Is curvature of the force-velocity relationship affected by oxygen availability? Evidence from studies in ex vivo and in situ rat muscles.

The power of shortening contractions in skeletal muscle is determined by the force-velocity relationship. Fatigue has been reported to either increase or decrease the force-velocity curvature depending on experimental circumstances. These discrepant findings may be related to experimental differences in oxygen availability. We therefore investigated how the curvature of the force-velocity relationship in soleus and gastrocnemius rat muscles is affected during fatigue, in both an ex vivo setup without an intact blood perfusion and in an in situ setup with an intact blood perfusion. Furthermore, we investigated the effect of reduced oxygen concentrations and reduced diffusion distance on the curvature of the force-velocity relationship in ex vivo muscles, where muscle oxygen uptake relies on diffusion from the incubation medium. Muscles were electrically stimulated to perform repeated shortening contractions and force-velocity curves were determined in rested and fatigued conditions. The curvature increased during fatigue in the soleus muscles (both in situ and ex vivo), and decreased for the gastrocnemius muscles (in situ) or remained unchanged (ex vivo). Furthermore, under ex vivo conditions, neither reduced oxygen concentrations nor reduced diffusion distance conferred any substantial effect on the force-velocity curvature. In contrast, reduced oxygen availability and increased diffusion distance did increase the loss of maximal power during fatigue, mainly due to additional decreases in isometric force. We conclude that oxygen availability does not influence the fatigue-induced changes in force-velocity curvature. Rather, the observed variable fatigue profiles with regard to changes in curvature seem to be linked to the muscle fiber-type composition.

Effects of manipulating tetanic calcium on the curvature of the force-velocity relationship in isolated rat soleus muscles.

AIM: In dynamically contracting muscles, increased curvature of the force-velocity relationship contributes to the loss of power during fatigue. It has been proposed that fatigue-induced reduction in [Ca++ ]i causes this increased curvature. However, earlier studies on single fibres have been conducted at low temperatures. Here, we investigated the hypothesis that curvature is increased by reductions in tetanic [Ca++ ]i in isolated skeletal muscle at near-physiological temperatures. METHODS: Rat soleus muscles were stimulated at 60 Hz in standard Krebs-Ringer buffer, and contraction force and velocity were measured. Tetanic [Ca++ ]i was in some experiments either lowered by addition of 10 µmol/L dantrolene or use of submaximal stimulation (30 Hz) or increased by addition of 2 mmol/L caffeine. Force-velocity curves were constructed by fitting shortening velocity at different loading forces to the Hill equation. Curvature was determined as the ratio a/F0 with increased curvature reflecting decreased a/F0 . RESULTS: Compared to control levels, lowering tetanic [Ca++ ]i with dantrolene or reduced stimulation frequency decreased the curvature slightly as judged from increase in a/F0 of 13 ± 1% (P = < .001) and 20 ± 2% (P = < .001) respectively. In contrast, increasing tetanic [Ca++ ]i with caffeine increased the curvature (a/F0 decreased by 17 ± 1%; P = < .001). CONCLUSION: Contrary to our hypothesis, interventions that reduced tetanic [Ca++ ]i caused a decrease in curvature, while increasing tetanic [Ca++ ]i increased the curvature. These results reject a simple causal relation between [Ca++ ]i and curvature of the force-velocity relation during fatigue.

European Stroke Organisation (ESO) guidelines for the management of spontaneous intracerebral hemorrhage

"BACKGROUND: Intracerebral hemorrhage (ICH) accounted for 9% to 27% of all strokes worldwide in the last decade, with high early case fatality and poor functional outcome. In view of recent randomized controlled trials (RCTs) of the management of ICH, the European Stroke Organisation (ESO) has updated its evidence-based guidelines for the management of ICH. METHOD: A multidisciplinary writing committee of 24 researchers from 11 European countries identified 20 questions relating to ICH management and created recommendations based on the evidence in RCTs using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. RESULTS: We found moderate- to high-quality evidence to support strong recommendations for managing patients with acute ICH on an acute stroke unit, avoiding hemostatic therapy for acute ICH not associated with antithrombotic drug use, avoiding graduated compression stockings, using intermittent pneumatic compression in immobile patients, and using blood pressure lowering for secondary prevention. We found moderate-quality evidence to support weak recommendations for intensive lowering of systolic blood pressure to <140 mmHg within six-hours of ICH onset, early surgery for patients with a Glasgow Coma Scale score 9-12, and avoidance of corticosteroids. CONCLUSION: These guidelines inform the management of ICH based on evidence for the effects of treatments in RCTs. Outcome after ICH remains poor, prioritizing further RCTs of interventions to improve outcome."

