Quadriceps neuromuscular function and self-reported functional ability in knee osteoarthritis

The purposes of this study were to determine 1) the relationships of self-reported function scores in patients with knee osteoarthritis (OA) to both maximal isometric torque and to isotonic power at a variety of loads, and 2) the degree to which muscle volume (MV) or voluntary activation (VA) are associated with torque and power measures in this population. Isometric maximal voluntary contraction (MVC) torque and isotonic power [performed at loads corresponding to 10, 20, 30, 40, and 50% MVC, and a minimal load ("Zero Load")] were measured in 40 participants with knee OA. Functional ability was measured with the Western Ontario and McMaster Osteoarthritis Index (WOMAC) function subscale. MV was determined with magnetic resonance imaging, and VA was measured with the interpolated twitch technique. In general, power measured at lower loads (Zero Load and 10-30% MVC, r(2) = 0.21-0.28, P < 0.05) predicted a greater proportion of the variance in function than MVC torque (r(2) = 0.18, P < 0.05), with power measured at Zero Load showing the strongest association (r(2) = 0. 28, P < 0.05). MV was the strongest predictor of MVC torque and power measures in multiple regression models (r(2) = 0.42-0.72). VA explained only 6% of the variance in MVC torque and was not significantly associated with power at any load (P > 0.05). Quadriceps MVC torque and power are associated with self-reported function in knee OA, but muscle power at lower loads is more predictive of function than MVC torque. The variance in MVC torque and power between participants is due predominantly to differences in MV and has little to do with deficits in VA.     

Plantar flexor activation capacity and H reflex in older adults: adaptations to strength training.

The purpose of this study was to investigate whether the voluntary neural drive and the excitability of the reflex arc could be modulated by training, even in old age. To this aim, the effects of a 16-wk strengthening program on plantar flexor voluntary activation (VA) and on the maximum Hoffman reflex (H(max))-to-maximum M wave (M(max)) ratio were investigated in 14 elderly men (65-80 yr). After training, isometric maximum voluntary contraction (MVC) increased by 18% (P < 0.05) and weight-lifting ability by 24% (P < 0.001). Twitch contraction time decreased by 8% (P < 0.01), but no changes in half relaxation time and in peak twitch torque were observed. The VA, assessed by twitch interpolation, increased from 95 to 98% (P < 0.05). Pretraining VA, also evaluated from the expected MVC for total twitch occlusion, was 7% higher (P < 0.01) than MVC. This discrepancy persisted after training. The interpolated twitch torque-voluntary torque relationship was fitted by a nonlinear model and was found to deviate from linearity for torque levels >65% MVC. Compared with younger men (24-35 yr), the H(max)- to M(max) ratio and nerve conduction velocity (H index) of the older group were significantly lower (42%, P < 0.05; and 29%, P < 0.001, respectively) and were not modulated by training. In conclusion, older men seem to preserve a high VA of plantar flexors. However, the impaired functionality of the reflex pathway with aging and the lack of modulation with exercise suggest that the decrease in the H(max)- to M(max) ratio and H index may be related to degenerative phenomena.     

Residual force enhancement following eccentric induced muscle damage

During lengthening of an activated skeletal muscle, the force maintained following the stretch is greater than the isometric force at the same muscle length. This is termed residual force enhancement (RFE), but it is unknown how muscle damage following repeated eccentric contractions affects RFE. Using the dorsiflexors, we hypothesised muscle damage will impair the force generating sarcomeric structures leading to a reduction in RFE. Following reference maximal voluntary isometric contractions (MVC) in 8 young men (26.5±2.8y) a stretch was performed at 30°/s over a 30° ankle excursion ending at the same muscle length as the reference MVCs (30° plantar flexion). Surface electromyography (EMG) of the tibialis anterior and soleus muscles was recorded during all tasks. The damage protocol involved 4 sets of 25 isokinetic (30°/s) lengthening contractions. The same measures were collected at baseline and immediately post lengthening contractions, and for up to 10min recovery. Following the lengthening contraction task, there was a 30.3±6.4% decrease in eccentric torque (P<0.05) and 36.2±9.7% decrease in MVC (P<0.05) compared to baseline. Voluntary activation using twitch interpolation and RMS EMG amplitude of the tibialis anterior remained near maximal without increased coactivation for MVC. Contrary to our hypothesis, RFE increased (～100-250%) following muscle damage (P<0.05). It appears stretch provided a mechanical strategy for enhanced muscle function compared to isometric actions succeeding damage. Thus, active force of cross-bridges is decreased because of impaired excitation-contraction coupling but force generated during stretch remains intact because force contribution from stretched sarcomeric structures is less impaired.     

