Wellcome Prize Lecture
Visual signals in the retina: from photons to synapses
- Leon Lagnado
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 1-15
-
- Article
- Export citation
-
The ability to see the world around us is an immediate and striking example of the abilities of the nervous system, and perhaps for this reason, vision is one of the most intensively studied aspects of brain function (Hubel, 1995). This paper examines some of the earliest steps in vision occurring in the retina (Dowling, 1987; Rodieck, 1998).
Research Article
Protective effect of HOE642, a selective blocker of Na+-H+ exchange, against the development of rigor contracture in rat ventricular myocytes
- Marisol Ruiz-Meana, David Garcia-Dorado, Margarita Juliá, Javier Inserte, Berthold Siegmund, Yuri Ladilov, Francesco Paolo Tritto, Miguel A. González, J. Soler-Soler
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 17-25
-
- Article
- Export citation
-
The objective of this study was to investigate the effect of Na+-H+ exchange (NHE) and HCO3--Na+ symport inhibition on the development of rigor contracture. Freshly isolated adult rat cardiomyocytes were subjected to 60 min metabolic inhibition (MI) and 5 min re-energization (Rx). The effects of perfusion of HCO3- or HCO3--free buffer with or without the NHE inhibitor HOE642 (7 µM) were investigated during MI and Rx. In HCO3--free conditions, HOE642 reduced the percentage of cells developing rigor during MI from 79 ± 1 % to 40 ± 4 % (P < 0.001) without modifying the time at which rigor appeared. This resulted in a 30 % reduction of hypercontracture during Rx (P < 0.01). The presence of HCO3- abolished the protective effect of HOE642 against rigor. Cells that had developed rigor underwent hypercontracture during Rx independently of treatment allocation. Ratiofluorescence measurement demonstrated that the rise in cytosolic Ca2+ (fura-2) occurred only after the onset of rigor, and was not influenced by HOE642. NHE inhibition did not modify Na+ rise (SBFI) during MI, but exaggerated the initial fall of intracellular pH (BCEFC). In conclusion, HOE642 has a protective effect against rigor during energy deprivation, but only when HCO3--dependent transporters are inhibited. This effect is independent of changes in cytosolic Na+ or Ca2+ concentrations.
Modulation of delayed rectifier potassium current, iK, by isoprenaline in rabbit isolated pacemaker cells
- Ming Lei, Hilary F. Brown, Derek A. Terrar
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 27-35
-
- Article
- Export citation
-
Permeabilized patch whole-cell voltage clamp methods were used to investigate the effects of isoprenaline (ISO) on total delayed rectifier potassium current, iK, in rabbit sino-atrial (SA) node pacemaker cells; total iK is composed of the rapidly activating iKr and the slowly activating iKs, but predominantly iKr in this species. ISO (20 nM) increased the amplitude of total iK and caused a negative shift of approximately 10 mV in the activation curve for iK, both in the absence and in the presence of 300 nM nisoldipine to block the L-type Ca2+ current, iCa,L. The same concentration (20 nM) of ISO increased the spontaneous pacemaker rate of SA node pacemaker cells by 16 %. In addition to increasing the amplitude of iK, ISO (20-50 nM) also increased the rate of deactivation of this current. The stimulation of iK by ISO was reversed by 10 µM H-89, a selective protein kinase A inhibitor, but not by 200 nM bisindolymaleimide I, a selective protein kinase C inhibitor. It therefore appears that the mechanisms by which β-adrenoceptor agonists increase pacemaking rate in sinoatrial node pacemaker cells include an increase in the rate of deactivation of iK in addition to the well-documented augmentation of iCa,L and the positive shift of the activation curve for the hyperpolarization-activated inward current, if. The observations are also consistent with a role for protein kinase A in the stimulation of iK by ISO in SA node cells.
