Saturday, February 14, 2009

Performance Research for February: Central Fatigue Round 2

I must be going crazy as now you have 2 blog posts in one day. I needed a break. Yes, I read studies to relax. I even take vacations to go to conferences on exercise physiology. Next up on that one is ACSM this May.

So my parents came by today to help clean my townhouse. Very much appreciated, but nothing like having your mom (love ya mom) run around asking "How did this get so dirty?" My answer is that I am a grad student, Teaching Assistant for Exercise Physiology and Human Physiology, run a separate training/nutrition business, work 24 hours a week for a medical device company (on call full time there too), and try to see Jodie on occasion too. Coffee is my best friend on most days and sleeping more than 7 hours is heaven!

So we move on and here are a few more studies on Round 2 of Central Fatigue.

Inflammatory and oxidative and nitrosative stress pathways underpinning chronic fatigue, somatization and psychosomatic symptoms.

Maes M. Clinical Research Centre of Mental Health (CRC-MH), Antwerp, Belgium.

PURPOSE OF REVIEW: The aim of this paper is to review recent findings on inflammatory and oxidative and nitrosative stress (IO&NS) pathways in chronic fatigue and somatization disorder. RECENT FINDINGS: Activation of IO&NS pathways is the key phenomenon underpinning chronic fatigue syndrome (CFS): intracellular inflammation, with an increased production of nuclear factor kappa beta (NFkappabeta), cyclo-oxygenase-2 (COX-2) and inducible NO synthase (iNOS); and damage caused by O&NS to membrane fatty acids and functional proteins.

These IO&NS pathways are induced by a number of trigger factors, for example psychological stress, strenuous exercise, viral infections and an increased translocation of LPS from gram-bacteria (leaky gut). The 'psychosomatic' symptoms experienced by CFS patients are caused by intracellular inflammation (aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection); damage caused by O&NS (aches and pain, muscular tension and fatigue); and gut-derived inflammation (complaints of irritable bowel). Inflammatory pathways (monocytic activation) are also detected in somatizing disorder.

CONCLUSION: 'Functional' symptoms, as occurring in CFS and somatization, have a genuine organic cause, that is activation of peripheral and central IO&NS pathways and gut-derived inflammation. The development of new drugs, aimed at treating those disorders, should target these IO&NS pathways.

My notes: Holy crap, what did they say? The big take away here is the body is ALL connected! See my post below about my theory of the body as a black box

The Body as a Black Box

Resistance exercise training enhances sympathetic nerve activity during fatigue-inducing isometric handgrip trials.

Saito M, Iwase S, Hachiya T. Applied Physiology Laboratory, Toyota Technological Institute, 2-12 Hisakata Tmpaku-ku, Nagoya 468-8511, Japan.

Just a note that the full study is up and finalized. I covered this one already below

Performance Research October: Sticking Needles in Nerves and Jumping Out of Planes

Last one for today below.

High-intensity running in English FA Premier League soccer matches.

Bradley PS, Sheldon W, Wooster B, Olsen P, Boanas P, Krustrup P. Department of Sport and Exercise Sciences, University of Sunderland, Sunderland, UK.

The aims of this study were to (1) determine the activity profiles of a large sample of English FA Premier League soccer players and (2) examine high-intensity running during elite-standard soccer matches for players in various playing positions. Twenty-eight English FA Premier League games were analysed during the 2005-2006 competitive season (n = 370), using a multi-camera computerised tracking system. During a typical match, wide midfielders (3138 m, s = 565) covered a greater distance in high-intensity running than central midfielders (2825 m, s = 473, P = 0.04), full-backs (2605 m, s = 387, P < 0.01), attackers (2341 m, s = 575, P < 0.01), and central defenders (1834 m, s = 256, P < 0.01). In the last 15 min of a game, high-intensity running distance was approximately 20% less than in the first 15-min period for wide midfielders (467 m, s = 104 vs. 589 m, s = 134, P < 0.01), central midfielders (429 m, s = 106 vs. 534 m, s = 99, P < 0.01), full-backs (389 m, s = 95 vs. 481 m, s = 114, P < 0.01), attackers (348 m, s = 105 vs. 438 m, s = 129, P < 0.01), and central defenders (276 m, s = 93 vs. 344 m, s = 80, P < 0.01).

There was a similar distance deficit for high-intensity running with (148 m, s = 78 vs. 193 m, s = 96, P < 0.01) and without ball possession (229 m, s = 85 vs. 278 m, s = 97, P < 0.01) between the last 15-min and first 15-min period of the game. Mean recovery time between very high-intensity running bouts was 72 s (s = 28), with a 28% longer recovery time during the last 15 min than the first 15 min of the game (83 s, s = 26 vs. 65 s, s = 20, P < 0.01). The decline in high-intensity running immediately after the most intense 5-min period was more evident in attackers (216 m, s = 50 vs. 113 m, s = 47, P < 0.01) and central defenders (182 m, s = 26 vs. 96 m, s = 39, P < 0.01).

CONCLUSION: The results suggest that high-intensity running with and without ball possession is reduced during various phases of elite-standard soccer matches and the activity profiles and fatigue patterns vary among playing positions. The current findings provide valuable information about the high-intensity running patterns of a large sample of elite-standard soccer players, which could be useful in the development and prescription of specific training regimes.

My notes: SAID principle 101---the coach needs to understand the needs/demands of his/her player's sport in order to optimal train them for it.