Journal of Applied Physiology (J APPL PHYSIOL)

Publisher: American Physiological Society (1887- ), American Physiological Society

Journal description

The Journal of Applied Physiology publishes original papers that deal with diverse areas of research in applied physiology, especially those emphasizing adaptive and integrative mechanisms. Adaptive physiology includes 1) inherent adaptations such as those related to development, aging, and pathophysiological conditions and 2) adaptations to the external environment such as those occurring with exercise, microgravity, hypoxia, hypo- and hyperbaria, and hypo- and hyperthermic conditions. Integrative physiology includes 1) horizontal integration across organ systems and 2) vertical integration from molecule to cell to organ. In all areas of applied physiology, the use of cutting-edge techniques including molecular and cellular biology is strongly encouraged.

Current impact factor: 3.43

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.434
2012 Impact Factor 3.484
2011 Impact Factor 3.753
2010 Impact Factor 4.232
2009 Impact Factor 3.732
2008 Impact Factor 3.658
2007 Impact Factor 3.632
2006 Impact Factor 3.178
2005 Impact Factor 3.037
2004 Impact Factor 2.824
2003 Impact Factor 3.027
2002 Impact Factor 2.72
2001 Impact Factor 2.581
2000 Impact Factor 2.297
1999 Impact Factor 2.081
1998 Impact Factor 2.122
1997 Impact Factor 1.77
1996 Impact Factor 2.05
1995 Impact Factor 1.947
1994 Impact Factor 1.852
1993 Impact Factor 1.799
1992 Impact Factor 1.959

Impact factor over time

Impact factor

Additional details

5-year impact 4.16
Cited half-life 0.00
Immediacy index 0.52
Eigenfactor 0.05
Article influence 1.24
Website Journal of Applied Physiology website
Other titles Journal of applied physiology (Bethesda, Md.: 1985), Journal of applied physiology
ISSN 8750-7587
OCLC 11603017
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Physiological Society

