Muscle Soreness? What’s going on?

Let’s just start this off immediately by addressing that lactic acid does not cause muscle soreness (Bebbert et al 1986). We’ve known that longer than I’ve been alive, but this myth still persists. Now that we got that out of the way, we can discuss what is really going on those days after a strenuous workout.

The predominate theory in the field blames delayed onset muscle soreness (DOMS) on microscopic “tears” in your muscles. Think of it almost as a small, controlled muscle strain of sorts (don’t’ worry, it’s a good thing). However, if you’ve ever strained (“pulled”) a muscle, you know that it hurts immediately, and DOMS really kicks in about 24-48 hours after exercising. So why the difference?

Ironically, it’s the repair process, rather than the damage itself, that is thought to cause DOMS. Since these micro-tears in the tissue exist, the body sends in specialized cells to clear out damaged tissue and mobilize a host of other types of cells to start the healing process. During this chaos of cell removal, repair and rebuilding nearby healthy cells are also damaged, allowing fluids to enter the cells and they begin to swell (inflammation). While all of this is happening other signaling chemicals are released to facilitate healing, but one in particular, called bradykinin, ends up causing an increase in nerve growth factor (NGF). This increase in NGF is what is associated with chronic pain conditions because it makes your nerve endings more sensitive to pain. NGF is predominately what is responsible for the pain during DOMS, while inflammation of the muscle, while occurring simultaneously, is only a fraction of what contributes to the pain you’re feeling (Murase 2010). This is still being debated in the exercise physiology world, but the amount of evidence is growing to support this claim.

Knowing this, once that workout is in the books, you’re doomed for DOMS. Additionally, there’s no shortage of promises for relief from DOMS, most of which actually have little to no effect on reducing DOMS. I’ll have a different post addressing many of these “remedies” more specifically. Knowing this, embrace the soreness! It’s a good thing that you pushed your body to that point, however uncomfortable it might feel at the time. In order for muscles to adapt and become bigger, stronger, and faster they need to be stressed, and DOMS is a normal reaction to that stress, indicating you’ve done enough to challenge that tissue.

So next time you’ve done all those sets of squats, and you’re cursing anytime you go down stairs, sit on a toilet, or get out of your car, remember this: you’re in the process of becoming a more awesome version of you.

 

References:

Bobbert, Maarten et all, 1986. “Factors in delayed onset muscular soreness of man.” Journal of Science and Medicine in Sports & Exercise. 18(1), 75-81.

Murase, Shiori et al., 2010. “Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness).” Journal of Neuroscience. 30(10), 3752-3761

American College of Sports Medicine Resources for the Personal Trainer, 4th Edition, 2014. Lippincott Williams & Wilkins. Pp. 366.

5 Fitness Myths and Truths About the Differences Between Men and Women

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Some of the most obvious sex differences we observe happen when we put on pair of shorts and hit the gym. It’s obvious that men are bigger than women, not only in height (usually) but also in muscle bulk (hopefully). The differences don’t stop there. In this post, which was a paper from my undergraduate years, I will discuss sex differences that relate to exercise, and briefly, differences in sport performance. Topics will include body composition, muscle strength, cardiovascular endurance, metabolic function, sport performance, and age-related changes in these areas. Some common myths will be used as guides to explore these topics. *Warning* – this post contains a lot of primary research, and is not at the “basic” level. If you are left with questions after reading, leave a comment and I’d be happy to reply.

 Myth #1 – Women are fatter than men: Body Composition

Are women fatter than men? There is no easy answer to this question. Body size and composition are similar in men and women during early childhood. During adolescence, women begin to accumulate more fat, while men begin to increase fat-free mass (muscle, bone, connective tissue, etc). This results in differences in body composition, which is the relative ratio between fat free body mass and fat mass. The reason for this change can be directly attributed to hormone changes during puberty. During puberty, the anterior pituitary (a gland in the base of the brain) secretes higher concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These hormones will result in sex organ development and steroid hormone secretion (estrogen in women, testosterone in men). Testosterone secretion will result in increased bone formation and increased protein synthesis[i]. This results in men developing larger muscles and larger bones. In adulthood, men will have greater muscle mass than women, as well as differing distribution of muscle mass. Men have a higher percentage of upper body muscle mass compared to women, 42.9% to 39.7% respectively[ii]. Estrogen influences broadening of the pelvis, breast development, and increased fat deposition1. These changes from estrogen result in increased body fat percentage in women compared to men. Estrogen can also stimulate bone growth, which explains why women typically stop growing only 2-4 years following puberty. The immediate growth brought on by the surge of estrogen during puberty forces the bones to grow very rapidly, allowing them to reach their final length sooner than in men. Men have a much longer growth rate following puberty, which allows them to grow to a greater height (on average). Because of these differences, mature men are typically 13 cm taller, 30-40 lbs heavier, 40-50 lbs heavier in fat free body mass, 7-13 lbs lighter in fat mass, and 6%-10% lower in relative body mass compared to fully mature women1.

