Inverse Association between Exercising Blood Pressure Response and Left Ventricular Chamber Size and Mass in Women Who Habitually Resistance Train.

Exercise is a major modifiable lifestyle factor that leads to temporarily increased systolic blood pressure (SBP), which is thought to influence left ventricular mass normalized to body surface area (LVM/BSA). This relationship has never been studied in women who habitually perform resistance exercise. PURPOSE: To determine if a direct correlation exists between the SBP response to resistance exercise (change from rest; eSBP) and LVM/BSA in young healthy women who habitually resistance train. METHODS: Leg extension resistance exercise was performed while continuously monitoring blood pressure using finger plethysmography. LVM was estimated using echocardiography. Data are shown as mean ± SD. RESULTS: Thirty-one women participated (age 23 ± 3 years, height 164 ± 7 cm, body mass 63.7 ± 10.3 kg). Resting SBP (110 ± 8 mmHg, r = 0.355, p = 0.049) was shown to be directly correlated to LVM/BSA (72.0 ± 28.4 g/m2). Conversely, eSBP (30.8 ± 14.6 ∆mmHg, r = -0.437, p = 0.014) was inversely related to LVM/BSA. eSBP was not correlated to interventricular septum width (0.88 ± 0.12 cm, r = -0.137, p = 0.463) or posterior wall thickness (0.91 ± 0.15 cm, r = -0.084, p = 0.654). eSBP was inversely related to left ventricle internal diameter during diastole (LVIDd) (4.25 ± 0.33 cm, r = -0.411, p = 0.021). CONCLUSION: Counter to the hypothesis, these data suggest an inverse association between eSBP during resistance exercise and LVM/BSA in healthy young women who resistance train. This relationship is due to a smaller LVIDd with greater eSBP.

Microbiota Mediate Enhanced Exercise Capacity Induced by Exercise Training.

PURPOSE: We investigated the effects of gut microbes, and the mechanisms mediating the enhanced exercise performance induced by exercise training, i.e., skeletal muscle blood flow, and mitochondrial biogenesis and oxidative function in male mice. METHODS: All mice received a graded exercise test before (PRE) and after exercise training via forced treadmill running at 60% to 70% of maximal running capacity 5 d·wk -1 for 5 wk (POST). To examine the role of the gut microbes, the graded exercise was repeated after 7 d of access to antibiotic (ABX)-treated water, used to eliminate gut microbes. Peripheral blood flow, mitochondrial oxidative capacity, and markers of mitochondrial biogenesis were collected at each time point. RESULTS: Exercise training led to increases of 60% ± 13% in maximal running distance and 63% ± 11% work to exhaustion ( P < 0.001). These increases were abolished after ABX ( P < 0.001). Exercise training increased hindlimb blood flow and markers of mitochondrial biogenesis and oxidative function, including AMP-activated protein kinase, sirtuin-1, PGC-1α citrate synthase, complex IV, and nitric oxide, all of which were also abolished by ABX treatment. CONCLUSIONS: Our results support the concept that gut microbiota mediate enhanced exercise capacity after exercise training and the mechanisms responsible, i.e., hindlimb blood flow, mitochondrial biogenesis, and metabolic profile. Finally, results of this study emphasize the need to fully examine the impact of prescribing ABX to athletes during their training regimens and how this may affect their performance.

Individuals with a previous symptomatic COVID-19 infection have altered heart rate and blood pressure variability during acute exercise.