Reduced short-interval intracortical inhibition after eccentric muscle damage in human elbow flexor muscles

The purpose of this study was to use paired-pulse transcranial magnetic stimulation (TMS) to examine the effect of eccentric exercise on short-interval intracortical inhibition (SICI) after damage to elbow flexor muscles. Nine young (22.5 ± 0.6 yr; mean ± SD) male subjects performed maximal eccentric exercise of the elbow flexor muscles until maximal voluntary contraction (MVC) force was reduced by ～40%. TMS was performed before, 2 h after, and 2 days after exercise under Rest and Active (5% MVC) conditions with motor-evoked potentials (MEPs) recorded from the biceps brachii (BB) muscle. Peripheral electrical stimulation of the brachial plexus was used to assess maximal M-waves, and paired-pulse TMS with a 3-ms interstimulus interval was used to assess changes in SICI at each time point. The eccentric exercise resulted in a 34% decline in strength (P < 0.001), a 41% decline in resting M-wave (P = 0.01), changes in resting elbow joint angle (10°, P < 0.001), and a shift in the optimal elbow joint angle for force production (18°, P < 0.05) 2 h after exercise. This was accompanied by impaired muscle strength (27%, P < 0.001) and increased muscle soreness (P < 0.001) 2 days after exercise, which is indicative of muscle damage. When the test MEP amplitudes were matched between sessions, we found that SICI was reduced by 27% in resting and 23% in active BB muscle 2 h after exercise. SICI recovered 2 days after exercise when muscle pain and soreness were present, suggesting that delayed onset muscle soreness from eccentric exercise does not influence SICI. The change in SICI observed 2 h after exercise suggests that eccentric muscle damage has widespread effects throughout the motor system that likely includes changes in motor cortex.     

Cardiopulmonary responses to combined rhythmic and isometric exercise in humans

A rhythmic (R) and an isometric (I) exercise were performed separately and in combination to assess their additive effects on arterial systolic (P(as)) and diastolic (P(ad)) blood pressures, heart rate (fc), and minute ventilation (VI). The isometric effort consisted of a 40% maximal voluntary handgrip contraction (MVC) performed for a duration of 80% of a previously determined 40% MVC fatiguing effort. The R effort consisted of a 13-min cycle effort at 75% maximum oxygen consumption (VO2max). For the combined efforts, I was performed starting simultaneously with or ending simultaneously with R. Data on nine subjects yield statistically significant evidence (P less than 0.05) that the effects of I and R are not additive for the following three cases: (1) P(as) when I and R are ended simultaneously (I alone = 4.9, SEM 0.5 kPa increase; R alone = no significant change from steady state; I + R = 1.2, SEM 0.4 kPa increase), (2) P(ad) when I and R are started simultaneously (I alone = 4.1, SEM 0.4 kPa increase; R alone = 0.7, SEM 0.3 kPa decrease; I + R = 1.9, SEM 0.4 kPa increase), and (3) P(ad) when I and R are ended simultaneously (I alone = 4.1, SEM 0.4 kPa increase; R alone = 0.3, SEM 0.5 kPa decrease; I + R = 0.8, SEM 0.3 kPa increase). For all other variables and cases, there is not sufficient evidence to conclude that the effects of I and R are not additive. We conclude that R and I exercises do not invariably produce strictly additive cardiopulmonary responses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms contributing to knee extensor strength loss after prolonged running exercise.

