I would like to thank Dr Baxter for her kind words regarding the
importance of my manuscript in highlighting the ambiguity in the use of
the term intensity in the exercise sciences. I also agree fully that more
careful definition might help to clarify the issue of its use. However, I
think that better clarification of the definition of the term only further
serves to highlight the issues associated with its use.
I would like to thank Dr Baxter for her kind words regarding the
importance of my manuscript in highlighting the ambiguity in the use of
the term intensity in the exercise sciences. I also agree fully that more
careful definition might help to clarify the issue of its use. However, I
think that better clarification of the definition of the term only further
serves to highlight the issues associated with its use.
In correspondence with another academic in this area it was pointed
out that my manuscript did not in fact discuss Intensity as defined under
the Systeme International d'Unites which is power transferred per unit
area (i.e. W.m-2). Further that in luminescence the term is defined
differently again (candela per square metre i.e. cd.m-2). A number of
manuscripts in previous years have discussed the misuse of Newtonian
mechanical constructs in describing exercise and yet have opted for the
continued use of intensity to describe the difficulty or 'hardness' of
exercise (Knuttgen, 1978; Winter & Fowler 2009). I maintain that
attempting to describe exercise in such a way is perhaps a wasted effort.
If, for example, we use 'Intensity' as defined under the Systeme
International d'Unites as power transferred per unit area, and it is
expressed as the unit watts per square metre (i.e. W*m-2), then
technically any use of the term outside of this strict definition would
constitute a misapplication, assuming it is taken to be the accepted
definition in that context. This would also apply to the suggestions made
by other authors (Knuttgen, 1978; Winter & Fowler 2009) more recently
to use the term to describe how 'hard' exercise is but to differ the unit
dependent on the context. Unless power per unit area is being measured or
discussed would it perhaps not be better to avoid the term altogether in
exercise science? If so then the word 'Intensity' could be avoided
completely by just using the phrase 'power per unit area'. Alternatively,
the problem appears to me that many within exercise science are probably
more likely to consider the OED definition of 'Intensity' and as noted in
my article the term becomes redundant once the construct being measured
(and preferably the unit of measurement) is made clear. Further, the
suggestion to avoid the word 'Intensity' entirely (unless referring to
power per unit area) in order to avoid confusion is exemplified by the
confusion that could occur from the situation (albeit unlikely) that the
magnitude of 'power per unit area' is being considered. Both the SI and
OED definition could be applied and result in curious statements such as
"Intensity (OED Definition) OF Intensity (SI Definition)" (i.e. "Intensity
OF W*m-2") which is very confusing (albeit rather amusing). Indeed,
another proverbial can of worms could be opened by noting that 'hardness'
is already considered a measurable variable in itself which refers to
either scratch, indentation or mechanical resistance of minerals. Perhaps
we should also leave this term alone as well except in colloquial verbiage
and 'difficulty' or 'challenge' might be better suited. These could be
defined along the lines of 'the overall demands of exercise relative to a
person's immediate ability to meet those demands'. Neither term to my
knowledge is currently under use with different application in other
scientific disciplines such to cause confusion.
I agree fully with Dr Baxter's comments that variables such as 'load'
and 'perception of effort' can indeed vary dependent upon the context.
However, this does not seem to me to be a terminological issue as it is
known that almost all dependent variables that can be measured may in fact
differ dependent upon manipulation of other independent and confounding
variables. For example, load measured by a 1RM may vary dependent upon
number of factors such as those noted by Dr Baxter and thus the 1RM should
be considered within the context of those factors. If one particular
context permits a higher 1RM than all others it may be fair to say that
this is indeed the individual's true maximum to the best of our knowledge.
In this case using Dr Baxter's example that in such instances where 1RM
may be reduced "...the (reported) intensity of the session would be higher
despite lower loading...", instead it could be said that the loading
relative to the true maximum was lower, however, relative loading under
the circumstances was still maximal (a 1RM under the current conditions)
despite a lower absolute loading. Similarly, perception of effort may
differ dependent upon a number of factors despite the same exercise
conditions being performed and indeed that many person's ability to rate
their perception of effort on a continuum is poor. Indeed a good example
of this, and which suggests even advanced trainees are not so good at
predicting how close they are to their maximum effort, is seen where such
trainees are asked to predict the number of repetitions they could perform
to momentary muscular failure and initially under predict (Hackett et al.,
2012). Perception of effort is also often confused with perceptions of
discomfort or other physical sensations, as noted in my manuscript, which
further confound this and suggests that the two should be differentiated
in measurement and in reference.