Electrode placement in bioimpedance spectroscopy: evaluation of alternative positioning of electrodes when measuring relative dehydration in athletes.

In order to maintain a homeostatic environment in human cells, the balance between absorption and separation of water must be retained. Imbalance will have consequences on both the cellular and organ levels. Studies performed on athletes have shown coherence between their hydration status and ability to perform. A dehydration of 2-7% of total body weight resulted in a marked decrease in performance. Measurement and monitoring of hydration status may be used to optimize athlete performance. Therefore, in this current study bioimpedance spectroscopy is used to determine the hydration status of athletes. Trials were made to investigate alternative ways of electrode placement when performing bioimpedance spectroscopy in order to measure relative dehydration. A total of 14 test subjects underwent measurements before, during, and after a cycle test of 3×25min. Electrodes where placed to measure body impedance in three different ways: wrist-ankle (recommended method), wrist-wrist, and transthoracic. Furthermore, the relative loss in weight of the subjects during the trial was registered. The study showed no relation between relative weight loss and the wrist-wrist and transthoracic placement method, using bioimpedance spectroscopy to measure relative dehydration. The inability of the method to detect such relative changes in hydration may be due to the bioimpedance spectroscopy technology being extremely sensitive to changes in skin temperature, movement artifacts, thoroughness in placing the electrodes, and the physiological impact on the human body when performing exercise. Therefore, further research into the area of bioimpedance spectroscopy is needed before this methodology can be applied in monitoring active athletes. Hence, a simple weight measurement still seems a more useful way of determining a relative change of hydration in an active setting.

Effects of sprint interval training on VO2max and aerobic exercise performance: A systematic review and meta-analysis.

Recently, several studies have examined whether low-volume sprint interval training (SIT) may improve aerobic and metabolic function. The objective of this study was to systematically review the existing literature regarding the aerobic and metabolic effects of SIT in healthy sedentary or recreationally active adults. A systematic literature search was performed (Bibliotek.dk, SPORTDiscus, Embase, PEDro, SveMed+, and Pubmed). Meta-analytical procedures were applied evaluating effects on maximal oxygen consumption (VO2max). Nineteen unique studies [four randomized controlled trials (RCTs), nine matched-controlled trials and six noncontrolled studies] were identified, evaluating SIT interventions lasting 2-8 weeks. Strong evidence support improvements of aerobic exercise performance and VO2max following SIT. A meta-analysis across 13 studies evaluating effects of SIT on VO2max showed a weighted mean effects size of g = 0.63 95% CI (0.39; 0.87) and VO2max increases of 4.2-13.4%. Solid evidence support peripheral adaptations known to increase the oxidative potential of the muscle following SIT, whereas evidence regarding central adaptations was limited and equivocal. Some evidence indicated changes in substrate oxidation at rest and during exercise as well as improved glycemic control and insulin sensitivity following SIT. In conclusion, strong evidence support improvement of aerobic exercise performance and VO2max following SIT, which coincides with peripheral muscular adaptations. Future RCTs on long-term SIT and underlying mechanisms are warranted.

Muscle fiber size increases following resistance training in multiple sclerosis.

