ATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, Rheb.

RATIONALE: Endoplasmic reticulum (ER) stress dysregulates ER proteostasis, which activates the transcription factor, ATF6 (activating transcription factor 6α), an inducer of genes that enhance protein folding and restore ER proteostasis. Because of increased protein synthesis, it is possible that protein folding and ER proteostasis are challenged during cardiac myocyte growth. However, it is not known whether ATF6 is activated, and if so, what its function is during hypertrophic growth of cardiac myocytes. OBJECTIVE: To examine the activity and function of ATF6 during cardiac hypertrophy. METHODS AND RESULTS: We found that ER stress and ATF6 were activated and ATF6 target genes were induced in mice subjected to an acute model of transverse aortic constriction, or to free-wheel exercise, both of which promote adaptive cardiac myocyte hypertrophy with preserved cardiac function. Cardiac myocyte-specific deletion of Atf6 (ATF6 cKO [conditional knockout]) blunted transverse aortic constriction and exercise-induced cardiac myocyte hypertrophy and impaired cardiac function, demonstrating a role for ATF6 in compensatory myocyte growth. Transcript profiling and chromatin immunoprecipitation identified RHEB (Ras homologue enriched in brain) as an ATF6 target gene in the heart. RHEB is an activator of mTORC1 (mammalian/mechanistic target of rapamycin complex 1), a major inducer of protein synthesis and subsequent cell growth. Both transverse aortic constriction and exercise upregulated RHEB, activated mTORC1, and induced cardiac hypertrophy in wild type mouse hearts but not in ATF6 cKO hearts. Mechanistically, knockdown of ATF6 in neonatal rat ventricular myocytes blocked phenylephrine- and IGF1 (insulin-like growth factor 1)-mediated RHEB induction, mTORC1 activation, and myocyte growth, all of which were restored by ectopic RHEB expression. Moreover, adeno-associated virus 9- RHEB restored cardiac growth to ATF6 cKO mice subjected to transverse aortic constriction. Finally, ATF6 induced RHEB in response to growth factors, but not in response to other activators of ATF6 that do not induce growth, indicating that ATF6 target gene induction is stress specific. CONCLUSIONS: Compensatory cardiac hypertrophy activates ER stress and ATF6, which induces RHEB and activates mTORC1. Thus, ATF6 is a previously unrecognized link between growth stimuli and mTORC1-mediated cardiac growth.

Increases in core temperature counterbalance effects of haemoconcentration on blood viscosity during prolonged exercise in the heat.

NEW FINDINGS: What is the central question of this study? The purpose of the present study was to determine the effects of exercise-induced haemoconcentration and hyperthermia on blood viscosity. What is the main finding and its importance? Exercise-induced haemoconcentration, increased plasma viscosity and increased blood aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell (RBC) deformability (e.g. RBC membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat. Previous studies have reported that blood viscosity is significantly increased following exercise. However, these studies measured both pre- and postexercise blood viscosity at 37 °C even though core and blood temperatures would be expected to have increased during the exercise. Consequently, the effect of exercise-induced hyperthermia on mitigating change in blood viscosity may have been missed. The purpose of this study was to isolate the effects of exercise-induced haemoconcentration and hyperthermia and to determine their combined effects on blood viscosity. Nine subjects performed 2 h of moderate-intensity exercise in the heat (37 °C, 40% relative humidity), which resulted in significant increases from pre-exercise values for rectal temperature (from 37.11 ± 0.35 to 38.76 ± 0.13 °C), haemoconcentration (haematocrit increased from 43.6 ± 3.6 to 45.6 ± 3.5%) and dehydration (change in body weight = -3.6 ± 0.7%). Exercise-induced haemoconcentration significantly (P < 0.05) increased blood viscosity by 9% (from 3.97 to 4.33 cP at 300 s(-1)), whereas exercise-induced hyperthermia significantly decreased blood viscosity by 7% (from 3.97 to 3.69 cP at 300 s(-1)). When both factors were considered together, there was no overall change in blood viscosity (from 3.97 to 4.03 cP at 300 s(-1)). The effects of exercise-induced haemoconcentration, increased plasma viscosity and increased red blood cell aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell deformability (e.g. red blood cell membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat.