In any case, it would appear that Dr Baxter along with most others
persistence that 'intensity' should be used, albeit in combination with
the unit of measurement being considered or "...defined in terms of
reliable measures with which to underpin the definition in the respective
study..." appears a redundant suggestion and a potentially confusing one.
If the term intensity to describe the 'hardness' (difficulty/challenge?)
of an exercise can be defined differently in different contexts dependent
upon the variable being examined it potentially opens up many to again
misinterpret its meaning. Why not instead just refer to the variable being
considered (e.g. load, effort, heart rate, force/torque etc.) whilst
considering the context under which it is being measured/examined?
References
1. Kunttgen HG. Force, work, power and exercise. Med Sci Sport
1978;10(3):227-228
2. Winter EM, Fowler N. Exercise defined and quantified according to
the Systeme International d'Unites. J Sports Sci 2009; 27(5):447-460
3. Hackett DA, Johnson NA, Halaki M, Chow CM. A novel scale to assess
resistance-exercise effort. J Sports Sci 2012;30:1405-1413
I fully agree with comments made by Masci regarding treatment for
tendinopathy.
I also practice at the coalface, treating tendon pain from elite to
recreational athletes.
The reality I face when prescribing exercise protocols is both a lack of
evidence base as to the optimum program, and the harsh reality that most
non-elite athletes will not strictly comply with complex home exercise
programs, particularly where there i...
I fully agree with comments made by Masci regarding treatment for
tendinopathy.
I also practice at the coalface, treating tendon pain from elite to
recreational athletes.
The reality I face when prescribing exercise protocols is both a lack of
evidence base as to the optimum program, and the harsh reality that most
non-elite athletes will not strictly comply with complex home exercise
programs, particularly where there is no rapid improvement in symptoms-
people have busy and complex lives and it is not possible to simplify a
complex life into a single tendon.
I frequently opt for platelet rich plasma injections, as do many of my
sports medicine colleagues.
Anecdotally these work well, which, despite failing the evidence base
test, passes the word of mouth test, and word of mouth is the source of
many of my referrals. This is perhaps the major difference between
research and the real world.
If we adhere strictly to the evidence base, we should stop treating
tendons altogether, and leave our patients in pain, as even the most
widely used treatment programs have questionable evidence behind them.
My approach is largely common sense based. Patients who are prepared to
reduce loading on a painful tendon and work on a graded and comprehensive
exercise program are offered that.
Those who state outright that they will not do an exercise program, but
wish to try PRP injections (because their friend/ relative/ sports
colleague had great benefit) are not turned away, but given the treatment.
I perform injections under ultrasound control, and treat gluteal and
rotator cuff tendons as well as Achilles, patellar, and elbow tendons.
Anecdotally most get better, and although this is not science, I am happy
to inhabit the large grey area of tendinopathy treatment. I am also happy
to follow the research, and change my approach as are knowledge evolves.
Clarification on the definition of use of the term 'intensity' as
raised by Steele certainly serves to highlight the continuing variation -
and confusion - around use of this term. Due to the ambiguity as to
whether intensity is a measured load or is synonymous with perceived level
of exertion, Steele recommended abandonment of intensity as a descriptive
word.
However it is my belief that the very dichotomy rai...
Clarification on the definition of use of the term 'intensity' as
raised by Steele certainly serves to highlight the continuing variation -
and confusion - around use of this term. Due to the ambiguity as to
whether intensity is a measured load or is synonymous with perceived level
of exertion, Steele recommended abandonment of intensity as a descriptive
word.
However it is my belief that the very dichotomy raised by Steele
emphasises the need to quantify and define the term through the
development and adoption of reliable and objective outcome measures, and
ones that capture the dichotomy: i.e. the psychological (perceived level
of exertion) and physiological (load) components of intensity.
Translation and definition of terms are fundamentally important in
the communication of science: in fact the imperative of research papers
reporting the details of the research methods employed depends in turn on
the definition and language used to communicate the methods.
While I acknowledge that there are inherent problems in translation
of the term intensity, I further believe there are issues surrounding the
choice of definition being either 'load', or 'perception of exertion'.
For example, an individual's maximum 'load', or 1RM, is not constant:
rather, it represents a hypothetical 'best'. It fails to recognise
differing circumstances, including human factors, and instead assumes a
mechanistic uniformity in ability for 1 RM. However, there are a number of
factors which may affect the ability of a individual to achieve a 1RM,
including stressors; injury or muscle tightness; pre-fatigue from other
lifts; DOMS (delayed onset muscle soreness); or even calorific deficit or
inadequate nutrition. In such instances the measured load of 1RM would be
altered (albeit transiently), but the (reported) intensity of the session
would be higher despite lower loading.
