Peak Po Research Articles

Responses to Exercise at the Critical Heart Rate vs. the Power Output Associated With the Critical Heart Rate.

Succi, PJ, Dinyer-McNeely, TK, Voskuil, CC, Abel, MG, Clasey, JL, and Bergstrom, HC. Responses to exercise at the critical heart rate vs. the power output associated with the critical heart rate. J Strength Cond Res XX(X): 000-000, 2023-This study examined the physiological (volume of oxygen consumption [V̇o2], heart rate [HR], power output [PO], respiration rate [RR], muscle oxygen saturation [%SmO2]), neuromuscular (electromyographic and mechanomyographic amplitude [EMG AMP and MMG AMP] and mean power frequency [EMG MPF and MMG MPF]), and perceptual (rating of perceived exertion [RPE]) responses during exercise anchored at the critical heart rate (CHR) vs. the PO associated with CHR (PCHR). Nine subjects (mean ± SD; age = 26 ± 3 years) performed a graded exercise test and 4 constant PO trials to exhaustion at 85-100% of peak PO (PP) to derive CHR and PCHR on a cycle ergometer. Responses were recorded during trials at CHR (173 ± 9 b·min-1, time to exhaustion [TLim] = 45.5 ± 20.2 minutes) and PCHR (198 ± 58 W, TLim = 21.0 ± 17.8 minutes) and normalized to their respective values at PP in 10% intervals. There were significant (p ≤ 0.05) mode (CHR vs. PCHR) × time (10%-100% TLim) interactions for all variables (p < 0.001-0.036) except MMG AMP (p > 0.05). Post hoc analyses indicated differences across time for CHR V̇o2 (%change = -22 ± 16%), PCHR V̇o2 (19 ± 5%), CHR RR (24 ± 23%), PCHR RR (45 ± 14%), CHR PO (-33 ± 11%), PCHR HR (22 ± 5%), CHR RPE (22 ± 14%), PCHR RPE (39 ± 6%), CHR %SmO2 (41 ± 33%), PCHR %SmO2 (-18 ± 40%), CHR EMG AMP (-13 ± 15%), PCHR EMG AMP (13 ± 13%), CHR EMG MPF (9 ± 8%), CHR MMG MPF (7 ± 11%), and PCHR MMG MPF (-3 ± 14%). The critical heart rate was more sustainable than PCHR but required adjustments in PO which traversed intensity domains and caused dissociations of the responses previously observed in exercise anchored to PO. These dissociations indicated the demands to exercise varied with anchoring scheme and provides an important consideration for practitioners prescribing endurance exercise.

Dantrolene Inhibition of Skeletal Muscle RYR in the Presence of CAM

Dantrolene is a muscle relaxant that has been used clinically as the treatment for malignant hyperthermia (MH). Our group recently reported that dantrolene inhibition of RyR1 and RyR2 required calmodulin (CaM)1. However, nothing more is known about the properties of dantrolene inhibition of RyR1 on single channels. Here, we characterized dantrolene inhibition on RyR1 in the presence of exogenous CaM at various cytosolic [Ca2+] and in the presence of other activators: ATP, halothane and domain peptide, DP4. RyR1 was isolated from rabbit skeletal muscle and incorporated into artificial lipid bilayers and their open probability, Po, was measured using single channel recording. Dantrolene caused inhibition of RyR1 and RyR2, but when CaM was presence in the cytoplasmic bath. In the presence of cytoplasmic [Ca2+] (100 nmol/l) and 2 mmol/l ATP, dantrolene inhibited both RyR1 and RyR2 with identical hyperbolic dose-responses with IC50 of 0.16 ± 0.03 μmol/l and with saturating Po of 52 ± 4 % of control. RyR1 has a bell-shaped cytoplasmic Ca2+ activation curve with half activation at 1.75 ± 0.62 μmol/l and half inhibition at 0.21 ± 0.02 mmol/l and a peak Po = 0.94 ± 0.06. Dantrolene reduced Po in sub-activating and inhibiting [Ca2+] but failed to reduce peak Po. Dantrolene caused 50-60% reduction in Po of RyR1 activated by cytoplasmic Ca2+ alone (100 nmol/l) or in conjunction with halothane (5 mmol/l) or DP4 (10 μmol/l). To conclude, dantrolene inhibits RyR1 activity by 1) decreasing RyR1 sensitivity to Ca2+ activation, 2) increasing sensitivity to Ca2+ inhibition and 3) decreasing channel activation halothane or by 4) reducing the effect of inter-domain disruption in the RyR1 protein.