Introduction: As the number of COVID-19 cases begin to diminish it is important to turn our attention to any long-term issues that may be associated with a prior infection. Cardiovascular defects have been noted following prior SARS-CoV-2 infections. However, less is known about how a previous infection alters the cardiovascular response to exercise. Further, differences may exist during exercise between previously SARS-CoV-2 positive individuals who had symptoms (symptomatic) relative to those who did not have symptoms (asymptomatic). We hypothesized that previously symptomatic (S) COVID-19 recoveries have an altered cardiovascular response to acute exercise relative to both control (CON; never infected), and previously COVID-19 positive asymptomatic (AS) individuals. Methods: Twenty-seven subjects (CON = 9; AS = 9; S = 9) underwent 30 min of submaximal treadmill exercise. During exercise, blood pressure was recorded on the brachial artery every 5 min and 3-lead electrocardiography was measured continuously. Indirect indicators of autonomic nervous system health: heart rate variability and blood pressure variability were measured during each session. Baseline mean arterial pressure (MAP) was taken prior to exercise in seated, standing and supine positions. Results: Blood pressure was similar (p > 0.05) amongst all three groups. There were no differences between average heart rate (HR; CON = 104 ± 4 BPM vs AS = 118 ± 6 BPM vs. S = 112 ± 3 BPM), mean arterial pressure (MAP; CON = 108 ± 4 mmHg vs. AS = 105 ± 13 mmHg vs. S = 108 ± 7 mmHg) or oxygen consumption (VO2) between groups during a bout of exercise. However, the standard deviation of the inter beat intervals of normal sinus beats, a measure of heart rate variability (HRV) (CON = 138 ± 2.8 m vs. AS = 156 ± 6 m vs. S = 77.7 ± 11 m; p < 0.05) and blood pressure variability (BPV; CON = 5.18 ± 1.1 vs. AS = 12.1 ± 0.88 mmHg vs. S = 10.2 ± 10.7 mmHg; p < 0.05) were different in our S group. Further, when HRV was assessed in the frequency domain the very low frequency was different during exercise in the S group relative to the other groups. Discussion: Collectively, these data suggest that a previous symptomatic SARS-CoV-2 infection may alter heart rate and blood pressure regulation during exercise.

Naltrexone alters cardiovascular function following acute forced swimming in mice.

Purpose: Naltrexone (NTX) is an opioid antagonist that can reverse the physiological effects of opioid receptors when bound. Opioid receptors have been found to play a role in cardiovascular (CV) function, and thus, binding of NTX may alter CV activity at rest and in response to acute and chronic exercise (EX). We hypothesized that opioid receptor blockade will alter the typical CV responses following acute EX. Methods: We assessed the effects of opioid receptor blockade on CV function via echocardiography in mice following an acute bout of forced swimming (FSw), a model of rodent EX. We administered opioid receptor antagonist, NTX, or saline in mice before FSw and in the absence of an FSw perturbation. Furthermore, we assessed how NTX can influence maximal EX capacity on a rodent treadmill. Results: Our data shows that NTX administration does not decrease maximal EX capacity in mice (P > 0.05). However, NTX attenuated cardiac output following FSw (FSw = 52.5 ± 2.5 ml/min vs. FSw + NTX = 32.7 ± 5.2 ml/min; P < 0.05) when compared with saline control (33.5 ± 3.8 ml/min). Further, the administration of NTX in the non-EX condition significantly (P < 0.05) reduced ejection fraction. Conclusion: These data suggest that normal opioid receptor activation is necessary for typical CV function following FSw.

Young healthy adults with a family history of hypertension have increased microvascular reactivity but decreased macrovascular function.

OBJECTIVE: To determine whether, like hypertensives, normotensive adults with a family history of hypertension (+FHH) display lower microvascular reactivity and conduit artery function than normotensive adults without a family history of hypertension (-FHH). METHODS: A forearm vascular occlusion test was performed on healthy normotensive adults while resting in the supine position. A near-infrared spectroscopy sensor placed on the forearm measured skeletal muscle oxygen saturation kinetics to determine microvascular reactivity. Simultaneously, an ultrasound probe placed on the brachial artery above the occlusion cuff was used to assess flow-mediated dilation; a test of macrovascular function. RESULTS: Twenty-two participants were included in this investigation (-FHH n = 13, +FHH n = 9). Following cuff release, the resaturation slope (1st 10 s median ± SD, -FHH 2.76 ± 2.10, +FHH 5.59 ± 2.47%/s; p = .036) was greater in +FHH when accounting for the magnitude and rate of the decrease in skeletal muscle oxygen saturation during occlusion. Conversely, flow-mediated dilation (median ± SD, -FHH 5.96 ± 5.22, +FHH 4.10 ± 3.17%∆; p = .031) was lower in +FHH when accounting for baseline artery diameter and shear rate. CONCLUSIONS: Young +FHH adults have altered microvascular and macrovascular reactivity compared with young -FHH adults.