'Load' also does not capture other factors which affect the 'load'
such as 'time'; if the lift is slowed down then there is more effort
exerted without altering the load. Other ways of increasing the intensity
of a lift without altering the load include reduced rest periods, more
repetitions and 'concentration' sets whereby the person is restricted to
main area of the workload (such as in squats the bottom half of range of
movement).
Similarly there are challenges in advocating intensity as being
synonymous with perceived level of exertion, which requires the objective
ability of the participant to distinguish with accuracy the effort
required in a given exercise session. This presents two problems: often
the complete novice participant has low experience in determining what
their effort is on a continuum, when compared to (say) that of the
experienced lifter/athlete. Further to this, there is the issue that, both
the novice and advanced lifter are inclined to responder bias in such
circumstances. Although for the advanced lifter their experience while
provide a more accurate quantification of perceived level of exertion
(perhaps due to more instances for comparison), in both cases the accuracy
is contingent on the responder (and their associated prior
agendas/preconceptions).
It is my recommendation that intensity is not a term that becomes
neglected or ceases to be used. The term must instead be defined in terms
of reliable measures with which to underpin the definition in the
respective study. These outcome measures should reflect the dual nature,
and therefore, ambiguity in translation: they should include both
physiological and psychological concepts, and measures. This would include
and capture the level of exertion used while providing a more scientific
foundation for replication.
Although good to see researchers putting forward hypotheses for improving rehabilitation protocols I do believe there needs to be a balance of promoting their own work published in another journal (Scandinavian Journal of Medicine & Science in Sports) with incomplete presentation in an editorial article of another. In the original paper there were no differences between groups at 1, 6, and 12 months. There was no mention of t...
Although good to see researchers putting forward hypotheses for improving rehabilitation protocols I do believe there needs to be a balance of promoting their own work published in another journal (Scandinavian Journal of Medicine & Science in Sports) with incomplete presentation in an editorial article of another. In the original paper there were no differences between groups at 1, 6, and 12 months. There was no mention of this in the editorial paper. At 12 months, the Foot Function Index was lower in the stretch group. So if all our patients were just interested in how they functioned at 3 months post commencement of treatment it may be more relevant. There could be a variety of reasons for a transient difference at 3 months including chance, the sensitivity of the instrument, sample size etc. There may have been no difference at 4 months and it was a transient 'blip in the data. Perhaps an explanation of reported improvements at 3 months but not at 1,6 & 12, should have been hypothesised in relation to the high-load' model. Self-interest promotion of one's own model will be considered more seriously by others if the authors objectively present the data. Too often we are told of the next great step in treatment based on limited science and then have to readjust it and confuse our patients yet again.
With great interest we read Sj?gren et al.'s contribution that
analyzed changes in telomere length in association to the time spent
exercising and the time spent sitting in a 6-month randomized controlled
trial in 49 older sedentary and overweight men and women. Sj?gren et al.
concluded that reduced sitting time was significantly associated with
telomere lengthening.
These findings are of great potential interest, as hi...
With great interest we read Sj?gren et al.'s contribution that
analyzed changes in telomere length in association to the time spent
exercising and the time spent sitting in a 6-month randomized controlled
trial in 49 older sedentary and overweight men and women. Sj?gren et al.
concluded that reduced sitting time was significantly associated with
telomere lengthening.
These findings are of great potential interest, as highlighted in the
accompanying press release. However, several questions remained for us
after carefully reading this contribution:
1. In Figure 1 the associations for change in exercise time and change in
telomere lengths for control and intervention group are given. When
looking only at those participants with no or positive changes in exercise
time, there seems to be a zero or even slightly positive association
between change in exercise time and change in telomere length. With regard
to the main hypothesis as laid down by the authors, we wonder why
participants with reduced exercise time over the course of the study show
highest values of lengthening. These are participants who exercised up to
500 minutes per week less at the end of the study than they did at
baseline. It would be interesting to see an ANCOVA analysis of both groups
combined including baseline telomere length values and baseline exercise
time values. This would account for differences in baseline values of each
subject and additionally for a possible curvilinear relationship between
the change in exercise time and the change in telomere length.
2. Sj?gren et al. stated that they did not find significant associations
between changes in steps per day and changes in telomere lengths. It would
be helpful to see some descriptive statistics and the test results for
that statement. Thus, the reader may get a more comprehensive picture of
the study result; e. g., non-significance may just be due to small sample
size.
3. The main result of the study is provided in figure 2: associations of
change in sitting time and change in telomere length by group.
Interestingly Sj?gren et al. only refer to the (significant) result in the
intervention group which compiles data from 12 individuals. There is
almost no association to be seen in the control group. This raises
additional questions: How would the authors explain the differential
results for the control and the intervention group? Was change in sitting
time related to changes in steps per day or to changes in exercise time?
