Exercises that overtrain your nervous system

[revexrevex]

For me its

1 Rep Max Deadlifts
20 Rep squats
Forced Reps on any exercise

Takes me a while to recover from these. What about you

 

[Liftbig]

nothing, im young, hahahahahaha

 

[revexrevex]

Just because you are young you never get overtrained?

 

[Mike_Rojas]

Training to failure on multiple sets kills my CNS.

 

[louden_swain]

high volume. . . .and several training days.

Which I never use. . thats why I like low volume.

 

[pwr_machine]

Ok? Overtraining your nervous system? Can you elaborate? In my 10 years of study in exercise science, I have never heard of such a thing. Please explain.

 

[revexrevex]

There is first time for everything. Now you heard of it.

Ok? Overtraining your nervous system? Can you elaborate? In my 10 years of study in exercise science, I have never heard of such a thing. Please explain.

 

[coolcolj]

heavy anything

but deadlifts of all types mostly

 

[pwr_machine]

There is first time for everything. Now you heard of it.

So, explain.

 

[louden_swain]

I feel that I have plenty of CNS damage accumulated through the years. . .I no longer feel muscle pain when I train. . .I just fail. . .thats how I know my set is finished.

 

[pwr_machine]

I feel that I have plenty of CNS damage accumulated through the years. . .I no longer feel muscle pain when I train. . .I just fail. . .thats how I know my set is finished.

Again, how do you accumulate CNS damage?

 

[anabolicmd]

Its gotta be squats. I dont think there is a more intense excercise. Heavy reps of near-max or max weights are truly taxing physically and psychologically.

 

[revexrevex]

General feeling of being drained, tired, unable to add weight the next workout, muscle soreness or perception of lasting for more than a week, feelings of exhaustion and unwillingness to workout during succeeding training days, overall feeling of heaviness, short term loss of appetite and sleep, these are just my personal definition of it, and that is what I was refering to.

 

[pwr_machine]

General feeling of being drained, tired, unable to add weight the next workout, muscle soreness or perception of lasting for more than a week, feelings of exhaustion and unwillingness to workout during succeeding training days, overall feeling of heaviness, short term loss of appetite and sleep, these are just my personal definition of it, and that is what I was refering to.

And how is that related to your nervous system?

 

[pwr_machine]

pwr_machine, the nervous system needs about 5x the amount of time of the muscles to recover. Not allowing them to recover, overtime, can lead to some undesireable side effects.

Have you ever experienced tremors or shakes from lifting a weight a certain way?

You know I need a reference.

 

[revexrevex]

You know I need a reference.

You will get them in 20 minutes.

 

[spatts]

pwr_machine, the nervous system needs about 5x the amount of time of the muscles to recover. Not allowing them to recover, overtime, can lead to some undesireable side effects.

Have you ever experienced tremors or shakes from lifting a weight a certain way?

 

[sinjinsmythe33]

constant heavy training on compound excercises....

accompanied by lack of sufficient sleep (deep rem sleep) and poor nutrition. nothing kills motivation and intensity than a lack of progress.

 

[spatts]

Actually I quotted this study in a recent article I wrote on active recovery. I'll look it up for you and get you a link to the abstract.

Otherwise, any neurology book ought to cover it. The neurons just don't fire as efficiently, so you stop getting the muscle response you want. The symptoms appear to be that of muscle overtraining, and they are, but not because the muscle itself needs recovery, but because the other end of the motor unit needs recovery...the nerve.

 

[pwr_machine]

I thought the neuromuscular fatigue you were talking about could only occur with extensive and exhaustive levels of muscle activity. It's not just a set of squats or even a max attempt.

 

[teen1216]

I thought the neuromuscular fatigue you were talking about could only occur with extensive and exhaustive levels of muscle activity. It's not just a set of squats or even a max attempt.

A set of squats probably won't cause it in most people. It is exhaustive muscle activity. I'd say working up to a true max in deads or squats is quite draining, and over time that adds up.

 

[louden_swain]

Again, how do you accumulate CNS damage?

Maybe damage was the wrong term to use, but maybe I have trained the CNS to adapt to pain.

Disregard damage. . . . . my mistake.

 

[coolcolj]

It's accumlation over several sessions usually.

basicly you get to a point where the muscles don't respond to the same amount of electrical current from the CNS, or the CNS doesn't discharge enough current to recruit

 

[pwr_machine]

I see where stimulation of the nerve fiber has to occur at rates greater than 100 times per second for several minutes to diminish the amount of Ach released so much that the impulses fail to pass into the muscle fiber.

 

[spatts]

I thought the neuromuscular fatigue you were talking about could only occur with extensive and exhaustive levels of muscle activity. It's not just a set of squats or even a max attempt.

That's correct, but at some point, because the CNS takes longer to recover than a muscle, you can reach a point where no matter how recovered your muscle is from a single bout of strain, you are still feeling "overtrained" because the neural part of the neuromuscular equation isn't working like it should.

When a light flickers in your car, you think you need a new bulb. No matter how often you replace the bulb, it will still flicker if the bulb is not being fired efficiently. It appears to be the bulb...you change the bulb, but it doesn't get better. The fuse is bad.

I don't know if revex was referring to the "shakes" of a single bout or the long term effects. Either way, we give too little credit to how much neural recovery we need.

 

[revexrevex]

There are many references in this study to neuronal activity, but I made bold whatever I thought was revelant. Enjoy.


Title: Autonomic imbalance hypothesis and overtraining syndrome.
Source: Medicine and Science in Sports and Exercise v. 30 no7 (July 1998) p. 1140-5 Journal Code: Med Sci Sports Exercise
Additional Info: United States
Standard No: ISSN: 0195-9131
Details: bibl il.
Language: English
Review: Peer-reviewed journal


Abstract: Part of a special section on athletic training and overtraining. The writers propose an autonomic or neuroendocrine imbalance as the underlying cause of the parasympathetic, Addison type, overtraining syndrome. In an early stage of overtraining syndrome, the decreased adrenal responsiveness is no longer compensated, despite increased pituitary ACTH release, and the cortisol response decreases. In an advanced stage of the syndrome, the pituitary ACTH release also reduces. Therefore, parasympathetic overtraining syndrome can be regarded as an ultimate negative feedback response to sustained levels of arousal, whether from long-term heavy exercise or other issues. Athletes and coaches should provide appropriate regeneration before the athlete's body does it independently. They should learn that performance incompetence and severe fatigue are symptoms to be respected rather than problems to be overcome.
SUBJECT(S)
Descriptor: Athletes -- Training.
Autonomic nervous system.






Autonomic imbalance hypothesis and overtraining syndrome.
Author: Lehmann, Manfred.; Foster, Carl. Dickhuth, Hans-Hermann. Source: Medicine and Science in Sports and Exercise v. 30 no7 (July 1998) p. 1140-5 ISSN: 0195-9131 Number: BGSI98036231 Copyright: The magazine publisher is the copyright holder of this article and it is reproduced with permission. Further reproduction of this article in violation of the copyright is prohibited.


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Definition, epidemiology, and pathogenesis of short-term overtraining (overreaching), long-term overtraining, and possibly resulting overtraining syndrome have already been described elsewhere (2,3,5,7,8,15,17,20,25,27,28,37). This overview focuses on long-term endurance overtraining, possibly resulting in overtraining syndrome, and the hypothesis of an underlying autonomic or neuroendocrine imbalance (15,17). An overall schematic presentation of factors likely to be related to the development of overtraining syndrome is given in Fig. 1.

From a clinical standpoint, Israel (15) distinguished between a parasympathetic or vagal type overtraining syndrome and a sympathetic type. The more frequently observed parasympathetic type may be called modern type of overtraining syndrome. It is characterized by persistent performance incompetence, altered immune, and reproductive function (4,5,10,20,25,27). According to anecdotal observations (15,27), the sympathetic or "classical" type overtraining syndrome is a less frequent problem in modern sports. It can be characterized by hyperexcitability, restlessness, and performance incompetence (15).

The parasympathetic type overtraining syndrome is assumed to be the consequence of an imbalance between long-term inappropriately high training volume in endurance sports and too little time for regeneration (besides other additional and more or less essential stress factors (5)). The sympathetic type overtraining syndrome may also be the consequence of such an imbalance but seems to be related to inappropriately intensive training sessions. This classification may be too simple and one-dimensional, as no sympathetic type overtraining syndrome was seen after intensive resistance (6) and after high-intensity endurance overtraining (26). Therefore, a sympathetic type overtraining syndrome may rather be the consequence of too much accompanying psycho-emotional stress, such as too many competitions and too many nontraining stress factors (social, educational, occupational, economical, nutritional, travel, and time stress).

ADDISON OR BASEDOW TYPE OVERTRAINING SYNDROME

From a clinical standpoint, the parasympathetic or vagal overtraining syndrome was also called Addison type, and the sympathetic was named Basedow type overtraining syndrome (15). Their clinical patterns were similar to adrenal insufficiency (Morbus Addison) and thyroidal hyperfunction (Morbus Basedow).