Protein kinase C-dependent inhibition of K+ currents in noradrenaline-induced depolarization of smooth muscle of guinea-pig vas deferens
- Noritaka Kamimura, Sechiko Suga, Kyoko Nakano, Takahiro Kanno, Teruko Takeo, Makoto Wakui
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 37-42
-
- Article
- Export citation
-
Ionic mechanisms and signal transduction underlying noradrenaline (NA)-induced depolarization in single smooth muscle cells of guinea-pig vas deferens were studied. NA caused depolarization followed by action potentials through activation of α1-adrenoceptors. In the presence of nifedipine, no action potential was generated, and the magnitude of the depolarization depended on the concentration of NA (0.1-100 µm). NA, through α1-adrenoceptor activation, reduced the magnitude of membrane currents in response to voltage ramp pulses from -90 to -30 mV in a concentration-dependent manner. The reversal potential of the current inhibited by NA changed proportionally to the change in the equilibrium potential of K+, suggesting that NA inhibited K+ channel activity. Treatment of cells with GDPβS, an inhibitor of G proteins, or bisindolylmaleimide (BIM), a selective protein kinase C (PKC) inhibitor, prevented the NA inhibition of the currents. Application of 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of PKC, mimicked the effect of NA. It is suggested that in the smooth muscle of guinea-pig vas deferens, activation of α1-adrenoceptors and the subsequent activation of PKC led to inhibition of K+ currents, which is responsible for the depolarization induced by NA.
Effects of shear stress on [Ca2+]i and membrane potential of vascular endothelium of intact rat blood vessels
- Sergey M. Marchenko, Stewart O. Sage
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 43-48
-
- Article
- Export citation
-
Shear stress is an important modulator of endothelial function which can affect vessel tone, endothelial morphology and gene transcription. However, the mechanism by which the endothelium detects changes in shear stress is the subject of conflicting reports. The possible contributions of changes in the cytosolic Ca2+ concentration ([Ca2+]i) and of membrane hyperpolarisation are disputed. Here we have investigated the effects of shear stress on these variables in native endothelium in situ in rat aorta and hepatic portal vein. Endothelial [Ca2+]i was recorded using the fluorescent indicator fura-2. The [Ca2+]i in unstimulated rat aortic endothelium was 86 ± 12 nM (n = 9). Acetylcholine (ACh) evoked relaxation of the aorta and a biphasic increase in endothelial [Ca2+]i. Shear stress that evoked relaxation comparable to that evoked by ACh did not affect the endothelial [Ca2+]i. Endothelial membrane potential was recorded using the patch clamp technique. The resting membrane potentials of rat aortic and portal vein endothelium were -47 ± 3.8 mV (n = 14) and -68 ± 4.5 mV (n = 9), respectively. Shear stress did not affect the endothelial membrane potential of rat aorta, but evoked a small (-1.6 ± 0.3 mV, n = 9) hyperpolarisation of the endothelium of rat portal vein in all preparations studied. These results suggest that neither changes in [Ca2+]i nor hyperpolarisation are involved in the reception of shear stress by native rat aortic endothelium in situ, but that shear stress induces small hyperpolarisations of endothelium of portal vein, a mechanism that may be present and of greater physiological significance in other parts of vascular system.