"The addition of naltrexone alters cerebral glucose uptake following acute forced swimming".

Endogenous opioid release has been linked to exercise. We investigated if opioid blockade following forced swimming, a common model of rodent exercise, influenced cerebral glucose metabolism in mice. PET scan was used to assess the uptake of Fludeoxyglucose (FDG-18), a marker of cerebral glucose metabolism in 19 regions of the interest in the brain following: forced swimming, an acute dose of the opioid receptor blocker naltrexone or a combination of both. Forced swimming increased glucose uptake in the cerebellum, while naltrexone + forced swimming increased glucose uptake in the hypothalamus, forebrain, septum and amygdala. This suggests that opioid blockade alters the typical pattern of cerebral glucose uptake following forced swimming in mice in certain areas of the brain.

Voluntary Wheel Running Attenuates Salt-Induced Vascular Stiffness Independent of Blood Pressure.

BACKGROUND: Excess dietary salt can lead to the development of arterial stiffness and high blood pressure (BP). Regular physical activity can protect against arterial stiffening and lower BP. Less is known regarding the role of exercise on the vasculature independent of BP under high salt (HS) conditions. The aim of the study was to determine whether wheel running protects against the development of dietary salt-induced arterial stiffness independent of BP. METHODS: Rats were maintained on either normal salt (NS; 0.49% NaCl) or HS (4.0% NaCl) diet for 6 weeks and further divided into a voluntary wheel running (NS-VWR, HS-VWR) or cage control group (NS, HS). Carotid-femoral pulse wave velocity (PWV) was measured using applanation tonometry at baseline (BSL) and 6 weeks. RESULTS: BP was measured weekly and remained unchanged among groups throughout the 6 weeks (P > 0.05). PWV was elevated at 6 weeks in HS compared to baseline (HS-BSL, 3.27 ± 0.17 vs. HS-6 week, 4.13 ± 0.26 m/s; P < 0.05) and was lower at 6 weeks in both VWR groups (NS-VWR, 2.98 ± 0.29, HS-VWR, 3.11 ± 0.23 m/s) when compared to HS at 6 weeks (P < 0.05). This was supported by a significant increase in aortic collagen I in the HS group alone and transforming growth factor beta (TGF-ß) was greater in the HS group compared to both NS groups (P < 0.05). Wheel running resulted in a greater aortic phosphorylated eNOS and SOD-2 in HS-WVR (P < 0.05) compared to HS. CONCLUSIONS: These data suggest that VWR may protect against collagen accumulation through a TGF-ß-mediated pathway by improving nitric oxide bioavailability and redox balance in rats.

Voluntary wheel running prevents salt-induced endothelial dysfunction: role of oxidative stress.