4. To gain a more comprehensive picture of the associations of interest,
additional information as outlined above would be helpful. Furthermore,
the role of confounders should be more thoroughly discussed, and results
from the entire trial included in the discussion. Generally, it should be
avoided to focus only on the subgroup with significant test results (Dwan
et al. 2008).
Getting the information to the points above would shine more light on
the association between time spent for sitting, exercising and telomere
lengths.
Reference:
Dwan K, Altman DG, Arnaiz JA, Bloom J, Chan AW, Cronin E, Decullier E,
Easterbrook PJ, Von Elm E, Gamble C, Ghersi D, Ioannidis JP, Simes J,
Williamson PR. (2008). Systematic review of the empirical evidence of
study publication bias and outcome reporting bias. PloS one, 3(8), e3081.
The article by Dr. Twaij and associates nicely covers the range of
thoracic outlet syndromes (TOS) seen in athletes. However, several
important points have been overlooked. The chief diagnostic tool for
neurogenic TOS is physical examination that includes four provocative
maneuvers: Upper limb tension test (ULTT}, elevated arm stress test
(EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the
authors...
The article by Dr. Twaij and associates nicely covers the range of
thoracic outlet syndromes (TOS) seen in athletes. However, several
important points have been overlooked. The chief diagnostic tool for
neurogenic TOS is physical examination that includes four provocative
maneuvers: Upper limb tension test (ULTT}, elevated arm stress test
(EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the
authors that pulse deficits by the Adson maneuver are too unreliable to
use.
The most important objective test is measurement of latency and
amplitute of the medial antebrachial sensory cutaneous nerve (MAC) on EMG.
2 (Machanic2008) For neurogenic TOS, the only imaging study of value is
the plain X-ray of the chest to reveal cervical or anomalous first ribs.
MRI is helpful for recognizing associated or differential diagnoses, such
as cervical spine or shoulder disease, but MRA to reveal arterial stenosis
is not helpful in diagnosing neurogenic TOS because it is relying on a
vascular sign to diagnose a neurologic condition. There are too many
false negatives and positives.
The underlying pathology in NTOS, is scarred muscle, not muscle
hypertrophy. This comes from the healing of torn muscle fibers from neck
trauma, which can be from a single acute accident or repetitive stress
injury. 3 (Sanders 1990).
The second observation in the article is failure to mention another
group of closely related diagnoses in athletes that have similar symptoms,
but lie below the clavicle in the subpectoral area--namely neurogenic
pectoralis minor syndrome (NPMS), as well as arterial pectoralis minor
syndrome (APMS) and venous pectoralis minor syndrome (VPMS). It is
important to recognize the subpectoral conditions, as when they are
present they can be treated by minimal risk surgical procedures, performed
as outpatients and have recovery times of only one or two weeks.
NPMS is a condition seen in athletes who use their arms above
shoulder level to throw or pull, such as swimming, baseball, volleyball,
gymnastics, and weight lifting. The pectoralis minor muscle (PMM)
attaches to the coracoid process of the scapula. As such, repetitive
actions of the shoulder that pull back the scapula stress the PMM. In
time, the PMM scars, tightens, and can put pressure on any of the three
structures in the axillary neurovascular bundle, but most often on the
cords and branches of the brachial plexus.
Symptoms of NPMS are the same as NTOS, pain, numbness, tingling, and
weakness in the upper extremity, pain over the trapezius, and a lesser
degree of neck pain and occipital headache. It is quite common for NPMS
to accompany NTOS.
Physical examination may reveal the same positive findings as NTOS,
but in addition, there are two findings specific for NPMS: Tenderness
over the PMM, just below the clavicle, and tenderness in the axilla.
These two findings are not from NTOS, but indicate NPMS.
A very helpful diagnostic test is a PMM muscle block with local
anesthetic. After this is performed, the physical examination is repeated
and the tenderness in those areas should temporarily disappear or be
greatly reduced; provocative maneuvers show improvement. 4 (Sanders 2010)
Arterial PMS is a condition seen almost exclusively in athletes who
use there arms for vigorous overhead throwing. Baseball pitchers and
volleyball players are the ones most often affected but it also can occur
in mechanics and laborers who work with their arms above their heads. The
pathology is either in the axillary artery or one of its branches, most
often the posterior circumflex humeral artery(PCHA). This artery
traverses the quadralateral space and wraps around the humeral head
increasing resistance within the artery and causing aneurysm formation at
the axillary-PGHA junction. These aneurysms tend to thrombose. When
thrombus breaks off, it enters the axillary artery and embolizes distally.
