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

Conflict of Interest:

None declared

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.

Conflict of Interest:

None declared

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.

Conflict of Interest:

None declared

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.

Conflict of Interest:

None declared