OBJECTIVE: To test the hypothesis that lower body progressive resistance training (PRT) leads to an increase of the muscle fiber cross-sectional area (CSA) and a shift in the proportion of fiber types in patients with multiple sclerosis (MS). METHODS: The present study was a two-arm, randomized controlled trial (RCT). Thirty-eight MS patients (Expanded Disability Status Scale (EDSS) 3-5.5) were randomized to a PRT group (Exercise, n = 19) or a control group (Control, n = 19). The Exercise group performed a biweekly 12-week lower body PRT program [five exercises progressing from 15RM (Repetition Maximum) towards 8RM], whereas the Control group maintained their usual daily activity level during the trial period. Muscle biopsies from vastus lateralis were taken before (pre) and after the trial (post). Thigh volume (TV) was estimated from anthropometric measurements. Isokinetic muscle strength of the knee extensors (KE) and flexors (KF) were evaluated at slow (90(°)/s) and fast (180(°)/s) angular velocities. RESULTS: In the Exercise group the mean CSA of all muscle fibers (7.9 ± 15.4% vs. -3.5 ± 9.0%, p = 0.03) and of type II muscle fibers (14.0 ± 19.4% vs. -2.6 ± 15.5%, p = 0.02) increased in comparison with the Control group. No changes occurred in the proportion of fiber types in the Exercise group. Neither was there any change in total TV. Isokinetic strength at KE180, KF90 and KF180 improved significantly after PRT when compared with the control group (10.2-21.3%, p ≤ 0.02). CONCLUSIONS: We conclude that progressive resistance training induces a compensatory increase of muscle fiber size in patients with the central nervous system disorder, multiple sclerosis.

Fatigue, mood and quality of life improve in MS patients after progressive resistance training.

Fatigue occurs in the majority of multiple sclerosis patients and therapeutic possibilities are few. Fatigue, mood and quality of life were studied in patients with multiple sclerosis following progressive resistance training leading to improvement of muscular strength and functional capacity. Fatigue (Fatigue Severity Scale, FSS), mood (Major Depression Inventory, MDI) and quality of life (physical and mental component scores, PCS and MCS, of SF36) were scored at start, end and follow-up of a randomized controlled clinical trial of 12 weeks of progressive resistance training in moderately disabled (Expanded Disability Status Scale, EDSS: 3-5.5) multiple sclerosis patients including a Control group (n = 15) and an Exercise group (n = 16). Fatigue (FSS > 4) was present in all patients. Scores of FSS, MDI, PCS-SF36 and MCS-SF36 were comparable at start of study in the two groups. Fatigue improved during exercise by -0.6 (95% confidence interval (CI) -1.4 to 0.4) a.u. vs. 0.1 (95% CI -0.4 to 0.6) a.u. in controls (p = 0.04), mood improved by -2.4 (95% CI -4.1 to 0.7) a.u. vs. 1.1 (-1.2 to 3.4) a.u. in controls (p = 0.01) and quality of life (PCS-SF36) improved by 3.5 (95% CI 1.4-5.7) a.u. vs. -1.0 (95% CI -3.4-1.4) a.u. in controls (p = 0.01). The beneficial effect of progressive resistance training on all scores was maintained at follow-up after further 12 weeks. Fatigue, mood and quality of life all improved following progressive resistance training, the beneficial effect being maintained for at least 12 weeks after end of intervention.

Resistance training improves muscle strength and functional capacity in multiple sclerosis.

OBJECTIVE: To test the hypothesis that lower extremity progressive resistance training (PRT) can improve muscle strength and functional capacity in patients with multiple sclerosis (MS) and to evaluate whether the improvements are maintained after the trial. METHODS: The present study was a 2-arm, 12-week, randomized controlled trial including a poststudy follow-up period of 12 weeks. Thirty-eight moderately impaired patients with MS were randomized to a PRT exercise group (n = 19) or a control group (n = 19). The exercise group completed a biweekly 12-week lower extremity PRT program and was afterward encouraged to continue training. After the trial, the control group completed the PRT intervention. Both groups were tested before and after 12 weeks of the trial and at 24 weeks (follow-up), where isometric muscle strength of the knee extensors (KE MVC) and functional capacity (FS; combined score of 4 tests) were evaluated. RESULTS: KE MVC and FS improved after 12 weeks of PRT in the exercise group (KE MVC: 15.7% [95% confidence interval 4.3-27.0], FS: 21.5% [95% confidence interval 17.0-26.1]; p < 0.05), and the improvements were better than in the control group (p < 0.05). The improvements of KE and FS in the exercise group persisted at follow-up after 24 weeks. Also, the exercise effects were reproduced in the control group during the 12-week posttrial PRT period. CONCLUSIONS: Twelve weeks of intense progressive resistance training of the lower extremities leads to improvements of muscle strength and functional capacity in patients with multiple sclerosis, the effects persisting after 12 weeks of self-guided physical activity. LEVEL OF EVIDENCE: The present study provides level III evidence supporting the hypothesis that lower extremity progressive resistance training can improve muscle strength and functional capacity in patients with multiple sclerosis.