Arterial PMS elicits the same symptoms as Arterial TOS: Coldness,
palor, arm claudication, and ischemic fingers. Diagnosis is by
arteriograms revealing arterial occlusion by emboli in the forearm or
hand. It also reveals a normal subclavian artery and may or may not
reveal a normal axillary artery. Other mechanisms of APMS are compression
of the axillary artery between the PMM and head of the humerus. This can
result in axillary artery stenosis or even occlusion. 5 (Atema 2012 )
Finally, venous PMS is rarely seen and caused by PMM compression of
the axillary vein. It is the result of repetitive overhead activities
with the upper extremities. Its symptoms are similar to venous TOS,
intermittent swelling and cyanosis of the upper extremity. To date, all
reported cases have been axillary vein obstruction without thrombosis.6
(Sanders 2007)
Treatment for neurogenic PMS initially is physical therapy which is
mainly stretching exercises of the PMM. If this fails, surgical treatment
is minimum risk, outpatient pectoralis minor tenotomy (PMT) with a short
recovery time. Treatment for venous TOS is also PMT.
Arterial PMS is a surgical problem. Physical therapy is not an
option. If the problem is stenosis of the axillary artery, PMT may be all
that is required. If the axillary artery is aneurysmal or too badly
scarred, repair by patch or replacement graft is required.7 (Duwayri 2011)
Above all, the most important point is to recognize whether the
pathology lies above the clavicle in the thoracic outlet area, or below
the clavicle in the pectoralis minor area.
References
1. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100
operations for pectoralis minor syndrome alone or accompanied by
neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.
3. Sanders RJ, Jackson CGR, Banchero N, Pearce WH: Scalene muscle
abnormalities in traumatic thoracic outlet syndrome. Am J Surg. 1990;
159:231-6.
4. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100
operations for pectoralis minor syndrome alone or accompanied by
neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.
5. Atema JJ, Unlu C, Reekers JA, Idu MM. Posterior circumflex
humeral artery (PCHA) injury with distal embolizaion in professional
volleyball players: Discussion of three cases. Eur J Vasc endovascular
Surg 2012;44:195-198.
6. Sanders RJ, Rao NM. Pectoralis minor obstruction of the axillary
vein: Report of six patients. J Vasc Surg 2007; 45:1206-1211.
7. Duwayri YM, Emery VB, Driskill MR, Earley JA, Wright RW, Paletta
GAJr, Thompson RS. Position compression of the axillary artery causing
upper extremity thrombosis and embolism in the elite overhead throwing
athlete. J Vasc Surg 2011;53:1329-1340.
We have read the respective article and we agreed with all great
findings. Nevertheless, we wish to emphasize the need to address the role
of some molecular and physiological markers that may elaborate and
possibly support the findings of the study. Intermittent hypoxia exposure
can enhance the generation of red blood cells, which may consequentially
increase hemoglobin concentration and hematocrit depending on the model...
We have read the respective article and we agreed with all great
findings. Nevertheless, we wish to emphasize the need to address the role
of some molecular and physiological markers that may elaborate and
possibly support the findings of the study. Intermittent hypoxia exposure
can enhance the generation of red blood cells, which may consequentially
increase hemoglobin concentration and hematocrit depending on the model of
IHE exposure and its effect on serum hypoxia inducible factors (HIF-1
alpha, HIF-2alpha and HIF-3 alpha), erythropointin (EPO) levels and some
signaling pathways (such as those mediated by the nuclear factor-kappa
light chain B: NF-kB for stress and inflammation examinations) [1].
Hypoxia-inducible factors (HIF-1 alpha, HIF-2alpha and HIF-3alpha) are
transcriptional regulatory factors that orchestrate cellular responses to
hypoxia and regulates oxygen homeostasis[2]. However hypoxic induction of
HIF-1alpha and HIF-2alpha leads to the transcriptional activation of HIF-
3alpha expression as a target gene, which in turn is involved in the
reverse negative regulation of other HIFs activities [3]. Less
intramuscular hypoxic shifts of metabolic parameters (lactate and pyruvate
concentration, lactate/pyruvate and NAD/NADH ratios) after IHT [4] are
accompanied by marked decrease of HIF-3alpha expression and increase in
the resistance to physical exercise (with up to 70% increase endurance and
25% oxygen pressure in muscle). This indicates the importance of
establishing the changes in HIFs system included in this study.