Because of the changes brought on from hormones, specifically during puberty and following this time, women tend to accumulate more body fat than men. However, increased body fat composition does not mean that women are larger, or “fatter” than men. Men should have less body fat than women, about 10% actually. Fat is necessary in reproductive functions, especially in women. When women have a body composition of that less than 12-15% body fat, they will stop menstruation (amenorrhea). However, men can remain healthy until they reach around 4-6% body fat, because of decreased dependence on body fat1.

Both men and women will see losses in total body mass, losses of fat mass, losses of relative fat, and gains in fat-free mass with sustained exercise. The losses that are seen are more related to total energy expenditure associated with the activities performed rather than sex differences. Both men and women can also see similar relative gains in lean mass (muscle mass) with sustained resistance training1. Other physiological changes, such as weight-bearing long bone density or connective tissue textile strength also adapt independent of sex. Simply put, men and women can lose fat at equal levels, as well as gain muscle mass at relatively equal levels.

Myth # 2 – Men are stronger than women: Muscular Strength

Are men stronger than women? Yes, but only for a few reasons. Women are approximately 40% – 60% weaker than men in upper body strength, and 25% – 30% weaker in lower body strength. When expressing strength relative to body weight, women are still 5% to 15% weaker in lower body strength. Women have a higher percentage of muscle mass in the lower body compared to men2. Women tend to use the muscles of the lower body more than the muscles of the upper body, compared to patterns of men. In fact, some average size women have lower body strength exceeding that of an average man.

The relative muscular strength compared between men and women is similar until puberty. During puberty, levels of sex hormones will begin to play a significant role in skeletal muscle development, just as hormones played a significant role in body composition. During puberty, men will increase the synthesis of testosterone, which will influence increases in muscle mass, primarily through the IGF-1 pathway. IGF-1 (Insulin-like Growth Factor-1) is a protein that plays in important role in cell growth, maturation, and multiplication. The increased muscle growth that we see in adolescent boys is due to this increase in IGF-1 regulation from increased levels of testosterone[iii].

While there are sex differences in muscle mass between men and women, there are also differences in the size of muscle fibers between the sexes. Muscle fibers contain areas called sarcomeres, which are the basic units involved in muscle contractions. There are various types of muscle fibers, which will be discussed later. There are significant differences in fiber area between men and women. When comparing sedentary men and women, the typical cross-sectional area of all fiber types is about 4500-5000 µm2 in men, while only 3500-4000 µm2 in women. In trained individuals, fiber areas for trained men is about 12,000-13,000 µm2, compared to around 7,000 µm2 for women. These sex-differences could be related to both testosterone levels and gene expression3.

So we know that muscle fiber size differs between men and women. What about individual types of fibers? Type I muscle fibers are the “fatigue resistant” muscle fibers, which are involved in aerobic exercise and contract at a slow rate, hence the layman term “slow-twitch” fiber. There are several Type II muscle fibers, which are commonly called “fast-twitch” fibers. Type IIa muscle fibers utilize oxygen for exercise, but less efficiently than type I. They contract faster than type I, but are slower than type IIb. Type IIb fibers do not utilize oxygen well, and are very prone to fatigue. However, these fibers generate large amounts of power because of the fast contractile speed (power = work/time). In men, the largest muscle fibers are IIa, followed by type I, then type IIb. In women, the largest muscle fibers are type I, followed by type IIa, then type IIb. These differences in muscle fiber type size result in differences in relative fiber type cross-sectional area in any particular muscle. While fiber type distribution is the same between sexes[iv], there are differences in the volume each fiber type occupies in any particular muscle. Since men have larger type IIa fibers, the muscle is generally better able to produce more power because of faster contractile speed. In women, larger type I fibers results in more area occupied by “fatigue resistant” fibers, which allows women to have slightly better endurance/resistance to fatigue than men4. Despite smaller fiber type size in women, capillarization (amount of blood flow in any given area) appears to be similar in both sexes[v].