Hackney et al. (12) observed reduced resting thyroid stimulating hormone (TSH), total T3 and free T3 concentrations in mountaineers subsequent to a Mt. McKinley expedition. Reduced resting TSH concentrations, reduced exercise-related TSH levels (by 40-50%), and approximately 20% reduced thyroid-releasing hormone-stimulated pituitary release of TSH were also observed in an early stage of the overtaining syndrome (26). Probably dependent on methodical problems, these changes did not reach the level of significance and have first to be confirmed. Data that can be related to an altered thyroidal function in an advanced stage of an overtraining syndrome are lacking at present anyway. Besides lacking confirmation of altered thyroidal function, decreased TSH (and TT3, fT3) levels could point to reduced hypothalamic TRH and pituitary TSH release owing to inhibitory effects caused by long-term increased sympathetic nervous system activity, metabolism, and body core temperature during prolonged training periods (11).

Persson et al. (33) described a reduced ACTH-stimulated adrenal cortisol release in chronically fatigued horses. These data, however, could not be confirmed by Kuipers (19). Contrary to untrained controls, Wittert et al. (40) observed significantly increased ACTH plasma concentrations in ultramarathoners during an early morning period between 3 and 8. Cortisol plasma levels or 24-h renal cortisol excretions did not show any significant differences. This study was performed 3-5 d after completion of the 1-d New Zealand coast-to-coast marathon. Corresponding to the findings presented by Persson et al. (33) in chronically fatigued horses, the findings of Wittert et al. (40) may point to decreased adrenal responsiveness to ACTH in these ultraendurance athletes. The decreased adrenal responsiveness can be the consequence of an overload during heavy preparatory training sessions before the ultramarathon, the ultramarathon stress itself, and incomplete regeneration. An incomplete regeneration may be assumed because a period of 3-5 d seems too short for complete regeneration. In this stage, the decreased adrenal responsiveness may still be compensated by increased ACTH levels (responses).

An approximately 60-80% higher pituitary corticotropin-releasing hormone (CRH)-stimulated ACTH response was also observed in experimentally overtrained athletes in an early stage of the overtraining syndrome (26). However, this increased response could no longer prevent a significantly reduced adrenal cortisol response compared to baseline. The findings lagged behind and were still amplified after 2 wk of incomplete regeneration (26,27). A decreased adrenal responsiveness was no longer completely compensated by increased pituitary ACTH response. In agreement with these findings, significantly (24) or tendentially (26) decreased exercise-related maximum cortisol levels were observed in overtrained distance runners (24) or recreational athletes (26) compared to baseline (397 (plus or minus) 119 vs 502 (plus or minus) 188 nmol/L, and 353 (plus or minus) 39 vs 389 (plus or minus) 166 nmol/L).

Barron et al. (1) additionally described a significantly decreased pituitary ACTH response related to insulin-induced hypoglycemia in overtrained distance runners. This was paralleled by clearly reduced adrenal cortisol response as also observed in chronically fatigued horses (33) and in overtrained human athletes (26,27). Besides the question of underlying different mechanisms (insulin-induced hypoglycemia vs CRH test), the findings of Barron et al. (1) additionally reflect a decreased hypothalamic and/or pituitary responsiveness, besides reduced adrenal responsiveness to ACTH. They also described a decreased pituitary release of growth hormone. This pattern may be characteristic of an advanced stage in the overtraining process. Recently, Gastmann et al. (9) also observed a reduced pituitary ACTH response to CRH in experienced road cyclists. This study was performed at the end of a heavy road pacing season after an additional 2-wk high-volume training stress without a preceding regeneration period.

Altogether, the majority of findings provide evidence of a reduced adrenal responsiveness to ACTH in the stage of overreaching or early overtraining syndrome. The reduced responsiveness is initially compensated by an increased pituitary ACTH response. However, it is no longer compensated in an early stage of a parasympathetic (Addison type) overtraining syndrome; the cortisol response decreases. A decreased hypothalamic/pituitary responsiveness (ACTH response) is added in an advanced stage of a parasympathetic overtraining syndrome (Fig. 2). There is additionally some evidence of a decreased pituitary release of thyroid-stimulating hormone (12,26); growth hormone release may be increased in an early stage (26,27) and decreased in an advanced stage of an overtraining syndrome (1).

At present, there is no valid experimental model of the genesis of the seldom observed sympathetic (Basedow type) overtraining syndrome. Because our knowledge concerning this type of overtraining syndrome mainly arises from anecdotal observations (15,27), the following sections therefore focus on the more common parasympathetic (Addison type) overtraining syndrome.

PARASYMPATHETIC TYPE OVERTRAINING SYNDROME AND BASAL RENAL CATECHOLAMINE EXCRETION

Basal renal (urinary) catecholamine excretion, the excretion of free catecholamines during overnight rest, is seen to reflect the intrinsic activity or tone of the sympathetic nervous system, as activating mechanisms are clearly reduced during night rest (18,22). Because noradrenaline concentrations in plasma and cerebrospinal fluid are quite similar (34,35), circulating and excreted noradrenaline may reflect the neuronal noradrenaline release in the brain.

Anecdotal observations in a top tennis player after too many matches, in track and road cyclists before the 1988 Games in Seoul (22,27), and during a follow-up of semiprofessional soccer players (22) give some support to Israel's hypothesis (15) of an autonomic imbalance and altered sympathetic nervous system activity in athletes suffering from parasympathetic type overtraining syndrome. The majority of these overtrained athletes showed an average 50-70% reduction in basal urinary catecholamine excretion. Such a finding was independently reported in soccer players by Naessens et al. (29). However, we believe this to be a "late" finding in the overtraining process during long-term high-volume training (22,27). Catecholamine excretion was negatively correlated to fatigue ratings (27) and showed normalization during a 2-3-wk regeneration period (22). There is also a negative correlation between basal catecholamine excretion and latency of REM sleep (r = -0.46; P < 0.01) in elite athletes (36). These correlations support the hypothesis that basal catecholamine excretion may reflect central mechanisms and that a clearly reduced basal catecholamine excretion may indicate central fatigue.

Altogether, there is some evidence that significantly reduced intrinsic activity of the sympathetic system, altered adrenal cortisol response, and potential alterations in thyroidal function can explain fatigue, demotivation, and performance incompetence in athletes suffering from a parasympathetic type overtraining syndrome. The decrease in sympathetic intrinsic activity is seen to depend on a negative feedback mechanism to increased concentration of circulating free catecholamines during prolonged heavy training sessions (Fig. 3). A plasma amino acid imbalance and altered brain neurotransmitter metabolism (30,31) is hypothesized to be involved in this process. An inhibitory effect of hypothalamic heat centers on hypothalamic sympathetic centers may have additional influence caused by increased body core temperature during prolonged training sessions.

PARASYMPATHETIC TYPE OVERTRAINING SYNDROME AND PLASMA CATECHOLAMINE LEVELS

During a prospective high-volume (moderate intensity) endurance overtraining study, final resting plasma norepinephrine (noradrenaline) levels before exercise and submaximum responses were significantly increased compared to baseline (23,24). Increased resting plasma norepinephrine levels were also observed by Hooper et al. (14) in overtrained elite swimmers. Increased submaximum norepinephrine responses were also described by Fry et al. (6) related to resistance overtraining. Increased plasma norepinephrine levels in overtrained athletes can indicate a loss in sensitivity of target organs to catecholamines, that is, a loss in training-dependent adaptation (32). But neither increased resting levels nor increased submaximum responses were observed after a 6-wk prospective high-intensity (moderate volume) overtraining study (26). Thus, inappropriately prolonged and monotonous daily training sessions may be an essential prerequisite for this loss in adaptation. Because catecholamine plasma clearance is not related to training (13), an increased response likely reflects an increased release and increased neuronal sympathetic activity because neuronal sympathetic activity is positively correlated to plasma norepinephrine levels (39,41).

A decreased intrinsic sympathetic activity (see above) as observed in the same affected athletes (23,24) and in other different groups of overtrained athletes (22,27,29) may not be seen as contradictory to increased submaximum plasma catecholamine responses, as plasma responses reflect acute stress-related changes in sympathetic activity rather than changes in intrinsic activity. Despite overtraining-related decreased intrinsic activity, stress-related responses are maintained and even amplified at identical absolute submaximum work load (27). From a common sense standpoint, this guarantees "flight or fight" even in fatigued subjects at least during early phases of overtraining. Related to a respective lowered absolute maximum work load in affected overtrained athletes, the final maximum plasma catecholamine responses were similar compared to baseline (23) or even decreased in more advanced stages of the overtraining process (17).