Successive normobaric hypoxia-reoxygenation cycles in intermittent hypoxia
exposure is associated with generation of cytosolic reactive oxygen
species (ROS) which aid in transduction of cellular signals by stabilizing
the HIF alpha subunits and promoting its translocation to nucleus and
subsequent dimeruization with its alpha subunit to form complexes that
binds to hypoxia response element (HRE) to express certain genes (e.g EPO,
VEGF, NOS/HO-1 etc) that mediate cellular oxygen adaptation mechanism
that will in the long run reflect on exercise performance and
endurance[5]. Erythropoiesis is a classic physiologic response to hypoxia
that is mediated by the HIFs through inducing cell-type specific gene
expression changes that result in increased erythropoietin (EPO)
production in kidney, liver and facilitates erythroid progenitor
maturation and proliferation. HIF-2 is the main transcription factor that
regulates EPO synthesis in the kidney and liver and plays a critical role
in the regulation of intestinal iron uptake [6].
Although the heart rate during graded swim test was found to be the same
before and after IHE, cardiac responses to hypoxia are quite dependent on
carotid body function, which is deeply affected by its oxygen sensing
capability. Tissue specificity of HIF-1 homolog (HIF-2alpha) may play an
important role in the stable heart rate observed because irrespective of
the wide expression of HIF-1 in many cells, including the carotid body
glomus cells, hypoxia elicits different responses in different cell types
[7]. Additionally, endurance training and intermittent hypoxia are
effective preventive strategies against stress induced cardiac and
mitochondrial dysfunction. There is need to support the findings of normal
heart rate with further studies on signaling pathways, consequent
metabolic and redox remodeling associated with a cardioprotective
phenotype. This could be achieved by analyzing the myocardial heat shock
proteins, cyclooxygenase-2 activity, endoplasmic reticulum stress
proteins, nitric oxide production, myocardial antioxidant capacity,
sarcolemmal and mitochondrial adenosine triphosphate (ATP)-sensitive
potassium channels [8]. In order to obtain a viable result, the inclusion
and exclusion criteria must address previous exposure ti intermittent
hypobaric hypoxia as it has been reported to decreases myocardial
infarction size, reduces the number of ventricular arrhythmias, and
improves the recovery of cardiac contractile function against acute
ischemia-reperfusion (I/R) injury [9]. The crucial role of mitochondria in
cellular energetics, metabolism and intracellular signaling processes
regulating cell death and survival [10] has made it important to assess
the role of mitochondria in the 4.8% and 1.6% performance declines
observed in middle-distance (MD) and long-distance (LD) subjects as
reported by the study.
References:
[1]. Zhang, C. Y., Zhang, J. X., L?, X. T., & Li, B. Y. (2009).
Effects of intermittent hypoxic exposure on the parameter of erythrocyte
and serum hypoxia inducible factor-1 alpha and erythropoietin levels. Xi
bao yu fen zi mian yi xue za zhi= Chinese journal of cellular and
molecular immunology, 25(10), 932.
[2]. Semenza, G. (2009). Regulation of oxygen homeostasis by hypoxia-
inducible factor 1. Physiology, 24:97-106.
[3]. Hara, S., Hamada, J., Kobayashi, C., Kondo, Y., Imura, N. (2001).
Expression and characterization of hypoxia-inducible factor (HIF)-3? in
human kidney: suppression of HIF-mediated gene expression by HIF-3?.
Biochemical and Biophysical Research Communications, 287:808-813.
[4]. Semenza, G.L. (2001). HIF-1 O2 and the 3 PHDs: how animal cells
signal hypoxia to the nucleus. Cell 107, 1-3.
[5]. Mankovskaya, I., Drevitskaya, T., Dosenko, V., Gavenauskas, B.,
Moiseenko E. (2006). Expression of transcriptional factor HIF subunits in
rat tissues under acute and intermittent hypoxia. Hypoxia Medical Journal,
35:1-2.
[6]. Haase, V. H. (2013). Regulation of erythropoiesis by hypoxia-
inducible factors. Blood reviews, 27(1), 41-53.
[7]. Lahiri, S., Di Giulio, C., & Roy, A. (2002). Lessons from chronic
intermittent and sustained hypoxia at high altitudes. Respiratory
physiology & neurobiology, 130(3), 223-233.
[8]. Kavazis, A.N. (2009). Exercise preconditioning of themyocardium.
Sports Med, 11:923-35
[9]. Ostadal, B. and Kolar, F. (2007). Cardiac adaptation to chronic high-
altitude hypoxia: beneficial and adverse effects. Respir Physiol
Neurobiol. 2(3):224-36.
[10]. Ascensao A, Magalhaes J, Soares JM, et al. Moderate endurance
training prevents doxorubicin-induced in vivo mitochondriopathy and
reduces the development of cardiac apoptosis. Am J Physiol Heart Circ
Physiol 2005;2:H722-31.