Decreased response of rat knee joint blood vessels to phenylephrine in chronic inflammation: involvement of nitric oxide
- Mohammad Badavi, Ali Khoshbaten, Sohrab Hajizadeh
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 49-55
-
- Article
- Export citation
-
The effect of chronic inflammation induced by Freund's Complete Adjuvant (FCA) on rat articular blood vessels and knee joint diameter was investigated. Blood flow changes in response to phenylephrine (an α1-adrenoceptor agonist) in FCA-treated and contralateral knee joints were studied over a 40 day period, using the laser Doppler flowmetery (LDF) technique. Unilateral injection of FCA (0.2 ml) increased the injected knee diameter on all days examined post-injection (P < 0.001) and its maximum increase (53 ± 2 %) was reached on day 3. After this, the diameter decreased gradually but did not return to its initial value. In control animals, topical application of 10-13-10- 7 mol phenylephrine onto the exposed joint capsule decreased blood flow dose dependently (11.1 ± 4.4 to 58.2 ± 4.5 %, respectively, P < 0.001). Unilateral injection with FCA attenuated the phenylephrine response in both ipsilateral and contralateral knees compared with the response of control animals (5.2 ± 1.6 to 48.3 ± 6.1 % and 1.9 ± 2.2 to 45.3 ± 5.6 %, respectively, P < 0.05). The reduction persisted for 3 weeks after FCA injection (ipsilateral for 21 days; contralateral for 30 days, P < 0.001). Subsequently the response returned towards normal. To avoid the influence of α2-adrenoceptors, yohimbine (an α2-adrenoceptor antagonist) was injected (0.5 mg kg-1, I.P.) 30 min before phenylephrine application. Yohimbine blocked the vasoconstrictor effect of 10-10-10-7 mol clonidine (an α2-adrenoceptor agonist, topical application) by 44-67.7 % inhibition, respectively (P < 0.001). Prazosin (an α1-adrenoceptor antagonist, 0.1 mg kg-1, I.P.) blocked the vasoconstrictor effect of phenylephrine (10-10-10-7 mol, topical application) effectively (42 to 69.8 % inhibition, respectively, P < 0.001). To assess the role of nitric oxide (NO) on the observed responses, N G-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) was applied topically (0.2 µmol) 5 min before phenylephrine application. L-NAME application at 7 and 14 days after FCA injection potentiated the vasoconstrictor response in the FCA-treated knee (P < 0.001) but had no significant effect on the contralateral knee. Blood pressure monitoring during phenylephrine, clonidine and L-NAME administration indicated that topical application of the drugs had no significant effect on the systemic blood pressure. These findings indicate that the vasoconstrictor response to phenylephrine was decreased in chronic inflammation and increased NO production could be involved.
Forskolin has a bimodal cAMP-independent effect on superoxide anion generation in isolated osteoclasts
- Christine E. M. Berger, Harish K. Datta
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 57-60
-
- Article
- Export citation
-
The mode of action of forskolin is of clinical and scientific interest since forskolin has been shown to have potentially therapeutic bone anti-resorptive and anti-hypertensive properties. Forskolin is thought to inhibit the bone resorptive activity of osteoclasts by elevating cytosolic cAMP and to mimic as well as augment the anti-resorptive effect of calcitonin (CT). Other studies have found that forskolin has a dose-dependent dual effect in mouse calavaria, stimulating bone resorption at low doses and having an inhibitory effect at high doses. However, the acute effect of forskolin on osteoclast functional modality has never been studied. The present investigation examined the effect of low (1 mM) and high doses (10 mM) of forskolin on superoxide anion (O2Σ-) generation in isolated bone-resorbing rat osteoclasts. Forskolin was found to have a bimodal cAMP-independent effect on O2Σ- generation, being stimulatory at a low dose and having an inhibitory effect at a higher dose. These findings also suggest that CT-induced inhibition of O2Σ- generation in the osteoclasts is likely to be mediated by cAMP-independent pathways, perhaps involving [Ca2+]i modulation.
Effects of capsaicin-induced sensory denervation on osteoclastic resorption in adult rats
- C. Adam, A. Llorens, B. Baroukh, M. Cherruau, J. L. Saffar
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 61-66
-
- Article
- Export citation
-
Many recent findings suggest that the nervous system has efferent effects on bone. A putative role of the sensory innervation has been assessed by using a synchronised rat model of bone resorption after treating adult animals with the neurotoxin capsaicin. Fourteen days after capsaicin treatment (50 mg kg-1) the right maxillary molars were extracted to activate a wave of resorption along the mandibular cortex. The rats were killed 4 days later (i.e. at the peak of resorption in this model), and their right mandibles were processed for histometric evaluation of resorption along the cortex and of calcitonin gene-related peptide (CGRP)- and substance P (SP)-immunoreactive (IR) fibres in the dental pulp. CGRP-IR and SP-IR fibres were significantly reduced in numbers by the capsaicin treatment (by 58 and 49 %, respectively), confirming the success of sensory denervation. The resorption surface was significantly reduced (P < 0.005) versus the sham-treated animals. Although the size of the osteoclast population recruited in the site was not modified, the number of actively resorbing osteoclasts was significantly reduced (P < 0.03). However, the activity of the resorbing cells was not modified. Non-specific esterase-positive osteoclast precursors were also significantly few after capsaicin treatment. These data show that the sensory nervous system is involved in the control of bone resorption at two different levels: (1) in the recruitment of osteoclast precursors, and (2) in regulating the access of recruited cells to the bone surface.