Because of the different distribution of muscle fiber types between the sexes, women have a greater resistance to fatigue compared to men. When subjects of different sexes maintain a constant force output, such as riding an exercise bike at a certain resistance level, at a given percentage of the maximal exercise output (e.g. VO2 max), women can maintain the constant force for longer periods of time. Women can do this for a few reasons. Women can recruit more fiber type I muscle fibers and utilize more fat during exercise, which allows for better utilization of energy sources[vi].

So why are women still not as strong as men when they are capable of comparable gains? For decades, women were not prescribed strength training programs, for both fear of masculinization and the belief that women were not able to gain significant strength because of low levels of testosterone. However, we now know that women are capable of significant strength gains when undergoing a strength training program. Often, these gains in strength are not accompanied with large increases in muscle size (bulk). Women’s smaller muscle size compared to men is correlated to women’s lower levels of testosterone[viii]. However, muscle size does not determine strength. Other factors, such as nervous innervation (amount of nerves stimulating a particular area of muscle fibers), play a very important role in muscle strength and action. Women have considerable potential to increase nervous innervation, which can significantly increase absolute strength. Keep in mind, some women are able to attain significant muscle hypertrophy (growth in muscle size). Many studies have shown that men and women see similar increases in fat-free mass, muscle volume, and hypertrophy of type I, type IIa, and type IIx muscle fibers following periods of resistance training.

Similar strength gains, nervous innervation, and rigorous exercise programs have still left sex-related gaps between absolute strength between the sexes. This can be easily observed when comparing world records in weightlifting. On average, men are considerably stronger at each weight classification for weightlifting. Men typically lifted at least 165 lbs more that women in records for total weight lifted (sum of snatch and clean & jerk). We must keep in mind, men typically have higher fat-free mass than women at any given body weight. Also, more men tend to participate in weightlifting events compared to women, giving more opportunity to have higher world records.

Myth # 3 – Men can run longer and faster than women: Cardiovascular & Respiratory Function

We now know that women are more capable of resistance to fatigue when it comes to strength training, compared to men. Is this true when concerning endurance and cardiovascular training? There are some similarities and differences when comparing cardiovascular function between the sexes. When subjects of each sex are placed on a cycle ergometer (exercise bike), where power output can be independently controlled based on body weight, women tend to have a higher heart rate (HR), lower stroke volume (SV), an similar cardiac output (Q) and maximum heart rate (HRmax) compared to men for any absolute sub-maximal power output. A power output is the rate at which someone is doing work, or more specifically speaking, the transformation of metabolic potential energy to work or heat. These changes are also seen at maximal levels of exercise, with the exception of HRmax[ix]. Higher HR in women will help compensate for the lower SV, allowing a similar Q between the sexes. The differences in these variables can be attributed to two factors. First, women have smaller hearts than men, due to both smaller overall body size and lower testosterone levels. Therefore, the smaller left ventricle has a lower SV. Lastly, women have a smaller blood volume compared to men. This is also related to smaller body size. However, a study showed that 7-9 year old boys and girls showed no sex differences in SV and HR during any absolute sub-maximal power output[x]. This further supports evidence that many sex differences related to cardiovascular function occur post-puberty, suggesting the influence of sex hormones.

During a given absolute power output of 50 W on a cycle ergometer, women had higher heart rates than men, and lower stroke volumes. However, cardiac output was the same, which means that men and women have comparable abilities to perform a given absolute power output. However, at any relative power output (based on %VO2 max), men have similar heart rates, but much higher stroke volumes. This leads to a higher cardiac output. A higher cardiac output means men are working at a harder rate than women, at that relative power output.