Increased plasma norepinephrine responses may also indicate the attempt to overcome overtraining-related peripheral or muscular fatigue. Because a decrease in b-adrenoreceptors on blood cells was observed in swimmers and distance runners (16) subsequent to prolonged high-volume training periods, increased plasma norepinephrine stress responses can be explained as consequence to decreased b-adrenoreceptor density. The decrease in b-adrenoreceptor density can be seen as a protective mechanism underlying the loss in sensitivity of target organs to catecholamines. This mechanism can explain overtraining-related "peripheral" fatigue in athletes after prolonged periods of high-volume training. This is supported by also decreased b-adrenoreceptor-mediated metabolic and cardiac effects in affected athletes after high-volume overtraining (23) (Fig. 4). The increased submaximum plasma norepinephrine responses were related to decreased submaximum heart rate, blood glucose, lactic acid, and free fatty acid responses (Fig. 4).

This pattern is identical to that following administration of b-blockers (21). An overtraining-related down-regulation of b-adrenoreceptors can be seen as a consequence to an increased concentration of circulating free catecholamines during prolonged, heavy, daily training sessions. The complete pattern of decreased intrinsic sympathetic activity, decreased b-adrenoreceptor density, decreased b-receptor-mediated effects, and increased norepinephrine levels/responses can only be expected after prolonged periods of daily training sessions of more than 2-3 h but not at a training load of <1 h d-1 (Fig. 4). Thus, after a 6-wk high-intensity (but moderate volume) overtraining study, decreased blood glucose and compromised performance ability were also observed (26). However, this was not paralleled by decreased sympathetic intrinsic activity, by significantly increased submaximum plasma norepinephrine, and by a complete pattern of decreased heart rate, lactic acid, and free fatty acid responses (Fig. 4). Therefore, the first step in the endurance overtraining process might be a significant decrease in stored energy-rich substrates such as glycogen (3), which is amplified or removed by down-regulation of b-adrenoreceptors during inadequately prolonged daily training sessions. An overtraining-related down-regulation in b-adrenoreceptors can be seen as protecting mechanism of target organs against overload-dependent irreversible damage. The transmission of ergotropic or catabolic signals becomes adapted to the reduced functional state of fatigued target organs.

Parasympathetic overtraining syndrome can thus be thought of as an ultimate negative feedback response to sustained levels of arousal, whether from long-term heavy exercise or other issues. Given both by the volume of training undertaken by contemporary athletes and the general pace of life today, the ability to enforce a reduction in the net stress to the system is, in fact, very adaptive. The unique problem for athletes and their coaches is to provide appropriate regeneration before the athlete's body does it independently. In this regard, athletes and coaches must learn that performance incompetence and severe fatigue are symptoms to be respected, not problems to overcome.

Added material.

MANFRED LEHMANN, CARL FOSTER, HANS-HERMANN DICKHUTH, and UWE GASTMANN.

University Hospital Ulm, Department of Sports and Performance Medicine, Steinhövelstrasse, 9, D-89075 Ulm, GERMANY; Milwaukee Heart Institute, Milwaukee, WI 53201-0342; University Hospital Tübingen, Department of Sports Medicine, D-72074 Tübingen, GERMANY.

Figure 1--Schematic overview of the genesis of overtraining syndrome in endurance sports related to long-term high-volume overtraining, as far as known at present. See text for further explanations and references.

Figure 2--Attempt of a schematic presentation of overtraining-dependent alterations in pituitary adrenocorticotropin (ACTH) and adrenal cortisol responses. There is a fluent transition between the different stages of short-term (overreaching) and long-term overtraining and a possibly resulting overtraining syndrome. According to Wittert et al. (40) and Lehmann et al. (27), it may be assumed that in the state of overreaching, a normal or slightly decreased cortisol response is guaranteed by a significantly increased ACTH response (release). In the state of an early overtraining syndrome, a further increase in ACTH release cannot completely prevent a further decrease in cortisol response, according to Lehmann et al. (27). In an advanced stage of the overtraining syndrome, both ACTH and cortisol responses are significantly reduced as described by Barron et al. (1).

Figure 3--Hypothesized mechanisms that may underly an endurance overtraining-related decrease in intrinsic activity (tone) of the sympathetic system are as follows: (i) a negative feedback mechanism to an increased concentration of circulating free catecholamines; (ii) a plasma amino acid and brain neurotransmitter imbalance (metabolic error signals) (30,31); (iii) an inhibitory effect of hypothalamic heat centers on hypothalamic sympathetic centers caused by increased body core temperature during prolonged heavy training sessions; and (iv) an afferent neuronal negative feedback using respective receptors of overloaded muscles (nociception, proprioception, metabo-receptors).

Figure 4--High-volume endurance overtraining (23,24,27) at average caloric demands of 4110 (plus or minus) 942 kcal d-1 (mean (plus or minus) SD) goes along with a decrease in intrinsic sympathetic activity compared to baseline as confirmed by Naessens et al. (29). A decreased b-adrenoreceptor density was described by Jost et al. (16) during high-volume training periods in distance runners and swimmers. b-Adrenoreceptor-mediated heart rate and metabolic responses were also reduced compared to baseline, whereas resting noradrenaline levels and submaximum responses were increased (23,24,27). Increased plasma noradrenaline levels were also observed by Hooper et al. (14) and Fry et al. (6), but decreased maximum noradrenaline responses were described by Kindermann (17) in an advanced stage. Besides decrease in intrinsic sympathetic activity, this pattern including decreased performance is identical to that following administration of b-blockers (21). During high-intensity but moderate-volume overtraining (26) at caloric demands of 2815 (plus or minus) 647 kcal d-1, these alterations in intrinsic sympathetic activity, plasma noradrenaline levels, or behavior of heart rate were not observed, and the pattern of metabolic alterations was less marked, respectively. This may indicate that intrinsic activity and b-adrenoreceptors are not affected by such overtraining on a level of approximately 1 h of daily intensive training load. Rest, before exercise; SM, submaximum workload; ME, maximum workload during maximum incremental ergometric testing.

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33. PERSSON, S. G. B., M. LARSSON, and A. LINDHOLM. Effects of training on adreno-cortisol function and red-cell in trotters. Zeitblatt für Veterinär Medizin 27:261-268, 1980.

34. PESKIND, E. R. Peripheral sympathectomy and adrenal medullectomy do not alter cerebrospinal fluid norepinephrine. Brain Res. 367:258-264, 1986.

35. SARMENTO, A. Adrenergic influences on the control of blood-brain barrier permeability. Naunyn-Schmiedebergs Arch. Pharmacol. 343:633-637, 1991.

36. STEINLE, H. Influence of Intensive Exercise on Sleep and Breathing Regulation in Athletes. Dissertation. University of Freiburg, 1997.

37. STONE, M. H., R. E. KEITH, J. T. KEARNEY, S. J. FLECK, G. D. WILSOND, and N. T. TRIPLETT. Overtraining: a review of signs, symptoms and possible causes. J. Appl. Sport Sci. Res. 5:35-50, 1991.

38. TOMEH, J. F., and P. E. CRYER. Biphasic adrenergic modulation of b-adrenergic receptors in man. J. Clin. Invest. 65:836-840, 1980.

39. WALLIN, B. G. Relationship between sympathetic outflow to muscles, heart rate and plasma norepinephrine in man. In: Catecholamines and the Heart, W. Delius, E. Gerlach, H. Grobecker, and W. Kuebler (Eds.). Berlin: Springer, 1981, pp. 11-17.

40. WITTERT, G. A., J. H. LIVESEY, E. A. ESPINER, and R. A. DONALD. Adaptation of the hypothalamopituitary-adrenal axis to chronic exercise stress in humans. Med. Sci. Sports Exerc. 28:1015-1019, 1996.

41. YAMAGUCHI, N., J. DE CHAMPLAIN, and R. NADEAU. Correlation between the response of the heart to sympathetic stimulation and the release of endogenous catecholamines into the coronary sinus of the dog. Circ. Res. 36:662-668, 1975.

 

[MsBeverlyHills]

General feeling of being drained, tired, unable to add weight the next workout, muscle soreness or perception of lasting for more than a week, feelings of exhaustion and unwillingness to workout during succeeding training days, overall feeling of heaviness, short term loss of appetite and sleep, these are just my personal definition of it, and that is what I was refering to.

also known as power cleans.