Acute normobaric hypoxia reduces body temperature in humans.

Anapyrexia is the regulated decrease in body temperature during acute exposure to hypoxia. This study examined resting rectal temperature (Trec) in adult humans during acute normobaric hypoxia (NH). Ten subjects breathed air consisting of 21% (NN), 14% (NH14), and 12% oxygen (NH12) for 30 min each in thermoneutral conditions while Trec and blood oxygen saturation (Spo2) were measured. Linear regression indicated that Spo2 was progressively lower in NH14 (p=0.0001) and NH12 (p=0.0001) compared to NN, and that Spo2 in NH14 was different than NH12 (p=0.00001). Trec was progressively lower during NH14 (p=0.014) and in NH12 (p=0.0001) compared to NN. The difference in Trec between NH14 and NH12 was also significant (p=0.0287). Spo2 was a significant predictor of Trec such that for every 1% decrease in Spo2, Trec decreased by 0.15°C (p=0.0001). The present study confirmed that, similar to many other species, human adults respond to acute hypoxia exposure by lowering rectal temperature.

Alterations in the rate of limb movement using a lower body positive pressure treadmill do not influence respiratory rate or phase III ventilation.

The purpose of this study was to determine the effect of alterations in rate of limb movement on Phase III ventilation during exercise, independent of metabolic rate, gait style, and treadmill incline. Subjects completed five submaximal exercise bouts on a lower body positive pressure treadmill (AlterG P 200). The percent body weight for the five exercise bouts was 100, 87, 75, 63, and 50% and each was matched for carbon dioxide production (V CO2 ). Naturally, to match the V CO2 while reducing the body weight up to 50% of normal required a significant increase in the treadmill speed from 3.0 ± 0.1 to 4.1 ± 0.2 mph, which resulted in a significant (P < 0.05) increase in the mean step frequency (steps per minute) from 118 ± 10 at 3 mph (i.e., 100% of body weight) to 133 ± 6 at 4.1 mph (i.e., 50% of body weight). The most important finding was that significant increases in step frequency did not significantly alter minute ventilation or respiratory rate. Such results do not support an important role for the rate of limb movement in Phase III ventilation during submaximal exercise, when metabolic rate, gait style, and treadmill incline are controlled.

Effect of air temperature on the rectal temperature gradient at rest and during exercise.

The purpose of the current study was to determine the effect of air temperature on the rectal temperature gradient at rest and during exercise. It was hypothesized that the rectal temperature gradient would be exacerbated in cold environments and attenuated in warm environments both at rest and during exercise. Each subject completed three exercise bouts on a motor driven treadmill at approximately 55% of their previously determined maximal oxygen uptake. Three different air temperatures (10, 22, 39°C) were used for the exercise bouts. Rectal temperature was measured at rest and every 5 min during each exercise bout using 4 temperature sensors affixed at 4, 7, 10 and 13 cm past the anal sphincter. Readings obtained from the 4-cm depth were significantly (p<0.05) lower than those obtained at deeper insertion depths both at rest and during exercise for all three air temperatures. Furthermore, the results showed that the rectal temperature gradient was exacerbated in cold environments and attenuated in warm environments both at rest and during exercise.

Specific exercise heat stress protocol for a triathlete's return from exertional heat stroke.

A triathlete collapsed with exertional heatstroke (EHS) during 2 races over 3 months. The American College of Sports Medicine recommends a heat tolerance test (HTT) following EHS if there is a concern with return to play. The classical walking HTT may not be the best test to evaluate elite triathletes' heat tolerance due to race intensity, nor is it suited to evaluate acclimation ability, which may play a role in risk of heat illness. Is the athlete capable of returning to racing or should he retire from sport due to heat intolerance? Up to 90 min of cycling (70% of V˙O2max; 36°C, 50% relative humidity) was followed by 9 d of exercise heat acclimation and a final identical exercise heat stress test. After acclimation, exercise duration before reaching a gastrointestinal temperature (Tgi) of 39.5°C increased 25 min, sweat rate increased 0.5 L·h, initial Tgi decreased 0.85°C, and rate of Tgi rise decreased 0.6°C·h. Adaptations were deemed acceptable, and the athlete was allowed to return to competition. The athlete has since raced in hot environments without incident.

