Mechanisms underlying extremely fast muscle V˙O2 on-kinetics in humans.

The time constant of the primary phase of pulmonary V˙O2 on-kinetics (τp ), which reflects muscle V˙O2 kinetics during moderate-intensity exercise, is about 30 s in young healthy untrained individuals, while it can be as low as 8 s in endurance-trained athletes. We aimed to determine the intramuscular factors that enable very low values of t0.63 to be achieved (analogous to τp , t0.63 is the time to reach 63% of the V˙O2 amplitude). A computer model of oxidative phosphorylation (OXPHOS) in skeletal muscle was used. Muscle t0.63 was near-linearly proportional to the difference in phosphocreatine (PCr) concentration between rest and work (ΔPCr). Of the two main factors that determine t0.63 , a huge increase in either OXPHOS activity (six- to eightfold) or each-step activation (ESA) of OXPHOS intensity (>3-fold) was needed to reduce muscle t0.63 from the reference value of 29 s (selected to represent young untrained subjects) to below 10 s (observed in athletes) when altered separately. On the other hand, the effect of a simultaneous increase of both OXPHOS activity and ESA intensity required only a twofold elevation of each to decrease t0.63 below 10 s. Of note, the dependence of t0.63 on OXPHOS activity and ESA intensity is hyperbolic, meaning that in trained individuals a large increase in OXPHOS activity and ESA intensity are required to elicit a small reduction in τp . In summary, we postulate that the synergistic action of elevated OXPHOS activity and ESA intensity is responsible for extremely low τp (t0.63 ) observed in highly endurance-trained athletes

Greater V˙O2peak is correlated with greater skeletal muscle deoxygenation amplitude and hemoglobin concentration within individual muscles during ramp-incremental cycle exercise.

It is axiomatic that greater aerobic fitness (V˙O2peak) derives from enhanced perfusive and diffusive O2 conductances across active muscles. However, it remains unknown how these conductances might be reflected by regional differences in fractional O2 extraction (i.e., deoxy [Hb+Mb] and tissue O2 saturation [StO2]) and diffusive O2 potential (i.e., total[Hb+Mb]) among muscles spatially heterogeneous in blood flow, fiber type, and recruitment (vastus lateralis, VL; rectus femoris, RF). Using quantitative time-resolved near-infrared spectroscopy during ramp cycling in 24 young participants (V˙O2peak range: ~37.4-66.4 mL kg-1 min-1), we tested the hypotheses that (1) deoxy[Hb+Mb] and total[Hb+Mb] at V˙O2peak would be positively correlated with V˙O2peak in both VL and RF muscles; (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in V˙O2peak Peak deoxy [Hb+Mb] and StO2 correlated with V˙O2peak for both VL (r = 0.44 and -0.51) and RF (r = 0.49 and -0.49), whereas for total[Hb+Mb] this was true only for RF (r = 0.45). Baseline deoxy[Hb+Mb] and StO2 correlated with V˙O2peak only for RF (r = -0.50 and 0.54). In addition, the deoxy[Hb+Mb] slopes were not affected by aerobic fitness. In conclusion, while the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) did not differ between fitness groups the capacity to deoxygenate [Hb+Mb] (index of maximal fractional O2 extraction) correlated significantly with V˙O2peak in both RF and VL muscles. However, only in the RF did total[Hb+Mb] (index of diffusive O2 potential) relate to fitness

The Songs Of Long Ago

Illustrations of plantation livinghttps://scholarsjunction.msstate.edu/cht-sheet-music/1629/thumbnail.jp

A Novel Waveform to Extract Exercise Gas Exchange Response Dynamics: The Chirp Waveform