Influence of the intracellular GluN2 C-terminal domain on NMDA receptor function

Excitatory neurotransmission mediated by N-methyl-d-aspartate receptors (NMDARs) is fundamental to learning and memory and, when impaired, causes certain neurological disorders. NMDARs are heterotetrameric complexes composed of two GluN1 [NR1] and two GluN2(A–D) [NR2(A–D)] subunits. The GluN2 subunit is responsible for subunit-specific channel activity and gating kinetics including activation (rise time), peak open probability (peak Po) and deactivation (decay time). The peak Po of recombinant NMDARs was recently described to be controlled by the extracellular GluN2 N-terminal domain (NTD). The cytoplasmic GluN2 C-terminal domain (CTD) could also be involved, because the Po of synaptic NMDARs is reduced in mice expressing C-terminally truncated GluN2 subunits. Here, we examined the role of the GluN2 cytoplasmic tail for NMDAR channel activity and gating in HEK-293 cells. C-terminal truncation of GluN2A, GluN2B or GluN2C did not change the subunit-specific rise time but accelerated the decay time of glutamate-activated currents. Furthermore, the peak Po was reduced by about 50% for GluN2A and GluN2B but not for GluN2C. These results indicated that the CTD of GluN2 has a modulating role in NMDAR gating even in the absence of interacting synaptic proteins. Reduction of peak Po and deactivation kinetics following GluN2 C-terminal truncation were reversed by re-introducing a CTD from a different GluN2 subunit. Thus, the CTDs of GluN2 subunits behave as constitutive structural elements required for normal functioning of NMDARs but are not involved in determining the subunit-specific gating properties of NMDARs.

Natural-orifice transluminal endoscopic surgery: low-pressure pneumoperitoneum is sufficient and is associated with an improved cardiopulmonary response (PressurePig Study)

The aim of this randomized trial in the acute porcine model was to compare the quality of transgastric peritoneoscopy with the use of low-pressure versus standard-pressure pneumoperitoneum and to evaluate the respective associated cardiopulmonary changes. For transgastric peritoneoscopy, carbon dioxide was insufflated via the endoscope for a constant intraperitoneal pressure of 6 mmHg or 12 mmHg in 9 pigs each. The quality of transgastric peritoneoscopy was rated on a visual analog scale (0 mm, min.; 100 mm, max.) by the endoscopist, who was blinded to the intraperitoneal pressure. The cardiac index and global end-diastolic volume index (GEDVI, reflecting preload) were measured every 3 minutes by transpulmonary thermodilution. The following were also recorded: heart rate, mean arterial pressure (MAP), systemic vascular resistance index (SVRI, reflecting afterload), peak inspiratory pressure (PIP), pH, PCO (2), and PO (2). The quality of transgastric peritoneoscopy with the use of low-pressure pneumoperitoneum was not inferior to that obtained using standard-pressure pneumoperitoneum (87.0 mm vs. 87.3 mm; P<0.05). In both groups we observed a statistically significant rise in MAP and SVRI. The increase in SVRI was less pronounced during low-pressure peritoneum ( P=0.042), indicating a reduced stress response in comparison to standard-pressure peritoneum. There were no relevant differences between the groups in relation to cardiac index, GEDVI, and heart rate. An intra-abdominal pressure of 6 mmHg also led to better oxygenation ( P=0.031 for difference in PO (2) between the two groups) due to lower peak inspiratory pressure ( P<0.001 for difference). There were only slight differences between the groups with regard to pH and PCO (2). Pneumoperitoneum of 12-16 mmHg is used for standard laparoscopy. For NOTES, low-pressure pneumoperitoneum is sufficient and is associated with an improved cardiopulmonary response compared to standard-pressure pneumoperitoneum.