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • NIH, Wellcome Trust, HHMI, MRC and BBSRC authors will on their behalf have the Publisher's version/PDF deposited in PubMed Central for release 12 months after publication
    • Publisher's version/PDF cannot be used
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: In the last few years, genetic and functional studies have provided important insight on the pathophysiology of excessive erythrocytosis (EE), the main sign of Chronic Mountain Sickness (CMS). The recent finding of the association of the CMS phenotype with a single-nucleotide polymorphism (SNP) in the SENP1 gene, and its differential expression pattern in CMS and non-CMS Andean highlanders, has triggered large interest in the high-altitude field because of the potential role of its gene-product in the control of erythropoiesis. The SENP1 gene encodes for a protease that regulates the function of hypoxia-relevant transcription factors such as HIF and GATA, and thus might have an erythropoietic regulatory role in CMS through the modulation of the expression of Epo or Epo receptors. The different physiological patterns in the Epo-EpoR system found among Andeans, even within CMS highlanders, together with their different degrees of erythropoietic response, might indicate specific underlying genetic backgrounds, which in turn might reflect different levels of adaptation to lifelong high-altitude hypoxia. This mini-review discusses recent genetic findings potentially underlying EE and CMS, and their possible physiological mechanisms in Andean highlanders. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 08/2015; DOI:10.1152/japplphysiol.00271.2015
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    ABSTRACT: Aim To assess the correlation between contraction-associated muscle kinematics as measured by velocity-encoded phase contrast MRI and EMG activity, and to construct a detailed three-dimensional map of the contractile behavior of the triceps surae complex from the MRI data. Methods Ten axial-plane velocity-encoded phase contrast MRI slices of the triceps surae and EMG data were acquired during submaximal isometric contractions in ten subjects. The MRI images were analyzed to yield the degree of contraction-associated muscle displacement on a voxel-by-voxel basis and determine the heterogeneity of muscle movement within and between slices. Correlational analyses were performed to determine the agreement between EMG and displacements. Results Pearson's coefficients demonstrated good agreement (0.84 < r < 0.88) between EMG and displacements. Comparison between different slices in the gastrocnemii muscles revealed significant heterogeneity in displacement values both in-plane and along the cranio-caudal axis, with highest values in the mid-muscle regions. In the soleus, by contrast, no significant differences between muscle regions were found. Substantial differences for displacements were also observed within slices, with those in static areas being only 17-39% (maximum) of those in the most mobile muscle regions. Conclusions The good agreement between EMG and displacements suggests that velocity-encoded phase contrast MRI may be used as a non-invasive, high-resolution tool to quantify and model muscle activity over the entire three-dimensional volume of muscle groups. Application to the triceps surae complex revealed substantial heterogeneity of contraction-associated muscle motion both within slices and between different cranio-caudal positions. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 06/2015; DOI:10.1152/japplphysiol.00275.2015
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    ABSTRACT: Acute hypoxia increases cerebral blood flow (CBF) and ventilation (VE). It is unknown if these responses are impacted with normal aging, or in patients with enhanced oxidative stress, such as chronic obstructive pulmonary disease (COPD). The purpose of the study was to 1) investigate the effects of aging and COPD on the cerebrovascular and ventilatory responses to acute hypoxia, and 2) to assess the effect of vitamin C on these responses during hypoxia. In 12 Younger, 14 Older, and 12 COPD, we measured peak cerebral blood flow velocity (VP; index of CBF), and VE during two 5-min periods of acute isocapnic-hypoxia, under conditions of: 1) saline-sham; and 2) intravenous vitamin C. Antioxidants (vitamin C, superoxide dismutase [SOD], glutathione peroxidase, and catalase), oxidative stress (malondialdehyde [MDA] and advanced protein oxidation product) and nitric oxide metabolism end-products (NOx) were measured in plasma. Following the administration of vitamin C, Vitamin C, SOD, catalase, and MDA increased, while NOx decreased. VP and VE sensitivity to hypoxia were reduced in Older by ~60% (P < 0.02). COPD patients exhibited similar VP and VE responses to Older (P > 0.05). Vitamin C did not have an effect on the hypoxic VE response, but selectively decreased the VP sensitivity in Younger only. These findings suggest a reduced integrative reflex (i.e., cerebrovascular and ventilatory) during acute hypoxemia in healthy older adults. Vitamin C does not appear to have a large influence on the cerebrovascular or ventilatory responses during acute hypoxia. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 06/2015; DOI:10.1152/japplphysiol.00389.2015