Carbachol-stimulated chloride secretion in mouse colon: evidence of a role for autocrine prostaglandin E2 release
- Mark A. Carew, Peter Thorn
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 67-72
-
- Article
- Export citation
-
We used the short-circuit current technique to investigate the possible facilitatory role of epithelium-derived prostaglandin E2 (PGE2) release on Cl- secretion in the mouse colon. Carbachol- (CCh)-stimulated Cl- secretion was reduced by pretreatment with either indomethacin (10 µM), or TTX (1 µM), and when added together, these inhibitors revealed net CCh-stimulated K+ secretion. CCh-stimulated Cl- secretion was partially restored to TTX/indomethacin-treated colons by addition of a subsecretory concentration of PGE2 (1 nM). In acutely isolated, unstimulated crypt cells, we measured PGE2 release at a similar level. We conclude that autocrine release of PGs from epithelial cells is sufficient to support the CCh-induced Cl- secretory response and is a likely co-factor in this response.
Effect of reproductive status on plasma oxytocin concentrations and the renal response to oxytocin in the conscious rat
- Yan Zhou, Mary L. Forsling
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 73-78
-
- Article
- Export citation
-
The magnitude of diuresis and natriuretis produced by oxytocin in the female rat has been shown to be dependent on the stage of the oestrous cycle. A study has been performed to determine the role of ovarian steroids in modulating the renal response to oxytocin infused at a rate of 100 fmol min-1 in hypotonic saline. Observations were performed on ovariectomised rats with and without steroid treatment and rats with suppressed oestrous cycles following treatment with the long-acting gonadotrophin-releasing hormone analogue Zoladex, given as a 100 mg S.C. depot, or the antioestrogen tamoxifen, given as three daily injections of 1 mg. Steroid treatment comprised a single dose of 10 µg oestradiol benzoate or 2.0 mg progesterone, or a combination of the two hormones given 30 h apart. Ovariectomy had no significant effect on plasma oxytocin concentrations, although progesterone treatment produced an increase. The natriuresis in ovariectomised animals of 27 % was smaller (P < 0.05) than that seen on the day of pro-oestrus and closer to that seen in the intact rat at oestrus. The responses in animals with suppressed oestrous cycles following treatment with tamoxifen were not significantly different from those observed following ovariectomy, neither was the diuresis following Zoladex. The renal responses were greater following treatment with oestradiol than in the ovariectomised group. Thus ovarian steroids do influence the renal responsiveness to oxytocin with oestradiol augmenting the response.