Increase in calf post-occlusive blood flow and strength following short-term resistance exercise training with blood flow restriction in young women

The response of calf muscle strength, resting (R (bf)) and post-occlusive (PO(bf)) blood flow were investigated following 4 weeks resistance training with and without blood flow restriction in a matched leg design. Sixteen untrained females performed unilateral plantar-flexion low-load resistance training (LLRT) at either 25% (n = 8) or 50% (n = 8) one-repetition maximum (1 RM). One limb was trained with unrestricted blood flow whilst in the other limb blood flow was restricted with the use of a pressure applied cuff above the knee (110 mmHg). Regardless of the training load, peak PO(bf), measured using venous occlusion plethysmography increased when LLRT was performed with blood flow restriction compared to no change following LLRT with unrestricted blood flow. A significant increase (P < 0.05) in the area under the blood time-flow curve was also observed following LLRT with blood flow restriction when compared LLRT with unrestricted blood flow. No changes were observed in R (bf) between groups following training. Maximal dynamic strength (1 RM), maximal voluntary contraction and isokinetic strength at 0.52 and 1.05 rad s(-1) also increased (P < 0.05) by a greater extent following resistance training with blood flow restriction. Moreover, 1 RM increased to a greater extent following training at 50% 1 RM compared to 25% 1 RM. These results suggest that 4 weeks LLRT with blood flow restriction provides a greater stimulus to increase peak PO(bf) as well as strength parameters than LLRT with unrestricted blood flow.

Physical fitness in people with a spinal cord injury: the association with complications and duration of rehabilitation

Objective: To assess the association between physical fitness and its recovery over time on the one hand, and complications and duration of phases of rehabilitation on the other. Design and setting: Prospective cohort study at eight rehabilitation centres. Subjects: People with a spinal cord injury were assessed four times: at the start of active rehabilitation (n = 110), three months later (n = 92), at discharge (n = 137) and a year after discharge from inpatient rehabilitation (n = 91). Main measures: Physical fitness was defined as aerobic capacity, determined at each occasion by the peak oxygen uptake (peak Vo2; L/min) and the peak power output (peak PO; W) during a maximal exercise test. On these occasions, spasticity, musculoskeletal and neurogenic pain were determined (1 = present; 0 = absent). During inpatient rehabilitation, complications (urinary tract infection, pulmonary infection or pressure sore) and bed rest were registered (1 = complication; 0 = no complications, and 1 = bed rest; 0 = no bed rest). Complications and bed rest occurring during the year after discharge were registered similarly. Results: Multilevel random coefficient analyses revealed associations in multivariate models (P ≤ 0.05). The peak oxygen uptake was negatively associated with complications after discharge. The recovery of peak power output over time was negatively associated with bed rest and spasticity. Both physical fitness and its recovery were negatively associated with the duration of active rehabilitation. Conclusion: Results suggest that limiting complications, spasticity or bed rest may improve fitness. A longer duration of active rehabilitation is not associated with an increase in physical fitness.

Effects of Oral ATP Supplementation on Anaerobic Power

1158 PURPOSE: We examined 4-d of oral ATP supplementation on indices of anaerobic capacity and muscular strength performance. METHODS: We assigned 27 healthy males to randomly receive orally, in a double–blind manner, a low (150 mg) or high dose (225 mg) of ATP, or matched placebo. To improve absorption characteristics, we enterically coated the ATP supplement. Total blood ATP (whole blood and plasma ATP) concentrations, two Wingate anaerobic power tests (30 s), and muscular strength (1RM and 3 sets of repetitions to fatigue at 70% of 1RM) were measured under three conditions: (i) baseline, (ii) acutely (7d later, no prior supplementation and 1 hour following ATP ingestion, and (iii) after 14 days of daily ingestion (post). RESULTS: Statistical analysis showed no significant between or within group treatment effects for whole blood ATP or plasma ATP concentrations for any treatment condition. We also did not observe any treatment effects for any Wingate testing parameter including peak PO, total work, average PO for 30 s or post Wingate lactate accumulation. Overall, we observed no significant between group treatment effects for any muscular strength parameter. We did observe several within group differences for the group ingesting the high ATP dosage including 1RM (6.6%; P < 0.04) and reps to fatigue during set one of acute testing (18.5%; P < 0.007) and total lifting volume at post; 28.2%; P < 0.003). However, we can credit those increases observed under acute conditions to two outliers showing large gains during that treatment phase. CONCLUSIONS: We conclude that enterically coated oral ATP supplementation shows only small “ergogenic” effects on muscular strength under some treatment conditions, though no distinctive pattern appears to exist.