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    ABSTRACT: In humans, enhanced joint range of motion is observed after static stretch training and results either from an increased stretch tolerance or from a change in the biomechanical properties of the muscle-tendon unit. We investigated the effects of an intermittent stretch training on muscle biomechanical and structural variables. The left plantarflexors muscles of seven anesthetized New Zealand (NZ) White rabbits were passively and statically stretched three times a week for 4 wk, while the corresponding right muscles were used as nonstretched contralateral controls. Before and after the stretching protocol, passive torque produced by the left plantarflexor muscles as a function of the ankle angle was measured. The left and right plantarflexor muscles were harvested from dead rabbits and used to quantify possible changes in muscle structure. Significant mass and serial sarcomere number increases were observed in the stretched soleus but not in the plantaris or medial gastrocnemius. This difference in adaptation between the plantarflexors is thought to be the result of their different fiber type composition and pennation angles. Neither titin isoform nor collagen amount was modified in the stretched compared with the control soleus muscle. Passive torque developed during ankle dorsiflexion was not modified after the stretch training on average, but was decreased in five of the seven experimental rabbits. Thus, an intermittent stretching program similar to those used in humans can produce a change in the muscle structure of NZ White rabbits, which was associated in some rabbits with a change in the biomechanical properties of the muscle-tendon unit. Copyright © 2015 the American Physiological Society.
    Journal of Applied Physiology 06/2015; 118(12):jap.00515.2014. DOI:10.1152/japplphysiol.00515.2014
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    ABSTRACT: Recent studies demonstrate that high dietary sodium (HS) impairs endothelial function in those with salt-resistant (SR) blood pressure (BP). The effect of HS on endothelial function in those with salt-sensitive (SS) BP is not currently known. We hypothesized that HS would impair brachial artery flow-mediated dilation (FMD) to a greater extent in SS compared with SR adults. Ten SR (age 42 ± 5 yr, 5 men, 5 women) and 10 SS (age 39 ± 5 yr, 5 men, 5 women) healthy, normotensive participants were enrolled in a controlled feeding study consisting of a run-in diet followed by a 7-day low dietary sodium (LS) (20 mmol/day) and a 7-day HS (300 mmol/day) diet in random order. Brachial artery FMD and 24-h BP were assessed on the last day of each diet. SS BP was individually assessed and defined as a change in 24-h mean arterial pressure (MAP) of >5 mmHg between the LS and HS diets (ΔMAP: SR -0.6 ± 1.2, SS 7.7 ± 0.4 mmHg). Brachial artery FMD was lower in both SS and SR individuals during the HS diet (P < 0.001), and did not differ between groups (P > 0.05) (FMD: SR LS 10.6 ± 1.3%, SR HS 7.2 ± 1.5%, SS LS 12.5 ± 1.7%, SS HS 7.8 ± 1.4%). These data indicate that an HS diet impairs brachial artery FMD to a similar extent in adults with SS BP and SR BP. Copyright © 2015 the American Physiological Society.
    Journal of Applied Physiology 06/2015; 118(12):jap.00023.2015. DOI:10.1152/japplphysiol.00023.2015
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    ABSTRACT: Positron Emission Tomography (PET) with [(18)F]-Fluorodeoxyglucose (FDG) is an established clinical tool primarily used to diagnose and evaluate disease status in patients with cancer. PET imaging utilizing FDG can be a highly valuable tool to investigate normal human physiology by providing a noninvasive, quantitative measure of glucose uptake into various cell types. Over the past years it has also been increasingly used in exercise physiology studies to identify changes in glucose uptake, metabolism, and muscle activity during different exercise modalities. Metabolically active cells transport FDG, an (18)fluorine-labelled glucose analogue tracer, from the blood into the cells where it is then phosphorylated, but not further metabolized. This metabolic trapping process forms the basis of this method's use during exercise. The tracer is given to a participant during an exercise task and the actual PET imaging is performed immediately after the exercise. Provided the uptake period is of sufficient duration and the imaging is performed shortly after the exercise, the captured image strongly reflects the metabolic activity of the cells utilized during the task. When combined with repeated blood sampling to determine tracer blood concentration over time, also known as the input function, glucose uptake rate of the tissues can be quantitatively calculated. This review provides an accounting of studies using FDG-PET to measure acute exercise induced skeletal muscle activity, describes the advantages and limitations of this imaging technique, and discusses it's applications to the field of exercise physiology. Copyright © 2014, Journal of Applied Physiology.