Diets high in salt can lead to endothelial dysfunction, a nontraditional risk factor for cardiovascular disease (CVD). Exercise is known to reduce CVD risk; however, it remains unknown whether chronic physical activity can attenuate salt-induced endothelial dysfunction independent of blood pressure (BP) and whether these changes are due to an upregulation in endogenous antioxidants. Eight-week-old Sprague-Dawley rats were fed either a normal (NS; 0.49%)- or a high (HS; 4.0%)-salt diet and further divided into voluntary wheel running (NS-VWR, HS-VWR) and sedentary (NS, HS) groups for 6 wk. BP was measured weekly and remained unchanged within groups ( P = 0.373). Endothelium-dependent relaxation (EDR) was impaired in the femoral artery of HS compared with NS (38.6 ± 4.0% vs. 65.0 ± 3.6%; P = 0.013) animals, whereas it was not different between NS and HS-VWR (73.4 ± 6.4%; P = 0.273) animals. Incubation with the antioxidants TEMPOL ( P = 0.024) and apocynin ( P = 0.013) improved EDR in HS animals, indicating a role for reactive oxygen species (ROS). Wheel running upregulated the antioxidant superoxide dismutase-2 (SOD-2) ( P = 0.011) under HS conditions and lowered NOX4 and Gp91-phox, two subunits of NADPH oxidase. Wheel running elevated phosphorylated endothelial nitric oxide synthase (eNOS) ( P = 0.014) in HS-fed rats, demonstrating a role for physical activity and eNOS activity under HS conditions. Finally, there was a reduction in EDR ( P = 0.038) when femoral arteries from NS-VWR animals were incubated with TEMPOL or apocynin, suggesting there may be a critical level of ROS needed to maintain endothelial function. In summary, physical activity protected HS-fed rats from reductions in endothelial function, likely through increased SOD-2 levels and reduced oxidative stress. NEW & NOTEWORTHY Our data suggest that voluntary wheel running can prevent impairments in endothelium-dependent relaxation in the femoral artery of rats fed a high-salt diet. This appears to be independent of blood pressure and mediated through a decrease in expression of NADPH oxidases as a result of physical activity. These data suggest that increased chronic physical activity can protect the vasculature from a diet high in salt, likely through a reduction in oxidative stress.

In Vivo Efficacy of Histatin-1 in a Rabbit Animal Model.

Purpose/Aim: Corneal abrasions and nonhealing corneal epithelial defects are common conditions that cause pain and sometimes are slow to heal. Histatins, a family of histidine-rich peptides, have been implicated in oral and skin epithelial wound healing, and have been shown to be effective in vitro in human corneal epithelial cells. The objective of this study was to test the efficacy of histatin-1 on corneal epithelial wound healing in rabbits. MATERIALS & METHODS: Twenty-two (22) rabbits were separated into four treatment groups, each containing 3-7 rabbits. Treatments included three histatin-1 formulations (0.1 ug/ml. 1 ug/ml, and 10 ug/ml) and one inactive vehicle, one drop given three times per day. Eight (8) mm circular wounds were created using 0.5 ml of 20% ethyl alcohol in the right eye of each rabbit. A masked observer photographed each eye twice daily using slit-lamp biomicrophotography. Wound area was analyzed by using ImageJ. Statistical analysis was conducted using Graphpad Prism. RESULTS: Wound recovery was faster in animals given 0.1 ug/ml, 1 ug/ml, and 10 ug/ml when compared to the vehicle solution at 6, 24, and 30 hours after wound creation (p < 0.01). No adverse events were observed in any eyes. When analyzing area under the curve, % recovered area was higher overall in the 0.1 ug/ml (p < 0.01), 1 ug/ml (p < 0.01), and 10 ug/ml (p < 0.001) groups when compared to the vehicle solution. Hourly healing rate was also observed to be faster in the 0.1 ug/ml, 1 ug/ml, and 10 ug/ml groups (p < 0.001) at 24 hours postinjury suggesting an accelerated healing process as compared to the vehicle group. CONCLUSION: This study represents the first in vivo experiment evaluating and confirming the efficacy of topical histatin on the corneal epithelium wound healing. Further studiesare warranted to better understand the mechanism and safety of topical histatin-1 in corneal epithelial wound-healing and its potential role for human disease treatment.

Enhanced longevity and metabolism by brown adipose tissue with disruption of the regulator of G protein signaling 14.

Disruption of the regulator for G protein signaling 14 (RGS14) knockout (KO) in mice extends their lifespan and has multiple beneficial effects related to healthful aging, that is, protection from obesity, as reflected by reduced white adipose tissue, protection against cold exposure, and improved metabolism. The observed beneficial effects were mediated by improved mitochondrial function. But most importantly, the main mechanism responsible for the salutary properties of the RGS14 KO involved an increase in brown adipose tissue (BAT), which was confirmed by surgical BAT removal and transplantation to wild-type (WT) mice, a surgical simulation of a molecular knockout. This technique reversed the phenotype of the RGS14 KO and WT, resulting in loss of the improved metabolism and protection against cold exposure in RGS14 KO and conferring this protection to the WT BAT recipients. Another mechanism mediating the salutary features in the RGS14 KO was increased SIRT3. This mechanism was confirmed in the RGS14 X SIRT3 double KO, which no longer demonstrated improved metabolism and protection against cold exposure. Loss of function of the Caenorhabditis elegans RGS-14 homolog confirmed the evolutionary conservation of this mechanism. Thus, disruption of RGS14 is a model of healthful aging, as it not only enhances lifespan, but also protects against obesity and cold exposure and improves metabolism with a key mechanism of increased BAT, which, when removed, eliminates the features of healthful aging.