 

[revexrevex]

Read Discussion section that I highlighted in Bold, it mentions some of the symptoms due to overreaching and overtraining of the nervous system


Title: Autonomic adaptations to intensive and overload training periods: a laboratory study.
Source: Medicine and Science in Sports and Exercise v. 34 no10 (Oct. 2002) p. 1660-6 Journal Code: Med Sci Sports Exercise
Additional Info: United States
Standard No: ISSN: 0195-9131
Details: bibl graph il tab.
Language: English
Review: Peer-reviewed journal


Abstract: Purpose: Looking for practical and reliable markers of fatigue is of particular interest in elite sports. One possible marker might be the autonomic nervous system activity, known to be well affected by physical exercise and that can be easily assessed by heart rate variability. Methods: We designed a laboratory study to follow six sedentary subjects (32.7 (plus or minus) 5.0 yr) going successively through 2 months of intensive physical training and 1 month of overload training on cycloergometer followed by 2 wk of recovery. Maximal power output over 5 min (Plim5'), VO2peak and standard indices of heart rate variability were monitored all along the protocol. Results: During the intensive training period, physical performance increased significantly (VO2peak: +20.2%, P < 0.01; Plim5'; +26.4%, P < 0.0001) as well as most of the indices of heart rate variability (mean RR, Ptot, HF, rMSSD, pNN50, SDNNIDX, SDNN, all P < 0.05) with a significant shift in the autonomic nervous system toward a predominance of its parasympathetic arm (LF/HF, LFnu, HFnu, P < 0.01). During the overload training period, there was a stagnation of the parasympathetic indices associated to a progressive increase in sympathetic activity (LF/HF, P < 0.05). During the week of recovery, there was a sudden significant rebound of the parasympathetic activity (mean RR, HF, pNN50, rMSSD, all P < 0.05). After 7 wk of recovery, all heart rate variability indices tended to return to the prestudy values. Conclusion: Autonomic nervous system status depends on cumulated physical fatigue due to increased training loads. Therefore, heart rate variability analysis appears to be an appropriate tool to monitor the effects of physical training loads on performance and fitness, and could eventually be used to prevent overtraining states. Reprinted by permission of the publisher.
SUBJECT(S)
Descriptor: Fatigue.
Biological markers -- Man.
Autonomic nervous system.
Heart beat.


Autonomic adaptations to intensive and overload training periods: a laboratory study.
Author: Pichot, Vincent.; Busso, Thierry . Roche, Frédéric. Source: Medicine and Science in Sports and Exercise v. 34 no10 (Oct. 2002) p. 1660-6 ISSN: 0195-9131 Number: BGSI02201385 Copyright: The magazine publisher is the copyright holder of this article and it is reproduced with permission. Further reproduction of this article in violation of the copyright is prohibited.


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Key Words: AUTONOMIC NERVOUS SYSTEM, HEART RATE VARIABILITY, FATIGUE, OVER-REACHING.

The analysis of heart rate variability is an efficient tool to evaluate the autonomic nervous activity and its sympathovagal balance (1,24). This tool has gained increasing popularity these last few years in the field of exercise (2,6,8,9,12,15,18,21-23,27,31).

A physical exercise bout determines instantaneous modifications of the autonomic nervous system activity. Heart rate variability progressively decreases all along an incremental exercise bout, leading to a progressive shift of the sympathovagal balance where the sympathetic activity takes over the progressively withdrawing parasympathetic activity (2,31). The recovery of the initial heart rate variability level after an exercise session needs a few minutes up to 24 h, depending on the intensity of the physical exercise (8,9).

Furthermore, regular physical training induces a long-term increase in heart rate variability resulting from changes in the autonomic nervous system basal activity and balance. One of the proposed explanations is a higher parasympathetic tone, which can be evidenced by an increase of the high-frequency peak of heart rate variability (6,12,23). Indeed, endurance athletes have a lower resting heart rate compared with sedentary people (6,23). In addition, a linear relationship between VO2peak and the parasympathetic indices of heart rate variability has been shown (12). Although these transversal studies have demonstrated differences in heart rate variability between athletes and sedentary subjects, longitudinal studies have however hardly shown any significant modification in heart rate variability after a training program despite a significant increase of VO2peak (10,17,18).

Training programs of elite athletes are usually built with the repetition of training cycles composed of high training load periods followed by shorter resting periods (7,29). The training periods induce fatigue states (over-reaching) (4,13) followed by an increase of the physical capacity after the recovery period (supercompensation) (7,21). The lack of an appropriate recovery period and/or the accumulation of too intensive training periods can result in an overtraining syndrome characterized by an advanced fatigue state, which can seriously compromise the competitive season of the athlete (13,14). Overtraining induces a long-lasting imbalance in autonomic nervous system activity (13,15,27), which is probably the excessive form of the previously described adaptation. In overtrained subjects, this imbalance is characterized by a dramatic predominance of the parasympathetic or the sympathetic activity, depending on the type of overtraining (13,15).

Thus, the prevention of overtraining syndrome remains a priority in intensive training in elite athletes (13). Many markers have already been proposed to assess fatigue in athletes (3,14,25,26,30) to avoid the emergence of an overtraining syndrome. The resting heart rate still remains the most used noninvasive index. However, the magnitude of variations of this parameter is tight and quite difficult to appreciate due to multiple interacting factors (14). In a previous study, we described the decrease of heart rate variability associated to physical fatigue during a training cycle of national-level, middle-distance runners (21). This field study led to the idea that heart rate variability indices could be used to monitor training and prevent overtraining states.

The goal of the present study was to assess the potential use of heart rate variability analysis as a biomarker in the control of the impact of successive increasing training loads on fitness and performance. Thus, we designed a laboratory protocol with sedentary subjects who underwent a first period of intensive training immediately followed by an overload training period and, finally, a recovery period. Training loads and physical performances of the subjects were all precisely quantified and correlated to the evolution of the nocturnal heart rate variability all along the intensive training period, the overload training period, and the recovery period.

MATERIAL AND METHODS

SUBJECTS

Six sedentary men were included in the study (age 32.7 (plus or minus) 5.0 yr, weight 83.5 (plus or minus) 12.6 kg, and height 1.82 (plus or minus) 0.08 m). They were free of any known cardiac abnormalities, and none of them were on any cardioactive medications. They were all volunteers and provided written informed consent. The protocol was approved by the local IRB.

EXPERIMENTAL PROTOCOL

A schematic representation of the protocol is presented Figure 1. Further explanation and description of the training protocol can be found in the paper of Busso et al. (4).

The experimental protocol was composed of five successive periods. A reference nonactive period, a height-week intensive training period, a 1-wk recovery transition period, a 4-wk overload training period, and a 2-wk recovery period.

Reference period (W0). Two weeks before starting training, maximal oxygen consumption (VO2peak) was measured in all subjects with a stepwise incremental maximal cycle ergometer test (Monark Model 818, Stockholm, Sweden). After collecting the data in a resting state, the subjects started pedaling at 100 or 150 W for 5 min, depending on their initial estimated level. The power was then incremented every 2 min by 20 or 30 W until they reached exhaustion. Expiratory gases were collected in a polyethylene bag (HP Production, Saint-Etienne, France) during the last 30 s of each 2-min period. The gas composition was measured with a paramagnetic analyzer for O2 (Servomex Series 1440, Crowborough, UK) and an infrared analyzer for CO2 (Datex Normocap, Helsinki, Finland). The VO2peak corresponded to the value measured during the last step just before the subjects reached exhaustion. On another day, the maximal power that the subjects could maintain during 5 min (Plim5') on a cycloergometer (Monark Model 829E) was measured. This test constituted the performance level of the subjects and was reevaluated all along the protocol. Also, on a different day, the heart rate variability indices were calculated using a 24-h Holter recorder to establish the basal autonomic nervous system status.

Intensive training period (W1 to W8). The training period covered 8 successive weeks. The subjects performed three training sessions per week (from Monday to Friday), followed by 2 d of rest (Saturday and Sunday). Each training session included four successive steps: 1) 10-min warm-up, cycling at a low intensity; 2) a maximal effort test, Plim5'; 3) 15-min low-intensity cycling recovery; and 4) four bouts of 5-min cycling at 85% of Plim5', each separated by a 3-min active recovery period, cycling at a low intensity. A Holter recording was performed twice a week, on Thursday night, after a training session, and on Sunday night after the 2 d of rest. We calculated the heart rate variability indices for each recording.

Transition recovery period (W9). During the week of transition, 2 d were dedicated separately to a Plim5' test and a VO2peak test. On another day, a Holter recording was also performed.

Overload training period (W10 to W13). The transition period was followed by a 4-wk overload training period in which the weekly training workload was multiplied by a factor of 5/3 compared with the previous intensive training period. On Monday, Wednesday, and Friday: the same training sessions than during the intensive training period. Tuesday and Thursday: 10 min of low-intensity cycling warm-up, five bouts of 5 min at 85% of Plim5' each separated by 3 min of low-intensity cycling active recovery. Saturday and Sunday: rest. Two Holter recordings were made each week during the 4 wk, one recording beginning on Thursday evening and one beginning on Sunday evening, after the 2 d of rest.

Recovery period (W14, W15). During the 2 wk after the 4 wk of overload, the subjects reduced their physical exercise volume to exercise tests only. During the first week, they performed three Plim5' tests on separated days, and during the second week, they performed two Plim5' tests and a VO2peak test on different days as well. A Holter recording was performed during week 14 (W14) on a different day from the tests, and an additional recording was performed 7 wk later, after the end of the overload period (W21).