Respiratory muscle recruitment and exercise performance in eucapnic and hypercapnic severe chronic obstructive pulmonary disease.

If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine V E, V O(2), V CO(2), and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi. Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl. Hypercapnic patients had lower FEV(1) (0.60 +/- 0.24 versus 0.95 +/- 0.31 L, p < 0.001), MVV (28 +/- 11 versus 41 +/- 13 L, p < 0.001), resting PO(2) (61 +/- 11 versus 70 +/- 11 mm Hg, p < 0.001), peak PO(2) (60 +/- 20 versus 75 +/- 22 mm Hg, p < 0.005), and V E(max) (24 +/- 10 versus 32 +/- 12 L/min, p < 0.001). Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), V O(2)max (0.58 +/- 0.30 versus 0.76 +/- 0.32 L/min), Watts (45 +/- 48 versus 71 +/- 59), V E/MVV (88 +/- 33 versus 79 +/- 14), and HRmax (117 +/- 17 versus 128 +/- 18 beats/min). PI(max) (67 +/- 28 versus 65 +/- 32 cm H(2)O) and PE(max) (98 +/- 34 versus 96 +/- 40 cm H(2)O) were also similar in both groups. VMR (DeltaPg/DeltaPpl) at rest (-0.28 +/- 0.51 versus 0 +/- 0.35) and during exercise (0.4 +/- 0.2 versus 0.39 +/- 0.15) was equally affected in both groups. We conclude that exercise capacity and ventilatory muscle recruitment are similarly impaired in eucapnic and hypercapnic patients with severe COPD. These findings make inability of the lung to increase ventilation and not respiratory muscle dysfunction a more attractive explanation for CO(2) retention in stable hypercapnic patients.

Respiratory Muscle Recruitment and Exercise Performance in Eucapnic and Hypercapnic Severe Chronic Obstructive Pulmonary Disease.

If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (Pco 2 40 ± 3 mm Hg), and 13 hypercapnic (Pco 2 52 ± 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine V˙ e, V˙ o 2, V˙ co 2, and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi. Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl. Hypercapnic patients had lower FEV1 (0.60 ± 0.24 versus 0.95 ± 0.31 L, p < 0.001), MVV (28 ± 11 versus 41 ± 13 L, p < 0.001), resting Po 2 (61 ± 11 versus 70 ± 11 mm Hg, p < 0.001), peak Po 2 (60 ± 20 versus 75 ± 22 mm Hg, p < 0.005), and V˙ e max (24 ± 10 versus 32 ± 12 L/min, p < 0.00...

Single calcium channels in resistance-sized cerebral arteries from rats.

Unitary currents through single calcium channels were measured from cell-attached patches on smooth muscle cells isolated from resistance-sized branches of posterior cerebral arteries from Wistar-Kyoto normotensive rats. Barium (80 and 10 mM) was used as the charge carrier, with and without the dihydropyridine calcium channel agonist BAY R 5417. Unitary currents decreased on membrane depolarization, with a slope conductance of 19.4 pS (80 mM barium). Channel open-state probability (Po) was steeply voltage dependent. Peak Po during test pulses from -70 mV increased e-fold per 4.5-mV depolarization. Mean peak Po at potentials positive to +10 mV was 0.44. Po at steady membrane potentials was also steeply voltage dependent, changing e-fold per 4.5 mV in the absence of inactivation. Steady-state Po at positive potentials was substantially lower than peak Po elicited by test pulses, suggesting that steady-state inactivation can reduce Po by as much as 10-fold. Membrane depolarization decreased the longest mean closed time but had little effect on the mean open time of single calcium channels measured during steady-state recordings. Lowering the external barium concentration from 80 to 10 mM reduced the single channel conductance to 12.4 pS and shifted the relationship between steady-state Po and membrane potential by about -30 mV. BAY R 5417 also shifted this relationship by about -15 mV.

Ca2(+)‐activated K+ current involvement in neuronal function revealed by in situ single‐channel analysis in Helix neurones.