Effects of placental insufficiency on the ovine fetal renin-angiotensin system
- David Y. Zhang, Eugenie R. Lumbers, Giuseppe Simonetta, June J. Wu, Julie A. Owens, Jeffrey S. Robinson, I. Caroline McMillen
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 79-84
-
- Article
- Export citation
-
We postulated that chronic placental insufficiency would be associated with reduced expression of renal renin and angiotensinogen genes in the fetal sheep. Placental development was restricted in ewes by removing the majority of caruncles prior to mating (placentally restricted (PR) group). The weights of PR fetuses were significantly reduced (P < 0.05, 2.98 ± 0.33 kg) compared to control fetuses (4.20 ± 0.30 kg). Kidney weights were also significantly reduced in the PR fetuses (P < 0.05, 8.4 ± 0.9 g) compared with control fetuses (12.2 ± 1.3 g). The ratios of renal renin β-actin mRNA levels were significantly reduced in PR fetuses (P < 0.001, 0.35 ± 0.02) when compared to control animals (0.98 ± 0.13). The renal angiotensinogen mRNA/18S rRNA ratio was significantly lower (P < 0.05, 0.28 ± 0.13) in PR fetuses compared with control fetuses (0.72 ± 0.10), while hepatic angiotensinogen was unaffected. There was a positive correlation between renal renin mRNA and renal angiotensinogen mRNA levels (r = 0.65, P < 0.05, n = 12). It is unlikely that these changes in renal angiotensinogen and renin mRNA were due to the small increment in plasma cortisol levels (< 5 nmol l-1). There was, however, a positive correlation between arterial PO2 and renal renin mRNA (r2 = 0.77, P < 0.01). Plasma renin levels were not different between the two groups. Thus, restriction of nutrient and oxygen supply throughout fetal life was associated with suppression of renal renin and renal angiotensinogen gene expression, with no effect on hepatic angiotensinogen mRNA levels. This specific suppression of fetal renal renin and angiotensinogen expression could alter the activity of the intrarenal RAS and so affect growth and development of the kidney.
Effect of maternal nutrient restriction in early gestation on responses of the hypothalamic-pituitary-adrenal axis to acute isocapnic hypoxaemia in late gestation fetal sheep
- Paul Hawkins, Clare Steyn, Hugh H. G. McGarrigle, Tsukuru Saito, Takashi Ozaki, Lori L. Stratford, David E. Noakes, Mark A. Hanson
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 85-96
-
- Article
- Export citation
-
Epidemiological and experimental evidence suggests that maternal undernutrition during pregnancy may alter development of fetal organ systems. We have demonstrated previously that fetal hypothalamic-pituitary-adrenal (HPA) axis responses to exogenous corticotropin-releasing hormone (CRH) + arginine vasopressin (AVP), or adrenocorticotrophin hormone (ACTH), are reduced in fetuses of mildly undernourished ewes. To examine these effects further we tested HPA axis responses to acute isocapnic hypoxaemia in fetal sheep at 114-129 days gestation (dGA), following 15 % reduction in maternal nutritional intake between 0 and 70 dGA. Fetuses from control (C) and nutrient-restricted (R) ewes were chronically catheterised and plasma ACTH and cortisol responses were determined at 114-115, 120-123 and 126-129 dGA during hypoxaemia (1 h) induced by lowering the maternal inspired O2 fraction (FI,O2). Basal plasma cortisol concentrations and HPA axis responses at 114-115 and 120-123 dGA did not differ between C and R fetuses. At 126-129 dGA, both plasma ACTH (P < 0.01) and cortisol (P < 0.05) responses were smaller in R fetuses compared to C fetuses. Fetal blood gas status, fetal body weight, body proportions and organ weights did not differ between the groups. We conclude that mild maternal undernutrition alters development of the fetal HPA axis producing a reduction in pituitary and adrenal responsiveness to endogenous stimuli.