Evaluation of the ventilatory effects of a restraint chair on human subjects.

BACKGROUND: Combative individuals often require physical restraint in the prehospital and law enforcement setting. Specialized restraint chairs have been utilized for this purpose in the latter case, but concern has arisen that restrained individuals are at risk for ventilatory compromise and asphyxiation. OBJECTIVE: We sought to determine if placement in a restraint chair results in alterations of respiratory or ventilatory function. METHODS: We conducted a randomized, cross-over, controlled experimental trial in 10 healthy human volunteers performed at a university exercise physiology laboratory. After exercise on a cycle ergometer to 85% of the age-predicted maximal heart rate, subjects were randomized to either a sitting position or restraint chair with arms, legs, and chest secured using standard law enforcement protocol. Subjects remained in each position for 30 min, during which pulmonary function testing of maximal voluntary ventilation (MVV) was performed at 11 and 30 min. Arterial oxygen saturation (O(2)sat) and end-tidal PCO(2) levels (PETCO(2)) were monitored continuously. Subjects repeated the experimental trial in the alternate position after a 45-min rest period. Measures between restraint and sitting positions were compared using a paired t-test at each time measurement. RESULTS: There was no evidence of hypoxemia. Mean PETCO(2) levels were not statistically different between the two groups at any time (p > 0.05), and there was no evidence of hypercapnia. CONCLUSION: In healthy subjects, placement in a restraint chair resulted in a small decrease in MVV, but did not result in any changes in O(2)sat or PETCO(2).

Skeletal muscle fatigue precedes the slow component of oxygen uptake kinetics during exercise in humans.

The mechanisms determining exercise intolerance are poorly understood. A reduction in work efficiency in the form of an additional energy cost and oxygen requirement occurs during high-intensity exercise and contributes to exercise limitation. Muscle fatigue and subsequent recruitment of poorly efficient muscle fibres has been proposed to mediate this decline. These data demonstrate in humans, that muscle fatigue, generated in the initial minutes of exercise, is correlated with the increasing energy demands of high-intensity exercise. Surprisingly, however, while muscle fatigue reached a plateau, oxygen uptake continued to increase throughout 8 min of exercise. This suggests that additional recruitment of inefficient muscle fibres may not be the sole mechanism contributing to the decline in work efficiency during high-intensity exercise.

ACTN3 and ACE genotypes in elite Jamaican and US sprinters.

UNLABELLED: The angiotensin-converting enzyme (ACE) and the alpha-actinin-3 (ACTN3) genes are two of the most studied "performance genes" and both have been associated with sprint/power phenotypes and elite performance. PURPOSE: To investigate the association between the ACE and the ACTN3 genotypes and sprint athlete status in elite Jamaican and US African American sprinters. METHODS: The ACTN3 R577X and the ACE I/D and A22982G (rs4363) genotype distributions of elite Jamaican (J-A; N = 116) and US sprinters (US-A; N = 114) were compared with controls from the Jamaican (J-C; N = 311) and US African American (US-C; N = 191) populations. Frequency differences between groups were assessed by exact test. RESULTS: For ACTN3, the XX genotype was found to be at very low frequency in both athlete and control cohorts (J-C = 2%, J-A = 3%, US-C = 4%, US-A = 2%). Athletes did not differ from controls in ACTN3 genotype distribution (J, P = 0.87; US, P = 0.58). Similarly, neither US nor Jamaican athletes differed from controls in genotype at ACE I/D (J, P = 0.44; US, P = 0.37). Jamaican athletes did not differ from controls for A22982G genotype (P = 0.28), although US sprinters did (P = 0.029), displaying an excess of heterozygotes relative to controls but no excess of GG homozygotes (US-C = 22%, US-A = 18%). CONCLUSIONS: Given that ACTN3 XX genotype is negatively associated with elite sprint athlete status, the underlying low frequency in these populations eliminates the possibility of replicating this association in Jamaican and US African American sprinters. The finding of no excess in ACE DD or GG genotypes in elite sprint athletes relative to controls suggests that ACE genotype is not a determinant of elite sprint athlete status.

Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35 degrees C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 +/- 22 vs. 138 +/- 17 beats/min; P = 0.0001) and rectal temperature (38.2 +/- 0.3 vs. 37.9 +/- 0.3 degrees C; P = 0.0003) and increased whole body sweat rate (0.70 +/- 0.29 vs. 1.06 +/- 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days (P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 +/- 0.20 vs. 0.66 +/- 0.22 mg x cm(-2) x min(-1)). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 +/- 0.21 mg x cm(-2) x min(-1) (P = 0.021) but decreased 52% to 0.32 +/- 0.18 mg x cm(-2) x min(-1) (P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

Physiologic effects of the TASER after exercise.

OBJECTIVES: Incidents of sudden death following TASER exposure are poorly studied, and substantive links between TASER exposure and sudden death are minimal. The authors studied the effects of a single TASER exposure on markers of physiologic stress in humans. METHODS: This prospective, controlled study evaluated the effects of a TASER exposure on healthy police volunteers after vigorous exercise, compared to a subsequent, identical exercise session that was not followed by TASER exposure. Subjects exercised to 85% of predicted heart rate (HR) on an ergometer and then were given a standard 5-second TASER activation. Measures before and for 60 minutes after the TASER activation included minute ventilation, tidal volume, respiratory rate, end-tidal pCO(2), oxygen saturation, HR, blood pressure (systolic BP/diastolic BP), 12-lead electrocardiogram, and arterialized blood for pH, pO(2), pCO(2), and lactate. Each subject repeated the exercise and data collection session on a subsequent data, without TASER activation. Data were analyzed using paired Student's t-tests with differences and 95% confidence intervals (CIs). Statistical significance was adjusted for multiple comparisons. RESULTS: A total of 25 officers (21 men and 4 women) completed both portions of the study. After adjusting for multiple comparisons, the TASER group was significantly higher for systolic BP at baseline (difference of 14.1, 95% CI = 8.7 to 19.5, p < 0.001) and HR at 5, 30, and 60 minutes with the largest difference at 30 minutes (difference of 7.0, 95% CI = 2.5 to 11.5, p = 0.004). There were no other significant differences between the two groups in any other measure at any time. CONCLUSIONS: A 5-second exposure of a TASER following vigorous exercise to healthy law enforcement personnel does not result in clinically significant changes in ventilatory or blood parameters of physiologic stress.

Translating physical activity recommendations into a pedometer-based step goal: 3000 steps in 30 minutes.

BACKGROUND: It is a public health recommendation to accumulate at least 150 minutes per week of moderate intensity physical activity. Although pedometers are widely used as a physical activity-monitoring tool, they are unable to measure activity intensity. Translating current physical activity recommendations into a pedometer-based guideline could increase the public health impact of physical activity interventions. METHODS: A community sample of 97 adults (60% women, with a mean age of 32.1 [+/-10.6] years and a mean BMI of 28.8 [+/-5.5]) completed four 6-minute incremental walking bouts on a level treadmill at 65, 80, 95, and 110 m x min(-1). A calibrated metabolic cart was used to measure energy expenditure at each speed. Steps were measured using a Yamax SW-200 pedometer. Step-rate cut points associated with minimally moderate-intensity activity (defined as 3 METs) were determined using multiple regression, mixed modeling, and receiver operating characteristic (ROC) curves. All data were collected and analyzed in 2006. RESULTS: For men, step counts per minute associated with walking at 3 METs were 92 step x min(-1) (multiple regression); 101 step x min(-1) (mixed modeling); and 102 step x min(-1) (ROC curve). For women, step counts per minute associated with walking at 3 METs were 91 step x min(-1) (multiple regression); 111 step x min(-1) (mixed modeling); and 115 step x min(-1) (ROC curve). However, for each analysis there was substantial error in model fit. CONCLUSIONS: Moderate-intensity walking appears approximately equal to at least 100 step x min(-1). However, step counts per minute is a poor proxy for METs, and so 100 step x min(-1) should be used only as a general physical activity promotion heuristic. To meet current guidelines, individuals are encouraged to walk a minimum of 3000 steps in 30 minutes on 5 days each week. Three bouts of 1000 steps in 10 minutes each day can also be used to meet the recommended goal.