Characterizing exercise gas exchange response dynamics reveals important information about physiological control processes and cardiopulmonary dysfunction. However, current methods for extracting exercise response dynamics typically use multiple step-wise transitions, limiting applicability of this technique. PURPOSE: We designed a new protocol (chirp waveform) to extract exercise gas exchange response dynamics in a single visit. We tested the hypothesis that gas exchange response dynamics extracted from chirp forcing would be similar to those extracted from step-wise transitions. METHODS: Thirty-one participants (14 young healthy, 7 older healthy, and 10 patients with chronic obstructive pulmonary disease) visited the laboratory on three occasions. On visit 1, participants performed a ramp incremental test to determine the gas exchange threshold (GET). On visits 2-3, participants performed either a chirp or step-wise protocol in a randomized order. Chirp forcing consisted of sinusoidal fluctuations in work rate with constant amplitude and progressive shortening of sine periods. Square protocol consisted of 3 square-wave transitions each of 6 min duration. Work rate amplitude (from 20 W to ~95% of the individual’s GET) and exercise duration (30 min) were the same in both protocols. The input-output relationship was characterized using a first-order linear transfer function containing a system gain (K) and time constant (τ) [G(s)= K/(τ×s+1)]. Parameter identification was performed in Matlab using the Matlab System Identification toolbox. Agreement between measures was established using Bland-Altman analysis and Rothery’s Concordance Coefficient (RCC). RESULTS: No systematic bias (mean difference of chirp minus square-wave; Δmean) and good reliability was found for V̇O2 K [Δmean: 0.25(1.03) mL/min/W, p=0.179; RCC: 0.773, p=0.004], V̇O2 τ [Δmean: 0.30(7.08) s, p=0.815; RCC: 0.837, p2 K [Δmean: -0.19(1.57) mL/min/W, p=0.512; RCC: 0.827, pp=0.009] and good reliability (RCC: 0.794, p2 τ. CONCLUSION: The chirp waveform allows extraction of gas exchange response dynamics similar to those obtained from standard methods, thus overcoming the need for multiple tests

SARS-CoV-2 RapidPlex: A Graphene-Based Multiplexed Telemedicine Platform for Rapid and Low-Cost COVID-19 Diagnosis and Monitoring

The COVID-19 pandemic is an ongoing global challenge for public health systems. Ultrasensitive and early identification of infection is critical in preventing widespread COVID-19 infection by presymptomatic and asymptomatic individuals, especially in the community and in-home settings. We demonstrate a multiplexed, portable, wireless electrochemical platform for ultra-rapid detection of COVID-19: the SARS-CoV-2 RapidPlex. It detects viral antigen nucleocapsid protein, IgM and IgG antibodies, as well as the inflammatory biomarker C-reactive protein, based on our mass-producible laser-engraved graphene electrodes. We demonstrate ultrasensitive, highly selective, and rapid electrochemical detection in the physiologically relevant ranges. We successfully evaluated the applicability of our SARS-CoV-2 RapidPlex platform with COVID-19-positive and COVID-19-negative blood and saliva samples. Based on this pilot study, our multiplexed immunosensor platform may allow for high-frequency at-home testing for COVID-19 telemedicine diagnosis and monitoring

SARS-CoV-2 RapidPlex: A Graphene-Based Multiplexed Telemedicine Platform for Rapid and Low-Cost COVID-19 Diagnosis and Monitoring

The COVID-19 pandemic is an ongoing global challenge for public health systems. Ultrasensitive and early identification of infection is critical in preventing widespread COVID-19 infection by presymptomatic and asymptomatic individuals, especially in the community and in-home settings. We demonstrate a multiplexed, portable, wireless electrochemical platform for ultra-rapid detection of COVID-19: the SARS-CoV-2 RapidPlex. It detects viral antigen nucleocapsid protein, IgM and IgG antibodies, as well as the inflammatory biomarker C-reactive protein, based on our mass-producible laser-engraved graphene electrodes. We demonstrate ultrasensitive, highly selective, and rapid electrochemical detection in the physiologically relevant ranges. We successfully evaluated the applicability of our SARS-CoV-2 RapidPlex platform with COVID-19-positive and COVID-19-negative blood and saliva samples. Based on this pilot study, our multiplexed immunosensor platform may allow for high-frequency at-home testing for COVID-19 telemedicine diagnosis and monitoring

Skeletal muscle power and fatigue at the tolerable limit of ramp-incremental exercise in COPD

Muscle fatigue (a reduced power for a given activation) is common following exercise in COPD. Whether muscle fatigue, and reduced maximal voluntary locomotor power, are sufficient to limit whole-body exercise in COPD is unknown. We hypothesized in COPD: 1) exercise is terminated with a locomotor muscle power reserve; 2) reduction in maximal locomotor power is related to ventilatory limitation; and 3) muscle fatigue at intolerance is less than age-matched controls. We used a rapid switch from hyperbolic to isokinetic cycling to measure the decline in peak isokinetic power at the limit of incremental exercise ('performance fatigue') in 13 COPD (FEV1 49±17 %pred) and 12 controls. By establishing the baseline relationship between muscle activity and isokinetic power, we apportioned performance fatigue into the reduction in muscle activation and muscle fatigue. Peak isokinetic power at intolerance was ~130% of peak incremental power in controls (274±73 vs 212±84W, p<0.05), but ~260% in COPD (187±141 vs 72±34W, p<0.05) - greater than controls (p<0.05). Muscle fatigue as a fraction of baseline peak isokinetic power was not different in COPD vs controls (0.11±0.20 vs 0.19±0.11). Baseline to intolerance, the median frequency of maximal isokinetic muscle activity was unchanged in COPD but reduced in controls (+4.3±11.6 vs -5.5±7.6%, p<0.05). Performance fatigue as a fraction of peak incremental power was greater in COPD vs controls and related to resting (FEV1/FVC) and peak exercise (V̇E/MVV) pulmonary function (r2=0.47, r2=0.55, p<0.05). COPD patients are more fatigable than controls, but this fatigue is insufficient to constrain locomotor power and define exercise intolerance