Heat shock protein translocation and expression response is attenuated in response to repeated eccentric exercise.

AIM: This study hypothesized that heat shock protein (HSP) translocation and upregulation is more probable to occur after eccentric exercise than after concentric exercise or repeated eccentric exercise. METHODS: Fourteen young, healthy, untrained male subjects completed two bench-stepping exercise bouts with 8 weeks between bouts, and were compared with a control group (n = 6). Muscle biopsies collected from m. vastus lateralis of both legs prior to and at 3 h, 24 h and 7 days after exercise were quantified for mRNA levels and/or for HSP27, alphabeta-crystallin and inducible HSP70 content in cytosolic and cytoskeletal protein fractions. RESULTS: The first bout of exercise reduced muscle strength and increased muscle soreness predominantly in the eccentric leg (P < 0.05). These responses were attenuated after the repeated eccentric exercise bout (P < 0.05), suggesting a repeated bout adaptation. Increases in inducible HSP70 and HSP27 protein content in cytoskeletal fractions were observed exclusively after eccentric exercise (P < 0.05). For HSP27, an approx. 10-fold upregulation after first-bout eccentric exercise was attenuated to a an approximately fourfold upregulation after the repeated eccentric exercise bout. mRNA levels for HSP70, HSP27 and alphabeta-crystallin were upregulated within approximately two to fourfold ranges at time points 3 and 24 h post-exercise (P < 0.05). This upregulation was induced exclusively by eccentric exercise but with a tendency to attenuated expression 3 h after the repeated eccentric exercise bout. CONCLUSION: Our results show that HSP translocation and expression responses are induced by muscle damaging exercise, and suggest that such HSP responses are closely related to the extent of muscle damage.

Low-intensity training dissociates metabolic from aerobic fitness.

This study investigated the effect of prolonged whole-body low-intensity exercise on blood lipids, skeletal muscle adaptations and aerobic fitness. Seven male subjects completed a 32-day crossing of the Greenland icecap on cross-country skies and before and after this arm or leg cranking was performed on two separate days and biopsies were obtained from arm and leg muscle, and venous blood was sampled. During the crossing, subjects skied for 342+/-42 min/day and body mass was decreased by 7.1+/-0.7 kg. Peak leg oxygen uptake (4.6+/-0.2 L/min) was decreased (P<0.05) by 7% whereas peak arm oxygen uptake (3.0+/-0.2 L/min) remained unchanged. Total and low-density lipoprotein cholesterol (5.0+/-0.2 and 3.20.2 mmol/L) were decreased by 8% and 20%, respectively. Muscle beta-hydroxy-acyl-CoA dehydrogenase activity was increased with 22% in arm (P=0.08) and remained unchanged in leg muscle. Hormone sensitive lipase activity was similar in arm and leg muscle prior to the expedition and was not significantly affected by the crossing. In conclusion, an improved blood lipid profile and thus metabolic fitness was present after prolonged low-intensity training and this occurred in spite of a decreased aerobic fitness and an unchanged arm and leg muscle hormone-sensitive lipase activity.

Expression patterns of atrogenic and ubiquitin proteasome component genes with exercise: effect of different loading patterns and repeated exercise bouts.