There is some evidence to suggest that there are sex-specific differences in arterial-venous oxygen difference ((a-v) O2 difference). What the heck is (a-v) O2 difference? The (a-v) O2 difference is the difference in oxygen content between arterial and venous blood at the tissue level. This difference reflects the amount of oxygen used by the body. Women tend to have less potential for increasing their peak (a-v) O­2 difference. Although, women tend to have a steeper increase in (a-v) O2 difference for a given power output[xii]. The decreased potential to increase peak (a-v) O2 difference may be attributed to lower hemoglobin content, which results in lower arterial oxygen content and reduced potential to use oxygen in muscle.

There are little differences between the sexes when it comes to respiratory function. Respiratory responses to exercise are largely attributable to body size differences (with men being larger). When comparing relative power output between the sexes, respiration frequency (number of breathes taken/minute) is not significantly different. However, when comparing absolute power output between the sexes, women will breathe more rapidly than men. This is no doubt attributed to an increase workload relative to body weight, with women working at a higher percentage of maximum exercise potential than men, therefore breathing more frequently. Women also have a smaller tidal volume and respiration frequency for both relative and absolute power outputs (including maximal levels), when compared to men. Tidal volume is the amount of air inspired or expired during a normal breathing cycle. These differences are once again associated with body size differences between men and women1.

Following consistent cardiovascular training, the body undergoes many major cardiovascular and respiratory adaptations. Many of these adaptations are not sex-specific. There are major increases in maximal cardiac output (Qmax) following such training. Maximum heart rate typically does not change, but there is a significant increase in stroke volume. But remember, men inherently have larger stroke volumes than women because men have both larger left ventricles and stronger myocardium producing a stronger contraction, thus ejecting more blood1. Large increases in cardiac output from endurance training will typically only result in small increases in (a-v) O2 difference, which is a major limiting factor in increasing VO2 max. This increase is seen because of the increased efficiency of the heart to distribute oxygen to working muscles. However, there are many other factors that influence VO2 max. Other adaptations that increase VO2 max are increasing muscle blood flow (through vasodilation) or increasing muscle capillary density. Both of these changes are seen in men and women. During any submaximal exercise, cardiac output shows little to no adaptive change. Resting heart rate is reduced, while stroke volume increases. This is seen in both men and women.

Myth # 4 – Men get more out of exercising than women: Metabolic Function

Metabolic function is traditionally measured by maximal oxygen consumption (VO2 max) during any specific cardiovascular exercise. Oxygen consumption is resultant from active muscles using oxygen in order to carry out work. The more work done, the more oxygen consumed. The measurement of VO2 max is the single best index to represent a person’s cardiovascular potential. There are observed cardiovascular differences between the sexes, as measured by metabolic consumption of oxygen. The average woman tends to reach her peak of VO2 max between the ages of 12 and 15. The average man will hit his peak between ages 17 and 21. Beyond puberty, an average woman’s VO2 max is only 70% to 75% of the average man’s1.

There has been considerable difficulty in measuring the differences between the sexes when comparing VO2 max. In 1965, a study that compared the physiological responses to sub-maximal and maximal exercise revealed that there was considerable overlap of VO2 max scores between the sexes. 76% of women nonatheletes’ VO2 max scores overlapped 47% of men nonathletes’ scores, and 22% of women athletes overlapped 7% of men athletes[xiii]. These overlaps show the importance of looking beyond the mean values of VO2 max, because no significant conclusions could be drawn from the data gathered (See Figure 3). There are also unfair comparisons drawn between the sexes. Many groups that are considered nonathlete are comparing relatively sedentary women and relatively active men.

The most reliable conclusions have been drawn when comparing highly trained women and men athletes. A study by Saltin and Astrand compared VO2 max values of women and men athletes from Swedish national teams. The study revealed that highly trained women had 15% to 30% lower VO2 max values compared to highly trained men[xv]. The study also suggests that future studies take into account several variables that would help scale these values. The authors suggest scaling height, weight, fat-free mass, and/or limb volume in an attempt to more objectively compare men’s and women’s values. Each of these variables could provide some benefit to a VO2 max score, depending on the test implemented.