Distinguishing Increased Adiposity and/or Aerobic Deconditioning as Moderators of Low VO2peak in Obese Men

Peak oxygen uptake (V̇O2peak) in a cardiopulmonary exercise test (CPET) is a strong predictor of morbidity, mortality, and quality of life. V̇O2peak in obese individuals is typically below the lower limit of normal (2 transport and utilization, i.e. aerobic deconditioning; or both. We hypothesized a modified CPET, to measure the fraction of maximum isokinetic power that can be supported by aerobic metabolism, will distinguish between adiposity and deconditioning effects on V̇O2peak. PURPOSE: To compare V̇O2peak and isokinetic neuromuscular performance in obese vs non-obese men. METHODS: A modified CPET with maximal (3 s) isokinetic cycling power at baseline and the limit of ramp-incremental (RI) exercise was used to calculate: A) baseline maximum isokinetic power (Piso); B) tolerance index (TI), % of Piso at V̇O2peak; C) fatigue index (FI), % reduction in Piso per RI-watt at V̇O2peak; D) power reserve (PR), isokinetic power available at V̇O2peak expressed as % RI-wattpeak. The FRIEND nomogram was used to predict V̇O2peak. Data are mean(SD) and were assessed by t-test. RESULTS: Compared to controls (n=24), obese men (n=20) were older (32(5) vs 26(7) yr), had greater BMI (38(6) vs 23(2) kg/m2), but were not different in stature (177(5) vs 180(7) cm) or predicted V̇O2peak (3.49(0.49) vs 3.58(0.36) L/min). Obese men had lower V̇O2peak (2.84(0.42) vs 3.71(0.45) L/min, p2peak (82(15) vs 104(12) %, pIndependent of body mass, obese men had preserved leg strength (normal Piso), but the fraction of maximum isokinetic power supported by aerobic metabolism at RI intolerance was reduced (low TI) with greater fatigability (high FI); each consistent with aerobic deconditioning. A modified CPET with maximal isokinetic power measurements can distinguish the effects of increased adiposity from aerobic deconditioning on V̇O2peak in obese men

Psychophysiological effects of synchronous versus asynchronous music during cycling

"This is a non-final version of an article published in final form in (https://journals.lww.com/acsm-msse/pages/articleviewer.aspx?year=2014&issue=02000&article=00024&type=abstract )"Purpose: Synchronizing movement to a musical beat may reduce the metabolic cost of exercise, but findings to date have been equivocal. Our aim was to examine the degree to which the synchronous application of music moderates the metabolic demands of a cycle ergometer task. Methods: Twenty-three recreationally active men made two laboratory visits. During the first visit, participants completed a maximal incremental ramp test on a cycle ergometer. At the second visit, they completed four randomized 6-min cycling bouts at 90% of ventilatory threshold (control, metronome, synchronous music, and asynchronous music). Main outcome variables were oxygen uptake, HR, ratings of dyspnea and limb discomfort, affective valence, and arousal. Results: No significant differences were evident for oxygen uptake. HR was lower under the metronome condition (122 T 15 bpm) compared to asynchronous music (124 T 17 bpm) and control (125 T 16 bpm). Limb discomfort was lower while listening to the metronome (2.5 T 1.2) and synchronous music (2.3 T 1.1) compared to control (3.0 T 1.5). Both music conditions, synchronous (1.9 T 1.2) and asynchronous (2.1 T 1.3), elicited more positive affective valence compared to metronome (1.2 T 1.4) and control (1.2 T 1.2), while arousal was higher with synchronous music (3.4 T 0.9) compared to metronome (2.8 T 1.0) and control (2.8 T 0.9). Conclusions: Synchronizing movement to a rhythmic stimulus does not reduce metabolic cost but may lower limb discomfort. Moreover, synchronous music has a stronger effect on limb discomfort and arousal when compared to asynchronous music

Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee-extension

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with (31)P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n = 14). Unlocalized (31)P spectra were collected from the quadriceps throughout using a dual-tuned ((1)H and (31)P) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min(-1)) or change in [PCr] (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min(-1); each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min(-1) (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P < 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min(-1), or 26 ± 30%; P < 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r(2) = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O)