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 +/- 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 +/- 25.2 to 142.7 +/- 29.7 N x m; P < 0.001) as did %VA (from 98.8 +/- 1.8 to 91.3 +/- 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated (R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant (P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 +/- 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit.     

Relationship between back muscle endurance and voluntary activation

There is some evidence that the Biering-Sorensen endurance test can discriminate low back pain sufferers from healthy individuals and can predict future back pain. This test relies on the subject's ability to voluntarily drive the back muscles. This neural drive, termed voluntary activation (VA) can be measured using the twitch interpolation technique. The aim of the current study was to investigate the relationship between back muscle endurance and VA. Twenty-one healthy volunteers (10 males) participated. Bilateral electromyographic recordings were obtained from erector spinae and rectus abdominis. Back extensor torque was recorded using a dynamometer. The protocol consisted of measurement of VA (using magnetic stimulation of the brain and assessment of the sizes of the evoked twitches) and measurement of endurance. There was a linear correlation (r(2)=1, P<0.01) between voluntary torque and VA. The mean (SEM) endurance time was 174.9 (12.8)s. There was no correlation between endurance and VA at either 100% MVC (r(2)=0.01, P=0.72) or at 50% MVC (r(2)=0.11, P=0.16). These findings indicate that the endurance of the back muscles, as assessed using this widely utilised test does not appear to be related to a subject's ability to drive their back muscles voluntarily either maximally or submaximally.     

Divergent roles of plasma osmolality and the baroreflex on sweating and skin blood flow

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (-40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ～10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP (P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions (P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated (P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.     

Differences in the log-transformed electromyographic–force relationships of the plantar flexors between high- and moderate-activated subjects

The present study examined the log-transformed electromyographic amplitude (EMG) versus force relationships for the medial gastrocnemius (MG) and soleus (SOL) in high- and moderate-activated subjects. Twenty-five (age = 21 ± 2 year; mass = 62 ± 12 kg) participants performed six submaximal contractions (30–90% maximal voluntary contraction [MVC]) with the interpolated twitch technique (ITT) performed at 90% MVC to calculate percent voluntary activation (% VA). Sixteen participants with > 90% VA at 90% MVC were categorized high-activated group; the remaining nine were the moderate-activated group. Linear regression models were fit to the log-transformed EMG–force relationships. The slope (b value) and the antilog of the Y-intercept (a value) were calculated. The b values from the MG EMG–force relationships were higher (P < 0.05) for the high-activated group (1.27 ± 0.13) than the moderate-activated group (0.88 ± 0.06). The a values and p–p M-wave amplitude values (collapsed across twitches [superimposed and potentiated]) were larger (P < 0.05) for the MG (1.17 ± 0.40 and 8.98 ± 0.46 mV) than the SOL (0.24 ± 0.07 and 4.48 ± 0.20 mV) when collapsed across groups. The b value from the log-transformed EMG–force relationships is an attractive model to determine if a subject has the ability to achieve high activation of their MG without muscle or nerve stimulation.     