Metabolic demands of simulated firefighting tasks.

Firefighters having higher cardiovascular fitness completed a series of simulated firefighting tasks more quickly than those having lower fitness. These results support the need of a high level of cardiovascular fitness for firefighters to ensure not only their safety, but that of fellow firefighters and rescue victims.

Electromyographic data do not support a progressive recruitment of muscle fibers during exercise exhibiting a VO2 slow component.

The origin of the slow component (SC) of oxygen uptake kinetics, presenting during exercise above the ventilatory threshold (VT), remains unclear. Possible physiologic mechanisms include a progressive recruitment of type II muscle fibers. The purpose of this study was to examine alterations in muscle activity through electromyography (EMG) and mean power frequency (MPF) analysis during heavy cycling exercise. Eight trained cyclists (mean +/- S.E.; age = 30 +/- 3 years, height = 1771 +/- 4 cm, weight = 73.8 +/- 6.5 kg, VO2max = 4.33 +/- 0.28 l min(-1)) completed transitions from 20W to a workload equaling 50% of the difference between V(T) and VO2max. VO2 was monitored using a breath-by-breath measurement system, and EMG data were gathered from surface electrodes placed on the gastrocnemius lateralis and vastus lateralis oblique. Breath-by-breath data were time aligned, averaged, interpolated to 1-s intervals, and modeled with non-linear regression. Mean power frequency (MPF) and RMS EMG values were calculated for each minute during the exercise bout. Additionally, MPF was determined using both isolated EMG bursts and complete pedal revolutions. All subjects exhibited a VO2 SC (mean amplitude = 0.98 +/- 0.16 l min(-1)), yet no significant differences were observed during the exercise bout in MPF or RMS EMG data (p > 0.05) using either analysis technique. While it is possible that the sensitivity of EMG may be insufficient to identify changes in muscle activity theorized to affect the VO2 SC, the data indicated no relationship between MPF/EMG and the SC during heavy cycling.

Fatigue and sleep quality in nurses.

Fatigue is a critical issue for nurses that may lead to medical errors, degradation in performance, decreased mental acuity, and social problems. Poor sleep quality is also a contributing factor in fatigue that nurses experience. Therefore, the purpose of this study was to examine the differences in perceptions of fatigue between night-shift and day-shift nurses, as measured by scores on the Brief Fatigue Inventory (BFI) and to examine differences in sleep quality between the two groups, as measured by responses on the Pittsburgh Sleep Quality Index (PSQI). Univariate analysis of variance showed significant differences between the two groups on the BFI, with the night-shift cohort reporting higher mean scores on the BFI. Significant differences were also found between the two groups on PSQI mean scores, with the night-shift cohort reporting higher mean scores. Findings from this study suggest that night-shift nurses, compared with day-shift nurses, perceived a much higher level of fatigue and had poorer sleep quality. Further research is needed to evaluate interventions that might decrease fatigue in nurses and improve their sleep quality.

Physiological effects of a conducted electrical weapon on human subjects.