Unaccustomed exercise is known to produce strength loss, soreness, and myocellular disruption. With repeated application of exercise stimuli, the appearance of these indexes of muscle damage is attenuated, the so-called "repeated bout effect." No direct connection has been established between this repeated bout effect and exercise-induced increases in protein turnover, but it appears that a degree of tolerance is developed toward exercise for both. The present study sought to investigate markers of protein degradation by determining the expression of components related to the ubiquitin-proteasome system (UPS) with repeated exercise bouts. Healthy men carried out 30 min of bench stepping, performing eccentric work with one and concentric work with the other leg (n = 14), performing a duplicate exercise bout 8 wk later. A nonexercising control group was included (n = 6). RNA was extracted from muscle biopsies representing time points preexercise, +3 h, +24 h, and +7 days, and selected mRNA species were quantified using Northern blotting. The exercise model proved sufficient to produce a repeated bout effect in terms of strength and soreness. For forkhead box O transcription factor 1 (FOXO1) and muscle RING finger protein-1 (MURF1), strong upregulations were seen exclusively with concentric loading (P < 0.001), while atrogin-1 displayed a strong downregulation exclusively in response to eccentric exercise (P < 0.001). For MURF1 transcription, the first bout produced a downregulation that persisted until the second bout (P < 0.01). In conclusion, the UPS is modulated differentially in response to varying loading modalities and with different time frames in a way that to some extent reflects changes in protein metabolism known to take place with exercise.

Localization and quantification of muscle damage by magnetic resonance imaging following step exercise in young women.

Eccentric exercise affects muscles differentially according to intensity, duration, and previous exposure to the specific exercise activity. We used T2-weighted magnetic resonance imaging sequences to localize and quantify muscle damage following step exercise and to determine correlations between transverse relaxation time (T2) and other markers of muscle damage. Eight women performed two-step exercise bouts (30 min) separated by 8 weeks. Blood samples, MR scans, measurements of muscle strength, and muscle soreness were obtained immediately before, after, and up to 9 days after each bout. Resting muscle T2 (40.3+/-0.6 ms) increased exclusively in m. Adductor magnus (AM) in the thigh performing eccentric contractions and peaked 3 days after bout 1 (73.5+/-9.7 ms, P<0.05). Plasma creatine kinase (CK) activity peaked on day 3 after bout 1 and correlated with T2 in AM (r=0.96, P<0.001). After bout 2 CK and T2 were almost unaffected. This indicates that T2-weighted MRI can be applied to identify muscles from which enzymes are being released into the circulation.

Experimental osteomyelitis: what have we learned from animal studies about the systemic treatment of osteomyelitis?

Clinical trials of systemic antibiotic treatment of osteomyelitis are difficult to perform for many reasons, such as low incidence rate of osteomyelitis, variety of anatomic locations, stage and etiologic agents. In this article, we reviewed the experimental studies on osteomyelitis available in the English medical literature since 1968, to ascertain their actual and potential impact on the treatment of human osteomyelitis. Major results are summarized and topics of major interest, such as reproducibility of animal models, predictive value of animal models, correlation of pharmacokinetics between different animals and humans, and the correlation of outcome between animal and clinical studies are discussed. Most of the reviewed animal models are reproducible and dependable. However, establishing the right dose regimen in animals appeared a critical factor, which might undermine the predictive value of the experimental study. Due to difficulties in comparing results of animal and human studies, the predictive value of animal studies about osteomyelitis is still unclear. However, animal models gave valuable information to the clinician for choosing the minimal duration of antibiotic treatment. Even though the use of antibiotic combinations was associated with better outcome in the majority of animal studies, such a finding seems to have limited impact on clinical practice.

D-amphetamine improves cognitive deficits and physical therapy promotes fine motor rehabilitation in a rat embolic stroke model.