HEART RATE VARIABILITY ANALYSIS

The heart rate variability was measured with 24 h Holter monitoring (Stratascan 563, Del Mar, Irvine, CA). Each RR interval was validated before the analysis. Then, we performed the heart rate variability analysis over the night periods to avoid variations originated by daily environmental factors. The mean RR interval, time domain indices and the Fourier transform indices of heart rate variability were standardized as previously described in the literature (24).

These indices of heart rate variability are assumed to represent the autonomic nervous system activity. The particular variables issued from the time domain analysis represent the parasympathetic activity (the percentage of differences between adjacent normal RR intervals more than 50 ms: PNN50, the square root of the mean of the sum of the squared differences between adjacent normal RR intervals: RMSSD) and the sympathetic activity (the standard deviation of all normal RR intervals: SDNN, the standard deviations of the mean of all normal RR intervals for 5-min segments: SDANN, and the mean of the standard deviation of all normal RR intervals for all 5-min segments: SDNNIDX) (24). In the frequency analysis, the total power of the spectrum (Ptot) indicates the global autonomic nervous system status; the VLF is notably an index of the regulation of the renin-angiotensin system, the thermoregulation, and parasympathetic activity; the high frequency of the spectrum expressed in absolute (HF) and in normalized value (HFnu = 100 HF/(Ptot - VLF)) represents the vagal activity; the low frequency expressed in absolute (LF) and in normalized value (LFnu = 100 LF/(Ptot - VLF)) contains both sympathetic and parasympathetic activities; and the LF/HF ratio represents the autonomic nervous system balance (1,24). Nocturnal mean heart rate (HR) was also calculated all along the study.

STATISTICAL ANALYSIS

The data were calculated and analyzed with the software MatLab 5 (Math Work Inc.®), and Staview 4.5 (SAS Institute®), on a Macintosh G3. The variables were compared using repeated ANOVA measures, and, when significant, further analysis was performed using paired t-test. P-value was taken as significant when equal or less than 0.05. This test was chosen to better fit the practical interest of the measure, i.e., significant differences between following weeks.

RESULTS

Intensive training period. The mean value of the VO2peak for the six subjects increased significantly from +20.2% during the 2-month training period (Table 1). Similarly, the Plim5' demonstrated a significant increase of +26.4% (Table 1).

The progressive modifications of the mean RR and of the indices of heart rate variability are illustrated in Figures 2 and 3. The 2-month intensive training period demonstrated an increase in the mean nocturnal RR from 0.92 (plus or minus) 0.13 s to 1.08 (plus or minus) 0.11 s, which represents a decrease in the mean nocturnal heart rate from 66.2 (plus or minus) 8.8 bpm to 56.5 (plus or minus) 5.6 bpm (P < 0.001) (Fig. 4). The time domain analysis of heart rate variability showed a significant increase of the pNN50, rMSSD, and SDNNIDX indices during the training period (from 10.0 (plus or minus) 12.3 to 18.3 (plus or minus) 8.4%, from 40.8 (plus or minus) 26.7 to 68.3 (plus or minus) 18.9 ms, and from 62.7 (plus or minus) 18.8 to 92.7 (plus or minus) 21.1 ms, respectively; all P < 0.001). The Ptot, HF, and HFnu indices of the frequency analysis increased significantly (from 3390 (plus or minus) 1046 to 5115 (plus or minus) 2084 ms2 Hz-1, from 386 (plus or minus) 368 to 747 (plus or minus) 465 ms2 Hz-1, and from 30.8 (plus or minus) 15.6 to 36.7 (plus or minus) 11.%), respectively; all P < 0.05), whereas the LF/HF ratio and LFnu decreased (from 4.0 (plus or minus) 2.1 to 2.4 (plus or minus) 1.1, and from 64.6 (plus or minus) 15.3 to 58.4 (plus or minus) 11.6%, respectively; both P < 0.01). Globally, there was a progressive increase of both the parasympathetic and sympathetic indices with a shift of the autonomic nervous system equilibrium toward a predominance of the parasympathetic arm simultaneously to an increase of the aerobic performance during the 2-month intensive training period.

Overload training period and the after recovery period. The mean nocturnal RR did not show further increase during the overload period (from 1.08 (plus or minus) 0.11 to 1.03 (plus or minus) 0.15 s, NS), and demonstrated a significant further increase during the week of in comparison with W13 (from 1.03 (plus or minus) 0.15 to 1.11 (plus or minus) 0.15 s, P < 0.05), corresponding to a concomitant decrease of -4.1 bpm in heart rate (Figs. 2 and 4).

There was a statistical stagnation with a clear visual tendency to decrease for most of the parasympathetic indices of heart rate variability (pNN50, rMSSD, SDNN, HF; all NS) during the overload period, followed by a significant increase of these indices during the recovery period (from 16.9 (plus or minus) 8.4 to 19.7 (plus or minus) 11.1%, from 60.5 (plus or minus) 24.6 to 76.9 (plus or minus) 40.2 ms, from 111.9 (plus or minus) 29.5 to 125.9 (plus or minus) 36.0 ms, and from 732 (plus or minus) 475 to 798 (plus or minus) 629 ms2 Hz-1), respectively; all P < 0.05) (Figs. 2 and 3). The LF/HF ratio representing the sympathovagal balance significantly increased during the overload period (from 2.4 (plus or minus) 1.4 to 2.7 (plus or minus) 1.4; P < 0.05) and significantly decreased during the week of recovery (from 2.7 (plus or minus) 1.4 to 2.4 (plus or minus) 1.4; P < 0.05) (Figs. 2 and 3). Globally, the autonomic nervous system balance shifted toward a predominance of its sympathetic arm during the overload period and bounced back toward a predominance of its parasympathetic arm during the recovery week.

We can already notice that most indices demonstrated their maximal variation during the third week of overload training. As a matter of fact, the fourth week did not follow exactly the trend of the first 3 wk of overload training, constituting an eventual transitory period.

Measurements 7 wk after the end of the protocol. When measured 7 wk after the end of the protocol, the nocturnal mean RR and heart rate variability were at an intermediate value between the basal and maximal values reached in the previous weeks. They still remained significantly different from the basal values for most of them (HR, RR, pNN50, rMSSD, SDNNIDX, VLF, HF, LFnu, Hfnu, and LF/HF; all P < 0.05) though. Especially, the LF/HF ratio, Lfnu, and HFnu, representative of the sympathovagal balance, were still close to the values obtained during the week of recovery, where the maximal rebound level was reached by the subjects.

Longitudinal relationship between heart rate variability and VO2peak. In addition to previous results, a significant longitudinal linear relationship was found between VO2peak on the one hand and, on the other hand, the mean nocturnal RR as well as the heart rate variability of the six subjects measured before training, after training, and after the recovery following the overload period (r2 = 0.638, P < 0.0001, and r2 = 0.596, P < 0.0002, respectively) (Fig. 5).

DISCUSSION

The changes in nocturnal heart rate variability during the 3 months of the study demonstrate, first, a significant increase of its indices during the 2 months of intensive training and, second, a slight decrease during the following month of overload training for finally rebounding significantly during the recovery period.

The subjects demonstrated a significant progressive increase of heart rate variability and a significant decrease of the mean resting heart rate all along the 2 months of intensive training. These modifications corresponded to a progressive significant increase of the parasympathetic drive of the autonomic nervous system. These results are different from previous studies suggesting that aerobic training does not increase heart rate variability (10,17,18). Only Seals and Chase (22) have found a moderate increase of the standard deviation of heart rate after a training program lasting 30 wk. As the training durations in these studies were similar or longer than ours, the intensity of training, which was higher in our study, appears to be the parameter inducing the modifications in the autonomic regulation. Usually, the training loads used in similar protocols are set between 40 and 80% of VO2peak measured at baseline. In our study, the training load was around 90% of VO2peak, and was repeatedly reevaluated each week to keep up with that intensity level to determine a progressive adapted increase of the training load for each subject. Thus, this longitudinal study confirms the parallel increase of parasympathetic activity and VO2peak that was only suggested by transversal studies (12,18,23). Moreover, it strengthens the importance of the participation of the parasympathetic drive in the bradycardia observed in subjects with high aerobic abilities as well (6,23).

