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What changes when we get "fitter"?

lister

Thinker
lister
Joined
Aug 27, 2005
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217
If I jogged 5 miles every day from now on, in a few months time I would be able to jog the distance in a much faster time, and my heart rate and breathing would return to normal faster after I finish.

I would become "fitter".

But can someone tell me exactly what physiological changes happen in my body to make this happen?

I can understand that the muscles in my legs would hypertrophy and so be able to propel me faster, but why am I able to recover more quickly?

And also, am I still using the same amount of energy to jog those 5 miles (presuming my weight stays the same, and presuming I deliberately paced myself to take the same time as when I first started?)
 
I cannot answer that question scientifically, but can most certainly assure you that a fitness routine will mean that your fitness level when you reach your 70s will be much higher than many of your contemporaries!
 
In essence (among many other changes), you develop better cardiac performance by "strengthening" of the cardiac muscles, which results in a much more efficient pumping of the heart. Also, your muscles respond by producing more myoglobin which responds by releasing more oxygen when put under anaerobic stress. Likewise, you lose fat mass which further reduces diversion of cardiac output to adipose tissue.

These are the main things that change and allow you to recover more quickly. There are also other cellular mechanisms that change (e.g., upregulation of glucose receptors, increase in efficiency of fat-burning mitochondria, etc.) that help with this.

All-in-all, exercise changes your physiology. And, that's a good thing.

-Dr. Imago
 
There is no system that remains unchanged. Muscular, skeletal, respiratory, digestive, etc. Even brain functions improve.
 
Dr. Imago said:
In essence (among many other changes), you develop better cardiac performance by "strengthening" of the cardiac muscles, which results in a much more efficient pumping of the heart. Also, your muscles respond by producing more myoglobin which responds by releasing more oxygen when put under anaerobic stress. Likewise, you lose fat mass which further reduces diversion of cardiac output to adipose tissue.

These are the main things that change and allow you to recover more quickly. There are also other cellular mechanisms that change (e.g., upregulation of glucose receptors, increase in efficiency of fat-burning mitochondria, etc.) that help with this.
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Thanks for the info. Much appreciated.

Can you tell me why such changes then change back again if I stop exercising? (ie I become unfit again).
I think I understand that the increased muscle mass in my legs and heart etc will require more calories to maintain, so if they're not used my body doesn't bother maintaining them.
Is it the same with the other things you mention (like glucose receptors etc)
 
Your muscles also produce more mitochondria as their usage goes up.
 
What you ask is essentially the subject of three (if not more) sciences: Exercise Physiology, Exercise Endocrinology and Exercise Biochemistry. This is a huge subject. I don't know how can one answer this in a general way on the molecular level. For example here's an excerpt from a review study on the plasticity of the skeletal muscle:

It has been shown that systematic endurance exercise training increases the steady-state level of a number of mRNAs encoding mitochondrial proteins in proportion to the increase in mitochondrial volume density (Puntschart et al. 1995a). Moreover, acute bouts of endurance exercise cause a significant rapid (0-4 h after exercise) transient increase in the mRNA level of several proteins involved in regulating mitochondrial functions (Pilegaard et al. 2000). Additionally, exercise seems to rapidly affect cellular trafficking, i.e. glut-4 and possibly small G proteins (Kraniou et al. 2000) (reviewed in Booth and Baldwin 1995). Endurance exercise training further causes a fine-tuning of the mRNA level of MCAD involved in beta oxidation of medium chain fatty acids (Vogt et al. 2001). This observation is compatible with the functional observation that endurance exercise shifts the functional capacity of mitochondria towards an increased use of lipids as a substrate (Holloszy and Booth 1976; Holloszy and Coyle 1984). Bicycling exercise also affects expression of genes involved in the modulation of muscle substrate supply, i.e. to an induction of key components of fatty acid transport (FAT/CD36, FABPpm, LPL) and -oxidation (CPTI) in human m. vastus lateralis during the recovery phase (Pilegaard et al. 2000; Tunstall et al. 2002b). Data from animal experiments support that LPL expression is at least in part controlled by local contractile activity (Hamilton et al. 1998). Activation of gene expression therefore appears to be the main mechanism for the accumulation of post-transcriptional micro-adaptations responsible for the subsequent structural and biochemical adaptations of the mitochondrial compartment in exercised skeletal muscle.
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