Disruption of adenylyl cyclase type 5 mimics exercise training.

Exercise training is key to healthful longevity. Since exercise training compliance is difficult, it would be useful to have a therapeutic substitute that mimicked exercise training. We compared the effects of exercise training in wild-type (WT) littermates with adenylyl cyclase type 5 knock out (AC5 KO) mice, a model of enhanced exercise performance. Exercise performance, measured by maximal distance and work to exhaustion, was increased in exercise-trained WT to levels already attained in untrained AC5 KO. Exercise training in AC5 KO further enhanced their exercise performance. The key difference in untrained AC5 KO and exercise-trained WT was the ß-adrenergic receptor signaling, which was decreased in untrained AC5 KO compared to untrained WT but was increased in WT with exercise training. Despite this key difference, untrained AC5 KO and exercise-trained WT mice shared similar gene expression, determined by deep sequencing, in their gastrocnemius muscle with 183 genes commonly up or down-regulated, mainly involving muscle contraction, metabolism and mitochondrial function. The SIRT1/PGC-1α pathway partially mediated the enhanced exercise in both AC5 KO and exercise-trained WT mice, as reflected in the reduced exercise responses after administering a SIRT1 inhibitor, but did not abolish the enhanced exercise performance in the AC5 KO compared to untrained WT. Increasing oxidative stress with paraquat attenuated exercise performance more in untrained WT than untrained AC5 KO, reflecting the augmented oxidative stress protection in AC5 KO. Blocking nitric oxide actually reduced the enhanced exercise performance in untrained AC5 KO and trained WT to levels below untrained WT, demonstrating the importance of this mechanism. These results suggest that AC5 KO mice, without exercise training, share similar mechanisms responsible for enhanced exercise capacity with chronic exercise training, most importantly increased nitric oxide, and demonstrate more reserve with the addition of exercise training. A novel feature of the enhanced exercise performance in untrained AC5 KO mice is their decreased sympathetic tone, which is also beneficial to patients with cardiovascular disease.

Intermittent parathyroid hormone administration attenuates endothelial dysfunction in old rats.

Aging is an independent risk factor for cardiovascular disease and is characterized by a decline in endothelial function. Parathyroid hormone (PTH) administration has been shown to increase endothelial nitric oxide synthase (eNOS) expression. The purpose of this investigation was to determine the effect of intermittent PTH administration on aortic endothelial function in old rodents. We hypothesized that intermittent PTH administration would improve endothelial function in older rodents. Old (24-mo-old) and young (4-mo-old) Fischer-344 rats were given 10 injections of PTH 1-34 (43 µg·kg-1·day-1) or phosphate-buffered saline (100 µl/day) over 15 days. Endothelium-dependent relaxation of aortic rings in response to acetylcholine (10-9 to 10-5 M) was significantly impaired in old control (OC) compared with young control (YC) as indicated by a reduced area under the curve (AUC, 100 ± 6.28 vs. 54.08 ± 8.3%; P < 0.05) and impaired maximal relaxation (Emax, 70.1 ± 4.48 vs. 92.9 ± 4.38%; P < 0.05). Emax was improved in old animals treated with PTH (OPTH) (OC, 70.1 ± 4.48 vs. OPTH, 85 ± 7.48%; P < 0.05) as well as AUC (OC, 54.08 ± 8.3 vs. OPTH, 82.5 ± 5.7%; P < 0.05) while logEC50 was not different. Endothelial-independent relaxation in response to sodium nitroprusside was not different among groups. Aortic eNOS protein expression was significantly decreased in OC compared with YC (P < 0.05). PTH treatment restored eNOS expression in OPTH animals (P < 0.05). These data suggest that PTH may play a role in attenuating age-related impairments in aortic endothelial function. NEW & NOTEWORTHY: We have demonstrated that intermittent parathyroid hormone administration can rescue age-related vascular dysfunction by improving endothelial-dependent dilation in the aorta of older rodents. This demonstrates a novel potential benefit of parathyroid hormone administration in aging.