BACKGROUND AND PURPOSE: The purpose of this study was to examine the effects of D-amphetamine (D-amph) and physical therapy separately or combined on fine motor performance, gross motor performance and cognition after middle cerebral artery thromboembolization in rats. METHODS: Seventy-four rats were trained in appropriate cognitive and motor behaviours. Thirteen animals were sham-operated and fifty-nine animals were embolized in the right carotid territory. Animals were randomly assigned to five groups: 1) SHAM (non-embolized, saline), 2) CONTROL (embolized, saline), 3) D-AMPH (embolized, D-amph), 4) THERAPY (embolized, saline + physical therapy) and 5) D-AMPH + THERAPY (embolized, D-amph + physical therapy). Rats of the groups 4-5 underwent d-amph or saline treatment on days 1, 3, 5 and 7 after surgery and were re-trained for 1 h starting 60 min after each treatment. During this time, rats were allowed to voluntarily engage in suitable cognitive or motor behaviours in order to obtain food. Animals from all groups were re-tested during days 21-28 after surgery. RESULTS: No differences in infarct volumes were observed between the groups of embolized animals. When evaluating performances on days 21-28 after surgery, rats of the SHAM and THERAPY groups had better fine motor performance than those of the CONTROL (P < 0.05), whereas rats of SHAM and D-AMPH groups achieved better cognitive performance than CONTROL rats (P < 0.05). No significant differences were observed between any groups regarding gross motor performance. CONCLUSIONS: After embolization, physical therapy improved fine motor performance and D-amph accelerated rehabilitation of cognitive performance as observed in the rats of the THERAPY and D-AMPH groups. As a result of the administration of a high dose of D-amph, the rats of the D-AMPH + THERAPY combination group failed to engage in physical therapy during D-amph intoxication, thereby limiting any promotion of rehabilitation by combining physical therapy and D-amph.

Evidence that the Na+-K+ leak/pump ratio contributes to the difference in endurance between fast- and slow-twitch muscles.

AIM: Muscles containing predominantly fast-twitch (type II) fibres [ext. dig. longus (EDL)] show considerably lower contractile endurance than muscles containing mainly slow-twitch (type I) fibres (soleus). To assess whether differences in Na+-K+ fluxes and excitability might contribute to this phenomenon, we compared excitation-induced Na+-K+ leaks, Na+ channels, Na+-K+ pump capacity, force and compound action potentials (M-waves) in rat EDL and soleus muscles. METHODS: Isolated muscles were mounted for isometric contractions in Krebs-Ringer bicarbonate buffer and exposed to direct or indirect continuous or intermittent electrical stimulation. The time-course of force decline and concomitant changes in Na+-K+ exchange and M-waves were recorded. RESULTS: During continuous stimulation at 60-120 Hz, EDL showed around fivefold faster rate of force decline than soleus. This was associated with a faster loss of excitability as estimated from the area and amplitude of the M-waves. The net uptake of Na+ and the release of K+ per action potential were respectively 6.5- and 6.6-fold larger in EDL than in soleus, which may in part be due to the larger content of Na+ channels in EDL. During intermittent stimulation with 1 s 60 Hz pulse trains, EDL showed eightfold faster rate of force decline than soleus. CONCLUSION: The considerably lower contractile endurance of fast-twitch compared with slow-twitch muscles reflects differences in the rate of excitation-induced loss of excitability. This is attributed to the much larger excitation-induced Na+ influx and K+ efflux, leading to a faster rise in [K+]o in fast-twitch muscles. This may only be partly compensated by the concomitant activation of the Na+-K+ pumps, in particular in fibres showing large passive Na+-K+ leaks or reduced content of Na+-K+ pumps. Thus, endurance depends on the leak/pump ratio for Na+ and K+.

Thrombolytic and anticoagulation treatment in a rat embolic stroke model.

OBJECTIVES: The effects of pentasaccharide (PENTA), given alone or combined with thrombolysis using recombinant tissue plasminogen activator (rt-PA), on infarct size and clinical outcome were evaluated in a rat embolic stroke model. MATERIALS AND METHODS: Ninety-two rats were embolized unilaterally and assigned to: (i). controls, (ii). rt-PA 6 mg/kg, (iii). PENTA 0.5 mg/kg, (iv). PENTA 0.5 mg/kg and rt-PA 6 mg/kg. After 2 days animals were killed, the brains removed and evaluated microscopically. RESULTS: The median infarct size measured in percentage of the affected hemisphere was 25% in the control group, 4% (P < 0.01, Mann Whitney) in group 2, 19% (n.s.) in group 3, and 10% (P < 0.05) in group 4. rt-PA, and rt-PA combined with PENTA also promoted functional recovery. CONCLUSION: The present study found no effect of 0.5 mg/kg PENTA treatment. Compared with rt-PA treatment alone, 0.5 mg/kg PENTA alone or combined with rt-PA did not significantly increase mortality or tendency for hemorrhage.