We have read the respective article and we agreed with all great
findings. But just need to emphasized on some thing very important and
crucial. We are working with adipocytes and adipose tissue is capable of
expanding many-fold during adulthood, therefore requiring the formation of
new vasculature to supply growing and proliferating adipocytes. The
expansion of the vasculature in adipose tissue occurs through
angiogenes...
We have read the respective article and we agreed with all great
findings. But just need to emphasized on some thing very important and
crucial. We are working with adipocytes and adipose tissue is capable of
expanding many-fold during adulthood, therefore requiring the formation of
new vasculature to supply growing and proliferating adipocytes. The
expansion of the vasculature in adipose tissue occurs through
angiogenesis, where new blood vessels develop from those pre-existing
within the tissue (Corvera et al., 2013). Previous studies indicated that
adipogenesis may be regulated by factors that drive angiogenesis.
Fundamental aspects of angiogenesis, including basement membrane
breakdown, vasculogenesis, angiogenic remodeling, vessel stabilization,
and vascular permeability. Critical angiogenic factors include vascular
endothelial growth factor (VEGF), VEGF receptors, angiopoietins (Ang),
ephrins, matrix metalloproteinases, and the plasminogen enzymatic system.
Vascular endothelial growth factor is the most critical factor because it
initiates the formation of immature vessels and disruption of a single
VEGF allele leads to embryonic lethality in mice. Expression of VEGF is
influenced by hypoxia, insulin, growth factors, and several cytokines
(Hausman et al., 2004). The VEGF has been reported to be modulated by
leptin and hCG (Islami et al., 2003) and more recently the expression of
angiogenic regulators, VGEF and leptin has been reported to be regulated
by the EGF/PI3K/STAT3 pathway (Cascio et al., 2009). These vital findings
reflects a regulation of secondary diseases related to obesity to be the
result of complex molecular events and adipose tissue vasculature as a
source of new targets for metabolic disease therapies. This gene is
located on chromosome 11q13 (7 exons). VEGFB has been reported to have a
role in endothelial targeting of lipids to peripheral tissues. Dietary
lipids present in circulation must be transported through the vascular
endothelium to be metabolized by tissue cells. Bioinformatic analysis
showed that VEGFB was tightly coexpressed with nuclear-encoded
mitochondrial genes across a large variety of physiologic conditions in
mice, pointing to a role for VEGFB in metabolism. VEGF specifically
controlled endothelial uptake of fatty acids via transcriptional
regulation of vascular fatty acid transport proteins. As a consequence,
Vegfb-/- mice showed less uptake and accumulation of lipids in muscle,
heart, and brown adipose tissue, and instead shunted lipids to white
adipose tissue. The co-expression of VEGFB and mitochondrial proteins
introduces a novel regulatory mechanism, whereby endothelial lipid uptake
and mitochondrial lipid use are tightly coordinated (Hagberg et al.,
2012). In our study, we are also looking in to identify the mutation(s) in
the VEGF-B gene in Malayisan Obese attributes towards CHD risk. We
hypothesized, if there is a mutation in VGEF-B, then the obese subject
will be predicted to have hypertension and if there will be no mutation
then signs of metabolic syndrome and diabetes type II will be predicted in
obese attribute in future. Most important the role of VEGF as major
autocrine mediator of FGF-2-induced angiogenesis and proliferation (Naim
et al 2005) should be considered by respective researchers in future.
References:
Cascio S, Ferla R, D'Andrea A, Gerbino A, Bazan V, Surmacz E, Russo
A. Expression of angiogenic regulators, VEGF and leptin, is regulated by
the EGF/PI3K/STAT3 pathway in colorectal cancer cells. J Cell Physiol.
2009
Oct;221(1):189-94. doi: 10.1002/jcp.21843.
Corvera S, Gealekman O. Adipose tissue angiogenesis: Impact on
obesity and type-2 diabetes. Biochim Biophys Acta. 2013 Jun 12. doi:pii:
S0925-4439(13)00211-1. 10.1016/j.bbadis.2013.06.003.
Hagberg CE, Mehlem A, Falkevall A, Muhl L, Fam BC, Orts?ter H,
Scotney P, Nyqvist D, Sam?n E, Lu L, Stone-Elander S, Proietto J,
Andrikopoulos S, Sj?holm A, Nash A, Eriksson U. Targeting VEGF-B as a
novel treatment for insulin resistance and type 2 diabetes. Nature. 2012
Oct 18;490(7420)
Islami D, Bischof P, Chardonnens D. Modulation of placental vascular
endothelial growth factor by leptin and hCG. Mol Hum Reprod. 2003
Jul;9(7):395-8.
