthropometric measurements. Compared with the control group, the exercise group MVC increased by about 20% and time to peak tension was slowed by about 11%. Also in the exercise group the peak rate of torque development of the potentiated twitch was reduced by about 10%. Twitch potentiation was substantial in both groups (about 140%) and unaffected by training. The 1 RM increased by about 30%, and there was a non-significant positive change of 8.6% in the muscle plus bone cross-sectional area in the exercise group. The results show that the force generating capacity of the triceps brachii in these men can be significantly improved for up to 24 weeks using concentric overload training. Furthermore, the finding of slowed twitch properties and no change in peak twitch amplitude substantiate and extend the limited data currently available on intrinsic contractile changes in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)

Contribution of sarcolemmal sodium-calcium exchange and intracellular calcium release to force development in isolated canine ventricular muscle.

The aim of this work was to determine the relationship between peak twitch amplitude and sarcoplasmic reticulum (SR) Ca2+ content during changes of stimulation frequency in isolated canine ventricle, and to estimate the extent to which these changes were dependent upon sarcolemmal Na(+)-Ca2+ exchange. In physiological [Na+]o, increased stimulation frequency in the 0.2-2-Hz range resulted in a positive inotropic effect characterized by an increase in peak twitch amplitude and a decrease in the duration of contraction, measured as changes in isometric force development or unloaded cell shortening in intact muscle and isolated single cells, respectively. Action potentials recorded from single cells indicated that the inotropic effect was associated with a progressive decrease of action potential duration and a marked reduction in average time spent by the cell near the resting potential during the stimulus train. The frequency-dependent increase of peak twitch force was correlated with an increase of Ca2+ uptake into and release from the SR. This was estimated indirectly using the phasic contractile response to rapid (less than 1 s) lowering of perfusate temperature from 37 degrees C to 0-2 degrees C and changes of twitch amplitude resulting from perturbations in the pattern of electrical stimulation. Lowering [Na+]o from 140 to 70 mM resulted in an increase of contractile strength, which was accompanied by a similar increase of apparent SR Ca2+ content, both of which could be abolished by exposure to ryanodine (1 x 10(-8) M), caffeine (3 x 10(-3) M), or nifedipine (2 x 10(-6) M). Increased stimulation frequency in 70 mM [Na+]o resulted in a negative contractile staircase, characterized by a graded decrease of peak isometric force development or unloaded cell shortening. SR Ca2+ content estimated under identical conditions remained unaltered. Rate constants derived from mechanical restitution studies implied that the depressant effect of increased stimulation frequency in 70 mM [Na+]o was not a consequence of a decreased rate of refilling of a releasable pool of Ca2+ within the cell. These results demonstrate that frequency-dependent changes of contractile strength and intracellular Ca2+ loading in 140 mM [Na+]o require the presence of a functional sarcolemmal Na(+)-Ca2+ exchange process. The possibility that the negative staircase in 70 mM [Na+]o is related to inhibition of Ca(2+)-induced release of Ca2+ from the SR by various cellular mechanisms is discussed.

Spontaneous Ca2+ release from the sarcoplasmic reticulum limits Ca2+-dependent twitch potentiation in individual cardiac myocytes. A mechanism for maximum inotropy in the myocardium.