The course of blood pressure in acute stroke is related to the severity of the neurological deficits.

OBJECTIVES: To evaluate how soon after stroke the diagnosis of hypertension could be established. METHODS: In a prospective study including 1192 patients with acute stroke within 6 h, blood pressure was measured serially at 2-h intervals during the first 24 h. Results are presented as mean arterial blood pressure (MAP). The Scandinavian Stroke Scale (SSS) assessed the neurological deficit. RESULTS: In 779 patients with mild to moderate ischaemic stroke or transient ischaemic attack (TIA) and SSS > 25, MAP was 118 mmHg (CI 95%: 116-119 mmHg) on admission and 109 mmHg (CI 95%: 108-110 mmHg) 4 h later (paired t-test, P < 0.001). No such early decrease was observed in 228 patients with severe cerebral infarction (CI). In mild to moderate ischaemic stroke or TIA, MAP at 24 h was not different from MAP at 3 months in paired t-test. CONCLUSIONS: Blood pressure 24 h after admission in patients with mild to moderate CI or TIA was representative of the patient's blood pressure 3 months after stroke. A diagnosis of arterial hypertension can be established a few days after stroke.

Protective effects of lactic acid on force production in rat skeletal muscle.

1. During strenuous exercise lactic acid accumulates producing a reduction in muscle pH. In addition, exercise causes a loss of muscle K(+) leading to an increased concentration of extracellular K(+) ([K(+)](o)). Individually, reduced pH and increased [K(+)](o) have both been suggested to contribute to muscle fatigue. 2. To study the combined effect of these changes on muscle function, isolated rat soleus muscles were incubated at a [K(+)](o) of 11 mM, which reduced tetanic force by 75 %. Subsequent addition of 20 mM lactic acid led, however, to an almost complete force recovery. A similar recovery was observed if pH was reduced by adding propionic acid or increasing the CO(2) tension. 3. The recovery of force was associated with a recovery of muscle excitability as assessed from compound action potentials. In contrast, acidification had no effect on the membrane potential or the Ca(2+) handling of the muscles. 4. It is concluded that acidification counteracts the depressing effects of elevated [K(+)](o) on muscle excitability and force. Since intense exercise is associated with increased [K(+)](o), this indicates that, in contrast to the often suggested role for acidosis as a cause of muscle fatigue, acidosis may protect against fatigue. Moreover, it suggests that elevated [K(+)](o) is of less importance for fatigue than indicated by previous studies on isolated muscles.

Activity-induced recovery of excitability in K(+)-depressed rat soleus muscle.

Increased extracellular K(+) concentration ([K(+)](o)) can reduce excitability and force in skeletal muscle. Here we examine the effects of muscle activation on compound muscle action potentials (M waves), resting membrane potential, and contractility in isolated rat soleus muscles. In muscles incubated for 60 min at 10 mM K(+), tetanic force and M wave area decreased to 23 and 24%, respectively, of the control value. Subsequently, short (1.5 s) tetanic stimulations given at 1-min intervals induced recovery of force and M wave area to 81 and 90% of control levels, respectively, within 15 min (P < 0.001). The recovery of force and M wave was associated with a partial repolarization of the muscle fibers. Experiments with tubocurarine suggest that the force recovery was related to activation of muscle Na(+)-K(+) pumps caused by the release of some compound from sensory nerves in response to muscle activity. In conclusion, activity produces marked recovery of excitability in K(+)-depressed muscle, and this may protect muscles against fatigue caused by increased [K(+)](o) during exercise.