Impact of severe deconditioning on muscle biology

Although I've put a link up to this information elsewhere, I reckon that it's important to put this info in full view.

Taken from: WAGENMAKERSC, ANTON J. M. (1999), 'Chronic fatigue syndrome: the physiology of people on the low end of the spectrum of physical activity?' Clinical Science 97, (pp.611–613) (link)

Severe deconditioning affects the blood flow to the muscles:

"...deconditioning plays an important, and so far under-appreciated, role in the abnormal physiology that is seen in CFS patients. Saltin et al. [9] have shown that 20 days of bed rest by healthy subjects reduced cardiac output and oxygen delivery to working muscles by 15–20%. Muscle blood flow during and following exercise is also reduced in elderly subjects [10]. This has, in part, been explained by a reduced vasodilatory capacity and in part by the decreased capillarization, which again is a consequence of the reduction in physical activity and deconditioning that are seen during ageing [10]. The development of abnormal autonomic or peripheral control of muscle blood flow is not limited to CFS patients [7,11] but also occurs in healthy subjects in the adaptation period to acute and long-term deconditioning."

Severe deconditioning adversely affects the biology of muscle and its ability to metabolise exertion:

".... some, but not all, patients with CFS show a severe loss of mitochondria. Six of the patients with the lowest mitochondrial activities performed a graded incremental exercise test on a cycle ergometer and had a dramatically reduced exercise capacity (maximal work rate 60–120 W; 20–50% of the normal controls). They nevertheless achieved heart rates and blood lactate concentrations normally found with maximal exercise [12,13]. These data indicate that these patients showed a metabolic adaptation to severe deconditioning, and that the adaptation to deconditioning may be as large as, but the reverse of that reported in trained subjects [14,15]. This implies that these patients experience the stress of maximal exercise during normal daily activities (20–80 W) and this again provides a reason to avoid exercise, so that they spiral down in a vicious circle of inactivity and exercise intolerance [12].

"One of the consequences of low mitochondrial density is a reduced oxidative capacity. This again leads to a reduced rate of resynthesis of creatine phosphate following high-intensity exercise [16]."

So, reduced blood flow to muscles, loss of mitochondira and the reduction in resynthesis of creatine phosphate (which is probably a consequence of the first 2 factors) all serve to cause deconditioned muscle to be fast fatiguing (i.e. significantly reduced endurance capacity) and slow recovering (i.e. requiring significantly longer to refuel and repair).

For further contextual information about creatine phosphate and its role in the biology of muscle fuelling and refuelling see: Link