First, numerous studies have shown that despite a lack of sarcolemma depolarisation or crossbridge cycling, a stretched muscle cell can not be considered metabolically dormant. In 1932, Feng (1932) showed that a passively stretched in vitro muscle was metabolically active. He found that passively stretched muscles exhibited increased heat production and oxygen consumption. Later research corroborated these findings; Clinch (1968) reported increased heat production, while Whalen and colleagues (1962) and Barnes (1987) added reports of increased oxygen consumption. In other related studies, passive stretch increased carbon dioxide production

( Eddy and Downs, 1921), increased glycogen breakdown RAD001 ( Barnes and Worrell, 1985), increased lactic acid production ( Barnes, 1987), and decreased phosphocreatine concentrations ( Barnes, 1987). Since increased metabolic activity is related to increased activation of the adenosine monophosphate kinase (AMPK) facilitated glucose transporter (GLUT 4) activation pathway ( Dohm, 2002), it is possible that the increased metabolic activity accompanying passive muscle stretching could have activated the incorporation of GLUT 4 into the stretched muscles. Other research also points to the possibility

of stretching increasing GLUT4 incorporation. For instance, protein kinase B activity Proteasome inhibitor partially controls GLUT 4 incorporation and activation, and Sakamoto and colleagues (2003) found that protein kinase B was stimulated by passively stretching isolated muscles for ten minutes. Second, mitogenactivated protein kinase activity stimulates muscle cell glucose uptake (Ho et al 2004), and the activity of mitogenactivated protein kinases directly reflects the magnitude of the mechanical stress (ie, actively or passively generated

Isotretinoin tension) applied to the muscle (Martineau and Gardiner, 2001). Third, exercise-induced increases in nitric oxide result in increased glucose transport (Roberts et al 1997), and nitric oxide released from excised soleus muscles can be increased 20% by a single two-minute passive stretch (Tidball et al 1998). Finally, ischaemia can increase GLUT 4 translocation to the sarcolemma as well as increasing glucose uptake (Sun et al 1994, Young et al 1997), and passive stretching has the potential to cause ischaemia (Poole et al 1997, Wines and Kirkebo 1976). Wisnes and Kirkebo (1976) found an increased resistance to blood flow during passive stretching. In addition, Poole and colleagues (1997) reported that muscle stretching reduces bulk blood delivery, alters capillary flow dynamics, and impairs blood tissue oxygen exchange. Regardless of the responsible mechanisms, it is clear that passive static stretching had a significant positive effect on blood glucose levels.