Voluntary wheel running augments aortic l-arginine transport and endothelial function in rats with chronic kidney disease.

Reduced nitric oxide (NO) synthesis contributes to risk for cardiovascular disease in chronic kidney disease (CKD). Vascular uptake of the NO precursor l-arginine (ARG) is attenuated in rodents with CKD, resulting in reduced substrate availability for NO synthesis and impaired vascular function. We tested the effect of 4 wk of voluntary wheel running (RUN) and/or ARG supplementation on endothelium-dependent relaxation (EDR) in rats with CKD. Twelve-week-old male Sprague-Dawley rats underwent ⅚ ablation infarction surgery to induce CKD, or SHAM surgery as a control. Beginning 4 wk following surgery, CKD animals either remained sedentary (SED) or received one of the following interventions: supplemental ARG, RUN, or combined RUN+ARG. Animals were euthanized 8 wk after surgery, and EDR was assessed. EDR was significantly impaired in SED vs. SHAM animals after 8 wk, in response to ACh (10(-9)-10(-5) M) as indicated by a reduced area under the curve (AUC; 44.56 ± 9.01 vs 100 ± 4.58, P < 0.05) and reduced maximal response (Emax; 59.9 ± 9.67 vs. 94.31 ± 1.27%, P < 0.05). AUC was not improved by ARG treatment but was significantly improved above SED animals in both RUN and RUN+ARG-treated animals. Maximal relaxation was elevated above SED in RUN+ARG animals only. l-[(3)H]arginine uptake was impaired in both SED and ARG animals and was improved in RUN and RUN+ARG animals. The results suggest that voluntary wheel running is an effective therapy to improve vascular function in CKD and may be more beneficial when combined with l-arginine.

The development of a repetition-load scheme for the eccentric-only bench press exercise.

The purpose of the present study was to develop a repetition-load scheme for the eccentric-only bench press exercise. Nine resistance trained men (age: 21.6 ± 1.0 years; 1-repetition maximum [RM] bench press: 137.7 ± 30.4 kg) attended four testing sessions during a four week period. During the first session each subject's 1-RM bench press load utilizing the stretch-shortening cycle was determined. During the remaining sessions they performed eccentric-only repetitions to failure using supra-maximal loads equivalent to 110%, 120% and 130% of their 1-RM value with a constant cadence (30 reps·min(-1)). Force plates and a three dimensional motion analysis system were used during these final three sessions in order to evaluate kinematic and kinetic variables. More repetitions were completed during the 110% 1-RM condition compared to the 130% 1-RM condition (p=0.01). Mean total work (p=0.046) as well as vertical force (p=0.049), vertical work (p=0.017), and vertical power output (p=0.05) were significantly greater during the 130% 1-RM condition compared to the 110% 1-RM condition. A linear function was fitted to the number of repetitions completed under each load condition that allowed the determination of the maximum number of repetitions that could be completed under other supra-maximal loads. This linear function predicted an eccentric-only 1-RM in the bench press with a load equivalent to 164.8% 1-RM, producing a load of 227.0 ± 50.0 kg. The repetition-load scheme presented here should provide a starting point for researchers to investigate the kinematic, kinetic and metabolic responses to eccentric-only bench press workouts.

Effect of cluster set configurations on mechanical variables during the deadlift exercise.