We hypothesized that the occurrence of spontaneous Ca2+ release from the sarcoplasmic reticulum (SR), in diastole, might be a mechanism for the saturation of twitch potentiation common to a variety of inotropic perturbations that increase the total cell Ca. We used a videomicroscopic technique in single cardiac myocytes to quantify the amplitude of electrically stimulated twitches and to monitor the occurrence of the mechanical manifestation of spontaneous SR Ca2+ release, i.e., the spontaneous contractile wave. In rat myocytes exposed to increasing bathing [Ca2+] (Cao) from 0.25 to 10 mM, the Cao at which the peak twitch amplitude occurred in a given cell was not unique but varied with the rate of stimulation or the presence of drugs: in cells stimulated at 0.2 Hz in the absence of drugs, the maximum twitch amplitude occurred in 2 mM Cao; a brief exposure to 50 nM ryanodine before stimulation at 0.2 Hz shifted the Cao of the maximum twitch amplitude to 7 mM. In cells stimulated at 1 Hz in the absence of drugs, the maximum twitch amplitude occurred in 4 mM Cao; 1 microM isoproterenol shifted the Cao of the maximum twitch amplitude to 3 mM. Regardless of the drug or the stimulation frequency, the Cao at which the twitch amplitude saturated varied linearly with the Cao at which spontaneous Ca2+ release first occurred, and this relationship conformed to a line of identity (r = 0.90, p = less than 0.001, n = 25). The average peak twitch amplitude did not differ among these groups of cells. In other experiments, (a) the extent of rest potentiation of the twitch amplitude in rat myocytes was also limited by the occurrence of spontaneous Ca2+ release, and (b) in both rat and rabbit myocytes continuously stimulated in a given Cao, the twitch amplitude after the addition of ouabain saturated when spontaneous contractile waves first appeared between stimulated twitches. A mathematical model that incorporates this interaction between action potential-mediated SR Ca2+ release and the occurrence of spontaneous Ca2+ release in individual cells predicted the shape of the Cao-twitch relationship observed in other studies in intact muscle. Thus, the occurrence of spontaneous SR Ca2+ release is a plausible mechanism for the saturation of the inotropic response to Ca2+ in the intact myocardium.

Effects of aminophylline, isoproterenol, and neostigmine on hypercapnic depression of diaphragmatic contractility.

We investigated the effects of aminophylline, isoproterenol, and neostigmine on decreased diaphragmatic contractility induced by hypercapnia. With the thorax open, the animal receiving mechanical ventilation, and a plaster cast around the abdomen, constant length and geometry of the diaphragm were maintained. Contractility was assessed by analysis of transdiaphragmatic pressure (Pdi) generated during supramaximal phrenic stimulation at different frequencies. Bilateral phrenectomy was performed to prevent spontaneous diaphragm movement. Hypercapnia (PaCO2, 85 mmHg) reduced Pdi by 10% at low and high frequencies of stimulation. Subsequently, aminophylline (20 mg/kg) restored Pdi to the control value at every frequency of stimulation (p less than 0.05), whereas neostigmine (0.25 and 1.0 mg) restored Pdi at low frequencies only (p less than 0.05). Isoproterenol did not improve Pdi at any frequency. Analysis of twitch characteristics revealed that hypercapnia reduced peak twitch amplitude by 17%, this being the underlying cause of the decrease in Pdi. Low and high doses of all 3 drugs significantly reversed this effect by improving peak twitch tension to values equal with or greater than control values (p less than 0.05). In addition, aminophylline (40 mg/kg) and neostigmine (0.25 and 1.0 mg) significantly increased time to peak tension of the twitch (p less than 0.05) and isoproterenol (5 and 20 micrograms/min) significantly decreased twitch half relaxation time (p less than 0.05). We conclude that aminophylline and neostigmine improve diaphragmatic contractility during hypercapnia by virtue of their potentiating effect on twitch amplitude, whereas isoproterenol does not increase contractility because the process underlying the decrease in twitch duration masks the effect of an improved twitch amplitude.

Effects of lanthanum on the coupling between membrane excitation and contraction of isolated frog muscle fibres.

AbstractThe effects of lanthanum on the electrical and mechanical activities of isolated muscle fibres from the frog were investigated. Lanthanum, in the range 0.05–0.3 mM, produced characteristic, concentration dependent changes of the isometric twitch. There was an increase in latent period, increase in rate of tension development, potentiation of peak twitch amplitude, and a prolongation of the relaxation period. Lanthanum produced no change of the resting potential, hut caused a graded reduction in rate of rise, amplitude, and rate of fall of the action potential. At concentrations of the metal ion exceeding 0.3 mM, the mechanical response was complicated by impaired excitation, leading to a diminution of the twitch response and failure to produce a fused tetanus. Exposure to still higher concentrations of lanthanum (≥ 0.5 mM) made the fibre electrically inexcitable. The lanthanum‐induced changes were completely reversible on removal of the metal ion from the bath. Lanthanum in a concentration of 0.1 mM could be used as a substitute for calcium to maintain a normal resting membrane potential and twitch response. The results suggest that lanthanum and calcium act on a common site in the membrane. The alterations in twitch kinetics produced by lanthanum are discussed in relation to changes of action potential and mechanical threshold.