During the overload training, the heart rate variability analysis demonstrated a nonsignificant decrease of the global autonomic nervous system tone with an imbalance toward a predominance of sympathetic activity. This was counterbalanced by a rebound in the parasympathetic activity during the week of recovery. In a recent study concerning elite middle-distance runners, we also evidenced a progressive decrease of the parasympathetic activity during 3 wk of over-reaching, a decrease that was greater than in the present study and that was also followed by a rebound of this parameter during the resting week (21). The more intensive training workload might explain the more pronounced decrease of heart rate variability during the over-reaching period. In the present study, in spite of the high training load, the subjects did not fall into an overtraining state that could impair their physical capacities for many weeks or months. Nevertheless, they presented mild symptoms of nervousness as well as mood state or sleeping disturbances that disappeared in the days after the end of the overload period. These evolutions were followed by a rebound in heart rate variability, reflecting an over-reaching state. This affirmation is reinforced by the fact that the calculated time to recover on the last week of the overload period was only 3.6 d (4). After greater workloads, as in elite athletes, time to recover from an over-reaching period may variate from 8 to 23 d (5,19,20).

The results concerning the fourth week of overload training remain to be discussed because some heart rate variability indices started to be reversed. Several explanations can be proposed. During the fourth week, the first measurement of heart rate variability was made on Friday, after the last overload training session, and the second one was made on Sunday, after 2 d of recovery. We expected to observe a further decrease in heart rate variability. However, the subjects were ending 4 months of a stressful heavy protocol, and we can suppose that they felt a strong relief at that moment, and, consequently, the sleep quality may have been improved as well as the heart rate variability (28). One explanation might therefore be a feeling of premature entrance in recovery. In a previous study (21), the results obtained with the middle-distance runners did not show such an interruption in heart rate variability decrease. The context was different though because these athletes were following an annual training program composed of monthly repeated training cycles.

Seven weeks after the last training session, the heart rate variability indices of the autonomic nervous system tended to return to their basal values while still at an intermediate level. Importantly, the autonomic nervous system balance as assessed by the LF/HF ratio still showed a strong predominance of the parasympathetic drive. In such a population, the effects of training, as measured by autonomic nervous system indices, were still significant 7 wk after the end of the protocol. These results may have potential impact on the short-term effects of training programs.

Interestingly, our protocol confirmed some of the main aspects of aerobic training and generally accepted training principles (15,29), namely supercompensation based on profound transient spontaneously reversible cycles of homeostasis disequilibrium and added quantification. In the first period of intensive training, there was a quick and large increase of heart rate variability and VO2peak. During the second period, the subjects were already pretrained, and the large increase in their training load, assessed to induce a transient decrease in heart rate variability, appears to be the drive for the following supercompensation period. These data, added to the study concerning the elite athletes (21), suggest that the higher the autonomic nervous system activity, the more one will be able to shift the homeostasis regulation and, consequently, induce a secondary rebound in physical performance. Studies on overtraining are difficult to manage as all measurements need to be repeated at least once a week during the athletic season. For that reason, previous studies mainly focused on the description of specific periods before or during overtraining as well as on short longitudinal periods of programmed overtraining (11,14,16,21,27). Heart rate variability analysis overcomes these practical difficulties because they are easy to use, therefore allowing an easy conduction of long-term prospective studies. Indeed, the analysis of the autonomic nervous system activity, which seems to be a crucial parameter in over-reaching and overtraining syndrome (13,15,21,27), could be helpful in finding optimal target values to optimize over-reaching as well as to assess threshold values beyond which there would be a risk of overtraining. Moreover, such an analysis could determine whether the parasympathetic and sympathetic types of overtraining are two different forms of overtraining or are two consecutive stages of overtraining.

In conclusion, this study has clearly demonstrated that a short period of 2 months of intensive training is able to increase both heart rate variability and VO2peak in sedentary subjects. These results underline important modifications of the autonomic nervous system global activity and equilibrium. Also, this study firms up the previous results concerning the interaction between an overload training period and an autonomic nervous system activity rebound. This could be helpful to better understand the physiological basis of overtraining states and, thus, be used for its prevention. Prospective studies have now to be done in top level athletes to determine whether it is possible to find heart rate variability thresholds between normal training fatigue and overtraining fatigue. Such parameters should prove to be efficient tools--noninvasive and easily used in free living situation--to follow up autonomic nervous system activity, and thus physical fitness all along the training periods. Further applications could include the monitoring of physical fatigue at the workplace, the benefits of rehabilitation programs in patients, as well as the effects of leisure activities or physical active lifestyles.

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26. URHAUSEN, A., T. KULLMER, and W. KINDERMANN. A 7-week follow-up study of the behaviour of the testosterone and cortisol during the competition period in rowers. Eur. J. Appl. Physiol. 50:528-533, 1987.

27. UUSITALO, A. L., A. J. UUSITALO, and H. K. RUSKO. Endurance training, overtraining and baroreflex sensitivity in female athletes. Clin. Physiol. 18:510-520, 1998.

28. VAUGHN, B. V., S. R. QUINT, J. A. MESSENHEIMER, and K. R. ROBERTSON. Heart period variability in sleep. Electroencephalogr. Clin. Neurophysiol. 94:155-162, 1995.

29. VIRU, A. The mechanism of training effects: a hypothesis. Int. J. Sports Med. 5:219-227, 1984.

30. WILSON, W. M., and R. J. MAUGHAN. Evidence for a possible role of 5-hydroxytryptamine in the genesis of fatigue in man: administration of paroxetine, a 5-HT re-uptake inhibitor, reduces the capacity to perform prolonged exercise. Exp. Physiol. 77:921-924, 1992.

31. YAMAMOTO, Y., R. L. HUGHSON, and J. C. PETERSON. Autonomic control of heart rate during exercise studied by heart rate variability spectral analysis. J. Appl. Physiol. 71:1136-1142, 1991.

 

[pwr_machine]

Ok, that works for endurance athletes but we're talking resistance exercise here.

 

[revexrevex]

Long term

 

[spatts]

I'm not sure these studies answer pwr_machine's question.

Revex, was the thread originally about the short term or long term effects?

 

[pwr_machine]

I'm not sure these studies answer pwr_machine's question.

Revex, was the thread originally about the short term or long term effects?

That's my point. Again, a set to failure or a max attempt does compare to the effects of long distance running.

 

[louden_swain]

Well I am not a physiologist or a doctor (I am a geoscientist), but what does it mean when you can no longer feel pain when you train to failure?

 

[pwr_machine]

I need science!

 

[spatts]

Perhaps I have missed the point entirely then...I agree with what you're saying from a scientific perspective, and I guess I'm just not sure what revex is getting at.

 

[spatts]

I need science!

 

[revexrevex]

Ok, it started out as a casual thread for people to communicate their experiences. I didn't go into scientific details and didn't try to specifically define what I meant by nervous system overtraining.

What I specifically meant was, "What exercise can add up to a point where overtraining could be experienced." I did not mean that a single set of 20 reps will cause overtraining, instead I meant what exercise is likely to cause overtraning if performed on consistent bases without sufficient recovery. As I mentioned before, based on personal experience, and experience of others, if I perform 1 rep Maxes of deadlift consistently every week, I experience overtraning by not progressing in weight and lacking the desire to even go to the gym on consistent bases.

 

[sinjinsmythe33]

way over my head...

getting back to the original topic, deadlifts from the floor are very taxing. my progress stalls when i do them too often, possibly because the load is realtively heavy. my best deadlift of 465 came after 25 days of no deads. i did two power clean workouts a week, 8 or 10 sets of two reps with a moderate weight, 135 to 185. never maxed, but when i went back to deads they were up forty pounds. during that 25 days i was also working squats with 185 to 275, working only the bottom portion, no lockouts. maybe its the ballistic nature of the clean? im no where near as knowlegeable as you guys, thats why im here listening intently!

 

[revexrevex]

Re: way over my head...

getting back to the original topic, deadlifts from the floor are very taxing. my progress stalls when i do them too often, possibly because the load is realtively heavy. my best deadlift of 465 came after 25 days of no deads. i did two power clean workouts a week, 8 or 10 sets of two reps with a moderate weight, 135 to 185. never maxed, but when i went back to deads they were up forty pounds. during that 25 days i was also working squats with 185 to 275, working only the bottom portion, no lockouts. maybe its the ballistic nature of the clean? im no where near as knowlegeable as you guys, thats why im here listening intently!

Same here. Deadlift is a unique lift, you can progress on it faster by taking longer rest periods then if you deadlift consistenly I think.

 

[pwr_machine]

There is first time for everything. Now you heard of it.

Be prepared to provide evidence for the theories you present. I think we're all looking for the best methods to train and how to recover from training. However, I'm not looking for hearsay; I want scientific evidence.

 

[spatts]

I only deadlift in competition, and never in the gym. It goes up about 20-40 pounds everytime I test it. I went from 365 to 405 to 430, each lift being 12 weeks apart. I do a lot of speed training (ballistic/explosive) movements too.

 

[revexrevex]

I showed you references of how exercise without sufficient recovery can cause NERVOUS SYSTEM overtraning. Are you saying that nervous system never gets overtrained? The references says otherwise

 

[spatts]

based on personal experience, and experience of others, if I perform 1 rep Maxes of deadlift consistently every week, I experience overtraning by not progressing in weight and lacking the desire to even go to the gym on consistent bases.

lol...spoken like Lou Simmons, himself.