Another variable considered to effect VO2 max is hemoglobin concentration. Remember, women have significantly lower hemoglobin concentrations compared to men, resulting in a lower (a-v) O2 difference, thereby less oxygen is available to muscles. Researchers have examined this difference between men and women in order to quantify the differences in VO2 max caused by hemoglobin concentration differences. In one study, researchers examined hemoglobin levels of 10 men and 11 women. After quantification, a specific amount of blood was withdrawn from men in order to equalize their hemoglobin concentrations with those of women. Each subject was measured for VO max, and significant reductions were found in the men participants. However, the reductions only accounted for a small portion of the sex differences in VO2 max. Men’s values were still significantly higher[xvi].

Why do we see this trend? I thought women had more endurance than men? An important consideration to remember is that at any absolute power output, women are working at a higher percentage of their VO2 max. This increased stress results in increased lactate production, raising blood lactate levels. Lactate threshold is the point during exercise at which blood lactate (lactic acid) begins to accumulate above resting levels. Basically clearance of lactic acid is slower than the accumulation during intense exercise. This accumulation is partially responsible for fatigue and muscle soreness following intense exercise. Researchers have shown that peak blood lactate thresholds are lower in active but untrained women than in active but untrained men. This same trend occurs when comparing trained women and men, with women having approximately 45% lower lactate thresholds compared to men[xvii]. This trend is only seen when examining absolute power outputs. When relative power outputs (relative %VO2 max) are taken into account, lactate threshold values are similar between the sexes. The lactate threshold appears to be related to mode of testing and to level of training of the participant.

During cardiorespiratory training, women will experience the same relative increase in VO2 max that is observed in men (about 15%-20% increase)1. The increase in VO2 max seen in the individual will depend on the intensity, duration, and frequency of training. Women experience all the adaptations to cardiorespiratory endurance training as men, but the magnitude is slightly different. Women reduce blood lactate levels during exercise, increase peak levels of lactate concentrations, and lactate threshold increases as well1. This means the individual can exercise at a higher intensity, for a longer period of time before fatigue is a problem. Men will see these same changes, but with slightly higher gains in blood lactate levels, peak lactate levels, and higher lactate thresholds.

Myth # 5 – Men are better at sports than women: Sport Performance

Bottom line… Maybe. Measuring differences in sport performance is a difficult, and sometimes an impossible task. Qualitative data can be subjective, so in order to observe differences in sport performance between the sexes, it can only be fair to examine sports that can be measured precisely by distance or time. Differences in sports such as shot put, swimming, and track events are key indicators of sex-related sport differences. To examine these differences, we must again examine current world records for each sex. Freestyle swimming can be a fair indicator of athletic performance between the sexes. As of 2006, the men’s world record for 400 m freestyle was 10.4% faster than the women’s world record. However, in years past, the gap between the sexes was much bigger. In the 1924 Olympic Games, the women’s winning time for the 400 m freestyle was 19% slower than the men’s. This was decreased to 15.9% in the 1948 Games, and again decreased to 7% in the 1984 Games. In fact, the fastest women’s 800 m freestyle swimmer in 1979 swam faster than the world record holding man for the 800 m freestyle in 19721. This shows that progressively over recent decades, women have narrowed the gap in sport performance. This change can be attributed to more opportunities to participate in sports and better coaching, facilities, and training techniques.

What to expect later in life…

Aging sucks. A lot. Especially when it comes to the gym. And there are only minimal means to do reduce the impacts of aging on dismantling your perfectly toned body into a blob of adipose tissue. As we age, body composition takes a turn for the worst. Between ages 25-45, weight tends to increase for both men and women. This is partially due to decreased levels of physical activity, but it is also due to excess caloric intake and decreased basal metabolic rate. We also shrink, usually around 5-7 cm in height[xviii]. This is often the result of years of compression of the intervertebral disks and poor posture. Not only that, but osteoporosis, a severe loss of bone mass with deterioration of the microarchitecture of bone leading to increased risk of bone fracture, also begins to set in. Osteoporosis has an earlier onset in women than it does in men, usually occurring between the ages of 40-50 in women and 50-60 in men. This difference is a direct result of decreased estrogen levels in women following menopause1. But wait, I’m not done yet. Fat-free mass also decreases progressively after age 40, with about 50% being the result of muscle loss. There is usually no decline in muscle mass before age 40, but after that the rate of decline increases, with a greater decline in men than in women2. The good news is endurance training can help slow these inevitable ends. Endurance trained athletes had much lower total body weight, relative body fat, and fat mass values compared to sedentary age matched individuals[xix]. Men experience greater changes in body composition compared to women, but these reasons are not fully understood.