三种手术入路显露男性后尿道的比较（英文）

目的：评价经耻骨上、耻骨下及会阴三种手术入路暴露尿道膜部的优劣。方法：对35具成年男性尸体标本解剖,测量并比较耻骨上缘中点（A）、耻骨下缘中点（B）及会阴部两坐骨结节连线中点（c）分男11到尿道球膜部连接处（D）、前列腺尖（E）及膀胱颈（F）的距离及相关角度;对另20具成年男性尸体标本分别经3种手术入路显露后尿道,标记可能损伤的组织器官并评分。结果：AD=（6．5±0．5）cm,BD=（2．2±0．5）cm,CD=（3．4±0．6）cm,其中BD〈CD〈AD（P〈0．05,SNK法）;AE=（6．6±0．5）cm,BE=（3．0±0．5）cm,CE=（4．4±0．7）cm,其中BE〈CE〈AE（P〈0．05,SNK法）;AF=（5．7±0．6）cm,BF=（4．5±0．5）cm,CF=（6．5±0．6）cm,其中BF〈AF〈CF（P〈0．05,SNK法）。各点连线所成角度中,ZEAD（仅。）=（9．3±2．0）。∠EBD（α2）=（17．4±3．8）°,ZECD（α3）=（9．2±1．6）°,其中α1与α2有显著性差异（P〈0．05,t=11．1）,α3与α2有显著性差异（P〈0．05,t=-12．1）,α1与α3无显著性差异（P〉O．05,t=-0．13）;∠FAE（β1）=（22．7±2．6）°,∠FBE（β2）=（32．9±6．4）°,∠FCE（β3）=（15．0±3．2）°,其中β2〉β1〉β3（P〈0．05,SNK法）。经耻骨上入路损伤评分为13分,经耻骨下为18分,经会阴为15分。结论：暴露从优到劣依次为经耻骨下、经耻骨上、经会阴;损伤从大到小依次为经耻骨下、经会阴、经耻骨上部分。     

Large differences in peak oxygen uptake do not independently alter changes in core temperature and sweating during exercise

The independent influence of peak oxygen uptake (Vo(? peak)) on changes in thermoregulatory responses during exercise in a neutral climate has not been previously isolated because of complex interactions between Vo(? peak), metabolic heat production (H(prod)), body mass, and body surface area (BSA). It was hypothesized that Vo(? peak) does not independently alter changes in core temperature and sweating during exercise. Fourteen males, 7 high (HI) Vo(? peak): 60.1 ± 4.5 ml·kg?1·min?1; 7 low (LO) Vo(? peak): 40.3 ± 2.9 ml·kg?1·min?1 matched for body mass (HI: 78.2 ± 6.1 kg; LO: 78.7 ± 7.1 kg) and BSA (HI: 1.97 ± 0.08 m2; LO: 1.94 ± 0.08 m2), cycled for 60-min at 1) a fixed heat production (FHP trial) and 2) a relative exercise intensity of 60% Vo(? peak) (REL trial) at 24.8 ± 0.6°C, 26 ± 10% RH. In the FHP trial, H(prod) was similar between the HI (542 ± 38 W, 7.0 ± 0.6 W/kg or 275 ± 25 W/m2) and LO (535 ± 39 W, 6.9 ± 0.9 W/kg or 277 ± 29 W/m2) groups, while changes in rectal (T(re): HI: 0.87 ± 0.15°C, LO: 0.87 ± 0.18°C, P = 1.00) and aural canal (T(au): HI: 0.70 ± 0.12°C, LO: 0.74 ± 0.21°C, P = 0.65) temperature, whole-body sweat loss (WBSL) (HI: 434 ± 80 ml, LO: 440 ± 41 ml; P = 0.86), and steady-state local sweating (LSR(back)) (P = 0.40) were all similar despite relative exercise intensity being different (HI: 39.7 ± 4.2%, LO: 57.6 ± 8.0% Vo(2 peak); P = 0.001). At 60% Vo(2 peak), H(prod) was greater in the HI (834 ± 77 W, 10.7 ± 1.3 W/kg or 423 ± 44 W/m2) compared with LO (600 ± 90 W, 7.7 ± 1.4 W/kg or 310 ± 50 W/m2) group (all P < 0.001), as were changes in T(re) (HI: 1.43 ± 0.28°C, LO: 0.89 ± 0.19°C; P = 0.001) and T(au) (HI: 1.11 ± 0.21°C, LO: 0.66 ± 0.14°C; P < 0.001), and WBSL between 0 and 15, 15 and 30, 30 and 45, and 45 and 60 min (all P < 0.01), and LSR(back) (P = 0.02). The absolute esophageal temperature (T(es)) onset for sudomotor activity was ～0.3°C lower (P < 0.05) in the HI group, but the change in T(es) from preexercise values before sweating onset was similar between groups. Sudomotor thermosensitivity during exercise were similar in both FHP (P = 0.22) and REL (P = 0.77) trials. In conclusion, changes in core temperature and sweating during exercise in a neutral climate are determined by H(prod), mass, and BSA, not Vo(? peak).     