 

[spatts]

Be prepared to provide evidence for the theories you present. I think we're all looking for the best methods to train and how to recover from training. However, I'm not looking for hearsay; I want scientific evidence.

What exactly is it you haven't heard of? You didn't know the CNS needs to recover?

 

[sinjinsmythe33]

spatts should break the womens record in a few years..

in the deadlift, think it was rebecca swanson, 630 maybe? must be the box squats and the sled? have to get me one of them boxes!!

 

[pwr_machine]

What exactly is it you haven't heard of? You didn't know the CNS needs to recover?

In theory, I can see how the CNS would need to recover. However, I don't think any of us are training that intensely. I think there are enough other feedback mechanisms that inhibit excessive CNS fatigue. I can see that with long distance running because you're pounding your body for a very, very long time. I don't see this with resistance exercise because we can't perform exercise that long. I'm not provoking an argument, I'm just looking for answers.

 

[spatts]

Re: spatts should break the womens record in a few years..

I'm working on it...believe me.



pwr_machine, the neural fatigue is from adaptation. It sound like you're looking for a study that compares neural fatigue for extended bouts vs short bouts. I will try to find something for you. Personally, it seems crazy to me that a distance runner would be experiencing more neural adaptation than me when I am in a circa max phase of speed squats. What if I'm new to it, and the distance runnner isn't? Will I require more adaptation, and therefore, more recovery time, irrespective of the type of exercise?

 

[pwr_machine]

I showed you references of how exercise without sufficient recovery can cause NERVOUS SYSTEM overtraning. Are you saying that nervous system never gets overtrained? The references says otherwise

You showed me references of how ENDURANCE exercise can cause overtraining. Are we cyclists? Are we runners? Do we have repeated days of the same exercises as a runner would (i.e. running)?

 

[pwr_machine]

pwr_machine, the neural fatigue is from adaptation. It sound like you're looking for a study that compares neural fatigue for extended bouts vs short bouts. I will try to find something for you.

That would be great!

My CNS is overtraining. I can't think much more.

 

[revexrevex]

The database I am using has very limited information on strength training specifically. However I saw many studies done in 1970's on olympic lifters that characterize overtraining. I am sure someone with more access than me can dig up the full studies.

 

[slobberknocker]

I only deadlift in competition, and never in the gym. It goes up about 20-40 pounds everytime I test it. I went from 365 to 405 to 430, each lift being 12 weeks apart.

Wait, spatts, you don't deadlift in the gym? At all?

 

[spatts]

Not a full ROM 1 rep max, no. In fact, the only full rom thing I do is speed deads, and I don't even really do those that often. Maybe every two weeks or so.

 

[slobberknocker]

Hmm. I guess squats really is the superior exercise then. Interesting.

 

[coolcolj]

Be prepared to provide evidence for the theories you present. I think we're all looking for the best methods to train and how to recover from training. However, I'm not looking for hearsay; I want scientific evidence.

Ok try this experiemnt yourself

get at weight around 85% of yoru 1RM - say squat or bench
do a single rest 1min and repeat up to 15 singles.

next workout add 5% to the bar if you make 15 singles,
and try and get 15 singles. If so add 5% as per before

By the 4th or 5th workout you should start to feel weaker, depending on your recovery levels. Things will start to feel heavy and you will go backwards.
Obviously your msucles are recovered, by each workout, the protein turnover is pretty small, so how do you epxlain feeling so trashed up?
I've trained like this before and it really kills your CNS!
The mental stress is immense. Every minute you gotta get under that bar and bang out another rep.


These are the kind of things studies should be doing, but they aren't!

 

[casualbb]

From the post, "Training theory by AnimalMass et al:"

***Begin***
ATP/Pc factors: Intramuscular levels of ATP fall rapidly during exercise...this is thought to be one of the major factors in fatigue...

Creatine Phosphate levels fall rapidly at the onset of exercise, after a period of roughly 30 secs levels may be as low as 5% of the prexercise concentration. Consequenlty there wont be optimal levels of CP to replenish ATP stores.
Creatine Phosphate fuels the ADP/ ATP conversion, as levels of CP decline levels of ATP get depleted.
The ATP/PC system fuels the first few seconds of exercise...after which anaerobic glycolysis takes place... a buy product of glycolysis is Lactic acid, which casues a build-up in the muscle cells of Hydrogen ions (H+) raising the p.H.... Which affects the process that exposes actin cross-bridging sites (troponin) and permit muscle contraction. ATP formation is also affected.
calcium ions (Ca++) are released from the sarcoplasmic reticulum by the T tubules during muscle contraction and returned by the Ca-Pump.

Reduced sarcoplasmic Ca++ concentrations has been linked to fatigue. Declines in force that can be produced have been linked to declined levels of CA++ (Calcium ions). This is because decreased Ca++ released reduces the number of actin/myosin cross-bridges that can be formed. This is most likely to be due to impairement of the T-tubule. While exercising potassium ions (K+)build up in the T-tubules, this is due to the inability of the Na+K+ ATPase (breaks down ATP) Pump (sodium, potassium atpase pump) to maintain the proper Na+/K+ balance at the T-tubules. This affects the conduction of the action potential (these cause movement to occur...like an electrical impulse) to the sarcoplasmic reticulum, consequently Ca++ release is inhibited affecting one's capacity to contract a muscle. lactic acid again builds yup here and once again intracellular H+ concentrations increase, this then slows the uptake of Ca++ by the sarcoplasmic reticulum, because the H+ affects the pump. Therefore there is a marked reduction in levels of Ca++

As should be obviuos ATP is broken and provides the energy for contraction (into ADP and Pi)this inorganic phosphate (Pi) builds up. Increased Pi levels are thought to inhibit further cross-bridges being formed between the filaments. As ATP is used to fuel the muscle contraction, Pi is released from the myosin head. Increased concentrations of Pi affects this from happening.
Intensity and Failure

That being said I can now continue...HIT popularized by Mike mentzer (hope this doesnt open up the proverbial can of worms!)is based on the premise that If you don't take your sets to failure, then you are not presenting your body with the stimulus to adapt because you can perform the appropriate amount of reps. Therefore as you take your reps to failure, you are presenting the stimulus by forcing your body to cope with something that it cannot do (remeber the original post!). Consequently you adapt because you have forced yourself to do something that it simply cannot do...seems logical and simple right! But you have to ask yourself, why are so many powerlifters muscular if they dont train to failure? as with olympic lifters!

...I take you back to the theory of rate coding..essentially you fail in an exercise because there are not sufficiently rested muscle fibres to perform the task...at the end of the set the only fibres that arent fatigued are the low threshold high endurance motor units..which dont have the neccessary force producing capabilities to perform the work.

I take you back now to the theory of supercompensation and the subesequent breakdown and buildup theory that dictates that muscle damage (catabolism) has to occur for the increase in proetin synthesis to occur!...

...Research has shown that the most muscle damage occurs during the negative paotion of the exercise (sarcomere popping!)...this is because less muscle fibres are recruited to perform the eccentric movemnt resulting in a greater stress on those fibres...consequently by increasing the time that the muscle fibres are under tension (most tension is generated during -ve portion) there in theory is a better stimulus for muscle growth! ... from this it seems that more tension can be generated by taking a set to failure than stopping short because it would take longer to perform! keep this in mind!

...Back to rate coding (seems pretty important doesnt it?) as the moment of failure draws closer the CNS will innervate all the motor units it can to perform the reps and fire them as often as it can...however as fatigue sets in there is a reduction in firing frequency (up to around 70-80% I think!), consequently the rate of twitching is not high enough to continue the exercise...thus failure occurs.

...back to neural factors...as a nueron fires it has to release the neurotransmitter Acetyl Choline so that the message can be carried...as mentioned previoulsy the electrical current is passed down the axon due to the na+ and K+ (when people refer to electrolites in sports drinks like gatorad, lucozade, these is what they are refering to), and the K+ Na+ atp ase pump... as failure approaches (lack of firing) the electrolites become taxed...as failure occurs these are virtually depleted...it is speculated that another of the major factors in fatigue is the inability of the motor neurons to create and release acetylcholine (ACh) fast enough so that transmission of the action potential can be maintained from the neron to the muscle...

It can be said that ability to produce force is dependant on power speed and frequency of the 'electrical impulse elicited by the CNS to contract a muscle...as fatigue develops there is a mared decrease in the speed of these signals, as this occurs inhibitory mechanisms (mentioned previuos) stop further contrcations occuring....

...However due to emotional factors lke psyching oneself up it is possible to extend the time until these inhibitory mechanisms take effect(fight or flight syndrome)...there is a ditinct relationship between this and catecholamine levels...