Because of these changes, especially in fat-free mass, muscular strength will also decrease with age. Strength can often decrease to the point where daily tasks become challenging or even impossible. In fact, the ability to stand up from a sitting position in a chair starts to be compromised at age 501. There is debate on whether or not muscle fiber distribution changes with aging. Cross-sectional studies have shown no change in fiber type distribution in the vastus lateralis (one of the quadriceps muscles) with aging[xx]. There may be a change in distribution if the amount or intensity of activity changes over time, which it normally always will. Runners who decreased their activity or become sedentary see a significantly greater proportion of type I fibers compared to when they were 18-22 years younger[xxi]. This results in a higher proportion of type I fibers. Strength training can, and should, reduce changes in fiber type distribution, as well as prevent muscle atrophy seen with aging. Elderly men and women can actually increase muscle mass with strength training[xxii]. However, as age increases, it becomes more and more difficult to offset the natural biological processes of aging, and strength training becomes only a means to lessen the impact of aging on muscle loss.

Cardiac functioning also decreases with age. The most notable change is decreased maximal heart rate. Typically, maximum heart rate will decrease slightly less than 1 beat/min per year. The reduction we see is seen across the board, whether you are sedentary or well-trained. This decrease in max heart rate can be attributed to several factors, including changed in cardiac morphology, electrophysiological alterations, and downregulation of β1 receptors in the heart. These receptors decrease sensitivity to hormone stimulation, so max heart rate is reduced. Another significant change occurs with peripheral blood flow, such as blood flow to the arms and legs. As we age, there is a significant reduction in leg blood flow to exercising muscles, about 10-15% actually[xxiii]. However, this reduction of blood flow is somewhat compensated by an increased (a-v) O2 difference. Remember what that is? “The (a-v) O2 difference is the difference in oxygen content between arterial and venous blood at the tissue level. This difference reflects the amount of oxygen used by the body.” So, even though blood flow is reduced to exercising muscles, the oxygen uptake by muscles is increased in order to extract more oxygen[xxiv]. This change is seen in both men and women.

Just as heart rate decreases with age, so does VO2 max. In a cross-sectional study of men and women, men will have an average decrease in VO2 max of .41 mL/kg/min per year (mL/kg/min is the standard unit to measure VO2 max). Women will only show a .30 mL/kg/min decrease per year[xxv]. Remember, women will typically have a VO2 max value 70%-75% less than that of men. This difference means that there is less opportunity for loss of maximum aerobic capacity, resulting in less annual changes due to age.

 

References:

[i] Wilmore, J., Costill, D., & Kenney, W. (2008) Sex Differences in Sport and Exercise. Physiology of Sport and Exercise. Human Kinetics: USA. pp 423-446.

[ii] Janssen, I., Heymsfield, S.B., Wang, Z., & Ross, R. (2000) Skeletal muscle mass and distribution in 468 men and women aged 18-88 yr. Journal of Applied Physiology. Vol 89. pp. 81-88.

[iii] Brown, M. (2004) Sex and hormonal influences on skeletal muscle; differentiation and contractile mechanisms. Principles of Sex-Based Differences in Physiology. Edited by Miller, V. & Hay, M. ElSevier: Amsterdam, The Netherlands. pp. 194-208.

[iv] Sharon, R.S. (1997) Human skeletal muscle fiber types: delineation, development and distribution. Can. J. Appl. Physiol. Vol 22. pp. 307-327.

[v] Porter, M.M., Stuart, S., Boij, M., & Lexell, J. (2002) Capillary supply of the tibialis anterior muscle in young, healthy, and moderately active men and women. Journal of Applied Physiology. Vol 92. pp. 1451-1457.

[vi] Hicks, A.L., Kent-Braun, J., & Ditor, D.S. (2001) Sex differences in human skeletal muscle fatigue. Exercise and Sport Sciences Reviews. Vol 29. pp. 109-112.

[vii] Gonzales, J. & Scheuermann, B. (2007) Absence of gender differences in the fatigability of the forearm muscles during intermittent isometric handgrip exercise. Journal of Sports Science and Medicine. Vol. 6. pp. 98-105

[viii] Mittendorfer, B., & Rennie, M.J. (2006) Swings and roundabouts for muscle gain and loss: Differences between sexes? Journal of Applied Physiology. Vol 100. pp. 375-376.