Neuromuscular adaptations to training

The purpose of this experiment was to determine whether there is a central adaptation to resistance overload. The right adductor pollicis muscle of each subject was trained with either voluntary (n = 9) or electrically stimulated contractions (n = 7), the contralateral muscle acted as an internal control, and seven other subjects acted as a control group. Training was the same in both groups: 15 contractions at 80% maximal voluntary contraction (MVC), 3 days/wk for 5 wk. Trained muscles in both groups increased MVC by approximately 15% (voluntary, P less than 0.01; stimulated, P less than 0.05). There was a small (9.5%) but significant (P less than 0.05) increase in MVC of the untrained muscles in the voluntary group. MVC did not change in the control group. Maximal electromyogram (EMG) was highly reproducible pre-to posttraining in the control group (r = 0.92, slope = 0.995) and did not change pre- to posttraining in the trained groups. Sensory adaptation to training caused a reduction in force sensation in the stimulated group (P less than 0.05) but not in the voluntary group. Because there was a small increase in MVC of the untrained muscle of the voluntary group (9.5%, P less than 0.05) but not in the stimulated group, it is possible that there is a central motor adaptation, but it is not manifested in increased neural drive (EMG). Moreover, this central adaptation may be responsible for the decrease in force sensation that follows training.     

Acute effects of a single warm-water bath on serum adiponectin and leptin levels in healthy men: A pilot study

To preliminarily assess the acute effects of a single warm-water bath (WWB) on serum adipokine activity, we measured serum adiponectin, leptin and other metabolic profiles before, immediately after and 30 minutes after WWB in seven healthy male volunteers (mean age, 39.7 ± 6.0 years; mean body mass index, 21.6 ± 1.8 kg/m(2)). The subjects were immersed in tap water at 41°C for 10 minutes. Two weeks later, the same subjects underwent a single WWB with a bath additive that included inorganic salts and carbon dioxide (WWB with ISCO(2)) by the same protocol as for the first WWB. Leptin levels significantly increased immediately after WWB with tap water and ISCO(2) (both P < 0.05), and remained significantly higher than those at baseline even 30 minutes after WWB with tap water (P < 0.05). Adiponectin levels showed a slight, but not significant, increase both immediately after and 30 minutes after WWB with tap water or ISCO(2). Some parameters, such as serum total cholesterol, red blood cell count, hemoglobin and hematocrit significantly increased immediately after WWB with tap water or ISCO(2) (all P < 0.05), but they all returned to the baseline levels 30 minutes after bathing under both conditions. The sublingual temperature rose significantly after 10 minutes of WWB with tap water (0.96 ± 0.16°C relative to baseline, P < 0.01) and after the same duration of WWB with ISCO(2) (1.24 ± 0.34°C relative to baseline, P < 0.01). These findings suggest that a single WWB at 41°C for 10 minutes may modulate leptin and adiponectin profiles in healthy men.     

Changes in H reflex and V wave following short-term endurance and strength training