...Therfore I hope that you can see that failure may not occur due to the peripheral (muscle) factors but the Central ones...failure may not be due to muscular fatigue but neural inhibition...the CNS does this for one simple reason: SO THAT IT CAN REST AND RECOVER!
***end***

I forget where he got this info. I think the book was titled "physiology."

 

[pwr_machine]

Ok try this experiemnt yourself

get at weight around 85% of yoru 1RM - say squat or bench
do a single rest 1min and repeat up to 15 singles.

next workout add 5% to the bar if you make 15 singles,
and try and get 15 singles. If so add 5% as per before

By the 4th or 5th workout you should start to feel weaker, depending on your recovery levels. Things will start to feel heavy and you will go backwards.

Yeah, I'll run out and try that now! NOT! No one trains that way! It's not realistic! I just don't believe our workouts cause that much of a problem for our CNS.

 

[pwr_machine]

...Back to rate coding (seems pretty important doesnt it?) as the moment of failure draws closer the CNS will innervate all the motor units it can to perform the reps and fire them as often as it can...however as fatigue sets in there is a reduction in firing frequency (up to around 70-80% I think!), consequently the rate of twitching is not high enough to continue the exercise...thus failure occurs.

...back to neural factors...as a nueron fires it has to release the neurotransmitter Acetyl Choline so that the message can be carried...as mentioned previoulsy the electrical current is passed down the axon due to the na+ and K+ (when people refer to electrolites in sports drinks like gatorad, lucozade, these is what they are refering to), and the K+ Na+ atp ase pump... as failure approaches (lack of firing) the electrolites become taxed...as failure occurs these are virtually depleted...it is speculated that another of the major factors in fatigue is the inability of the motor neurons to create and release acetylcholine (ACh) fast enough so that transmission of the action potential can be maintained from the neron to the muscle...

It can be said that ability to produce force is dependant on power speed and frequency of the 'electrical impulse elicited by the CNS to contract a muscle...as fatigue develops there is a mared decrease in the speed of these signals, as this occurs inhibitory mechanisms (mentioned previuos) stop further contrcations occuring....

...However due to emotional factors lke psyching oneself up it is possible to extend the time until these inhibitory mechanisms take effect(fight or flight syndrome)...there is a ditinct relationship between this and catecholamine levels...

...Therfore I hope that you can see that failure may not occur due to the peripheral (muscle) factors but the Central ones...failure may not be due to muscular fatigue but neural inhibition...the CNS does this for one simple reason: SO THAT IT CAN REST AND RECOVER!
***end***

Cl- ions have more negative potential than the resting neuronal membrane. When the Cl- channels open, allowing the ions to move inside, that will make the membrane potential more negative than normal. Opening the K+ channels will allow those ions to pass to the outside which will also make the membrane potential more negative than usual. The degree of intracellular negativity increases and is called hyperpolarization. This inhibits the neuron because the membrane potential in now further away than ever from the threshold for excitation. It is not because "the electrolites become taxed...as failure occurs these are virtually depleted." That's not possible! I don't want quotes from friends and relatives, I want real scientific data. I could spend a weekend making up theories too, but I don't!

 

[coolcolj]

Yeah, I'll run out and try that now! NOT! No one trains that way! It's not realistic! I just don't believe our workouts cause that much of a problem for our CNS.

I do

Well maybe not you, but my workouts sure kick my ass sometimes! Especially the oly lifts, high levels of CNS arousal required.

 

[pwr_machine]

I do

Well maybe not you, but my workouts sure kick my ass sometimes!

DON'T MAKE THIS PERSONAL!

Especially the oly lifts, high levels of CNS arousal required.

If you really train so much that it taxes your CNS, then you're negating everything that was said above. Why train like this if you can't recover?

 

[SAGAT]

Re: Re: way over my head...

Same here. Deadlift is a unique lift, you can progress on it faster by taking longer rest periods then if you deadlift consistenly I think.

agreed. to get back on topic, the exercise that taxes my body the most (i think this is what the thread was originally about, not too sure anymore though) is definitely the squat. although the fact that i have no squat rack and have to get the weight on my back by myself might have something to do with that.

 

[teen1216]

If you really train so much that it taxes your CNS, then you're negating everything that was said above. Why train like this if you can't recover?

Yes, it taxes his CNS so he must allow ample time for that to recover as well as his muscles. You can recover from it obvously.

 

[casualbb]

pwr: I'd be interested in the answer to your question as well. Do you have any texts that might address it?

 

[pwr_machine]

pwr: I'd be interested in the answer to your question as well. Do you have any texts that might address it?

Which question was that?

I have a Guyton & Hall's Texbook of Medical Phsyiology. I'll dig it out and read more about everything when I find the time.

 

[casualbb]

I mean what is the physiological mechanism for motor unit fatigue

 

[pwr_machine]

I mean what is the physiological mechanism for motor unit fatigue

Oh, I'll try to get back to you on that one later this afternoon.

 

[argent]

I thought the neuromuscular fatigue you were talking about could only occur with extensive and exhaustive levels of muscle activity. It's not just a set of squats or even a max attempt.

No but if you are training balls to the wall every workout, multiple times a week, your CNS will be overtaxed. That is one reason why periodization works. Thats why a lot of guys come back and feel stronger after taking a short lay-off (7 days).

 

[coolcolj]

DON'T MAKE THIS PERSONAL!

If you really train so much that it taxes your CNS, then you're negating everything that was said above. Why train like this if you can't recover?

There is a time and place for everything

There are periods of loading and unloading.
I treat a whole week like some people treat a single workout. ie I don't fully recover from workout to workout.
Most performance and sports training is setup like this.
Only BB'ers and Powerlifters don't train like this.

 

[pwr_machine]

No but if you are training balls to the wall every workout, multiple times a week, your CNS will be overtaxed. That is one reason why periodization works. Thats why a lot of guys come back and feel stronger after taking a short lay-off (7 days).

It seems to me that recognizable symptoms of overtraining would occur prior to reaching CNS overtaxation.

 

[pwr_machine]

Guyton and Hall state that under normal functioning conditions fatigue in the neuromuscular junction occurs rarely and even then only at the most exhausting levels of muscle activity.

 

[pwr_machine]

I mean what is the physiological mechanism for motor unit fatigue

When excitatory synapses are repetitively stimulated at a rapid rate, the number of discharges by the postsynaptic neuron is at first very great, but it becomes progressively less in succeeding milliseconds or seconds. This is called fatigue of synaptic transmission.

The motor unit is a motor neuron and all the muscle fibers it innervates. If the action potential doesn't reach a specific mV threshold, then it doesn't innervate the muscle fiber. I don't think that's due to fatigue, but due to other mechanisms such as the actions of the Cl- and K+ channels that I mentioned earlier that keep it from happening.

 

[revexrevex]

When excitatory synapses are repetitively stimulated at a rapid rate, the number of discharges by the postsynaptic neuron is at first very great, but it becomes progressively less in succeeding milliseconds or seconds. This is called fatigue of synaptic transmission.

The motor unit is a motor neuron and all the muscle fibers it innervates. If the action potential doesn't reach a specific mV threshold, then it doesn't innervate the muscle fiber. I don't think that's due to fatigue, but due to other mechanisms such as the actions of the Cl- and K+ channels that I mentioned earlier that keep it from happening.

Is this in reference to one workout, or the accumulation of fatigue over a specific time period (lets say few weeks)?

 

[pwr_machine]

Is this in reference to one workout, or the accumulation of fatigue over a specific time period (lets say few weeks)?

This can happen in a matter of seconds.

 

[JollyRogers]

I always overtrain doing 1 rm deads, I need to get used to them more..lol

 

[casualbb]

but due to other mechanisms such as the actions of the Cl- and K+ channels that I mentioned earlier that keep it from happening.

From somewhere (don't remember), I was under the impression that basically the motor unit is unable to recharge, that the action potential may exist but it can't keep up with ion transport, or something to that effect. Is that correct?

 

[IronLion]

ok then.....another geek thread

 

[casualbb]

hey, this stuff is important!

 

[crew9]

Just when you think you've finally escaped college Anatomy and Physiology you read a thread like this.

 

[IronLion]

i'm just mad cause i can't read all the big words

 

[Naeem]

High volume deadlifts and squats there murder

 

[pwr_machine]

From somewhere (don't remember), I was under the impression that basically the motor unit is unable to recharge, that the action potential may exist but it can't keep up with ion transport, or something to that effect. Is that correct?

I gather that, yes, the action potential exists. But, when it reaches the terminus it is inhibited by the Cl- and K+ actions and cannot continue beyond the synaptic cleft.

 

[pwr_machine]

ok then.....another geek thread

Brains and muscle. You know, I think that's how I landed a beautiful wife!

 

[casualbb]

I think the important thing to take away from this is that nothing about failure training is related to growth.

 

[slobberknocker]

ok then.....another geek thread

 

[Mike_Rojas]

Revenge of the Nerds

 

[slobberknocker]

Revenge of the Nerds

hahahaha