Naim R, Chang RC, Sadick H, Bayerl C, Bran G, Hormann K. Effect of
vascular endothelial growth factor on fibroblasts from external auditory
canal cholesteatoma. Arch Med Res. 2005 Sep-Oct;36(5):518-23. PubMed PMID:
16099332.
Having taught medical students about the benefits of PA for the past
20 years and lived through WHO's 2002 World health day on PA, I had the
belief that PA was now integrated and implemented in everyday practice.
This nice little piece of research reminds us how difficult it is to
change "routine" and how uncomfortable some of us feel when encouraging
people to change their behaviour.
Back to the drawing board...
Having taught medical students about the benefits of PA for the past
20 years and lived through WHO's 2002 World health day on PA, I had the
belief that PA was now integrated and implemented in everyday practice.
This nice little piece of research reminds us how difficult it is to
change "routine" and how uncomfortable some of us feel when encouraging
people to change their behaviour.
Back to the drawing board...
The article suggests that using fat as an energy source is how to
fuel endurance events.
Why is it that top marathons runners and the SKY/GB team don't do
this but have a good balance of mainly carbohydrate and protein?
Because using fat requires 3% more oxygen for the same amount of
energy. Thus energy release is slower and it is why top athletes train
specifically to perform glycogen depleted. If you...
The article suggests that using fat as an energy source is how to
fuel endurance events.
Why is it that top marathons runners and the SKY/GB team don't do
this but have a good balance of mainly carbohydrate and protein?
Because using fat requires 3% more oxygen for the same amount of
energy. Thus energy release is slower and it is why top athletes train
specifically to perform glycogen depleted. If you understand the
physiology it is so wrong. Why do cyclists consume carbohydrate during
long stages
I would like to thank Dr Baxter for her kind words regarding the importance of my manuscript in highlighting the ambiguity in the use of the term intensity in the exercise sciences. I also agree fully that more careful definition might help to clarify the issue of its use. However, I think that better clarification of the definition of the term only further serves to highlight the issues associated with its use.
...
I fully agree with comments made by Masci regarding treatment for tendinopathy. I also practice at the coalface, treating tendon pain from elite to recreational athletes. The reality I face when prescribing exercise protocols is both a lack of evidence base as to the optimum program, and the harsh reality that most non-elite athletes will not strictly comply with complex home exercise programs, particularly where there i...
Clarification on the definition of use of the term 'intensity' as raised by Steele certainly serves to highlight the continuing variation - and confusion - around use of this term. Due to the ambiguity as to whether intensity is a measured load or is synonymous with perceived level of exertion, Steele recommended abandonment of intensity as a descriptive word.
However it is my belief that the very dichotomy rai...
With great interest we read Sj?gren et al.'s contribution that analyzed changes in telomere length in association to the time spent exercising and the time spent sitting in a 6-month randomized controlled trial in 49 older sedentary and overweight men and women. Sj?gren et al. concluded that reduced sitting time was significantly associated with telomere lengthening. These findings are of great potential interest, as hi...
The article by Dr. Twaij and associates nicely covers the range of thoracic outlet syndromes (TOS) seen in athletes. However, several important points have been overlooked. The chief diagnostic tool for neurogenic TOS is physical examination that includes four provocative maneuvers: Upper limb tension test (ULTT}, elevated arm stress test (EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the authors...
We have read the respective article and we agreed with all great findings. Nevertheless, we wish to emphasize the need to address the role of some molecular and physiological markers that may elaborate and possibly support the findings of the study. Intermittent hypoxia exposure can enhance the generation of red blood cells, which may consequentially increase hemoglobin concentration and hematocrit depending on the model...
We have read the respective article and we agreed with all great findings. But just need to emphasized on some thing very important and crucial. We are working with adipocytes and adipose tissue is capable of expanding many-fold during adulthood, therefore requiring the formation of new vasculature to supply growing and proliferating adipocytes. The expansion of the vasculature in adipose tissue occurs through angiogenes...
Having taught medical students about the benefits of PA for the past 20 years and lived through WHO's 2002 World health day on PA, I had the belief that PA was now integrated and implemented in everyday practice. This nice little piece of research reminds us how difficult it is to change "routine" and how uncomfortable some of us feel when encouraging people to change their behaviour. Back to the drawing board...
...The article suggests that using fat as an energy source is how to fuel endurance events.
Why is it that top marathons runners and the SKY/GB team don't do this but have a good balance of mainly carbohydrate and protein?
Because using fat requires 3% more oxygen for the same amount of energy. Thus energy release is slower and it is why top athletes train specifically to perform glycogen depleted. If you...
Pages