Heat shock protein expression is increased in cardiac and skeletal muscles of Fischer 344 rats after endurance training
- T. R. Samelman
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 97-102
-
- Article
- Export citation
-
Heat shock proteins (HSPs) are expressed when cells are exposed to various types of stress and they may provide protection against cellular insult. Previous data have shown increases in HSP expression following acute exhaustive exercise in rats (Locke et al. 1990, 1995; Salo et al. 1991) and humans (Liu et al. 1999); however, it is not known if chronic exercise will increase resting levels of HSPs. The purpose of this study was to determine if basal protein levels of HSP 72/73 and HSP 60 are increased in cardiac and skeletal muscle of endurance trained Fischer 344 rats. Heart, soleus (SOL) and lateral gastrocnemius (LG) muscles were removed and hearts were sectioned into left ventricle (LV), right ventricle (RV) and atria (AT). Endurance training improved myocardial citrate synthase activity by 88, 90 and 77 % and cytochrome c oxidase activity by 58, 51 and 89 % in LV, RV and AT, respectively. LV and RV oxidative enzyme activities were greater when compared to AT for both trained and untrained rats (P < 0.05). HSP 72/73 expression was significantly greater (P < 0.05) in LV, RV and SOL from endurance trained versus from control rats (26, 45 and 67 %, respectively). HSP 60 was also increased (P < 0.05) in LV, RV and SOL in trained relative to untrained rats. HSP 72/73 and HSP 60 were unchanged in AT and LG after training. These results indicate that endurance training increases the basal expression of stress proteins and this observation is consistent with the hypothesis that endurance training may activate a protective mechanism to stress.
Exercise training enhances relaxation of the isolated guinea-pig saphenous artery in response to acetylcholine
- J. K. Choate, K. Kato, R. M. Mohan
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 103-108
-
- Article
- Export citation
-
The effects of exercise training were investigated on the vascular responses in the isolated guinea-pig saphenous artery. Exercising animals swam 5 days week-1 for 6 weeks (60 min day-1 for weeks 1 and 2; 75 min day-1 for weeks 3 and 4; 90 min day-1 for weeks 5 and 6), while control animals were placed into shallow water for the same duration. Trained animals had significantly higher ventricular:body weight ratios, increased citrate synthase activity in the latissimus dorsi, and enhanced Na+ pump concentrations in the latissimus dorsi and gastrocnemius muscles (P < 0.05). In vitro isometric techniques were used to measure constriction and relaxation responses of saphenous artery rings from trained and control animals. There were no significant differences in the constriction responses to KCl (50 mm) and phenylephrine (0.3-100 µM) in arterial rings from control versus trained animals. Relaxation responses to acetylcholine (10 µM; ACh-relaxation), following preconstriction with phenylephrine (10 µM), were significantly enhanced in rings from trained animals (P < 0.05). Acetylcholine relaxed the vessels to 47 ± 6 % (control) and 18 ± 3 % (trained) of the preconstriction responses to phenylephrine. The nitric oxide synthase inhibitor N G-nitro-L-arginine (L-NA; 50 µM) significantly attenuated the ACh-relaxation in control and trained animals (P < 0.05). The effect of L-NA on the ACh-relaxation was significantly larger in trained (change in ACh-relaxation with L-NA = 29 ± 9 %) than control (14 ± 3 %) animals (P < 0.05). In conclusion, exercise training enhanced the ACh-relaxation of the isolated guinea-pig saphenous artery. Inhibition of nitric oxide synthase attenuated the ACh-relaxation of rings from control and trained animals, but this effect was significantly larger in the vessels from trained animals. These results are consistent with the idea that nitric oxide could contribute to the enhanced ACh-relaxation of the saphenous artery with exercise training.