The purpose of the present study was to investigate the effects of different configurations of repetitions within a set of deadlifts on the mechanical variables of concentric force, concentric time under tension, impulse, work, power, and fatigue. Eleven resistance trained men (age: 21.9 ± 1.0 years; deadlift 1 repetition maximum: 183.2 ± 38.3 kg) performed four repetitions of the deadlift exercise with a load equivalent to 90% of 1 repetition maximum under three different set configurations: Traditional (continuous repetitions); Doubles cluster (repetitions 1 and 2, and 3 and 4 performed continuously with a 30 s rest inserted between repetitions 2 and 3); Singles cluster (30 s rest provided between repetitions). The order of the sessions was counterbalanced across the subjects and the mechanical variables were calculated during each repetition from the synchronized signals recorded from force platforms and a motion analysis system. Relative to the Traditional set, the insertion of rest periods in the cluster set configurations resulted in greater time under tension (p < 0.001) and therefore, greater impulse (p < 0.001) during the repetitions. Reductions in power were observed during the cluster sets compared to the Traditional set (p = 0.001). The Doubles cluster set resulted in greater fatigue scores for power compared to the Traditional set (p = 0.04). The influence of cluster sets on mechanical variables appears to be mediated by the mechanical characteristics of the exercise (i.e. stretch-shortening cycle) and the competing physiological mechanisms of fatigue and potentiation.

The effects of load on system and lower-body joint kinetics during jump squats.

To investigate the effects of different loads on system and lower-body kinetics during jump squats, 12 resistance-trained men performed jumps under different loading conditions: 0%, 12%, 27%, 42%, 56%, 71%, and 85% of 1-repetition maximum (1-RM). System power output was calculated as the product of the vertical component of the ground reaction force and the vertical velocity of the bar during its ascent. Joint power output was calculated during bar ascent for the hip, knee, and ankle joints, and was also summed across the joints. System power output and joint power at knee and ankle joints were maximized at 0% 1-RM (p < 0.001) and followed the linear trends (p < 0.001) caused by power output decreasing as the load increased. Power output at the hip was maximized at 42% 1-RM (p = 0.016) and followed a quadratic trend (p = 0.030). Summed joint power could be predicted from system power (p < 0.05), while system power could predict power at the knee and ankle joints under some of the loading conditions. Power at the hip could not be predicted from system power. System power during loaded jumps reflects the power at the knee and ankle, while power at the hip does not correspond to system power.

Familiarization, reliability, and evaluation of a multiple sprint running test using self-selected recovery periods.

The aims of the present study were to investigate the process of self-selected recovery in a multiple sprint test with a view to using self-selected recovery time as a means of reliably quantifying an individual's ability to resist fatigue in this type of exercise. Twenty physically active exercise science students (means ± SD for age, height, body mass, body fat, and VO2max of the subjects were 21 ± 2 yr, 1.79 ± 0.09 m, 83.7 ± 10.8 kg, 16.6 ± 3.9%, and 52.7 ± 7.2 ml·kg·min, respectively) completed 4 trials of a 12 × 30 m multiple sprint running test under the instruction that they should allow sufficient recovery time between sprints to enable maximal sprint performance to be maintained throughout each trial. Mean recovery times across the 4 trials were 73.9 ± 24.7, 82.3 ± 23.8, 77.6 ± 19.1, and 77.5 ± 13.9 seconds, respectively, with variability across the first 3 trials considered evidence of learning effects. Test-retest reliability across trials 3 to 4 revealed a good level of reliability as evidenced by a coefficient of variation of 11.1% (95% likely range: 8.0-18.1%) and an intraclass correlation coefficient of 0.76 (95% likely range: 0.40-0.91). Despite no change in sprint performance throughout the trials, ratings of perceived exertion increased progressively and significantly (p < 0.001) from a value of 10 ± 2 after sprint 3 to 14 ± 2 after sprint 12. The correlation between relative VO2max and mean recovery time was 0.14 (95% likely range: -0.37-0.58). The results of the present study show that after the completion of 2 familiarization trials, the ability to maintain sprinting performance in a series of repeated sprints can be self-regulated by an athlete to a high degree of accuracy without the need for external timepieces.