[ix] Proctor, D.N., Beck, K.C., Shen, P.H., Eickhoff, T.J., Halliwill, J.R., & Joyner, M.J. (1998) Influence of age and gender on cardiac output-VO2 relationships during submaximal cycle ergometry. Journal of Applied Physiology. Vol 84. pp. 599-605.

[x] Turley, J.M. & Wilmore, J.H. (1997) Cardiovascular responses to submaximal exercise in 7- to 9-yr. old boys and girls. Medicine and Science in Sports and Exercise. Vol 29. pp. 824-832.

[xi] Wilmore, J.H., Stanforth, P.R., Gagnon, J., Rice, T., Mandel, S., Leon, A.S., Rao, D.C., Skinner, J.S., & Bouchard, C. (2001). Cardiac output and stroke volume change with endurance training: The HERITAGE Family Study. Medicine and Science in Sports and Exercise. Vol. 33. pp. 99-106.

[xii] Fagard, R.H., Thijs, L.B., & Amery, A.K. (1995). The effect of gender on aerobic power and exercise hemodynamics in hypertensive adults. Medicine and Science in Sports and Exercise. Vol 27. pp. 29-34.

[xiii] Drinkwater, B.L. (1973) Physiological responses of women in exercise. Exercise and Sport Sciences Reviews. Vol 1. pp. 125-153.

[xiv] Hermansen, L, & Anderson, K.L. (1965) Aerobic work capacity in young Norwegian men and women. Journal of Applied Physiology. Vol 20. pp. 425-431.

[xv] Saltin, B., & Astrand, P.O. (1967) Maximal oxygen uptake in athletes. Journal of Applied Physiology. Vol 23. pp. 353-358.

[xvi] Cureton, K., Bishop, P., Hutchingson, P., Newland, H., Vickery, S., & Zwiren, L. (1986) Sex differences in maximal oxygen uptake: Effect of equating haemoglobin concentration. European Journal of Applied Physiology, Vol 54, pp 656-660.

[xvii] Pollock, M.L. (1977) Submaximal and maximal working capacity of elite distance runners: Part I. Cardiorespiratory aspects. Annals of the New York Academy of Sciences. Vol 301. pp. 310-322.

[xviii] Spirduso, W.W. (1995). Physical dimensions of aging. Champaign, IL: Human Kinetics.

[xix] Kohrt, W., Malley, M. ,,Dalsky, D., % Holloszy, J. (1992) Body composition of healthy sedentary and trained, young and older men and women. Medicine and Science in Sports and Exercise. Vol 24. pp. 832-837.

[xx] Johnson, M., Polgar, J., Weihtmann, D., & Appleton, D. (1973). Data on distribution of fiber types in thirty-six human muscles: An autopsy study. Journal of Neurological Science. Vol 1. pp. 111-129.

[xxi] Trappe, S., Costill, D., Fink, W., & Pearson, D. (1995) Skeletal muscle characteristics among distance runners: A 20-yr follow-up study. Journal of Applied Physiology. Vol 78. pp. 823-829.

[xxii] Lexell, J., Downham, D., Larson, Y., Bruhn, E., & Morsing, B. (1995) Heavy-resistance training in older Scandinavian men and women: Short- and long-term effects on arm and leg muscles. Scandinavian Journal of Medicine and Science in Sports. Vol 5. pp. 329-341.

[xxiii] Saltin, B. (1986) The aging endurance athlete. In J.R. Sutton & R.M. Brock (Eds.), Sports medicine for the mature athlete. Indianapolis: Benchmark Press. pp. 59-80

[xxiv] Proctor, D., Shen, P., Dietz, N., Eickhoff, T., Lawler, L., Ebersold, E., Loeffler, D., & Joyner, M. (1998) Reduced leg blood flow during dynamic exercise in older endurance-trained men. Journal of Applied Physiology. Vol 85. pp. 68-75.

[xxv] Buskirk, E. & Hodgson, J (1987) Age and aerobic power: The rate of change in men and women. Federation Proceedings. Vol 46. pp. 1824-1829.