Influence of muscle fibre type and fitness on the oxygen uptake/power output slope during incremental exercise in humans
- Thomas J. Barstow, Andrew M. Jones, Paul H. Nguyen, Richard Casaburi
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 109-116
-
- Article
- Export citation
-
We recently reported that a higher percentage of type I fibres in vastus lateralis and a greater peak oxygen uptake ([Vdot]O2) were associated with a greater initial rise in [Vdot]O2 (Δ[Vdot]O2 /ΔW, where W is work rate) following the onset of heavy constant power output exercise (above the lactate threshold, LT). It was unclear if these results were true only for heavy exercise, or if the association between fibre type and/or fitness and Δ[Vdot]O2 /ΔW would also be seen for moderate (< LT) exercise. The purpose of the present study was to compare the relationships between fibre type or peak [Vdot]O2 and Δ[Vdot]O2 /ΔW determined for moderate (< LT) and heavy (> LT) exercise intensities during incremental exercise. Nine healthy subjects performed an incremental ramp test on a cycle ergometer. The [Vdot]O2 /Wslope was calculated for the domain of power outputs up to the LT (S1), from the LT towards peak [Vdot]O2 (S2), and over the entire linear portion of the Δ[Vdot]O2 /ΔW response (ST), and compared to fibre type distribution determined from biopsy of the vastus lateralis, and to peak [Vdot]O2 (as ml kg-1 min-1). Significant correlations between Δ[Vdot]O2 /ΔW and the proportion of type I fibres were found for each exercise domain (r is 0.69, 0.71 and 0.84 for S1, S2 and ST, respectively, P < 0.05). S1 ranged between about 9 ml min-1 W-1 for a low proportion of type I fibres and 11 ml min-1 W-1 for a high proportion of type I fibres. Similar correlations were also found between S2 (r = 0.70) and ST (r = 0.76) and peak [Vdot]O2. These results are consistent with our previous findings during > LT constant power output exercise, and suggest that the proportion of type I fibres, and possibly fitness as indicated by peak [Vdot]O2, is associated with greater Δ[Vdot]O2 /ΔW during the initial adjustment to < LT as well as > LT exercise. These results do not appear to be explained by classical descriptions of the kinetics of adjustment of [Vdot]O2 following the onset of ramp or constant power output exercise. They might reflect enhanced motor unit recruitment in subjects with a greater percentage of type I fibres, and/or who are more aerobically fit. However, the underlying mechanism for these findings must await further study.
Human muscle power generating capability during cycling at different pedalling rates
- Jerzy A. Zoladz, Arno C. H. J. Rademaker, Anthony J. Sargeant
-
- Published online by Cambridge University Press:
- 25 January 2001, pp. 117-124
-
- Article
- Export citation
-
The effect of different pedalling rates (40, 60, 80, 100 and 120 rev min-1) on power generating capability, oxygen uptake ([Vdot]O2) and blood lactate concentration [La]b during incremental tests was studied in seven subjects. No significant differences in [Vdot]O2,max were found (mean ± S.D., 5.31 ± 0.13 l min-1). The final external power output delivered to the ergometer during incremental tests (PI,max) was not significantly different when cycling at 60, 80 or 100 rev min-1 (366 ± 5 W). A significant decrease in PI,max of ∼60 W was observed at 40 and 120 rev min-1 compared with 60 and 100 rev min-1, respectively (P < 0.01). At 120 rev min-1 there was also a pronounced upward shift of the [Vdot]O2-power output ([Vdot]O2-P) relationship. At 50 W δ[Vdot]O2 between 80 and 100 rev min-1 amounted to +0.43 l min-1 but to +0.87 l min-1 between 100 and 120 rev min-1. The power output corresponding to 2 and 4 mmol l-1 blood lactate concentration (P[La]2 and P[La]4 ) was also significantly lower (> 50 W) at 120 rev min-1 (P < 0.01) while pedalling at 40, 60, 80 and 100 rev min-1 showed no significant difference. The maximal peak power output (PM,max) during 10 s sprints increased with pedalling rate up to 100 rev min-1. Our study indicates that with increasing pedalling rate the reserves in power generating capability increase, as illustrated by the PI,max/PM,max ratio (54.8, 44.8, 38.1, 34.6, 29.2 %), the P[La]4/PM,max ratio (50.4, 38.9, 31.0, 27.7, 22.9 %) and the P[La]2/PM,max ratio (42.8, 33.5, 25.6, 23.1, 15.6 %) increases. Taking into consideration the [Vdot]O2,max, the PI,max and the reserve in power generating capability we concluded that choosing a high pedalling rate when performing high intensity cycling exercise may be beneficial since it provides greater reserve in power generating capability and this may be advantageous to the muscle in terms of resisting fatigue. However, beyond 100 rev min-1 there is a decrease in external power that can be delivered for an given [Vdot]O2 with an associated earlier onset of metabolic acidosis and clearly this will be disadvantageous for sustained high intensity exercise.