1. The properties of single calcium-activated potassium channels (or C-channels) were studied in cell-attached patches using the patch-clamp technique. Experiments were performed on identified Ca2(+)-dependent U cells in juvenile specimens (1-2 months old) of Helix aspersa. 2. The criteria used to identify C-channels were based on comparison between macroscopic C-currents and currents reconstructed from unitary recordings. Both currents had a slow activation rate at large positive potentials which turned into fast activation after large Ca2+ entries. Both currents were blocked by intracellularly injected EGTA. 3. The unitary conductance in normal (5 mM) or reduced (0.5 mM) [K+]o ranged from 24 to 65 pS (mean +/- S.D., 48 +/- 13; n = 64). With 85-110 mM [K+]o, which is approximately equal to the internal [K+], the conductance was 64 pS and the reversal potential was approximately 0 mV. 4. C-channels in U cells were distributed in clusters of three to ten channels (mean 5.05 channels in seventy-five patches). Calcium channels were present in patches containing clustered C-channels. C-channels within clusters behaved independently. 5. With patch electrode containing 8 mM-calcium, C-channels opened transiently upon patch depolarization. Reopenings in quiescent depolarized patches were induced by whole-cell spikes triggered by current pulses applied to an intracellular electrode. Apparent inactivation of C-channels in depolarized patches was in fact due to a decrease in [Ca2+]i resulting from inactivation of Ca2+ channels. 6. Calcium-free saline solutions in the patch electrodes prevented C-channels from opening upon patch depolarization. Entry of calcium through the surrounding membrane induced delayed openings in the patch. Peak opening probability Po occurred 330 +/- 30 ms after a brief Ca2+ entry with a lag period of 50-80 ms. With patch electrodes filled with Ca2(+)-containing saline solutions and under conditions which maximized C-channel opening, peak Po was reached in 20-50 ms. The same value was observed for the whole-cell C-current. 7. The peak Po at a given patch potential and in response to a whole-cell spike was not altered by a previous long-lasting patch depolarization, or by producing several successive Ca2+ entries. Thus, C-channels did not appear to be inactivated by depolarization or increase in [Ca2+]i. 8. C-channels were found to be relatively highly voltage dependent, with an e-fold increase in Po per 14.9 mV increase in potential.(ABSTRACT TRUNCATED AT 400 WORDS)

The maturation of the central auditory conduction in preterm infants until three months post term. I. Composite group averages of brainstem (ABR) and middle latency (MLR) auditory evoked responses.

Brainstem (ABR) and middle latency (MLR) auditory evoked responses were obtained sequentially in 49 preterm infants until three months post term date. In addition, the records of 16 preterm infants, obtained at different conceptional age levels, were included. The recording of these responses was performed successively in one procedure, together with auditory cortical evoked responses. The infants were divided into 5 groups according to their gestational age, i.e. the term at birth. Composite group averages were determined, showing the group stable components of the 5 gestational age groups at 8 different conceptional age levels, i.e. term at the time of the recording. The intra group stable components could thus be determined for further study of developmental trends in the responses. The group averages also serve as a reference in the visual analysis of the individual records. The averaged ABRs showed that with increasing conceptional age increasingly better identifiable waveforms were obtained. These were particularly outstanding for peaks I and V ipsilateral to stimulation, and peaks IIc and Vc contralateral to stimulation. This enabled the measurement of the central conduction times. The MLRs were especially remarkable for their latency changes which occurred in peak PO and the troughs Na and Nb. The results indicated that the conduction of the subcortical auditory afferent signals can be measured successfully in groups of very premature infants with ABRs and MLRs.

Relationship between intraoral air pressure and vocal intensity in children and adults.

Intraoral air pressure (Po) varies as a function of age. Specifically, children produce significantly higher Po values than adults. The higher Po produced by children has been discussed in relation to age-related volumetric differences of the subglottal and vocal tract, to lung compression differences, and to the fact that children's "comfortable" speaking level might exceed that of adults. The present study was undertaken to evaluate the hypothesis that children (vs. adults) and women (vs. men) produce higher Po values when sound pressure level (SPL) is held constant. Measurements were made of Po generated by children and adults during a connected speech task completed at three intensity levels. The findings of the study indicated that peak Po values increased as vocal intensity increased for all subject groups, peak Po values were higher for voiceless stops than for voiced stops, and peak Po values were not significantly different for adults than for children or for men than for women. These results were interpreted to show that despite physical and physiological differences between male and female, and between adult and child vocal tracts, all groups use the same Po mechanism for achieving a given vocal intensity level.