This study examined the effects of 3 wk of either endurance or strength training on plasticity of the neural mechanisms involved in the soleus H reflex and V wave. Twenty-five sedentary healthy subjects were randomized into an endurance group (n = 13) or strength group (n = 12). Evoked V-wave, H-reflex, and M-wave recruitment curves, maximal voluntary contraction (MVC), and time-to-task-failure (isometric contraction at 40% MVC) of the plantar flexors were recorded before and after training. Following strength training, MVC of the plantar flexors increased by 14.4 ± 5.2% in the strength group (P < 0.001), whereas time-to-task-failure was prolonged in the endurance group (22.7 ± 17.1%; P < 0.05). The V wave-to-maximal M wave (V/M(max)) ratio increased significantly (55.1 ± 28.3%; P < 0.001) following strength training, but the maximal H wave-to-maximal M wave (H(max)/M(max)) ratio remained unchanged. Conversely, in the endurance group the V/M(max) ratio was not altered, whereas the H(max)/M(max) ratio increased by 30.8 ± 21.7% (P < 0.05). The endurance training group also displayed a reduction in the H-reflex excitability threshold while the H-reflex amplitude on the ascending limb of the recruitment curve increased. Strength training only elicited a significant decrease in H-reflex excitability threshold, while H-reflex amplitudes over the ascending limb remained unchanged. These observations indicate that the H-reflex pathway is strongly involved in the enhanced endurance resistance that occurs following endurance training. On the contrary, the improvements in MVC following strength training are likely attributed to increased descending drive and/or modulation in afferents other than Ia afferents.     

A comparison of adductor pollicis fatigue in older men and women

Sex differences in fatigue resistance of the adductor pollicis (AP) muscle were studied in 24 older adults who were divided into three groups: 12 older men (69.8 +/- 4.60 years), 6 older women not on hormone replacement therapy (HRT) (70.2 +/- 4.02 years), and 6 older women on HRT (68.7 +/- 6.47 years). Fatigue in the AP muscle was induced using an intermittent (5 s contraction, 5 s rest) submaximal voluntary contraction (50% of maximal voluntary contraction (MVC)) protocol, which was continued until exhaustion (i.e., when subjects could either no longer maintain a 5-s contraction at 50% MVC or when the MVC was deemed to be lower than the target force). There was no effect of HRT on MVC or time to fatigue (TTF); therefore, the older women were pooled as one subject group. At baseline, men were stronger than women for MVC (75.9 +/- 18.8 N in men vs. 56.8 +/- 10.0 N in women; P < 0.05) and evoked twitch force (7.3 +/- 1.7 N in men vs. 5.2 +/- 0.8 N in women; P < 0.05). There was no difference in TTF between men and women (14.77 +/- 7.06 min in men vs. 11.53 +/- 4.91 min in women; P > 0.20), nor was there a significant relationship between baseline muscle force and TTF (r = 0.14). There was also no difference in the pattern of fatigue and recovery between the men and women. These results suggest that there is no difference in endurance or fatigue characteristics of the AP muscle in men and women over the age of 65 years, and that baseline muscle force does not predict fatigue resistance in this muscle.     

Effects of wearing a cooling vest during the warm-up on 10-km run performance

The purpose of this study was to examine whether wearing a cooling vest during an active warm-up would improve the 10-km time trial (TT) performance of endurance runners. Seven male runners completed 3 10-km TTs (1 familiarization and 2 experimental) on a treadmill after a 30-minute warm-up. During the warm-up of the experimental TTs, runners wore either a t-shirt (control [C]) or a cooling vest (V), the order of which was randomized. No differences were found between the C and V conditions for the 10-km TT times (2,533 ± 144 and 2,543 ± 149 seconds, respectively) (p = 0.746) or any of the 2-km split times. Heart rate (HR) at the start of the TT equaled 90 ± 17 b·min for C and 94 ± 16 b·min for V. The HR peaked at 184 ± 20 b·min in C and 181 ± 19 b·min in V. At the start of the TT Tc was 37.65 ± .72°C in C and 37.29 ± .73°C in V (p = 0.067). In C, Tc gradually increased until 39.34 ± 0.43°C while in V is reached 39.18 ± 0.72°C (p = 0.621). Although rating of perceived exertion (RPE) and Thermal sensation (TS) increased during both experimental TTs, there were no differences between V and C. Findings suggest wearing a cooling vest during a warm-up does not improve 10-km performance. The use of cooling vests during the warm-up did not produce any physiological (HR and Tc) or psychological (RPE and TS) benefit, perhaps accounting for the lack of improvement.     