    Journal of Applied Physiology 03/2015; 118(10):jap.01070.2014. DOI:10.1152/japplphysiol.01070.2014
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    ABSTRACT: A computer model of skeletal muscle bioenergetic system is used to study the background of the slow component of the V'O2 on-kinetics in skeletal muscle. Two possible mechanisms are analyzed: inhibition of ATP production by anaerobic glycolysis by progressive cytosol acidification (together with a slow decrease in ATP supply by creatine kinase) and gradual increase of ATP usage during exercise of constant power output. It is demonstrated that the former novel mechanism is potent to generate the slow component. The latter mechanism further increases the size of the slow component. It also moderately decreases metabolite stability and has small impact on muscle pH. An increase in anaerobic glycolysis intensity increases the slow component, elevates cytosol acidification during exercise and decreases PCr and Pi stability, although slightly increases ADP stability. A decrease in the P/O ratio during exercise cannot be also excluded as a relevant mechanism, although this issue requires further study. It is postulated that both the progressive inhibition of anaerobic glycolysis by accumulating protons (together with a slow decrease of the net creatine kinase reaction rate) and gradual increase of ATP usage during exercise, and perhaps decrease in P/O, contribute to the generation of the slow component of the V'O2 on-kinetics in skeletal muscle. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 03/2015; 118(10):jap.00027.2015. DOI:10.1152/japplphysiol.00027.2015
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    ABSTRACT: The mechanisms responsible for exercise-induced reductions in baseline heart rate (HR), training bradycardia, remain controversial. Therefore, changes in cardiac autonomic regulation and intrinsic sinoatrial nodal (SAN) rate were evaluated using dogs randomly assigned to either a 10-12 wk exercise training (Ex, n = 15) or an equivalent sedentary period (Sed, n = 10). Intrinsic HR was revealed by combined autonomic nervous system (ANS) blockade (propranolol + atropine, i.v.) before and after completion of the study. At the end of the study, SAN function was further evaluated by examining the SAN recovery time (SNRT) following rapid atrial pacing and the response to adenosine in anesthetized animals. As expected, both the response to submaximal exercise and baseline HR significantly (P<0.01) decreased and heart rate variability (HRV, e.g. high frequency R-R interval variability) significantly (P<0.01) increased in the Ex but did not change in the Sed group. Atropine also induced significantly (P <0.01) greater reductions in HRV in the Ex as compared to the Sed group; propranolol elicited similar HR and HRV changes in both groups. In contrast, neither intrinsic HR (Ex pre: 141.2 ± 6.7; post 146.0 ± 8.0 vs. Sed: pre 143.3 ± 11.1; post 141.0 ± 11.3 bpm), the response to adenosine, corrected SNRT, nor atrial fibrosis and atrial fibrillation inducibility differed in the Ex vs. the Sed groups. These data suggest that in a large animal model training bradycardia results from an enhanced cardiac parasympathetic regulation and not from changes in intrinsic properties of the sinoatrial node. Copyright © 2014, Journal of Applied Physiology.
    Journal of Applied Physiology 03/2015; 118(11):jap.01111.2014. DOI:10.1152/japplphysiol.01111.2014
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    ABSTRACT: High altitude (HA) exposure facilitates a rapid contraction of plasma volume (PV) and a slower occurring expansion of hemoglobin mass (Hbmass). The kinetics of the Hbmass expansion has never been examined by multiple repeated measurements and this was our primary study aim. The second aim was to investigate the mechanisms mediating the PV contraction. Nine healthy, normally-trained sea-level (SL) residents (8 males, 1 female) sojourned for 28 days at 3,454 m. Hbmass was measured and PV estimated by carbon monoxide re-breathing at SL, on every fourth day at HA, and one and two weeks upon return to SL. Four weeks at HA increased Hbmass by 5.26 % (range 2.5 - 11.1 %; p<0.001). The individual Hbmass increases commenced with up to 12 days delay and reached a maximal rate of 4.04 ± 1.02 g.d(-1) after 14.9 ± 5.2 days. The probability for Hbmass to plateau increased steeply after 20-24 days. Upon return to SL Hbmass decayed by -2.46 ± 2.3 g.d(-1), reaching values similar to baseline after two weeks. PV, aldosterone concentration and renin activity were reduced at HA (p<0.001) while the total circulating protein mass remained unaffected. In summary the Hbmass response to HA exposure followed a sigmoidal pattern with a delayed onset and a plateau after ~3 weeks. The decay rate of Hbmass upon descent to SL did not indicate major changes in the rate of erythrolysis. Moreover, our data supports that PV contraction at HA is regulated by the renin-angiotensin-aldosterone axis and not by changes in oncotic pressure. Copyright © 2014, Journal of Applied Physiology.
    Journal of Applied Physiology 03/2015; DOI:10.1152/japplphysiol.01121.2014