STUDY OBJECTIVE: Sudden death after a conducted electrical weapon exposure has not been well studied. We examine the effects of a single Taser exposure on markers of physiologic stress in healthy humans. METHODS: This is a prospective trial investigating the effects of a single Taser exposure. As part of their police training, 32 healthy law enforcement officers received a 5-second Taser electrical discharge. Measures before and for 60 minutes after an exposure included minute ventilation; tidal volume; respiratory rate (RR); end-tidal PCO2; oxygen saturation, pulse rate; blood pressure (systolic blood pressure/diastolic blood pressure); arterialized blood for pH, PO2, PCO2, and lactate; and venous blood for bicarbonate and electrolytes. Troponin I was measured at 6 hours. Data were analyzed using a repeated-measures ANOVA and paired t tests. RESULTS: At 1 minute postexposure, minute ventilation increased from a mean of 16 to 29 L/minute, tidal volume increased from 0.9 to 1.4 L, and RR increased from 19 to 23 breaths/min, all returning to baseline at 10 min. Pulse rate of 102 beats/min and systolic blood pressure of 139 mm Hg were higher before Taser exposure than at anytime afterward. Blood lactate increased from 1.4 mmol/L at baseline to 2.8 mmol/L at 1 minute, returning to baseline at 30 minutes. pH And bicarbonate decreased, respectively, by 0.03 and 1.2 mEq/L at 1 minute, returning to baseline at 30 minutes. All troponin I values were normal and there were no EKG changes. Ventilation was not interrupted, and there was no hypoxemia or hypercarbia. CONCLUSION: A 5-second exposure of a Taser X26 to healthy law enforcement personnel does not result in clinically significant changes of physiologic stress.

Sodium ion concentration vs. sweat rate relationship in humans.

The purpose of this study was to determine the effect of active heat acclimation on the sweat osmolality and sweat sodium ion concentration vs. sweat rate relationship in humans. Eight healthy male volunteers completed 10 days of exercise in the heat. The mean exercising heart rate and core temperature were significantly decreased (P < 0.05) by 18 beats/min and 0.6 degrees C, respectively, following heat acclimation. Furthermore, sweat osmolality and the sweat sodium ion concentration vs. sweat rate relationships were shifted to the right. Specifically, the slopes of the relationships were not affected by heat acclimation. Rather, heat acclimation significantly reduced the y-intercepts of the sweat osmolality and sweat sodium relationships with sweat rate by 28 mosmol/kgH(2)O and 15 mmol/l, respectively. Thus there was a significantly lower sweat sodium ion concentration for a given sweat rate following heat acclimation. These results suggest that heat acclimation increases the sodium ion reabsorption capacity of the human eccrine sweat gland.

Ventilatory and metabolic demands during aggressive physical restraint in healthy adults.

We investigated ventilatory and metabolic demands in healthy adults when placed in the prone maximal restraint position (PMRP), i.e., hogtie restraint. Maximal voluntary ventilation (MVV) was measured in seated subjects (n=30), in the PMRP, and when prone with up to 90.1 or 102.3 kg of weight on the back. MVV with the heaviest weight was 70% of the seated MVV (122+/-28 and 156+/-38 L/min, respectively; p<0.001). Also, subjects (n=27) were placed in the PMRP and struggled vigorously for 60 sec. During the restrained struggle, ventilatory function (V(E)/ MVV) was 44% of MVV in the resting PMRP. While prone with up to 90.1 or 102.3 kg on the back, the decrease in MVV was of no clinical importance in these subjects. Also, while maximally struggling in the PMRP, V(E) was still adequate to supply the ventilatory needs.

Effect of pedaling technique on muscle activity and cycling efficiency.

The purpose of this study was to examine the acute effect of talocrural joint position on muscle activity and gross mechanical efficiency (GE). Eleven trained cyclists participated in three randomized 6-min cycling bouts at approximately 80% of maximal aerobic capacity on an electromagnetically braked cycle ergometer while oxygen consumption and muscle activity (EMG) were monitored during the subject's self-selected pedaling technique (control) and while using a dorsi- and plantarflexed pedaling technique. The mean differences in range of motion of the dorsi- and plantarflexed technique from the control position were 7.1 +/- 4.4 and 6.9 +/- 5.4 degrees , respectively. Gastrocnemius EMG activity was higher with the dorsiflexion technique than when using the self-selected control position (33.2 +/- 13.0 and 24.2 +/- 8.4 microV s, respectively; P < 0.05). Moreover, GE was 2.6% lower while riding with the dorsiflexion technique than the control position (19.0 +/- 1.2 and 19.5 +/- 1.3%, respectively; P < 0.05). The data suggested that introducing more dorsiflexion into the pedal stroke of a trained cyclist increases muscle activity of the gastrocnemius lateralis and decreased GE when compared to the self-selected pedal stroke.