Oral atorvastatin therapy increases nitric oxide-dependent cutaneous vasodilation in humans by decreasing ascorbate-sensitive oxidants

Elevated low-density lipoproteins (LDL) are associated with cutaneous microvascular dysfunction partially mediated by increased arginase activity, which is decreased following a systemic atorvastatin therapy. We hypothesized that increased ascorbate-sensitive oxidant stress, partially mediated through uncoupled nitric oxide synthase (NOS) induced by upregulated arginase, contributes to cutaneous microvascular dysfunction in hypercholesterolemic (HC) humans. Four microdialysis fibers were placed in the skin of nine HC (LDL = 177 ± 6 mg/dl) men and women before and after 3 mo of a systemic atorvastatin intervention and at baseline in nine normocholesterolemic (NC) (LDL = 95 ± 4 mg/dl) subjects. Sites served as control, NOS inhibited, L-ascorbate, and arginase-inhibited+L-ascorbate. Skin blood flow was measured while local skin heating (42°C) induced NO-dependent vasodilation. After the established plateau in all sites, 20 mM ?ngname? was infused to quantify NO-dependent vasodilation. Data were normalized to maximum cutaneous vascular conductance (CVC) (sodium nitroprusside + 43°C). The plateau in vasodilation during local heating (HC: 78 ± 4 vs. NC: 96 ± 2% CVC(max), P < 0.01) and NO-dependent vasodilation (HC: 40 ± 4 vs. NC: 54 ± 4% CVC(max), P < 0.01) was reduced in the HC group. Acute L-ascorbate alone (91 ± 5% CVC(max), P < 0.001) or combined with arginase inhibition (96 ± 3% CVC(max), P < 0.001) augmented the plateau in vasodilation in the HC group but not the NC group (ascorbate: 96 ± 2; combo: 93 ± 4% CVC(max), both P > 0.05). After the atorvastatin intervention NO-dependent vasodilation was augmented in the HC group (HC postatorvastatin: 64 ± 4% CVC(max), P < 0.01), and there was no further effect of ascorbate alone (58 ± 4% CVC(max,) P > 0.05) or combined with arginase inhibition (67 ± 4% CVC(max,) P > 0.05). Increased ascorbate-sensitive oxidants contribute to hypercholesteromic associated cutaneous microvascular dysfunction which is partially reversed with atorvastatin therapy.     

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

End-tidal carbon dioxide tension (Pet(CO(2))) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on Pet(CO(2)) being an accurate surrogate for arterial carbon dioxide tension (Pa(CO(2))), the latter being the physiologically relevant variable. This study tested the hypothesis that Pet(CO(2)) provides an accurate assessment of Pa(CO(2)) during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress (N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in Pet(CO(2)) (N = 7). Pet(CO(2)) and Pa(CO(2)) decreased during heat stress (P < 0.001); however, there was no group difference between Pa(CO(2)) and Pet(CO(2)) (P = 0.36) nor was there a significant interaction between thermal condition and measurement technique (P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, Pet(CO(2)) and Pa(CO(2)) at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between Pa(CO(2)) and Pet(CO(2)) while normothermic (P = 0.14) and following a 1.0 ± 0.2°C (P = 0.21) and 1.4 ± 0.2°C (P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of Pet(CO(2)) and Pa(CO(2)) were similar (P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in Pet(CO(2)) (7.5 ± 2.8 mmHg) and Pa(CO(2)) (6.6 ± 3.4 mmHg) were similar (P = 0.31). These data indicate that mean Pet(CO(2)) reflects mean Pa(CO(2)) during the evaluated conditions.     

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O(2) consumption (PVA-MVo(2)) framework. AM (15 ng·kg(-1)·min(-1), n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg(-1)·min(-1)) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% (P < 0.05, AM-EPI interaction) compared with 13 ± 12% (P < 0.05 vs. baseline) and 18 ± 31% (P = not significant) with EPI. LV systolic capacitance decreased by -37 ± 22% and peak positive derivative of LV pressure (dP/dt(max)) increased by 32 ± 7% with AM-EPI (P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. -11 ± 10%, P = not significant). PVA-MVo(2) relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.